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Conferences and Medical Updates

Steinberg and one line board curiosities

One line questions – curiosities
Sunday, September 9, 2018

  • acinar cell carcinoma of pancreas. Panniculitis, second most common, rx surgery poor outcome

AIP – type 1, sausage shaped pancreas, not duct centric, path LPSP, relapses, systemic, igG4 elevated 65% time, stringy duct, (may have clinical scenario or parotid affected)
Type 2. Duct centric, local, IgG4 normal, bx granulocyte epithelial lesion, associated with UC, low recurrence rate, rx steroids

MCT- women, 50,s, size critical 3cm, calcification in wall, If communicates with duct IPMN. high cea in MCT
Serous cystadenoma – central scar in 20% of cases

Fertility Workup and pancreatitis, CYSTIC fibrosis, recessive and sweat chloride test

PRSS or abn cationic trypsinogen gene, hereditary pancreatitis, AD (autosomal dominant). SPINK – tropical pancreatitis AR

Schwachman Diamond syndrome SDS – second most common inherited pancreatic insufficiency, respiratory tract infection and bone marrow issues including AML. AR

Bilirubin more than 4 and dilated ducts ERCP

Skin lesion plus hypervascular mass – glucaganoma of pancreas – gallium scan, glucagon level, necrolytic migratory erythema is characteristic (but not specific)

Pancreatic cancer screening in PJ syndrome, lynch, BRAC mutations with family history (one FDR or 2 any family), p16 with FDR

Hypercontractile esophagus – DCI between 5000 to 8000 rx SSRI or TCA

Diffuse esophageal spasm,- normal IRP, but low latency and high DCI and few normal peristalsis

Gastric band – pseudoachalasia

Pancreatico – biliary maljunction – do cholecystectomy. (pancreas takes off from distal cbd). Slightly higher cholangiocarcinoma also.

Simvastatin protects against gallstones formation

Bouveret syndrome – gb-duodenal fistula. Heals on its own. Endoscopic removal of stone

AIDS choangiopathy – do ERCP, stent placement

Hep C is RF for cholangioca

Thailand – parasite Opsithorcosis and Chlonorsis, cholangio ca

Milwaukee classification for SOD – type 1 ( typical pain, ALT x2x ULN and cb more than 8 – Rx ercp
Type 2 – 2/3 do manometry and ercp if abnormal
Type 3 functional

S typhi chronic – rf for gb cancer

Endoscopic ampullectomy can be done for ampullary polyps upto 4 cm

Porcelain GB – incomplete calcification GB cancer risk. Complete calcification does not have gb cancer risk

HIV choangiopathy is from HIV, cryptosporidium (commonest), microsporidium, cyclospora and MAI

PSC strictures – FISH more than once with polysomy is concerning, not if just once

GB polyps – commonest cholesterol – size less than 1 cm. Size more than 1 cm – adenomyomatosis nd maybe carcinogenic. Adenoma is last type and always carcinogenic.

Carolis disease. Type 5 – just has hepatic -intra and extrahepatic – dot sign – dots in cbd. Carolis syndrome when extra hepatic manifestations and have hepatic fibrosis. Rxx of carolis is liver transplant or resection to prevent cancer
Type 1 or type 4 Rx is reux hepaticojejunostomy high risk of cancer (extrahepatic cyts and other is both intra and extra hepatic cysts)
Type 3 less risk of cancer, presents as pancreatitis
Type 2 – is a diverticulum, rx is diverticulectomy

Multiple bile duct strictures post OLT – hepatic artery compromised.)usually in first 3 months

PBC – worse outcomes in younger age, males and fatigue

Pediatric liver conditions
Criggler Najjar 1 – high bilirubin, neonates Rx OLT fatal, and from UGT1A1 abnormality, unconjugated bilirubin Type 2 rx barbiturates, can be older rx is stimulation of UGTA1 activity
Progressie familial intrahepatic cholestasis PFIC – 3 types. Type 3 is in adults, genetic ABCB4, duct proliferation on bx of liver and high GGT. Type 1 and 2 younger age and normal GGT.
Type 1 is Bylers disease and homozygous for ATP1B8. BRIC is heterozygous for ATP1B8, milder and normal GGT. Common in AMISH

Gallstones – 3 types cholesterol – commonest
Black pigment – hemolysis, cirrhosis, ileal resection. Radioopaque
Brown pigment – radiolucent, biliary strictures, chlonorchis infections

Alagille syndrome – JAG 1 gene, characteristics skeletal, cardiac and facial features with jaundice and ductopenia

Biliary cyst adenoma – rx is surgery, turns into cancer, ovarian tissue lining, calcifications in lining (similar to MCT?)

Rx for biliary infections – chlonorchis – praziquental
Strongyloides – Ivermectin
Fasciola hepatica – triclabendazole
Ascariasis – albendazole
Cryptosporidium – nitazoxanide

HCV – highest risk of cirrhosis and cancer type 3

IBD rx immuno suppression – HBV – HB sAg positve and HBc Ab + – highest risk. Moderate risk 1-10% reactivation – HBcA+ and HBsAg – – treat with tenofovir. Prednisone more than 20 mg for more than 4 weeks is also a high risk. AZT and methotrexate use is low risk less than 1 %. Once on treatment continue for 12 more months after the offending medication is not used

In solid organ transplant Rx HEV IgG due to relapse. HEV is from game meat, pork and mussels, Rx is ribavarin

Hep B with PAN (polyarteritis nodosa), – arthritis, myalgia, hypertension, rash and renal issues. Rx tenofovir if mild. If moderate steroids and severe cyclophosphamide. ANCA positive

HCV – lichen planus, lymphoma, diabetes,cholangioca, PCT

HBV with cirrohsis – Rx no matter what ALT or DNA level is. Risk of lactic acidosis is there

HCC screening in HBV – every 6 months. Asian male more than 40, asian female more than 50 and african americans more than 20 age

HSV hepatitis – ground glass appearance and history of steroid / immunosuppression use

EBV infection and splenomegaly – avoid sports for 4 weeks.

HIV and HBV together – treat both

AFLP – LCAD def. Mother is heterozygous and fetus is homozygous. Microvesicular steatosisj (other causes are tetracycline, reyes syndrome, valproic acid). Reyes syndrome – MCAD medium chain fatty disorder precipitated with flu and salicylate

Alcoholic hepatitis – worst prognosis with hepatic encephalopathy. Also they can get HRS without cirrhosis

Best transplant survival is in PBC.

AIH dosing – prednisone 60 mg or 30 mg with AZT 50 mg

Africa american patient with elevated ACE level, high alk phos – sarcoidosis

Tegretol decreasis the efficacy of OLT drugs (calcineurin). Causes acute cellular rejection

High Hb is PV and which leads to BCS (budd chiari)

Budd chiari treatment – anticoagulation, then thrombolysis, then TIPS and then OLT

Acute onset hepatomegaly,ascites, edema and jaundice – can be SOS (sinusoidal obstruction syndrome or veno occlusive disease, post liver transplant, herbal medications. Similar to budd chair but obstruction is at sinusoids and venules and not in hepatic vein or IVC as in BCS). Azathioprine can do it and treatment for Bone marrow transplant,

HH – target ferritin 50-100 and do liver biopsy if ferritin is more than 1500 (to rule out cirrhosis)

Alcoholic hepatitis – good response to prednisone is drop in Bil at day 7 or lille score less than 0.45

CHF – cholestsis of liver

High isolated AST – rhabdo

PSC – can be large duct or small duct. Small duct needs liver biopsy

Gilberts mild def of bilirubin UDP glucoronotransferase.

Conjugated bilirubin abnormalities are dubin johnson and rotors syndrome

CREST is higher in PBC (not any other autoimmune)

PBC – fatigue not improved with treatment, osteoporosis is common, hypothyroidism, and high cholesterol (not TG). Rx for pruritis is questran, rifampicin and naltrexone (naltrexone can cause chronic pain like syndrome, rare hepatotoxicity). Uros does not help itching. AMA targets enzymes that catalyze oxidative decarboxylation of keto acid

GVHD – close HLA match causes it. So liver is spared but develop immune reaction in skin, pancytopenia etc
However AGVHD with bone marrow transplant affects the liver – attacking the bile duct and cholestatic picture

AATD – PAS diastase resistant globules. Classical case emphysema also. However if A1AT is null / null, no liver damage since the abnormal protein is totally absent (so no abnormal A1AT polymerization in the liver cells)Be careful about checking A1AT levels after transfusion. False neg. Ground glass in liver cells is the hep B

Glycogen storage disease presents as hypertension and can cause HCC. Rx is starch Only type 3 causes cirrhosis, others do not

Gauchers disease – erlenmeyer flask deformity and glucocerebrosidease def leading to its deposition in the macrophages.

NASH biggest mortality is from cardiovascular abnormality

Non cirrhotic portal hypertension common in HIV treatment esp with didoinosine drugs, higher chance of variceal bleed. It is presinusoidal

Large EGV – do not use beta blocker if pt is diabetic or has asthma

TIPS mortality high if bilirubin more than 4, meld more than 15-18, advanced age, low sodium

Hospital acquired SBP – use zosyn or extended spectrum carbapenem

Increasing creatinine in cirrhosis – hold diuretics, volume expansion with albumin. If Cr does not improve or Cr rises more than 1.5, then type 1 HRS. Then consider octreotide and midodrine.

HE – sodium benzoate can be considered.

Clubbing and hypoxemia in cirrhosis – hepatopulmonary syndrome from shunting, do contrast echo. Portopulmonary HTN has vascular resistance more than 240, Pa pressures more than 25 and wedge less than 15. Occurs from splanchnic vasoconstrictors bypassing the liver, loud P2 and no hypoxia

Post OLT – hepatic artery thrombosis is in 7 days, 2-12% of cases and if with high lactate, AST more than 3000, need another liver immediately

High cancers post transplant include skin, respiratory and lymphoma

Ascites – fluid restriction if sodium low. Restrict salt, new ascites occurs about 7% per year.

A1AT does not recur after OLT

Best regimen is reduced dose tacrolimus with Everolimus or sirolimus an mTOR inhibitor. Well tolerated, less rejection

Post transplant hep B – consider tenofovir plus emtricitabine

Primary hyperoxaluria – def alanine-glyxolate aminotransferase, leads to renal failure, and death. Rx is transplant both kidneys and liver.

Living donor – small size for syndrome can occur. Avoid it by having graft to recepient ratio is more than 80. Smaller the size of remnant liver, faster the regeneration in the donor. Both lobes regenearate at same rate.

Lack of social support – no OLT. Compensated cirhosis and single less than 5 cm HCC, local resection

Thiamine def can cause – cerebellar degeneration, marchiafava – bignani (affects the corpus collusum with delirium, pyramidal signs), Werneckis and korsakofs.

Like new onset ascites, risk of varices to bleed is around 10% too

Annual GB surveillance in PSC patients. High risk of gb cancer

Amyloid variant TTR rare AD disease – bad prognosis if malnutrition. It’s a cause of cirrhosis and needs OLT

Post transplant avoid pregnancy for first 1 year. Higher chance of ACR (acute cellular rejection)

IBD patients high chance of budd chiari

Once ascites develops 5 year survival is down to 44%. Give 8 gm/l of albumin for every liter removed.

Varices if present, repeat EGD every year. IF offending agent removed EGD every 2 years

GOV 2 – no bleed NSSB and if bleed TIPS

RF on tacrolimus – switch to an mTOR

TACE and sorafenib is palliative. Curative are OLT, RFA and local resection
mTOR inhibitors and mycophenalate are contraindications to pregnancy. Tacrolimus causes diabetes,sirolimus causes high lipids.

Dysynergic defecation – less than 20% relaxation of the basal sphincter pressure plus failure of balloon expulsion or inadequate propulsive forces on anal manometry. Rx is biofeedback
Incontinence – urge or overflow. Urge rx is biofeedback. Normal resting sphincter but reduced squeeze pressure or duration.
Overflow – reduced resting pressures and suggests an internal anal sphincter pressure or from reduced rectal vault from inflammation, surgery, fibrosis

IPAA reduces fertility

Active peri anal disease – do C section

Hepatic adenoma – if more than 5 cm, RFA prior to pregnancy

ICP in pregnancy, 2 trimester, check bile salts level, rx urso, premature delivery risk

Mild to moderate nausea in pregnancy -use B 6 pyridoxine

HELLP – high LDH and peripheral smear shows microangiopathic hemolytic anemia.
AFLP – hypoglycemia, higher PT, PTT and creatinine

Rumination syndrome – behavorial therapy. Regurgitation and no retching prior to regurgitation.

Linzess side effect is headache, diarrhea

Slow transit constipation – once a week or less, no straining and minimal bloating and discomfort

Incontinence in pregnancy occurs with fetal weight more than 4 kg, prolonged second phase of labor and third or fourth degree tear

Endometriosis in colon – rectosigmoid, submucosal mass and needs EUS FNA

Hemangiomas are hyperechoic on US

Hyperemesis gravidarum is associated with liver abnormality but bilirubin elevation is low (less than 4)

Deli meat in pregnancy – listerosis. Rx ampicillin, high chance of fetal death. Second line is bactrim, erythromycin

SIBO – folate, vitamin K goes up. Thiamine, B 12 and iron can go down

PI-IBS RF – female, young age, fever, anxiety or depression

C jejuni – 70% of GBS have C jejuni, risk is 100 times more in infected patients, not associated with severity, worse prognosis if C jejuni and GBS

Osmotic gap : osmotic diarrhea more than 50, usually more than a 100, Normal is less than 50. Calculation 290 oolminus 2 x (K plus Na)

Non responsive microscopic diarrhea – rule out spure. 5% incidence of microscopic colits in sprue

Salmonella – treat if immunocompromised or age over 50

Stool Mg more than 90, factitious diarrhea

IBS-D rule out sprue, not FCP

BAD – 4 types – 1. Ileal dysfunction with (growth factor abnormality). 2. No obvious cause. 3. In patients with SIBO, spure, chronic pancreatitis 4. Increased bile synthesis in liver from medications

Biofeedback for pelvic dyssynergia. If no improvement, repeat balloon expulsion and manometry. If manometry normal – defecogram. If balloon expulsion normal – colon transit time AJG – 2014 (109-8) 1141-57

Linzess plus high fat breakfast – worse diarrhea

Mechanism of action – lubiprostone chloride channel activator, Linaclotide -GC-C, alosetron 5HT3 antagonist, Proculopride 5HT4 agonist

Methylnaltrexone – contraindicted in obstruction, PUD, diverticular dis, metastasis In abdomen

Colchicine can be used for chronic constipation if normal Cr and not on any CYP3A4 inhibitors

SRUS – do defecography and obliteration of fibromuscular layer in lamina propria

Constipation can occur with lasix and zofran

MAI can cause diarrhea. Diagnose with EgD bx

Crofelemer for HIV diarrhea and acts on the CFTR chloride receptor. Lymphoma in HIV can cause diarrhea too

Zinc rash not photosensitive. Carcinoids – niacin – pellagra, 3 D’s. Selenium cardiotoxicity

Carbohydrate malabsorption – high osmolar gap, and acarabose diarrhea, low stool pH

Lactulose breath test – avoid high fiber diet, smoking, exercise 2 hours before test, things that constipate you, and starch food that is hard to digest like potato. These things increase hydrogen in breath. Positive is more than20 ppm of H2 in 2 hours.

Xylose absorption – SIBO, nothing absorbed so no xylose in blood and not in urine in 4-5 hours.

Dilantin commonly causes constipation

Erythritol (stevia), is a carb, produces pH in stool less than 6, and osmotic diarrhea.(carb malabsorption causes low pH)

Functional outlet constipation – normal anal sphincter, but fails to relax. Rx biofeed back if alert otherwise tap water enema

Lactulose for constipation in pregnancy

Scleroderma can cause peptic stricture

GLP1- secreted from L cells in ileum, and released in response to fat in ileum. Slows gastric motility (puts a break)

Gastric pacemaker, only changes accomodation. Not gastric emptying.

Low dose nocturnal octreotide helps scleroderma by increasing motility (MMC) sweep and getting rid of bacteria causing SIBO Also helps chronic intestinal pseudo obstruction

Scleroderma of internal anal sphincter – weak tone, and normal balloon expulsion, normal squeeze of IAS

Ultrashort Hirschsprungs – Dx with anal manometry.

Colonic neuropathy – absence of wake response, low high amplitude contractions, and absent post prandial response

Achalasia dilatation only improves dysphagia after dilatation. It causes sq. cell ca, even though distal

10% of babies with Downs have Hirschsprung’s

Lung cancer – anti Hu or anti neuronal nuclear antibody – ANNA causing pseudoobstruction / dilatation

C jejuni – resistant to pcn and cephalosporin. Azithromycin is drug of choice. Increasing resistance to quinolones

Listeria – amp plus gent, or bactrim

Sushi – high MCV, diphylobotrium latum, Praziquental

Travelers diarrhea – Rx if fever, not responding and BM more than 4 with pus, blood or mucos.Azithromycin in children and pregnant women

Crypto diarrhea in HIV – improve CD4 by HAART is the treatment

Yersinia – right LQ, undercooked food, port and water. Also causes pharyngitis. No treatment needed. IF adenitis and severe symptoms, can use doxy, cipro, gent or bactrim

Diarrhea plus eosinophils in HIV – cysto-isospora infection (protozoan) and use bactrim

Hookworm – Rx albendezole, may have a rash in remote history and iron def. anemia

Campy and salmonella – poultry. Viral usually nausea predominant. Toxins – usually nausea vomiting Listeria and shigella, deli meat

Cholera – doxycycline, single dose

Paralytic shellfish – neurological symptoms in hours
Cigauatera fish – reef fish, like barracuda., GI symptoms and then 72 hours later cardiac, neurological symptoms and painful urination, dysesthesias etc

Scromboid fish poisoning – rapid chilling of fish to below 40 F is needed to prevent it. Rash is feature. Rx benadryl and histidine to histamine in fish

Seafood – hypotension – bullous skin lesions – Vibrio vulfinicus more common in cirrhosis

Botulism – cranial nerves, canned food, descending paralysis

FMT exclusions for donors diabetes, increased age, IBS, UK for more than 3 months due to CJ virus, obesity

Giardia – symptoms a week later, Nitazoxinide for 3 days or metronidazole, or tinidazole, or quinacrine. Stool antigen and relapse is high and 50% develop chronic symptoms

Ulcer bleed risk factors – age more than 65, NSAID, ASA and prior history of ulcer

Post polypectomy bleed – use of anticoagulation (ASA is not in the list), obesity, right polyp, size of polyp, hypertension, advanced age

Idiopathic ulcer without NSAID or HP treat with PPI indefinately. 42% will have a second bleed otherwise

IF INR less than 2.5 ok to EGD for active bleed without FFP

Blatchford score for bleeding – BUN, Hb, BP, are 3 main ones others are melena, syncope, cardiac or hepatic issues and tachycardia

Variceal bleed mortality – AIMS 65 – low albumin, high INR, mental status change, systolic pressure and age more than 65

Lvassist Device 20% have bleeding, usually from AVM or Deaulafoys

COX 2 causes coronary issues

Calcium oxalate stones and carbohydrate malabsorption (with subsequent d lactic acidosis) occurs when fat is mal absorbed (in short gut) and the colon is intact.

Why iron def in crohns ? – Normally, iron def, leads to decreased hepcidin in liver, and this stimulates increased ferroportin and transfer of iron from cells to body.
In crohns , hepcidin increases from acute phase inflammation , decreased ferroportin and less iron is taken from cell to body. Also , decreased pick up of iron in lumen to enterocytes due to inflammation.

Goblet cell mucin depletion suggests chronic inflammation

Very high TPMT levels – imuran gets metabolized to 6 MMP, the toxic pathway. Medicine wont work

Pouchitis more likely in indeterminate colitis, use of NSAID perioperative, PSC patients, pANCA postive, tobacco use and perioperative EIM symptoms. Fulminant colitis is protective

Predictors of poor response in UC flare up are TC colon diameter more than 5.5, albumin less than 3, higher BM frequency, and no drop in CRP on steroid treatment

IBD risk – 5% if one parent has CD, 2%if one parent has UC and 35 % of both parents have IBD

Microscopic colitis – NSAID, PPI, SSRI, statins, celiac and thyroid disease

TNF induced psoriasis – more in women and CD. Rx topical steroids and change to stelara

pANCA more common in UC and left sided CD. ASCA + and neg pANCA 93% specific for CD, cBir + and pANCA + CD much more likely than UC

NOD2/Card 15 – more common in CD with SB stricture and early surgery.

More severe UC in younger patients

Methotrexate – hypersensitivity pneumonitis, hepatotoxicity, nephrotoxicity, stomatitis, fever, alopecia, BM suppression, fatigue, nausea

High risk GIST recurrence (scandanavian study) 10 cm and 10/50 HPF mitosis or more than 5 cm and 5/50 mitosis , surgery and 36 months imatinib. Surgery if GIST is more than 2 cm and 5/50 mitosis

5 FU does not work in lynch

Risks with Lynch – 30 years on wards endometrial eval, antral and ampullary eval and urine for ureteric cancer all yearly except ampullary is every 2 years

Hereditary diffuse gastric cancer – CDH1 gene

Serrated polyp annual colon – Any poly more than 2 cm and serrated, or 5 serrated polyps with 2 more than 1 cm or family history of serrated polyp and patient has one serrated polyp proximal to sigmoid

FAP tumors – thyroid, brain, colon, duodenum, gastric jejunal

Rare complication of sprue – Enteropathy associated T cell lymphoma, 5 year survival 20%

Family history of HCC and hep B – screening US irrespective of age

Liver lesion less than 1 cm, US every 3 months for 2 years

Any pancreatic cyst with a solid component – EUS with FNA

Hemosuccus pancreaticus – artery communicating between splenic artery and PD

Copper def – muscle weakness and gait disturbance similar to B12, microcytic anemia. Zinc and copper compete with each other. Over ingestion of zinc causes copper def. Ingestion of iron makes copper def and anemia worse.

Zinc def – acrodermatitis (rash around orifice), dysgeusia, diarrhea, , delayed wound healing, growth retardation, low alk phos and night blindness, can occur in liver diseases,

Niacin – photophobia and burning mouth and glossitis

Vitamin C def – bleeding gums, history of alcoholics, crohns disease, petechiae, pedal edema, periorbital edema, dry skin

Reduced ghrelin – reduced appetite,
Reduced peptide YY ( from TI ), decreased insulin resistance and causes satiety
Sleeve gastrectomy causes reduced ghrelin, reduced peptide YY and increased GLP 1

Marginal ulcer – smoking, DM, NSAID, Hp and steroids

Severe pancreatitis – enteral TF is not tolerated and higher mortality. Then use TPN

Intestinal transplant indications- frequent sepsis, thrombolysis of TPN venous site more than 2 x, frequent dehydrtion and liver failure from TPN

PLE (protein losing enteropathy) – can be from obstructed lymphatics. Check A1AT in stools since it is not destroyed by proteases. Can check clearance – more than 24 without diarrhea or more than 56 with diarrhea.
Obstructed lymphatics can present this way also. (after cardiac surgery). Treatment is high protein low fat and MCT supplements (which is absorbed directly to the portal system)

Ghrelin levels rise with fasting, and reduced with rise in CCK and leptins

Refeeding syndrome – sudden death from feeding a starved individual. Occurs from K, Mg and phosphate def

Thiamine def – can occur with hyperemesis. Causes nystagmus, ataxia, confusion, delirium, and beriberi chf symptoms, mamillary hemorrhage in brain

Leptin – increase in level causes satiety by MSH hormone and peptide Y by targeting the hypothalamus

Binge eating disorder – binge eating once a week for more than 3 months, eat alone, fast depression after eating. Can co exist with anorexia nervosa

Latex allergy – banana, avocado, kiwi causes symptoms. Oropharyngeal symptoms or crampy non bloody diarrhea

Puffered fish poisoning – tetradotoxin , lethal

Buried bumper syndrome (BBS) – occurs with obesity, rapid weight gain, placing multiple gauzes. Check CT, presents as blockage of tube, or dripping.

Manganese deposits in the globus pallidum causing parkinsons syndrome. Usually too much in TPN

Oristat is a pancrease lipase inhibitor – Lose weight with fat malabsoprtion. 8% weight loss

Locaserin – affects serotonin 2 c. Cannot be used with MAOI, SSRI and triptans

Phenteramine – causes fetal abnormality

Niacin – 4 Ds, diarrhea dermatitis, dementia death. Photosensitive so rash on distal arms and legs

Chromium def causes insulin resistance

Keshan syndrome – selenium def, vegetarians who eat food from selenium def. soil, from TPN with low selenium

25-30 Kcal /day is normal intake

Refractory crohns disease – two types 1 and 2. In 2, there is aberrant T lymphocytes more than 20%, do flow cytometry and associated with t cell lymphoma

Zinc def common in sprue

AIE – auto immune enteropathy, similar to sprue, but no lymphocytes on biopsy, associated with RA and autoimmune thyroiditis, rx steroids

Tropical sprue – asia, peurto rico, – rx tetracycline, similar to celiac, diarrhea and other sprue

Whipples disease 49-55 male, sewer worker, joint, GI eye, heart, neurological features, PAS staining

Systemic mastocytosis – rash, syncope, flushing, c-KIT abnormality, bone marrow and elevated tryptase

Common variable immune def – presents similar to celiac or IBD, increased lymphocytes with villous blunting, rx is prednisone,gamma globlulin makes it worse

Primary amyloidosis – congo red with apple – green birefringence on staining

Menetriers disease, rx octreotide

IgA def – chronic giardia, Metronidazole

Double ballon endoscopy – rf for pancreatitis

Tropical sprue tetracycline and folate rx

Short bowel less than 180 cm and if less than 60 cm, will need TPN

Just like collagenous colitis there is a collagenous sprue. Rx steroids

PJ small bowel monitoring – video capsule every 3 years

BBPS – boston bowel prep system – right, left and transverse. 0-3, with 3 no stool seen, 2, minor liquid, 1 a lot of liquid and 0 with adherent stool. Less than 5 polyp detection 24% more than 5 40% detection

Risk of polyp recurrence – based on size more than 40 mm, bleeding during procedure and high grade dysplasia

The NICE classification describes criteria to differentiate conventional adenomas from serrated class lesions (sessile serrated polyps and hyperplastic polyps). Large open pits, irregular shape, indistinct edges, and a “cloud-like” appearance to the polyp surface are the WASP criteria that distinguish sessile serrated polyps from hyperplastic polyps.

To achieve a neutral posture for the range of endoscopists, the endoscopy gurney should be adjustable to allow holding of the endoscope between elbow height and 10 cm below elbow height to minimize forward flexion of the back and shoulder abduction. To accommodate the elbow height of the 5th percentile female to the 95th percentile male, the examination bed should be adjustable between 85 and 120 cm.

esophageal dilation, sclerotherapy of varices, instrumentation of obstructed bile ducts, EUS-FNA of cystic lesions, and percutaneous feeding tube placement. Patient factors that should raise concern for need for prophylactic antibiotics include the following: neutropenic patients (ANC <500 cells/mm3), those with advanced hematologic malignancies, cirrhosis with concurrent GI bleeding, or synthetic vascular grafts within 6 months of placement. Currently, there are no cardiac conditions that warrant prophylaxis unless the patient has a documented infection at time of procedure. ANTIBIOTIC PROPHYLAXIS

To immediately help the patient’s hypotension, placing the patient in the Trendelenburg position will help increase venous return to the heart, increasing cardiac output, and vital organ perfusion. The prolonged case and spasm requiring excessive use of air insufflation with associated bradycardia should prompt consideration of a vasovagal reaction, a well-described complication with identified risk factors including higher doses of sedation and presence of moderate-severe diverticulosis. Additionally, the use of air insufflation over CO2 or water infusion has been associated with higher rates of pain and vagal reactions.

Specifically, guidelines from the American Association for the Study of Liver Diseases (AASLD) recently updated their recommendations and state that patients with chronic liver disease with a liver stiffness measurement of <20 kPA on transient elastography and platelet count of >150,000 x 10 (9)/L have very low probability (<5%) of high risk varices, and thus EGD variceal screening can be circumvented

Most recently, a multi-center study of targeted stretching micro-breaks (TSMB) integrated into the surgical suite demonstrated that TSMB improved surgeon postprocedure pain scores in the neck, lower back, shoulders, upper back, wrists/hands, knees, and ankles without increasing operative time. Surgeons reported improved physical performance (57%) and mental focus (38%), with the majority (87%) planning to continue TSMB. Micro-breaks in endoscopy should involve relieving the static load of the endoscope and the overall body posture. Static loads occur when muscles are contracting without significant movement

Use of the Functional Lumen Imaging Probe (FLIP) could also be considered here to assess EGJ distensibility; however, manometry would be the first step in most institutions.

Importantly, histamine 2 receptor antagonists (H2RA) have shown to reduce esophageal hypersensitivity to both chemical and mechanical intra-esophageal stimuli. In this patient, an H2RA would work as a good neuromodulator therapeutic option to improve symptoms

Elimination of dairy and wheat, followed by “step up” with additional elimination of egg and soy if there is no response, followed by another step up with elimination of nuts and seafood if there is no response

Patients with an LS <20 kPa and platelet count >150,000/mm3 have a very low probability (<5%) of having high-risk varices, and EGD can be circumvented.

Patients with bloating can be sorted into 3 categories: gastric bloaters, small bowel bloaters, and constipated bloaters. These are sorted out by the time that it takes to develop symptoms after eating and whether or not constipation is present. Gastric bloaters develop symptoms in <30 minutes and may have gastric outlet obstruction, gastroparesis, and disordered gastric accommodation or functional dyspepsia as underlying causes. Small bowel bloaters develop symptoms in >30 minutes and may have dietary carbohydrate intolerance, small bowel obstruction, celiac disease, small intestinal bacterial overgrowth, or functional bloating as underlying causes.

n a recent ACG clinical guideline regarding the management of pancreatic cysts, the Charlson comorbidity index was recommended as a useful parameter to measure an individual patient’s status. In this case, the Charlson score is 10 and the patient’s predicted 10-year survival is 0% based on her history of end stage renal disease, peripheral vascular disease, prior TIA, myocardial infarction, and her age >70.

Distal intestinal obstruction syndrome (DIOS) is characterized by partial or complete obstruction due to fecal material in the ileocecal/right colon region. Differentiating DIOS from constipation can be difficult but DIOS is more often associated with acute obstruction involving the ileocecal area whereas constipation is more gradual with stool burden throughout the colon. Risk factors for DIOS include genotype, pancreatic insufficiency and prior episodes of DIOS.

Propranolol – osmotic diarrhea

Balloon hyperinflation has recently been described as a rare complication of saline-filled IGBs. It could lead to compression of surrounding organs including the pancreas. Antacid therapy may be associated with IGB bacterial and fungal overgrowth that could lead to overgrowth of gas-forming organisms inside the gastric balloon.

Specialized diets are one of the most effective treatment options, and include an elemental diet that can induce remission in the majority of patients with EGE. A 6-food elimination diet is easier to adhere to and may be effective as well for maintenance. Systemic steroids are also effective at induction, but should be tapered after 6-8 weeks and would not be a good option for long-term treatment due to side effects. Studies with biologic agents have yielded suboptimal results. Mepolizumab, an anti-IL 5 agent, improved tissue eosinophilia but did not have significant improvement in clinical symptoms. Similarly, omalizumab, an anti-IgE drug, can reduce tissue eosinophilia but do not work as well as specialized diets in EGE.

The patient meets criteria for absent contractility based on the lack of contractile activity in 10 swallows and the IRP below 15 mmHg. However, in the revised Chicago Classification, an IRP that is above 10 mmHg in the context of absent contractility should raise suspicion for achalasia since the pressure dynamics of bolus emptying may not allow an elevated IRP with a poorly functioning esophageal body. Additionally, esophageal pressurization (seen in the fourth swallow), should alert one to the possibility of achalasia. Given this issue, it is recommended that the patient undergo a timed barium esophagram (TBE) to rule out achalasia. If there is significant bolus retention, the patient should be managed similar to achalasia and treatment should be targeted at relieving the obstruction at the esophagogastric junction if this is revealed on the timed barium esophagram. If emptying is normal on the TBE, the patient should be considered to have absent contractility and this could potentially be related to an early presentation of a collagen vascular disorder. Endoscopic ultrasound would be helpful if there was still some doubt as to the diagnosis and some suspicion of pseudoachalasia based on presentation or endoscopic findings. Empiric dilation would not be helpful in a patient with a normal IRP and no evidence of mechanical obstruction. Going directly to surgical myotomy would be incorrect until the contractility abnormality can be more fully assessed and characterized.

Reflux treatment – There is no strong evidence about the efficacy of avoiding caffeine, alcohol, and certain foods.

Buspirone is a 5HT 1A receptor agonist used in the treatment of anxiety. In a dose-dependant manner, this drug was found to relax the proximal stomach and delay gastric emptying of liquids and solids, in healthy volunteers. In a small, randomized clinical trial in patients with functional dyspepsia, buspirone was shown to significantly improve overall symptom severity and the individual symptoms of early satiation, postprandial fullness, and upper abdominal bloating. The therapeutic effect was associated with a slowed liquid gastric emptying and enhanced gastric accommodation.

The Advisory Committee on Immunization Practices (ACIP) recommends the use of hepatitis B vaccination for all unvaccinated adults aged 19-59 years upon diagnosis with type 1 or type 2 diabetes mellitus, in whom an increased risk for acute hepatitis B has been reported by the Centers for Disease Control and Prevention (CDC). Unvaccinated adults age 60 years or older may be vaccinated at the discretion of the treating physician after individualized assessment of risk and likelihood of mounting an adequate immune response to HBV vaccination.

Using this model, the patient’s MELD score is 8, and his 30-day operative mortality is estimated to be 2.4%. Because the patient is undergoing a laparoscopic procedure, the actual mortality rate could be lower. A low serum sodium and low serum albumin would increase the risk. Note that based on the MELD score, the patient’s predicted 5-year mortality rate is 29%. If his MELD were higher, his operative risk and mortality would be higher. For example, if his MELD score were 12, his predicted 30-day operative mortality would be at least 12%, and his predicted 5-year mortality rate would be >70%.

The MRI demonstrates all of the diagnostic features of HCC including washout and delayed rim enhancement. The Liver Imaging Reporting and Data System (LI-RADS) is used by radiologists to assess the likelihood that a liver mass is HCC. Patients with LI-RADS 1 are definitely not HCC. LI-RADS 2 is probably benign. LI-RADS 3 is possibly HCC. LI-RADS 4 is likely to be HCC and LI-RADS 5 is definite HCC. Patients with LI-RADS category 4 and 5 do not require a biopsy of the liver mass to confirm HCC in the proper clinical situation, as this could cause seeding and spread of the HCC. If this occurs, the patient would no longer be a candidate for a liver transplant. Patients with LI-RADS category 1 and 2 also do not require liver biopsy because these lesions are benign or very likely benign. Patients with LI-RADS category 3 are generally the only patients who may require a biopsy because of the equivocal nature of the mass.

LI-RADS assesses the likelihood that a lesion is HCC. This is different than the actual staging of the HCC. The staging of HCC is based upon the size and number of lesions present. Stage 1 is a single lesion less than 2 cm. Stage 2 is a single lesion less than 5 cm or up to 3 lesions in the same lobe with total diameter less than 5 cm. Stage 3 HCC is any single lesion greater than 5 cm, more than 3 lesions or lesions within both lobes of the liver. Stage 4 HCC includes evidence of vascular invasion within the liver or metastatic disease outside the liver. Patients with stage 2 HCC are eligible for automatic MELD upgrade points for liver transplantation. Surgical resection and HCV treatment should not be considered in this patient because of the risk of hepatic decompensation in this patient with advanced liver disease (with ascites, low albumin, and thrombocytopenia).

HCV manifestations – Chronic hepatitis C is associated with a spectrum of extrahepatic manifestations such as mixed type cryoglobulinemia, porphyria cutanea tarda, vitiligo, lichen planus, membranous glomerulonephritis, membranoproliferative glomerulonephritis (MPGN), Hodgkin’s and non-Hodgkin’s lymphoma, diabetes mellitus, peripheral neuropathy, and Sjogren’s syndrome, among others. Of these conditions, mixed-type cryoglobulinemia represents a well-documented manifestation of chronic HCV infection due to its effect on B-cell lymphoproliferation, and may result in the precipitation and deposition of cold-insoluble immune complexes in the skin, kidneys, and peripheral nerves, resulting in characteristic rashes, neuropathy, and membranoproliferative glomerulonephritis.

EGV surveillance The AASLD Practice Guidelines for prevention and management of gastroesophageal varices state that patients with decompensated cirrhosis but no varices should have screening endoscopy on an annual basis. First-degree variceal prevention with non-selective beta-blockers showed no benefit in preventing development of varices and a suggestion of harm in a randomized controlled trial.

The patient has Peutz-Jeghers (PJ) syndrome, characterized by an STK11 mutation and the classic findings seen on the oral mucosa. Patients with PJ are at high risk for gastrointestinal tract, breast, testicular, and pancreatic malignancies. Answer A is correct – colonoscopy and EGD should be performed beginning at age 8. Capsule endoscopy should also be started at age 8. Males need testicular screening, but it should begin at birth. Breast MRI should begin at age 25.

When mesenteric panniculitis (MP) is ultimately diagnosed, the major symptom at presentation is pain, which is seen in 54.3% of patients, and may include low back pain, abdominal pain, and flank pain. Other common symptoms include weight loss and nausea with or without vomiting. Elevated inflammatory markers, such as an erythrocyte sedimentation rate and c-reactive protein, are seen in 42 and 52% of patients, respectively.

On CT scan, mesenteric panniculitis appears as a mass-like area of heterogeneously increased fat attenuation that may displace local bowel loops, but typically does not displace the surrounding mesenteric vascular structures. Mesenteric lymph nodes are often seen within the region of segmental mesenteric stranding and nodes may be greater than 1 cm in some cases. Lymph nodes greater than 1.2 cm together with the absence of the fat ring sign (halo of fat surrounding mesenteric vessels) are predictors of a diagnosis of malignancy in patients with MP.

Patients with HP not only have a higher prevalence of associated malignancies, but also have a greater chance of developing a malignancy at a 5-year follow-up compared to controls. In most cases, tumors are discovered before the diagnosis of MP. They include carcinomas (breast, colorectal, gynecological, renal and gastric as well as prostate) and hematological malignancies (non-Hodgkins lymphomas and plasma cell tumors). The time period during which a new malignancy was discovered ranged from 7 months to 3 years.

Mesenteric panniculitis is a fibroinflammatory process. It can regress spontaneously, run a stationary course, or progress to varying degrees of fibrosis. The disease is generally believed to be benign in the majority of cases, but needs to be followed given the increased association with malignancy. In the setting of progressive fibroinflammatory disease, a combination of prednisone and tamoxifen has been found to demonstrate improvement.

MCT of pancreas – ovarian stroma, mucos on ErCP

Serous cyst adenoma – cuboidal glycogen lining, honeycomb appearance, rarely becomes malignant

Solid pseudopapillary tumor in pancreas – woman in 30’s, hypoechoic solid lesion

CVID – recurrent respiratory infection and sprue like picture, low IgG , G A and M types

Patients taking PPIs are 2.46 times more likely to have SIBO than those not taking this medication. Given this patient’s chronic use of PPIs, answer A is incorrect

The addition of measuring methane in addition to measuring hydrogen in breath testing is believed to increase the accuracy of these tests by identifying the 20-30% of the population who produce methane as a main product of fermentation of carbohydrates. SIBO is a relapsing disease, especially when there are underlying factors that predispose to this condition. Relapse may be seen in 44% of patients at 9 months after induction of remission with rifaximin,

Extraintestinal symptoms are frequent in non-celiac wheat sensitivity and are increasingly being recognized as a hallmark of this disease. These extraintestinal symptoms include tiredness, lack of well-being, and neuropsychiatric symptoms such as headache, anxiety, “foggy mind,” arm/leg numbness, depression, and dermatologic manifestations. The majority of patients with NCGS report more than 2 associated gastrointestinal or extraintestinal symptoms, with the most frequent being bloating and abdominal pain (80%). Only 50% report diarrhea. There is strong evidence that non-celiac wheat sensitivity is caused by an innate immune response to wheat proteins, while celiac disease and wheat allergies are TH1 and TH2 cell mediated inflammatory diseases, respectively. Clinically, wheat allergies and FODMAP intolerance are usually characterized by a quick onset of symptoms after ingestion of the offending foods (minutes to a few hours), whereas non-celiac wheat sensitivity has a slower onset, with symptoms appearing hours to a few days after ingestion. The onset of symptoms after ingestion also helps set these entities apart from celiac disease in which symptom onset can take days to weeks after onset of gluten challenge.

This woman most likely has autoimmune enteropathy (AIE), which is a rare condition characterized by significant diarrhea, weight loss, and histologic changes on small intestinal biopsy (villous blunting, apoptotic bodies, lymphocytic infiltration, presence of plasma cells, absent goblet or Paneth cells). While patients may have anti-enterocyte or anti-goblet cell antibodies, they are not included as diagnostic criteria. For most patients, immunosuppressive medications are needed for treatment. IPEX (immunodysregulation polyendocrinopathy enteropathy X-linked syndrome) and APECED (autoimmune phenomena, polyendocrinopathy, candidiasis, and ectodermal dystrophy) are systemic forms of AIE. The negative IgA TTG and the histologic findings would make celiac disease unlikely. Patients with combined variable immunodeficiency (CVID) typically have a paucity of plasma cells noted in small bowel biopsy samples. Those with small intestinal bacterial overgrowth (SIBO) may have similar symptoms, but the histology noted in this case should not be seen in patients with SIBO.

Hyperplastic gastric polyps are associated with an increased risk of cancer. As such, large hyperplastic polyps should be excised.

Eighty-six percent of patients who remained transfusion dependent after APC had success with a mean of 2 ablation sessions using RFA, with no further need for transfusion out to 6 months.

When fundic gland polyps are found in large quantity (≥20) in a young patient (<40 years of age), it is important to consider familial adenomatous polyposis syndrome.

Gastroparesis testing other 2 options are the wireless motility capsule as well as C-13 breath testing, which was just recently approved.

Colon ischemia – he patient also has the most significant risk factor for colon ischemia, which is COPD. Finally, the image shows the “single stripe sign,” the colonoscopic finding most commonly associated with colon ischemia. The most common distribution of colon ischemia involves the left colon, specifically the rectosigmoid colon.

Submucosal invasion in LST polyps – The prevalence of SMI in LSTs stratified by endoscopic LST subtype were: 31.6% in pseudodepressed nongranular LSTs, 10.5% in nodular mixed granular LSTs, 4.9% in flat elevated nongranular LSTs, and 0.5% in homogenous granular LSTs. Within that study, SMI was also more common in distal rather than proximal LSTs and the proportion of SMI increased with lesion size (10-19 mm, 4.6%; 20-29 mm, 9.2 %; ≥30 mm, 16.5%).

According to the 2012 U.S. Multi-Society Task Force recommendations, patients who have advanced findings (adenoma ≥1 cm, adenoma with villous elements or high-grade dysplasia, or 3 or more adenomas) should have a colonoscopy in 3 years. Those with 1 or 2 tubular adenomas with low-grade dysplasia (low-risk findings) should have a repeat colonoscopy in 5-10 years. Those with advanced findings who reach 5 years should stay at 5-year intervals, even when colonoscopy is normal. Those with low-risk adenomas (and no prior high-risk findings) who have normal colonoscopic follow-up at 5 years could return to a 10-year screening interval.

Use of the Functional Lumen Imaging Probe (FLIP) could also be considered here to assess EGJ distensibility; however, manometry would be the first step in most institutions.

Esophageal lichen planus has been postulated to result from immune-mediated mechanisms involving activated T cells, particularly CD8+ T cells, directed against basal keratinocytes. Hepatitis C infection, autoimmune disorders, and medications have been putative risk factors for esophageal lichen planus. However, history of head and neck cancer has not been reported as a risk factor for esophageal lichen planus.

Turmeric exhibits an inhibitory effect on platelet aggregation. Therefore, patients who are maintained on agents such as aspirin, clopidogrel, or ticlopidine should be closely monitored if prescribed this complementary therapy to avoid the possibility of a bleeding complication.

Oral contraceptives have been implicated in the development of inflammatory bowel disease and possible exacerbation of Crohn’s disease, but not ulcerative colitis.

In patients with compensated cirrhosis without esophageal varices on initial screening examination, endoscopy should be repeated every 2 years if there is ongoing liver injury such as untreated hepatitis C virus infection or continued alcohol use, and repeated every 3 years if liver injury is not active (e.g., successful cure of chronic hepatitis C virus, alcohol abstinence). Patients with compensated cirrhosis and small esophageal varices identified on endoscopy should have a repeat endoscopy every year if there is ongoing liver injury, and repeated every 2 years if liver injury is not active, provided that primary prophylaxis with beta blockers is not initiated.

Hepatic adenoma recommendation : guidelines recommend follow-up imaging to be considered once every 6 months for at least 2 years to establish any growth patterns and monitor for malignant transformation. Annual imaging can be performed after this period based on the growth patterns and stability of the lesion.

EGV Mx. Once endoscopic variceal band ligation is performed, a repeat examination for additional banding is recommended every 2-8 weeks until complete variceal eradication is confirmed (e.g., no further endoscopic variceal band ligation is possible). Once eradication is confirmed, the next follow-up surveillance examination is recommended in 3-6 months after eradication and every 6-12 months thereafter. Current data does not support the use of combination therapy with beta-blockers and endoscopic variceal band ligation for primary prophylaxis,

Normal ALT. The 2017 ACG guidelines on the evaluation of abnormal liver chemistries proposed a new upper limit of normal for ALT of 29-33 U/L for males and 19-25 U/L for females. This proposal was based on the fact that this appears to be the true healthy upper limit of normal for ALT. In addition, there is an increase in mortality in persons with ALT exceeding these levels. Thus, even though her ALT is “normal” according to the reference lab, her ALT level of 52 U/L is actually elevated and should be further evaluated. Given the fact that it is only mildly elevated, the guidelines suggest confirming that the value is correct prior to ordering additional testing.

The ALT divided by Alk P (both expressed as multiples of ULN) or the R ratio should be less than 2.0, but may be higher at the time of onset, as the Alk P usually rises during the first week or two of injury.

Cholestatic liver injury DILI – The course and outcome are compatible with severe cholestatic hepatitis with partial vanishing bile duct syndrome (VBDS). The most predictive factor of poor outcome was the degree of bile duct loss on liver biopsy. Bile duct loss during acute cholestatic hepatitis is an ominous early indicator of possible VBDS, for which at present there are no known means of prevention or therapy. Pseudoxanthomatous change and copper accumulation are seen with chronic cholestasis. The presence of fibrosis may be indicative of underlying chronic liver disease with early fibrosis but is not predictive of outcome

In a recent study by Romero-Gomez, et al, a weight loss of 7% is associated with a 50% regression of hepatic fibrosis, a 64% resolution of NASH, and a 76% improvement of steatosis. Weight loss has not been associated with a 100% normalization of transaminases or a decrease in the risk of the development of hepatocellular carcinoma.

AFLP diagnosis Swanson criteria

Risk of EGV very low if Patients with an LS <20 kPa and platelet count >150,000/mm3 have a very low probability (<5%) of having high-risk varices, and EGD can be circumvented.

Anterior Cutaneous Nerve Entrapment Syndrome (ACNES), and gives a typical history for this condition. Key historical features are localization to a single spot on the abdomen, sharp quality of the pain, and aggravation by lying on the same side as the pain or daily activities, along with lack of association with meals, bloating, or abnormal stool consistency.

The risk of extrapyramidal effects are highest in patients who are: 1) under 20 years of age; 2) on high-dose therapy; and 3) on prolonged therapy. Tardive dyskinesia more likely to occur with use longer than 3 months, and the FDA recommends the drug be used short-term, ideally less than 12 weeks. In 2009, the FDA issued a black box warning for those with chronic or high-dose use given the concern over tardive dyskinesia. Before the black box warning, 69.8% of patients received metoclopramide for gastroparesis, compared with 23.7% after the warning.

Patients with bloating can be sorted into 3 categories: gastric bloaters, small bowel bloaters, and constipated bloaters. These are sorted out by the time that it takes to develop symptoms after eating and whether or not constipation is present. Gastric bloaters develop symptoms in <30 minutes and may have gastric outlet obstruction, gastroparesis, and disordered gastric accommodation or functional dyspepsia as underlying causes. Small bowel bloaters develop symptoms in >30 minutes and may have dietary carbohydrate intolerance, small bowel obstruction, celiac disease, small intestinal bacterial overgrowth, or functional bloating as underlying causes. Constipation also may be accompanied by bloating which may resolve with effective management of constipation. Patients with aerophagia also may complain of bloating, but often have belching or tympany on physical examination.

STW-5, or Iberogast, has been used in the management of functional dyspepsia and irritable bowel syndrome. It is made up of 9 ingredients, including: extracts of bitter candytuft, peppermint herb, angelica root, milk thistle fruit, celandine herb, caraway fruit, licorice root, balm leaf, and chamomile flower. In 2016, there was a first report of hepatotoxicity requiring transplant (and found to be a “probable” association with the supplement) in a 37-year-old man who had been on STW-5 for 2 weeks.

Copper deficiency can cause a microcytic anemia and a rare myeloneuropathy, and has been reported to occur in patients with celiac disease at rates that vary between 6-33%.

persistent nausea and vomiting following weight loss surgery is the classic setting for thiamine deficiency, referred to as “bariatric beriberi.” The patient may deteriorate further if he does not receive thiamine replacement prior to concurrently with any glucose infusion.

persistent nausea and vomiting following weight loss surgery is the classic setting for thiamine deficiency, referred to as “bariatric beriberi.” The patient may deteriorate further if he does not receive thiamine replacement prior to concurrently with any glucose infusion.

In cirrhosis – encephalopathy Mimic is vitamin E deficiency.
When vitamin E (tocopherol) is deficient, patients can present with classic symptoms of ataxia and gait disturbance. These patients can also have peripheral neuropathy and hyporeflexia, which can also suggest hepatic encephalopathy. For this reason, it is especially important to check levels of vitamin E when you encounter neurologic symptoms in a patient with cholestatic liver disease – and not just assume that they are caused by encephalopathy. Fat soluble vitamins are often deficient in cholestatic diseases.

Mucinous cystic neoplasms (MCNs) have 3 classic features: (1) they occur almost exclusively in women; (2) they are almost always located in the body or tail of the pancreas; and (3) they are single cysts. Like IPMNs, they classically have a high cyst fluid CEA (>192 ng/mL), and have mucin on cytology. Unlike branch-duct IPMNs, there is no communication, or connection, between the cyst and the main pancreatic duct. Similar to IPMNs, they may have a mutation in the KRAS gene, but do not have a mutation in GNAS, which is only seen in IPMNs. The absence of communication between the cyst and the main pancreatic duct, and absence of a GNAS mutation, are used to differentiate IPMNs from MCNs.

DIOS. GI findings, including constipation, in the cystic fibrosis (CF) population are common. Distal intestinal obstruction syndrome (DIOS) is characterized by partial or complete obstruction due to fecal material in the ileocecal/right colon region. Differentiating DIOS from constipation can be difficult but DIOS is more often associated with acute obstruction involving the ileocecal area whereas constipation is more gradual with stool burden throughout the colon. Risk factors for DIOS include genotype, pancreatic insufficiency and prior episodes of DIOS. The differential diagnosis for DIOS includes appendicitis, volvulus, and intussusception.

propranolol is a well-described cause of osmotic diarrhea, and highlights the need to consider commonly prescribed drugs which might prompt consistent change in bowel habits. The other listed choices are associated with predominantly inflammatory diarrhea (NSAIDs), constipation (butalbital-acetaminophen-caffeine combination), or no predictable effect (rizatriptan).

Balloon hyperinflation has recently been described as a rare complication of saline-filled IGBs. It could lead to compression of surrounding organs including the pancreas. Antacid therapy may be associated with IGB bacterial and fungal overgrowth that could lead to overgrowth of gas-forming organisms inside the gastric balloon.

This is a patient with eosinophilic gastroenteritis (EGE), a rare inflammatory gastrointestinal disorder. There are several proposed management options, although most have not been studied extensively due to the rarity of this condition. Specialized diets are one of the most effective treatment options, and include an elemental diet that can induce remission in the majority of patients with EGE. A 6-food elimination diet is easier to adhere to and may be effective as well for maintenance. Systemic steroids are also effective at induction, but should be tapered after 6-8 weeks and would not be a good option for long-term treatment due to side effects.

Heat stroke can cause abnormal LFT

Obese women more likely to get diverticulitis

Repeat diverticulitis unusual

Small duct pancreatitis -no calcification, (alcohol causes large duct), less likely to have secretin positive test

Hp can cause ITP

Air in portal vein – ischemic bowel

Colon ischemia – rule out Factor V leyden

Low Mg can cause seizure

Mesalamine causes pancreatitis

MYH is AR (recessive)

Migraine and cyclical vomiting commonly associated

Hp and NSAID are additive

Young patient less than 40 with iron def, more likely to have Small bowel polyps, lymphoma and carcinoids

Biliary colic recurrence is more than 20% but recurrent cholecystitis is less common

Pregnant woman viral hepatitis is still the most common

To change TPMT pathway, use lower dose of allopurinol

Post cholecystectomy, higher change of right colon cancer

Onion skinning on liver biopsy – small vessel PSC

Wilsons disease look at urine total copper not copper concentration

Class. B esophagitis – continue PPI

Acute caustic ingestion – check airway also

Mirizzis syndrme – no pancreatitis

Hemodialysis – Hep b vaccination is not very effective

Beta blocker plus banding better for secondary prophylaxis

AIP – neurological problems (porphyria). Rx Haemin

High TG from – beta blocker, thiazides, vitamin A and alcohol

Mallory bodies in NASH, amiodarone, alcohol, jejunal bypass

RF from DILI – alcohol, female, age more than 60 and prior DILI

Insulinomas are usually sporadic not part of MEN, rx surgery

HFE patients die from HCC

IV contrast dye – do not use gastrograffin

OWR- usually bleeding before 40, no AVM in colon, can cause liver problems

Best treatment for gastroparesis – strict sugar control

Malnutrition and oxalate stones require more than 100 cm of TI removed

GIST CD117 and CD3

LNs and small bowel inflammation – anthrax

Failure of HBV immunization -Hep b s Ag positive

Autosomal dominant disorder
Lifetime CRC risk of about 50% to 80%
Early development of CRC (average 44 years)
CRC predominantly locates proximal to the splenic flexure
Germline mutation in one of several DNA mismatch repair genes (90% have mutations in the MLH1 or MSH2 genes)
Microsatellite instability (MSI) is found in 90% of tumors from patients with HNPCC syndrome (versus in only 15% of sporadic CRCs)
Low levels of expression of the protein products of the MLH1 or MSH2 genes
Histologically, cancers are often poorly differentiated, mucinous, and have large numbers of tumor-infiltrating lymphocytes
Extracolonic cancers:
Small bowel
Hepatobiliary tract
Upper uroepithelial tract
Brain (Turcot variant)
Sebaceous adenomas/carcinomas (Muir-Torre variant)

Polyp recurrence of large polyps

The Sydney EMR recurrence tool (SERT) can be used to risk stratify large laterally spreading lesions for risk of adenoma recurrence after piecemeal EMR. The clinical tool incorporates three factors and assigns a score to each risk factor:

Risk Factor Score
LSL Size >=40 2
Intraprocedural bleeding 1
High-grade dysplasia 1
Total 4

In the study by Tate et al, a lesion with a SERT score of 0 (no identified risk factors) had an incidence of endoscopically detected recurrence (EDR) of 8.7% and of histologically detected recurrence (HDR) of 8.0% at four- to five-month follow-up colonoscopy, versus an EDR of 25.9% and HDR of 30.6% for lesions with SERT scores 1-4.

Management options for large flat lesions
• Surgery: Until recently, the only curative therapy for large (>20 mm) laterally spreading sessile colon adenomas was surgery.
• EMR: EMR (Figures 2 and 3, Video 2) gained widespread acceptance and has become the main treatment option. However, risks include incomplete removal and local recurrence with EMR. Ideally, all adenomatous tissues should be removed during the initial EMR.
• ESD: ESD adopts the surgical principle of en bloc resection of the neoplasms. Although ESD has not been widely adopted in the West, endoscopists in Japan have embraced this technique for more than 10 years. Recently, Saito et al reported their single-center experience on the outcomes and adverse events with colonic EMR (n = 228) versus ESD (n = 145). They found that ESD provided a higher en bloc resection rate (84% versus 33%, P < .0001), less tumor recurrence (2% versus 14%, P < .0001), higher perforation risk (6.2% versus 1.3%, P = NS), and a similar risk of delayed bleeding (1.4% versus 3.1%, P = NS). Besides the higher perforation risk, ESD requires special endoscopic skills and is time-consuming.

In irritable pouch syndrome, patients have symptoms of pouchitis, but no endoscopic or histologic evidence of inflammation. The syndrome is characterized by presence of visceral hypersensitivity. Pouchoscopy, therefore, helps differentiate pouchitis and irritable pouch syndrome, though other entities should be considered prior to making this functional diagnosis including celiac disease, lactose intolerance, and small bowel bacterial overgrowth.

• Familial Adenomatous Polyposis. Caused by germline pathogenic variants in the APC gene; associated with increased risk for colon, small bowel, and thyroid cancer, colon polyps, and extracolonic physical features.
• Hereditary Breast and Ovarian Cancer. Caused by germline pathogenic variants in the BRCA1 and BRCA2 genes; associated with increased risk for breast, ovarian, pancreatic, and prostate cancer, as well as melanoma (hence answer B is incorrect).
• Familial Multiple Mole Melanoma-Pancreatic Cancer syndrome. Caused by germline pathogenic variants in the CDK4 and CDKN2A genes; associated with increased risk for melanoma and pancreatic cancer (the patient described in answer option C).
• Lynch syndrome. Caused by germline pathogenic variants in the MLH1, MSH2, MSH6, PM2S, and EPCAM genes; mainly associated with an increased risk for colon and endometrial cancer.
• Peutz-Jeghers syndrome. Caused by germline pathogenic variants in the STK11 genes; mainly associated with increased risks for breast, colon, stomach, ovarian, and pancreatic cancer.
• Li-Fraumeni syndrome. Caused by germline pathogenic variants in the TP53 gene; core cancers include premenopausal breast cancer, sarcomas, adrenocortical carcinomas, and brain tumors.
• Mutations in the ATM or PALB2 genes. (Moderate penetrance genes); associated with increased risks for breast, ovarian, and pancreatic cancers.
• Hereditary pancreatitis due to mutations in PRSS1.
• Familial pancreatic cancer. Defined as a familial with at least two first-degree relatives with pancreatic cancer, which does not fulfill the diagnostic criteria for an inherited tumor syndrome. (the patient described in answer option A).

LVAD bleed from lowering of von Willebrand factor . Rx is thalidomide

This can be done by giving fresh frozen plasma and/or intravenous vitamin K or prothrombin protein concentrates (PCC). The current recommendation is to use PCC if rapid reversal is needed as this is the most effective treatment and has a low associated volume. FFP has relatively high volume, which can cause volume overload and pulmonary edema in a heart failure patient. In patients with valvular heart disease, vitamin K is not recommended as it can cause a hypercoagulable state.

When vitamin E (tocopherol) is deficient, patients can present with classic symptoms of ataxia and gait disturbance. These patients can also have peripheral neuropathy and hyporeflexia, which can also suggest hepatic encephalopathy. For this reason, it is especially important to check levels of vitamin E when you encounter neurologic symptoms in a patient with cholestatic liver disease – and not just assume that they are caused by encephalopathy. Fat soluble vitamins are often deficient in cholestatic diseases.

Risk in Investigational Treatment Group: 30/1000 = 0.03
Risk in Placebo Group: 150/3000 = 0.05
Absolute Risk Reduction: Absolute Value of Risk in Investigational Treatment Group – Risk in Placebo Group = | 0.03 – 0.05 | = | – 0.02 | = 0.02.
Number Needed to Treat: 1 / Absolute Risk Reduction = 1 / 0.02 = 50.

Budesonide requires dose reduction in Childs B cirrhosis and should not be prescribed in Child’s C cirrhotics due to impaired first pass metabolism and increased systemic exposure

This is pyoderma gangrenosum. While numerous immunosuppressives are useful for treatment, the patient cannot tolerate further infliximab based on severe infusion reaction. Most consider systemic steroids as a first-line therapy.

Baseline, 6 month and annual screening after bariatric surgery
Nutrient Biomarker(s) Primary symptoms of deficiency
Vitamin B1 Serum thiamin Ophthalmoplegia, nystagmus, ataxia, encephalopathy, rapid visual loss (Wernicke encephalopathy)
Isolated peripheral neuropathy
Vitamin B12 Serum vitamin B12 Anemia, neurological dysfunction, visual loss
Folate Red blood cell folate
Consider plasma homocysteine Anemia
Iron Serum, ferritin, total iron binding capacity, complete blood count with differential Microcytic anemia
Vitamin D Serum 25(OH) vitamin D, calcium, phosphorus, parathyroid hormone Decreased bone mineral density
Secondary hyperparathyroidism
Protein Serum albumin Edema, excessive alopecia, poor wound- healing
Additional annual screening after BPD and BPD-DS
Vitamin A Plasma retinol Reduced night vision, visual impairment
Vitamin E Plasma alpha-tocopherol Neuropathy, ataxia
Vitamin K Prothrombin time Bleeding, easy bruising
Screen after any bariatric procedure if suggestive symptoms
B6 (pyridoxine) Plasma pyridoxal-5′-phosphate Anemia, neurological symptoms
Copper Serum copper Anemia, neuropathy
Zinc Plasma zinc Acrodermatitis enteropathica-like rash, taste alterations
General supplementation recommendations
Supplement Daily Recommendations
Multivitamin (contains folic acid) AGB/VSG
BPD-DS One daily
One to two daily
Two daily
Calcium citrate with vitamin D3 AGB
RYGB and BPD-DS 1200–1500mg/day
1800 mg/day
Vitamin D3 RYGB
BPD-DS consider 1000 IU/day
2000 IU/day
Vitamin B12 RYGB

BPD-DS crystalline 500 μg/day oral or 1000 μg/month
monitor and start if needed.
Elemental iron RYGB and BDP-DS 65 mg elemental iron in menstruating females
Vitamin B1 All procedures consider once daily in first 6 months
Vitamin A, K BPD-DS 10,000 IU vitamin A and 300 μg/vitamin K

The course and outcome are compatible with severe cholestatic hepatitis with partial vanishing bile duct syndrome (VBDS). The most predictive factor of poor outcome was the degree of bile duct loss on liver biopsy. Bile duct loss during acute cholestatic hepatitis is an ominous early indicator of possible VBDS, for which at present there are no known means of prevention or therapy. Pseudoxanthomatous change and copper accumulation are seen with chronic cholestasis. The presence of fibrosis may be indicative of underlying chronic liver disease with early fibrosis but is not predictive of outcome.

The Advisory Committee on Immunization Practices (ACIP) recommends the use of hepatitis B vaccination for all unvaccinated adults aged 19-59 years upon diagnosis with type 1 or type 2 diabetes mellitus, in whom an increased risk for acute hepatitis B has been reported by the Centers for Disease Control and Prevention (CDC). Unvaccinated adults age 60 years or older may be vaccinated at the discretion of the treating physician after individualized assessment of the risk and likelihood of mounting an adequate immune response to HBV vaccination.

Asian American patients, HBeAg positive or negative, with HBV DNA levels >2,000 IU/mL (>104 copies/mL) and ALT values above normal are candidates for anti-viral therapy. HBeAg negative patients with HBV DNA >2,000 IU/mL and normal ALT levels but who have either serum albumin <3.5 g/dL or platelet count <130,000 mm3, basal core promoter (BCP) mutations, or who have first-degree relatives with HCC should be offered treatment

HEllP complication hepatic infarct or rupture. This woman has HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome with hepatic complications. Hepatic infarct, hematoma, and rupture are all associated with HELLP. Cross-sectional imaging is indicated when ALT or AST is >1,000 U/L or abdominal pain radiates to the right shoulder. CT and MRI could be considered. Most hematomas require only supportive management unless enlarging at which time surgery or embolization is indicated.

This patient is presenting with acute esophageal necrosis (AEN), also known as black esophagus. AEN presents with characteristic circumferential black appearance of the esophagus, involving the distal esophagus and stopping abruptly at the gastroesophageal junction. Extension into proximal esophagus is also seen. AEN occurs in the setting of ischemia in addition to acid reflux. Also, it has been described in the setting of infection, antibiotic use, gastric volvulus, diabetic ketoacidosis, and aortic dissection. Management is supportive and involves control of underlying etiology, aggressive hydration, and intravenous proton pump inhibitors. Oral intake should be avoided initially and nasogastric tubes (NGT) should be withheld to avoid further damage.

There are two types of esophageal strictures:
• Refractory esophageal stricture is defined as one in which there is an inability to successfully remediate the anatomic problem to a diameter of 14 mm over five sessions at 2-week intervals.
• Recurrent esophageal stricture is defined as one in which there is an inability to maintain a satisfactory luminal diameter for four weeks once the target diameter of 14 mm has been achieved.
The etiology of most refractory strictures includes the following:
• Radiation therapy
• Caustic ingestion
• Surgical anastomoses
The following endoscopic options could be used in patients who fail to respond to balloon or bougie dilation of refractory esophageal strictures:
• Intralesional injection of steroids or mitomycin C followed by dilation.
• Short refractory strictures (anastomotic strictures and Schatzki rings) could be managed by endoscopic incision with a needle-knife or endoscopic scissors.
• Long refractory strictures could be managed with the insertion of self-expanding metal or plastic stents, but results are mixed, and this should be approached with caution, especially in patients with history of radiation. Self-dilation is also considered an option.
Metallic stent placement for benign refractory strictures has disappointing results and is not typically recommended. Long-term clinical resolution of the stricture with self-expandable metal stents is achieved in less than 50% of patients. SEMS placement is associated with complications including migration, bleeding, fistula, erosion into vital structures, recurrent strictures and death.

• Non-dysplastic Barrett’s esophagus: Surveillance endoscopy every 3 – 5 years
• Low-grade dysplasia: Esophagogastroduodenoscopy every year until no more low-grade dysplasia x 2 or consider endoscopic ablation. If visible lesion is present, endoscopic mucosal resection (EMR) should be performed first.
• High-grade dysplasia: EMR of nodule followed by endoscopic ablation of the remainder of Barrett’s esophagus.
• T1a (intramucosal cancer): EMR of nodular cancer followed by endoscopic ablation of the remainder of Barrett’s esophagus.
• T1b adenocarcinoma: Referral to surgeon for esophagectomy.

The diagnosis of infectious esophagitis is made through endoscopic-guided biopsy. HSV usually occurs in the first 4 weeks after transplant, whereas CMV incidence peaks four to six months after transplant. HSV ulcers classically are well-circumscribed and crater-like with intervening normal mucosa, but often can have exudates, plaques, or a diffuse erosive esophagitis. CMV typically presents as deep linear ulcers. Biopsy specimens for HSV should be obtained from the edge of the ulcer because it localizes in the squamous epithelium, whereas CMV yield is best obtained from the ulcer base. Immunohistochemical stains, viral culture, and polymerase chain reaction on biopsy specimens may improve biopsy yield.

This patient presents with typical findings of esophageal intramural pseudodiverticulosis (EIPD). EIPD is a rare condition affecting predominately older individuals in the sixth and seventh decades of life. It is believed to be more common in patients with diabetes, alcohol use, liver disease, or malnutrition. The typical presentation is a patient with GERD and associated dysphagia or chest pain, and endoscopic findings may reveal multi-focal outpouchings of the esophageal wall. These pseudodiverticula are epithelium-lined cystic dilations of excretory elements in submucosal glands. 80%-90% of patients will develop esophageal strictures, most commonly in the distal esophagus. Esophagogastroduodenoscopy is typically the first line test, but findings can be subtle and often are better highlighted with a barium esophagram (Figure 3). These patients are at risk of pulmonary abscess and bronchoesophageal fistula formation. Treatment is with optimal management of underlying conditions, such as GERD and Candida esophagitis. Endoscopic dilation is recommended for associated strictures.

This patient has evidence of dermatomyositis as characterized by progressive myopathy, the ‘shawl’ sign (new V-shaped rash on her back), and Gottron papules (violaceous plaques on distal interphalangeal joints). She presents with progressive dysphagia, reflux, and weight loss as well. Recognizing that dermatomyositis affects predominantly skeletal muscle, this patient would have weak peristalsis in the proximal one-third of the esophagus that consists of skeletal muscle on esophageal manometry.

After successful endoscopic ablation, surveillance endoscopy with biopsy should be performed every 3 to 6 months during the first two years, and the surveillance interval can be increased afterward. Recent guidelines recommend endoscopic surveillance every three months during the first year after completion of therapy, every six months during the second year of therapy, and annually thereafter. Long-term follow-up of patients enrolled in a sham-controlled dysplasia trial (AIM dysplasia trial) for radiofrequency ablation (RFA) of non-nodular dysplastic Barrett’s esophagus reported a 32% recurrence of BE and a 17% recurrence of dysplasia after a mean follow-up of 3.6 years per patient. Recurrence of dysplasia was higher in the first year after completion of therapy.

Intestinal metaplasia of the GE junction is a distinct entity from Barrett’s esophagus and is associated with a much lower risk of cancer. Intestinal metaplasia in the cardia can be difficult to distinguish based on histopathological evaluation. Barrett’s esophagus requires both an endoscopic appearance of pink salmon-colored mucosa (columnar-lined esophagus) and intestinal metaplasia on histopathology. In this patient, the z-line appeared regular; therefore, the biopsies represent intestinal metaplasia of the cardia. Current guidelines do not recommend surveillance endoscopies for intestinal metaplasia of the cardia.

Alkali causes damage to the esophagus by liquefactive necrosis, whereas acid ingestion affects the stomach more with a coagulative necrosis. Patients usually present with oropharyngeal pain, chest pain, epigastric discomfort, and dysphagia. Hoarseness, stridor, or shortness of breath suggests injury to the epiglottis, larynx, or airway.

nclusion criteria include:
• Diagnosis of CCA by brush cytology or intraductal biopsy
• CA19-9 >100 mg/ml and a mass on cross-sectional imaging/cholangiogram
• Aneuploidy on FISH testing
• Unresectable tumor above the cystic duct
• Resectable CCA in the setting of PSC
• Tumor < 3 cm in diameter
• Absence of intra- and extra-hepatic metastases
• Candidate for liver transplantation

Biliary anastomotic strictures are common after liver transplantation, occurring in 10-15% of cases and typically present several months after surgery. The etiology is usually technical, but can also reflect an ischemic injury. The biliary tree is supplied by the hepatic artery, so any interruption can lead to stricturing. In addition, a leak at the biliary anastomosis is strongly associated with the subsequent development of a stricture. Presentation can often be asymptomatic and is usually suggested by cholestatic liver enzymes. Jaundice is rarely a presenting feature and ductal dilation can be absent initially.

Duodenal varices. Bleeding from duodenal (ectopic) varices occurs infrequently, but is a potentially fatal condition. Duodenal variceal bleeding accounts for 0.4% of all variceal bleeding encountered by gastroenterologists, but the mortality can be up to 40%. The etiology of duodenal varices can be divided into that from intrahepatic portal hypertension (cirrhosis) and that from extrahepatic portal hypertension. Knowing the cause of the formation of duodenal varices is important to access the potential outcome of the bleeding and optimal management of the patient. An attempt at endoscopic treatment of these duodenal varices is warranted, although such treatment often does not have durable success.

Ischemic cholangiopathy occurs after liver transplantation in two main situations: use of a DCD liver or after a hepatic artery thrombosis. Due to the donor organ shortage, the use of DCD organs is fairly common in the United States and the outcome is generally good, particularly when young (age <40 years) donors are used. The biliary tree relies on hepatic arterial supply and is very susceptible to ischemic injury which can occur after the donor heart stops beating, or related to hepatic artery thrombosis.

In untreated cirrhotic patients with PVT, imaging follow-up every three months is recommended. Anticoagulation is recommended in case of progression.

PSC patients get hepaticojejunostomy with OLT.
This young man has developed significant gastrointestinal bleeding after a recent liver transplant. The most likely diagnosis is bleeding from the entero-enteric anastomosis of the Roux limb. The clue is in the etiology of the liver disease. He has PSC, and so a duct-to-duct biliary anastomosis is not always an option if the PSC affects the extra-hepatic bile duct. Even if the extra-hepatic duct is normal, some surgeons will always perform a Roux-en-Y hepaticojejunostomy because of the very small risk of cholangiocarcinoma in the remnant recipient duct.

Bleeding from the Roux limb can occur in up to 5% of cases post liver transplantation. It typically occurs in the early phase after transplant at the staple line of the biliary anastomosis, and can lead to significant morbidity and risk of graft loss. It can present a difficult management problem for the gastroenterologist. Accessing the limb will not be possible with a standard gastroscope, and may not be possible at all if the entero-enteric anastomosis is very distal in the jejunum. Gastroenterologists should use a pediatric colonoscope to try and access the Roux limb. Another approach is to use a single or double balloon enteroscope to prevent coiling of the scope and allow deeper access. It is important to identify hemostatic instruments of appropriate length and diameter that will fit the working channel of the chosen scope, such as endoscopic clips or cautery probes.

GAVE cause GAVE may present with iron deficiency anemia in a subset of females > 40 years of age. It occurs in the antrum with characteristic linear strips radiating out from the pylorus, and is also called watermelon stomach. It can be seen in the setting of collagen vascular disease. The pathophysiology of GAVE is idiopathic. One of the hypotheses for the etiology of GAVE is that it is a disorder of peristalsis leading to distal gastric mucosa prolapse through the pylorus resulting in the formation of ectatic vessels. Treatment is usually with the use of argon plasma coagulation over multiple sessions. Medical therapy with estrogen and progesterone, proton pump inhibitors, or octreotide is not nearly as effective. At times, it may be difficult to differentiate GAVE from portal hypertensive gastropathy. The latter is not likely in this patient without known liver disease.

Blakemore details
The Sengstaken Blakemore tube is a balloon tamponade that consists of gastric and esophageal balloons (see Figure 1). The patient is usually endotracheally intubated and placed supine with the head at 45 degrees. Balloons are checked for leaks and compliance prior to insertion. The tube is then inserted via the nose or mouth and correct position is confirmed with a chest X-ray showing the gastric balloon in the stomach. The gastric balloon is inflated using 50 ml increments up to 250-300 ml. The balloon is pulled up against the gastric fundus and then secured to a traction device, such as a 500 ml bag of intravenous fluids. Inflation of the esophageal balloon is not performed unless esophageal variceal bleeding appears refractory to inflation of the gastric balloon. Some tubes have a middle port which allows aspiration from the esophagus; otherwise, a second orogastric tube can be placed through the mouth into the esophagus to allow aspiration of blood for assessment of cessation of bleeding. Major complications associated with a SBT are aspiration and esophageal perforation or rupture. Minor complications include pain, pressure necrosis of the nose, and pharyngeal and esophageal ulcerations. Balloon tamponade is only a temporary measure and should not be used for over 24 hours. A recent development has been the use of self-expanding metal stent for variceal tamponade. A recent randomized control trial compared the placement of a self-expanding metal stent versus a Sengstaken Blakemore tube and found stenting to be as effective as the tube with less side effects and morbidity.

Retained material of cyanoacrylate could be the potential cause of her recurrent fever. Retained material may act as infective foci with subsequent cast breakdown, intermittently releasing colonized microbes into the bloodstream. Embolized glue may persist beyond 24 weeks and cause recurrent infection, which may necessitate the need for prolonged antibiotics. FEVER FROM GLUE

Infectious proctitis and enteritis due to chlamydia, syphilis, gonorrhea, giardia, and cryptosporidium may be differentiated from one another, as well as inflammatory and functional bowel disease by clinical presentation, histology, and appropriate laboratory tests. Awareness of their distinct features avoids missed and incorrect diagnosis.

Pouchitis treatment. Some patients may require long-term maintenance therapy. Probiotics and continuous antibiotics may be effective maintenance therapy in cases of chronic pouchitis. Cases of chronic pouchitis may be antibiotic-dependent or refractory. However, in antibiotic refractory cases, 5-ASA therapy, topical steroids, topical tacrolimus, or anti-tumor necrosis factor (TNF) therapy may be effective. Anti-TNF therapy is the most effective option in antibiotic-refractory pouchitis. Where medical therapy fails, surgical intervention with diverting ileostomy or pouch resection may be necessary.

he US Multi Society Task Force on Colorectal Cancer (CRC) recently published updated guidelines on colonoscopy surveillance after cancer resection:
• Patients with CRC should undergo a high-quality perioperative clearing with colonoscopy to evaluate for synchronous lesions. The procedure should be performed preoperatively, or within a 3- to 6-month interval after surgery in the case of obstructive CRC. (strong recommendation, low-quality evidence)
• Patients who have undergone curative resection of either colon or rectal cancer receive their first surveillance colonoscopy after one year (either one year after surgery or one year after the clearing perioperative colonoscopy). (strong recommendation, low-quality evidence)
• After the 1-year colonoscopy, the interval to the next colonoscopy should be three years (ie, four years after surgery or perioperative colonoscopy) and then five years (ie, nine years after surgery or perioperative colonoscopy). Subsequent colonoscopies should occur at 5-year intervals until the benefit of continued surveillance is outweighed by diminishing life expectancy. If neoplastic polyps are detected, the intervals between colonoscopies should be in accordance with published guidelines for polyp surveillance intervals. These intervals do not apply to patients with Lynch syndrome. (strong recommendation, low-quality evidence)
• Patients with obstructive CRC precluding complete colonoscopy, the USMSTF recommends CTC as the best alternative to exclude synchronous neoplasms. Double-contrast barium enema is an acceptable alternative if computed tomographic colonography (CTC) is not available. (strong recommendation, moderate-quality evidence)
• Patients with localized rectal cancer who have undergone surgery without total mesorectal excision, those who have undergone transanal local excision (ie, transanal excision or transanal endoscopic microsurgery), or endoscopic submucosal dissection, and those with locally advanced rectal cancer who did not receive neoadjuvant chemoradiation and then surgery using total mesorectal excision techniques, are at increased risk for local recurrence. In these situations, the US Multi-Society Task Force suggests local surveillance with flexible sigmoidoscopy or endoscopic ultrasound every three-to-six months for the first two-to-three years after surgery. These surveillance measures are in addition to recommended colonoscopic surveillance for metachronous neoplasia. (weak recommendation, low-quality evidence)

UC dysplasia This patient has a raised, endoscopically visible dysplastic lesion (previously referred to as dysplasia-associated lesion or mass). It should be removed endoscopically and the surrounding mucosa should be sampled to ensure that the margins do not have flat or invisible dysplasia. It is also now generally accepted that patients who undergo complete resection of a visible dysplastic lesion with low-grade dysplasia do not require colectomy, provided there are no areas of endoscopically invisible dysplasia. Tattooing will aid in subsequent surveillance and/or resection.

Hemorrhoid management.

Based on the degree of prolapse, internal hemorrhoids can be classified in four grades/degrees:

Grade I (Video 4) Bleed, but do not prolapse.
Grade II (Video 1) Prolapse, but spontaneously reduce.
Grade III Prolapse and require manual reduction.
Grade IV (Video 3) Prolapse, but cannot be reduced.

Non-surgical management of internal hemorrhoids:
Non-surgical management of internal hemorrhoids include the following:
• Sclerotherapy
• Rubber-band ligation
• Infrared photocoagulation
• Electrocoagulation
• Cryotherapy
• Low-voltage direct current
Sclerotherapy is effective for first- and second-degree hemorrhoids, although rare adverse events including mucosal necrosis, abscess, prostatitis, erectile dysfunction, and portal pyemia have been reported.

Rubber-band ligation is an effective procedure and can be performed with either flexible or rigid endoscopes. In a study of 45 patients with chronic rectal bleeding secondary to second- and third-degree internal hemorrhoids randomized to RBL or bipolar coagulation therapy, success was higher with RBL (92% vs 62%, P < .05) with a similar safety profile. Experts caution against RBL of internal hemorrhoids in sedated patients because significant pain can occur with errant band placement too close to or below the dentate line. Usually, no more than three hemorrhoidal groups are banded in one session, although some experts advocate placing only one band at a time to minimize symptoms. Hemorrhoidal disease requiring the placement of four or more bands was associated with a trend toward higher failure rates and a greater need for subsequent operative hemorrhoidectomy. After RBL, the rectal bleeding and symptoms resolved in this patient, along with improved endoscopic findings during follow-up sigmoidoscopy (Figure 5, Video 5).

Contraindications to endoscopic therapy:
The contraindications to endoscopic treatment of internal hemorrhoids include the following:
• Acute thrombosis
• Severe, pre-existing rectal pain
• Portal hypertension
• Coagulopathy/thrombocytopenia
• Anorectal inflammatory bowel disease
• Rectal prolapse
• Grade IV hemorrhoids
• Immunodeficiency

Features of chronic radiation proctopathy include the following:
• They occur from 9 months to 30 years (typically within two years) after pelvic radiation.
• Symptoms may include hematochezia, tenesmus, diarrhea, and defecatory urgency.
• Endoscopic findings range from diffuse, friable angioectatic lesions to frank ulceration.
• A majority (95%) of the cases are mild and temporary, and require no therapy.
• Up to 5% of patients are refractory to conservative management.
• Treatment of radiation proctopathy that is found incidentally on endoscopy is not usually indicated.

APC for angioectasia. In patients with anemia or history of gastrointestinal bleeding, angioectasia in the gut should be ablated. A single session of argon plasma coagulation (APC) at 20 W and a 0.8 L/min flow rate will be sufficient to ablate the cecal angioectasia (Video 2). Submucosal injection of saline solution before APC has been shown to decrease the risk of deeper thermal injury to the cecum in experimental studies. For large vascular lesions (>10 mm) in the right side of the colon, it may be safer to inject saline solution submucosally before APC ablation. Mechanical hemostasis with endoscopic clips can also be utilized and avoids the potential transmural injury that can occur with thermal therapy. There are currently no comparative trials between thermal therapy and endoscopic clips for the management of bleeding colonic angioectasias. Injection of epinephrine is not appropriate in this situation since it will not provide durable hemostasis. Angioembolization has a very limited role in this situation.

Endoscopic balloon dilation has been shown to be effective in the treatment of strictures resulting from both surgical anastomoses and inflammatory bowel disease. TTS balloons can be used for dilations from 8 mm to 20 mm, based on stricture size. Balloon inflation can be performed once or twice for one minute, with a resting interval of 30 seconds between inflations. Success is defined as an anastomotic lumen wide enough to allow passage of a standard 13-mm-diameter colonoscope, with resolution of symptoms. With balloon dilators, the entire dilating force is delivered radially and over the entire length of the stricture, thereby significantly reducing shear stress. Poor candidates for endoscopic dilation include patients with ischemic strictures and Crohn’s disease with deep ulcers or fistulas.

HNPCC has the following features:
• Autosomal dominant disorder
• Lifetime CRC risk of about 50% to 80%
• Early development of CRC (average 44 years)
• CRC predominantly locates proximal to the splenic flexure
• Germline mutation in one of several DNA mismatch repair genes (90% have mutations in the MLH1 or MSH2 genes)
• Microsatellite instability (MSI) is found in 90% of tumors from patients with HNPCC syndrome (versus in only 15% of sporadic CRCs)
• Low levels of expression of the protein products of the MLH1 or MSH2 genes
• Histologically, cancers are often poorly differentiated, mucinous, and have large numbers of tumor-infiltrating lymphocytes
• Extracolonic cancers:
o Endometrium
o Ovary
o Stomach
o Small bowel
o Hepatobiliary tract
o Upper uroepithelial tract
o Brain (Turcot variant)
o Sebaceous adenomas/carcinomas (Muir-Torre variant)

Amsterdam II criteria
• At least three relatives with any LS-associated cancer.
• One should be a first-degree relative of the other two.
• At least two successive generations should be affected.
• At least one should be diagnosed before age 50.
• FAP should be excluded in the CRC case(s).
• Tumors should be verified by pathological examination.
Genetic testing

Currently, microsatellite instability (MSI) testing and immunohistochemical staining for MLH1 and MSH2 gene products on CRC tissue are recommended for screening patients clinically suspected to have HNPCC. The finding of MSI and low-gene protein expression in a tumor should then prompt genetic testing of the affected individual for germline mutations in the mismatch repair genes. If a mutation is identified, the first-degree relatives should then undergo genetic testing. If tumor tissue is not available, genetic testing should be performed in the affected individual. Genetic testing should be done along with expert genetic counseling.

The most appropriate step for removal of this large polyp is epinephrine injection into the stalk and head of the polyp; resect it on withdrawal from cecum. Large colon polyps (>3 cm) on a stalk can pose difficult challenges for the endoscopist. Due to the size of the polyp, it is often difficult to visualize the full extent of the lesion to facilitate polypectomy.

SRUS. SRUS is a disorder of defecation, typically affecting young adults. Possible contributing factors in SRUS include overt or occult mucosal prolapse, paradoxical pelvic floor muscle contraction during defecation, rectal hypersensitivity causing sensation of incomplete evacuation, and repeat straining. These factors produce increased rectal pressures with resultant rectal mucosa trauma. Despite its name, solitary ulceration is a less common manifestation than alternative pathology that may be identified endoscopically, including mucosal hyperemia, presence of a broad polypoid mass, or development of multiple ulcers. The polypoid variant is present in up to 32% of patients.

The Sydney EMR recurrence tool (SERT) can be used to risk stratify large laterally spreading lesions for risk of adenoma recurrence after piecemeal EMR. The clinical tool incorporates three factors and assigns a score to each risk factor:

Risk Factor Score
LSL Size >=40 2
Intraprocedural bleeding 1
High-grade dysplasia 1
Total 4

In the study by Tate et al, a lesion with a SERT score of 0 (no identified risk factors) had an incidence of endoscopically detected recurrence (EDR) of 8.7% and of histologically detected recurrence (HDR) of 8.0% at four- to five-month follow-up colonoscopy, versus an EDR of 25.9% and HDR of 30.6% for lesions with SERT scores 1-4.

Management options for large flat lesions
• Surgery: Until recently, the only curative therapy for large (>20 mm) laterally spreading sessile colon adenomas was surgery.
• EMR: EMR (Figures 2 and 3, Video 2) gained widespread acceptance and has become the main treatment option. However, risks include incomplete removal and local recurrence with EMR. Ideally, all adenomatous tissues should be removed during the initial EMR.
• ESD: ESD adopts the surgical principle of en bloc resection of the neoplasms. Although ESD has not been widely adopted in the West, endoscopists in Japan have embraced this technique for more than 10 years. Recently, Saito et al reported their single-center experience on the outcomes and adverse events with colonic EMR (n = 228) versus ESD (n = 145). They found that ESD provided a higher en bloc resection rate (84% versus 33%, P < .0001), less tumor recurrence (2% versus 14%, P < .0001), higher perforation risk (6.2% versus 1.3%, P = NS), and a similar risk of delayed bleeding (1.4% versus 3.1%, P = NS). Besides the higher perforation risk, ESD requires special endoscopic skills and is time-consuming.

Management of Rectal Carcinoid Tumors:

• Small rectal carcinoid tumors (<1 cm): As in this case, most small rectal carcinoid tumors are found incidentally during routine screening or surveillance colonoscopy or when unrelated lower gastrointestinal symptoms are investigated. There are data to support the recommendation for local surgical or endoscopic excision of small (<1 cm) rectal carcinoids given the low rate of metastatic spread. Endoscopic treatment is sufficient for tumors that are small, for tumors limited to the submucosa, and when the margin is negative for tumor. Transanal excision (TAE) should be considered when margins of endoscopic resection are positive. Endoscopic ultrasonography may be useful in determining whether lesions can be removed endoscopically; however, histopathological confirmation of complete resection is essential. Repeat sigmoidoscopy and/or endoscopic ultrasonography are not indicated when complete excision can be demonstrated on histopathological review of the endoscopic specimen. Similarly, surgical excision of the area or lymph node sampling is not useful. Radionuclide scanning for metastatic disease is not indicated in sub-centimeter rectal carcinoid due to the extremely low yield. • Rectal carcinoid tumors (11-19 mm): The management of these intermediate-sized lesions is somewhat controversial. EUS or endorectal magentic resonance imaging (MRI) should be performed for locoregional staging. For T1 lesions (confined to mucosa or submucosa), TAE or advanced endoscopic resection techniques, such as cap EMR or endoscopic submucosal dissection (ESD), can be performed. These minimally invasive techniques may be adequate for low-grade lesions; however, more radical surgery, such as low anterior resection (LAR) or abdominoperineal resection (APR), may be required in higher-grade lesions (elevated mitotic rate or ki-67 index, lymphovascular invasion, or size >1.5 cm). For T2-T4 lesions, patients should have a metastatic work-up to evaluate for distant spread. If this is negative, usually LAR or APR is indicated.
• Rectal carcinoid tumors (>20 mm): Radical surgery (low anterior resection or abdominoperineal resection) should be considered.

Topical application of a calcium channel blocker is the most appropriate recommendation for this patient. If the patient fails to respond to a topical calcium channel blocker, botulinum injection could be considered. Topical calcium channel blocker is preferred over nitroglycerine because of better side-effect profile, and is preferred over botulinum injection because of cost.

Anal fissure:
Anal fissure is characterized by pain and bleeding with defecation due to a tear in the anal mucosa below the dentate line resulting from local trauma to the anal canal because of the passage of a hard stool. Other predisposing conditions include hypertension of the internal anal sphincter, multiparity, or previous surgery. Anal fissures are also associated with Crohn’s disease (Figure 3 and Video 2).

Characteristic symptoms include “tearing” pain with bowel movements. An acute fissure appears as a laceration, whereas a chronic fissure appears as a linear white-based lesion with horizontally oriented fibers.

There are conservative management options, medical therapy, and surgical options available to treat anal fissures:

Conservative management includes increased fluid intake, dietary fiber supplementation (5 g, 3 times a day), warm sitz baths, and use of stool softeners and topical analgesics.

Medical therapy includes topical nitrates, calcium channel blockers, or botulinum toxin to reduce the sphincter tone and allow healing by improving circulation:
• Topical calcium channel blocker cream (nifedipine or diltiazem) should be recommended as first-line treatment in the management of anal fissure (Level 1, Grade A; it has similar efficacy to Nitroglycerin but with fewer side effects. Patients should be warned about pruritis ani).
• Topical nitroglycerin cream (0.2-0.4%) heals anal fissures better than placebo, irrespective of dose (Level 1, Grade A), but is associated with headache in 25% of patients. Mechanism of action is by increasing local blood flow and reducing pressure in the internal anal sphincter.
• Botulinum toxin is associated with a similar rate of healing of anal fissures as nitroglycerin but is more expensive and invasive. It may be used for a fissure resistant to topical treatment. Botulinum toxin injection induces muscle relaxation by inhibiting the release of acetylcholine. Reported healing rates with botulinum toxin injection vary widely, ranging from 37% to 92%.

Acute graft-versus-host disease (GVHD) is a common adverse event of allogenic bone marrow transplantation. GVHD is categorized into acute and chronic forms and can involve any part of the gastrointestinal tract. Histologically, glandular epithelial apoptosis, or villous or mucosal atrophy can be observed (Figure 3).

In acute form, GVHD affects the skin, liver, and gastrointestinal tract. The patients usually present with secretory diarrhea in the first three months after transplantation.

Gastrointestinal manifestations include the following:
• Diarrhea, usually severe
• Bleeding
• Nausea and vomiting
• Abdominal pain
Endoscopic findings in GVHD include the following:
• Normal mucosa
• Erythema
• Edema
• Erosions
• Ulcerations
• Mucosal sloughing

Crohns stricture.
Endoscopic treatment options:
• Endoscopic balloon dilation is useful in the management of short (less than 4-5 cm) benign small bowel, ileocolonic, or colonic strictures. Typically, the stricture is dilated to 18 mm to 20 mm, which results in short-term improvement in 71% to 100% of patients and long-term improvement in 50% to 100% of patients. Symptomatic recurrence is common (13%-100%).
• Endoscopic needle-knife stricturoplasty or stricturotomy can be considered in refractory benign ileocolonic and ileal pouch strictures. Doppler ultrasound helps to minimize the risk of bleeding associated needle-knife therapy.
• Endoscopic stent placement (biodegradable and self-expandable metal stents) could be considered in patients with longer strictures. Stent migration is an issue.

Although self-expandable metal stents (SEMS) have longer patency rates than plastic biliary stents for malignant obstruction, stent occlusion can occur in patients who are expected to have longer survival. More than 50% of SEMS become occluded after six months.

Causes of stent occlusion include clogging by stone/sludge/food impaction, tumor ingrowth, and tumor overgrowth. Occlusion caused by sludge/stones and food debris can be cleared by mechanical cleaning of the SEMS. Tumor ingrowth and overgrowth are best treated by placement of an additional stent within the previously placed SEMS. Placement of a second SEMS placed within the original metal stent has been shown to have increased patency with a decreased number of subsequent endoscopic retrograde cholangiopancreatographies (ERCPs) compared with plastic stents. Covered, partially covered, or uncovered SEMS can be used in such situations. Covered SEMS are thought to improve patency by preventing tumor ingrowth. In this patient, who is young with a good performance status and no evidence of metastatic disease, a SEMS is the correct option.

The patient’s clinical picture is consistent with Mirizzi syndrome. The MRCP and EUS images demonstrate a large stone in the cystic duct. The ERCP image is highlighting the corresponding filling defect at the level of the common hepatic duct. This syndrome is defined as common hepatic duct compression due to an impacted stone in the cystic duct or Hartmann pouch of the gallbladder. The most appropriate next step in the management of this patient is plastic stent insertion in conjunction with surgical referral.

The standard of management in these patients is endoscopic temporizing stent across the narrowing caused by the stone followed by definitive surgical treatment. Surgery allows treating and removing the inflamed gallbladder, and removing the cystic duct and the impacted stone. Controversy exists as to whether all patients with Mirizzi syndrome need open surgery versus whether Mirizzi syndrome can be treated with laparoscopic surgery. Because of the altered anatomy, edema, and adhesions, laparoscopic surgery may increase the risk of bile duct injury. In poor surgical candidates, endoscopic removal of the stone from the cystic duct may be attempted with the aid of extracorporeal shock wave lithotripsy (ESWL) or electrohydraulic lithotripsy (EHL).

Biliary papillomatosis is the most likely diagnosis. It is a rare disease consisting of multifocal, diffuse, and superficially spreading intraluminal papillary tumors of the intra- and extrahepatic biliary tree, analogous to the intraductal papillary mucinous neoplasm of the pancreas. The disease is indolent, but has a risk of malignant transformation as high as 41% in some series. In its initial presentation, it often mimics choledocholithiasis, presenting as cholangitis or presents in association with choledocholithiasis. It is classified as either mucin-hypersecreting or non-mucin-producing. It is more common in men in the sixth to seventh decade with a male/female ratio of 2:1. Its cause and pathogenesis are unknown, but possible factors include recurrent pyogenic cholangitis, congenital choledochal cysts, clonorchis infestation, and chronic irritation by lithiasis, infection, or pancreatic juice.

patients with a gallbladder polyp of 10 mm or greater have increased risk of malignancy and cholecystectomy is recommended if patients are fit for and accept surgery. In patients with a gallbladder polyp of 6-9 mm, along with increased risk of malignancy (age greater than 50 years, primary sclerosing cholangitis, Indian ethnicity, or sessile polyp including focal wall thickening of greater than 4 mm), cholecystectomy is also recommended if patients are fit for and accept surgery.

patients with a gallbladder polyp of 10 mm or greater have increased risk of malignancy and cholecystectomy is recommended if patients are fit for and accept surgery. In patients with a gallbladder polyp of 6-9 mm, along with increased risk of malignancy (age greater than 50 years, primary sclerosing cholangitis, Indian ethnicity, or sessile polyp including focal wall thickening of greater than 4 mm), cholecystectomy is also recommended if patients are fit for and accept surgery.

Sliding hiatal hernias are a contraindication for balloon placement.

Buried bumper syndrome (BBS) was first described in 1988. The incidence of BBS is 0.3%-2.4%. It occurs due to tight apposition of the external bolster of the PEG tube against the abdominal wall. The internal bolster of the PEG tube slowly erodes into the abdominal wall as tension is created on the PEG tube tract. To avoid this from occurring, it is critical to loosen the outer bumper after the first 24 hours.

The risk factors for BBS are obesity, rapid weight gain, patient manipulation, gauze placement beneath the external bumper instead of over it, chronic cough, tube manipulation by inexperienced personnel, and malnutrition.

Typical symptoms and signs of a buried bumper include PEG tube pain, poorly functioning tube, peristomal leakage of food, purulent discharge, peristomal bulging, or a PEG tube that fails to move easily in and out of the tract.

Endoscopic findings of a buried bumper include a dimple as seen in Figure 3, an ulcer-like mucosal defect as seen in Figure 4, and a fistulous orifice or a sunken internal bumper as seen in Figure 5. A CT of the abdomen will show dislodgement of the internal bumper of the PEG tube into the abdominal wall outside the peritoneum.

Endoscopic therapy of buried bumper syndrome depends upon the type of PEG tube and the depth of migration into the gastric wall. If the internal bolster is collapsible, such as with externally removable PEG tubes, the PEG tube can be removed by simple external traction. Some tubes may separate from the internal bolster, which then acts as a foreign body and is a source for chronic infection. If the internal bumper on the PEG tube is rigid, such as with tubes designed for endoscopic removal only, the PEG tube may have to be removed by dissection of the PEG tract with a needle-knife (or a polypectomy snare or argon plasma coagulation in one or multiple sessions) before using the push-pull T-technique or starting with the push-pull T-technique. This latter technique includes the following steps:
• The PEG tube is cut near the external bolster.
• A snare is passed through the shortened PEG tube from the gastric lumen to the outside of the patient.
• A cut 3 to 4 cm section of the excess PEG tube is grasped with the snare external to the patient.
• This separate piece of PEG tube is pulled by the snare against the external end of the “buried” PEG tube in a “T” configuration.
• This T-piece is grasped by a hemostat.
• The endoscope and snare are pulled at the same time the hemostat is pushed, mobilizing the buried PEG tube from within the abdominal wall to the gastric cavity where it can be easily removed.
Avoid pulling the PEG tube out and replacing it with a replacement tube at the bedside without endoscopic guidance as this could result in PEG tube tract disruption and untoward septic adverse events.

Prevention of BBS requires good nursing care and patient education. The external bolster of the PEG tube should be left 1-2 cm from the abdominal wall. The PEG tube should always be able to rotate and be freely mobile within the tract.

• Increased output in End Jejunostomy
• Exclude/treat causes other than a short bowel (for example, infection [intra- or extraluminal], partial obstruction, abrupt stopping of drugs) (grade C).
• Correct dehydration with intravenous saline solution while the patient takes nothing by mouth for 24–48 hours. This stops thirst and thus the desire to drink (grade C).
• Reduce oral hypotonic fluids to 500 mL/day. This is the most important measure (grade B).
• Give glucose/saline solution to sip (sodium concentration at least 90 mmol/L). Most stomal/fistula losses (except from the colon) have a sodium concentration of about 100 mmol/L (grade B).
• Add sodium chloride to any liquid feeds to make the sodium concentration approximate100 mmol/L while keeping osmolality near 300 mOsmol/kg (grade B).
• Give drugs to reduce motility; loperamide 2–8 mg (before food). Occasionally, addition of codeine phosphate further reduces stomal output (grade B).
• If there is a net “secretory” output (generally more than 3 L/24 hours), add drugs that reduce gastric acid secretion (H2 antagonists or proton pump inhibitors) or if unable to absorb oral drugs, octreotide can reduce stomal output by 1–2 L/24 hours (grade A).
• Correct hypomagnesemia.
• Intravenous magnesium sulfate can be started initially and then oral magnesium oxide and/or 1-alpha cholecalciferol (grade B). Other measures include:
o Separating solids and liquids (that is, having no drink for half an hour before or after food) (grade C)
o Using salt capsules instead of glucose/saline solutio

Zinc is important in growth and development, as well as immune and reproductive function. Zinc is absorbed along the whole length of the small bowel. Zinc deficiency can be determined by plasma concentration, although it can be affected by inflammation, pregnancy, and oral contraceptive use. Risk factors for deficiency include chronic diarrhea, short bowel syndrome, cystic fibrosis, pancreatic insufficiency, cirrhosis, chronic renal failure, and use of the drug D-penicillamine. Zinc deficiency can also be associated with poor wound healing. Patients with fistulizing Crohn’s disease (CD) have significantly lower zinc levels than non-fistulizing CD. A scaly red rash involving the face, groin, and hands may occur, which in CD is called acrodermatitis enteropathica (see Figure 1). Acrodermatitis enteropathica is a combination of facial skin lesions (around mouth and nose) and skin lesions around the tips of exposed skeletal parts (eg, fingers, joints). The deficiency can be supplemented with zinc gluconate 20-40 mg/day, 176 mg zinc sulfate daily, or 220 mg daily in divided doses. Excess zinc ingestion can lead to copper deficiency.

Necrotizing fasciitis (necrosis of the fascia layers) is a rare adverse event of PEG placement. Patients with diabetes, wound infections, malnutrition, or who are immunosuppressed are at an increased risk. Additionally, traction and pressure on the PEG wound may predispose the patient to the development of necrotizing fasciitis.

One study demonstrated that patients who had their PEG tube external bolster set directly against the abdominal wall were more likely to develop wound infection, peristomal drainage, and fasciitis when compared with patients whose external PEG bolster was left 3 cm from the abdominal wall. However, necrotizing fasciitis may develop after any injury, even minor, to the abdominal wall surface.
Successful treatment of necrotizing fasciitis requires early detection, immediate surgical debridement, and intravenous antibiotics.

Migration of foley replacing PEG can cause obstruction and nausea and vomiting

Vitamin B12, vitamin D, and iron deficiency can occur in up to 40% of patients without lifelong supplementation. Most deficiencies occur between 12 and 15 months post-operatively, but vitamin D3 deficiency occurs significantly earlier at 9.7 months. Hypocalcemia with or without vitamin D deficiency, and resulting osteoporosis can also occur without lifelong supplementation. These deficiencies are due to the surgery, which bypasses most of the stomach, all of the duodenum, and the proximal jejunum. The following are recommended supplements: iron 325 mg twice daily, vitamin B12 as part of a multivitamin, folate as part of a multivitamin, and 1200 to 1500 mg of calcium in divided doses over the day (calcium citrate is better absorbed in low-acid environments). Oral treatment of post-operative vitamin B12 and vitamin D3 deficiencies was successful in more than 80% of the patients, in contrast to oral treatment of anemia which was only successful in 62.5% of the patients.

He is asymptomatic and, hence, the most likely answer is a gastro-gastric fistula. This occurs due to an abnormal connection between the gastric pouch and the excluded stomach. The typical presenting symptom is weight re-gain or inability to lose weight as food does not bypass the remnant stomach. Pain, reflux, nausea, emesis, and marginal ulceration are also often reported. The diagnosis is most reliably made by upper gastrointestinal series or upper endoscopy, although cross-sectional imaging can also demonstrate this finding; there is a high false positive rate with oral contrast studies, as contrast can reflux into the remnant stomach from the duodenum. Hence, endoscopy with visualization of the actual fistula is required.

Gastroparesis is a common indication for direct percutaneous endoscopic jejunostomy (DPEJ) placement. Common indications for jejunal placement include gastroparesis, gastric resection, gastric outlet obstruction, failed percutaneous endoscopic gastrostomy, pancreatitis, feeding intolerance, improved nutrient delivery, and increased aspiration risk. The advantages that a DPEJ offers is greater stability than percutaneous endoscopic gastrostomy with jejunal extension (PEGJ), decreased kinking and migration, more distal jejunal access, and larger diameter tubes allowing for better infusion and less clogging.

Dumping syndrome is a complication of gastric resection and bypass. Early symptoms occur 15 minutes after ingestion of large amounts of simple carbohydrates. The food hyperosmolality causes fluid shifts from plasma into the bowel resulting in gastrointestinal symptoms (ie, abdominal pain, diarrhea bloating, and nausea) and vasomotor changes (ie, flushing, palpitations, perspiration, tachycardia, hypotension, and syncope).

Obstructed PEG

Warm water is the most effective and safe method to unclog a PEG tube. In the event of a PEG tube obstruction with yellow material, as shown in Figure 1, a number of simple steps could be undertaken to unclog the obstruction:
• Warm water – Flush the tube with a 60-mL syringe filled with warm water, which is superior to other fluids such as juices or colas. Allow to sit in the tube for 5 to 20 minutes and then repeat flush actions. Flushing should be done with a gentle back-and-forth motion with the plunger of the syringe without using a lot of force so as not to rupture the feeding tube.
• Non-enteric coated pancreatic enzyme- Dissolve the tablet in a bicarbonate solution and allow it to dwell within the PEG tube prior to water flushing.
• PEG tube brush – If the above techniques fail, gently pass a PEG tube brush into the tube to clear out the debris.
Prevention of clogging is important and there are several basic rules that should be followed:
• Always flush the tube immediately before and after feedings with at least 30 mL of water since medications and enteral formula feeds typically clog the PEG tube.
• Never mix medicine with tube feeding.
• Dissolve all medications in water or deliver in liquid form, if available.
• Flush the tube with at least 30 mL of water before and after all medications.
• Flush tube with at least 5 mL of water between each medication if more than one is given.

The most likely diagnosis is a PEG tube tract rupture, a known adverse event with the use of an obturator-driven gastrostomy replacement device. This is seen soon after the placement procedure.
There are two types of replacement PEG devices:
• Balloon tip PEG replacements: These are easy to insert through an existing stoma tract and are associated with few adverse events. However, the balloons have a shorter lifespan that may make these types of replacement PEG tubes less convenient for patients and caregivers due to need to change more often.
• Obturator type PEG replacement: This tube has a distensible tip that requires an obturator, which “stretches” the distensible tip in order to pass it through the stoma tract. These tubes have a much longer lifespan than a balloon replacement tube. However, the obturator can cause damage, such as PEG tube tract rupture, because it is blindly passed through the existing PEG stoma and, hence, it may be preferable to place these under endoscopic guidance.

ERCP with pancreatic duct stent placement is the best single treatment to manage this problem. This patient has a traumatic pancreatic duct disruption secondary to a motor vehicle accident resulting in a large intra-abdominal fluid collection and a pancreaticopleural fistula. A history of abdominal trauma and the subsequent finding of an amylase rich pleural effusion suggest the diagnosis.

Afferent loop syndrome is the most likely diagnosis. This scenario and imaging are typical of afferent loop syndrome, which is a late complication of pancreaticoduodenectomy and other foregut surgeries requiring intestinal anastomoses. The median time to diagnosis is 1.2 years (range 0.03 – 12.3 years). The most common clinical presentation is obstructive jaundice or cholangitis followed by abdominal pain and nausea or vomiting. The reported etiologies include malignant obstruction or radiation enteropathy. Treatment includes endoscopic decompression by balloon dilation or stenting of the anastomosis. Recently, there have been reports of creating a gastrojejunal anastomosis with lumen apposing metal stents. Other therapeutic options include percutaneous drains or surgical revision.

The inherited predisposition to pancreatic cancer include the following syndromes:
• Familial Adenomatous Polyposis. Caused by germline pathogenic variants in the APC gene; associated with increased risk for colon, small bowel, and thyroid cancer, colon polyps, and extracolonic physical features.
• Hereditary Breast and Ovarian Cancer. Caused by germline pathogenic variants in the BRCA1 and BRCA2 genes; associated with increased risk for breast, ovarian, pancreatic, and prostate cancer, as well as melanoma (hence answer B is incorrect).
• Familial Multiple Mole Melanoma-Pancreatic Cancer syndrome. Caused by germline pathogenic variants in the CDK4 and CDKN2A genes; associated with increased risk for melanoma and pancreatic cancer (the patient described in answer option C).
• Lynch syndrome. Caused by germline pathogenic variants in the MLH1, MSH2, MSH6, PM2S, and EPCAM genes; mainly associated with an increased risk for colon and endometrial cancer.
• Peutz-Jeghers syndrome. Caused by germline pathogenic variants in the STK11 genes; mainly associated with increased risks for breast, colon, stomach, ovarian, and pancreatic cancer.
• Li-Fraumeni syndrome. Caused by germline pathogenic variants in the TP53 gene; core cancers include premenopausal breast cancer, sarcomas, adrenocortical carcinomas, and brain tumors.
• Mutations in the ATM or PALB2 genes. (Moderate penetrance genes); associated with increased risks for breast, ovarian, and pancreatic cancers.
• Hereditary pancreatitis due to mutations in PRSS1.
• Familial pancreatic cancer. Defined as a familial with at least two first-degree relatives with pancreatic cancer, which does not fulfill the diagnostic criteria for an inherited tumor syndrome. (the patient described in answer option A).

• If patient is not pacemaker dependent, then no reprogramming is necessary.
• If the patient is pacemaker dependent, then they should be considered for pacemaker reprogramming prior to the planned endoscopic procedure as in our patient who has a third-degree heart block and prolonged electrocautery may be required (correct answer: B).
• Electrocautery factors which increase the risk for pacemaker interference include longer duration of electrocautery, proximity to the pacemaker, and monopolar electrosurgical current (eg, snare electrocautery, sphincterotomy, or argon plasma coagulation) compared to multipolar devices (eg, bipolar electrocoagulation or radiofrequency ablation).
• The ACCF/AHA differ from the ASGE in their views on perioperative management of pacemaker-dependent patients undergoing electrosurgery. The ACCF/AHA guidelines specifically recommend that the pacemaker be reprogrammed to an asynchronous mode (pacemaker codes VOO or DOO) throughout the entire procedure. External pacing can also be effective as long as it is set to the asynchronous mode that will be unaffected by cautery. Asynchronous pacing refers to regular, uninhibited pacing in which the pacemaker has no sensing capability. Therefore, any interference detected as a result of electrosurgery will not result in a pacemaker response. Asynchronous pacing can be achieved by programming the pacemaker in the VOO mode, in which a single ventricle generates, or in DOO mode, in which both the atrium and ventricle generate a fixed interval rate with no relationship to a spontaneous rhythm. Conversely, the ASGE guidelines indicate that reprogramming is only needed in pacemaker-dependent patients in whom prolonged electrocautery is anticipated, such as in the treatment of gastric antral vascular ectasia (correct answer: B) or radiation proctitis.

• A1. Bleeding: Low-risk procedures: Diagnostic endoscopy (esophagogastroduodenoscopy, colonoscopy, flexible sigmoidoscopy) including mucosal biopsy, endoscopic retrograde cholangiopancreatography with stent or papillary balloon dilation without sphincterotomy, endoscopic ultrasound (EUS) without fine-needle aspiration (FNA), enteroscopy and diagnostic balloon-assisted enteroscopy, capsule endoscopy, enteral stent placement (without dilation), argon plasma coagulation, and Barrett’s ablation.
• A2. Bleeding: Higher-risk procedures: Polypectomy, biliary or pancreatic sphincterotomy, therapeutic balloon-assisted enteroscopy, cystgastrostomy, treatment of varices, EUS-guided FNA (EUS-FNA of solid masses on acetylsalicylic acid or aspirin (ASA)/non-steroidal anti-inflammatory drugs is low-risk), endoscopic hemostasis, pneumatic or bougie stricture dilation, percutaneous endoscopic gastrostomy (PEG) placement (PEG on ASA or clopidogrel therapy is low-risk, but does not apply to dual antiplatelet therapy), ampullary resection, endoscopic mucosal resection, endoscopic submucosal dissection, percutaneous endoscopic jejunostomy, and tumor ablation.
• B1. Thromboembolism: Low-risk conditions: Uncomplicated or paroxysmal nonvalvular atrial fibrillation, bileaflet aortic valve prosthesis without atrial fibrillation and no other risk factors for cerebrovascular accident, and venous thromboembolism that occurred > 12 months prior with no other risk factors. • B2. Thromboembolism: Medium-risk conditions: Bileaflet aortic valve prosthesis and one or more of the following risk factors: atrial fibrillation, prior cerebrovascular accident or transient ischemic attack, hypertension, diabetes mellitus, congestive heart failure, age 75 or older, venous thromboembolism within the past 3-12 months, non-severe thrombophilia (heterozygous factor V Leiden or prothrombin gene mutation), recurrent venous thromboembolism, or active cancer.
• B3. Thromboembolism: Higher-risk conditions*: Any mitral valve prosthesis, any caged-ball or tilting disc aortic valve prosthesis, recent (within 6 months) cerebrovascular accident or transient ischemic attack, recent (within 3 months) venous thromboembolism, and severe thrombophilia (deficiency of protein C, protein S or antithrombin; antiphospholipid antibodies; multiple abnormalities).
*Patients classified as high-risk have a >10% annual risk for thromboembolism, patients classified as moderate-risk have a 5% to 10% annual risk for thromboembolism, and patients classified as low-risk have a <5% annual risk for thromboembolism.

Specific anticoagulation considerations:
• Novel oral anticoagulants (NOACs):
o Include the direct thrombin inhibitor dabigatran and the direct factor Xa inhibitors (eg, rivaroxaban, apixaban, edoxaban).
o There is no reliable serum assay to assess the degree of anticoagulant activity with these agents at this time.
o In the peri-endoscopic period, there are three important pharmacodynamics considerations when holding and restarting an anticoagulant: (1) time to maximum effect, (2) half-life, and (3) excretion of the drug.
o To minimize the risk of bleeding, these medications should be stopped for at least two half-lives before high-risk procedures, and their dosing should be adjusted in the setting of renal impairment.
o These medications do not have reversal agents at this time.
• Warfarin: There are two factors to consider related to warfarin:
o The decision to obtain a pre-procedure international normalized ratio (INR) should be individualized.
o The administration of vitamin K should be avoided since it delays therapeutic anticoagulation once anticoagulation is resumed in the nonbleeding patient.
• Delay elective procedures: The guidelines recommend that elective procedures should be delayed when possible if the indication for the anticoagulation is temporary (eg, deep venous thrombosis).
• Reinstitution of Anticoagulants:
o Reinstitution of warfarin can usually be done within 24 hours of the procedure. The benefits of immediate re-initiation of antithrombotic therapy in preventing thromboembolic events is weighed against the risk of hemorrhage and the decision is dependent on procedure-specific circumstances. As an example, a delay would be reasonable after endoscopic retrograde cholangiopancreatography with endoscopic sphincterotomy or removal of a large sessile polyp.
o Reinstitution of NOAC after high-risk endoscopic procedures should be delayed until adequate hemostasis is ensured, given their rapid onset of action and lack of reversal agents. If therapeutic doses of NOACs cannot be restarted within 12 to 24 hours after a high-risk endoscopic procedure, thromboprophylaxis (ie, unfractionated heparin bridge) should be considered to decrease risk of thromboembolism, given the short half-life of the NOAC agent, in those with a high risk for thromboembolism.
The American Society for Gastrointestinal Endoscopy (ASGE) guidelines state that dilation of strictures is a high-risk procedure for hemorrhage, and atrial fibrillation in the absence of valvular heart disease is a low-risk condition for thromboembolic complications. In this setting of a high-risk endoscopic procedure with a low risk for thromboembolism, warfarin and novel oral anticoagulant (NOAC) therapy should be discontinued for the appropriate drug-specific interval in the peri-endoscopic period.

A is incorrect. Dilation of strictures is a high-risk procedure for hemorrhage; therefore, continuing rivaroxaban would be incorrect.

C and D are incorrect. Atrial fibrillation in the absence of valvular heart disease is a low-risk condition for thromboembolism and does not require bridge therapy.

The ASGE guidelines take into account the procedure-related risk of bleeding and the patient’s risk for thromboembolic complications. The guidelines are general recommendations and may need to be adapted to the patient’s clinical condition and the estimated risk associated with the specific procedure. These recommendations are summarized in Figures 1 and 2 from ASGE’s Standards of Practice.

(Figure 1)

(Figure 2)

Peutz-Jeghers syndrome (PJS) is an autosomal dominant disease affecting 1 in 50,000 to 200,000 patients. Hamartomatous polyps have a typical histological appearance, and they are scattered throughout the gastrointestinal tract. Over 95% of patients have associated perioral and buccal mucocutaneous pigmentations, which are usually < 5mm, and can sometimes be found in the intestinal lumen. Most symptoms are related to polyp load and size. Intussusception may be the initial presentation, occurring in 50% of patients by age 20, and is usually associated with polyps at least 35 mm in size. Polyp obstruction, infarction, ulceration, or bleeding can also occur.

Most polyps occur in the jejunum, followed by the ileum, and finally the duodenum. Intestinal malignancies are more common in the colo-rectum, followed by the stomach and then by the small bowel. Malignancies also occur in the pancreas, breast, ovary, uterus, cervix, testes, and lungs, so they are targets for surveillance.

Current guidelines recommend endoscopies, and small-bowel imaging by magnetic resonance or video capsule starting at age 8, and then every three years starting at age 18. Computed tomography enterography can help identify polyps above 10 mm, but radiation exposure is a concern.

The goal of endoscopy is to reduce polyp burden, focusing on polyps 15 mm and above. This decreases the risk of intussusception and obstruction, but it is not clear how this approach affects the risk of intestinal malignancy.

The patient’s history and endoscopic findings are suggestive of lymphangiectasia with protein-losing enteropathy. Endoscopic features seen in the small bowel include chylous exudate, white swollen villi, and filliform-like polyps. Whitish villi and reticular pattern are a manifestation of dilated lymphatic vessels in the wall of the intestine. Small bowel biopsy (Figure 2) demonstrates lacteal dilation, confirming the presence of lymphatic obstruction. The most appropriate treatment for this patient is a low-fat diet with medium-chain triglyceride (MCT) supplementation.

Lymphangiectasia occurs as a result of lymphatic obstruction that may be due to primary or secondary causes. Primary intestinal lymphangiectasia is an unusual cause of protein losing enteropathy due to congenital malformation or obstruction of lymphatics of intestine. Secondary causes of lymphangiectasia include constrictive pericarditis, radiation or chemotherapy induced retroperitoneal fibrosis, obstructive adenopathy, celiac disease, Whipple disease, intestinal tuberculosis, sarcoidosis, surgical repair of complex congenital cardiac disease (eg, Fontan procedure), thoracic duct damage, and malignancy. Dilated lacteals in the mucosa, submucosa, or subserosa cause rupture of the lacteals with significant loss of lymphatic fluid into the intestinal lumen and disruption of long chain fatty acids leading to hypoproteinemia, steatorrhea, hypogammaglobulinemia, and lymphopenia.

Decreasing lacteal-absorption requirements can help reduce pressures and leakage. This is accomplished by replacement of dietary fat with medium-chain triglycerides, which do not require lymphatic transport. Fat-soluble vitamins, however, will require parenteral replacement unless the underlying enteropathy can be corrected. Associated vitamin deficiencies can result in hyperparathyroidism and elevated INR as demonstrated by this patient. Segmental disease may be treated by surgery, and a few patients have demonstrated a favorable response to octreotide and antiplasmin.

his patient is suffering an active small-bowel bleed, where the yield of endoscopy will be highest. The previous capsule study suggested active mid small-bowel bleeding which should be reachable by device-assisted enteroscopy. Water immersion (WI) enteroscopy may hold benefits over using CO2 or air insufflation. In cases of gastrointestinal (GI) bleeding, blood streaming into the water may improve localization of the bleeding site, and a continuous infusion can help expose the bleeding site which would otherwise be obscured by massive bleeding.

WI may improve enteroscope depth of insertion by reducing small-bowel looping. In cases of recent surgical intestinal anastomosis, WI in contrast to air insufflation may reduce the risk of provoking anastomotic leaking. As with WI colonoscopy, WI enteroscopy helps flatten the muscularis propria, separating it from the mucosa and submucosa allowing large endoscopic mucosal resection. Theoretical risks of WI may include volume overload and serum electrolyte abnormalities but there are no case reports of this complication.

Aortoduodenal fistulas are rarely primary, and usually associated with patients who have undergone aortic graft or endoluminal stent placement, but any previous vascular surgery, even with no graft, can be associated with this complication. Primary aortoduodenal fistulas are most commonly due to an aortic aneurysm, but have been associated with Behçet disease, retroperitoneal malignancy, radiation therapy, trauma, syphilis, tuberculosis, or septic aortitis.

CT is probably the single-most sensitive diagnostic test for aortoduodenal fistula. Disappearance of the fat plane between the duodenum and the aorta and retroperitoneal air are suggestive of a fistula. Intravenous contrast in the bowel provides a definitive diagnosis.

Endoscopic diagnosis may require an extended upper endoscopy with a pediatric colonoscope or enteroscope in order to visualize the third and fourth portions of the duodenum where aortoduodenal fistulas commonly occur due to its retroperitoneal location, but other parts of the bowel may be involved. Endoscopy may show the graft itself in the duodenal lumen, but may also show only clot, active bleeding, or an apparent submucosal lesion, as shown in this case. Endoscopy also enables other sources of gastrointestinal blood loss to be excluded.

Afferent loop syndrome is a postoperative complication that may occur following pancreatico-duodenectomy or gastrectomy with Billroth II anastomosis. It can occur in approximately 13% of patients undergoing a Whipple procedure for pancreatic cancer and it is typically caused by recurrent malignancy, radiation enteropathy, or severe bowel angulation leading to obstruction of the afferent limb. This may cause chronic abdominal pain, cholestasis, cholangitis, pancreatitis, and/or biliary fistulae. In addition to symptoms, CT provides evidence of a dilated afferent jejunal limb, supporting the diagnosis (Figure 2).

Treatment has traditionally required surgery, which entails significant morbidity. Advances in radiological and endoscopic techniques have led to novel options for non-surgical management of this complication with favorable outcomes. Percutaneous biliary or jejunal drainage and endoscopic balloon dilation followed by the placement of trans-stenotic plastic or metal stents have been reported. The recent availability of LAMS has enabled endoscopists and interventional radiologists to create a true entero-enteric anastomosis between the occluded jejunal loop and another gut segment (usually the stomach or jejunum) under endoscopic ultrasound and/or fluoroscopic guidance. Case reports and small series have suggested that these interventions can lead to the resolution of symptoms or complications associated with the afferent loop syndrome, including cholangitis. However, long term impact of the intervention is unclear.

Eosinophilic gastroenteritis (EGE) is a rare, benign inflammatory disorder that predominantly affects the stomach and small intestine. The disease is classified based on the involved intestinal layer in mucosal, submucosal, and serosal subtypes—although these subgroups frequently overlap. The mucosal layer is affected in the vast majority of patients, with a prevalence ranging between 88% and 100% in some series, but multiple biopsies (at least six), including of normal small-bowel mucosa, are recommended in order to increase the sensitivity. Infrequently, in patients with a high level of suspicion, but with negative biopsies, a full-thickness small-intestinal biopsy may be required, particularly in patients with serosal involvement.

Between 70% and 90% of patients have peripheral eosinophilia, but this does not correlate with symptom severity. Instead, patients with serosal involvement tend to have higher peripheral eosinophil count and respond more substantially to steroids. Although up to 40% of cases experience spontaneous remission, corticosteroid treatment is necessary in the majority of cases of EGE, with response rates in excess of 90% in some series.

Based on anecdotal evidence and expert opinion, the recommended initial dose of prednisone is 0.5-1 mg/kg followed by a taper over six to eight weeks. Relapse is common and patients with mucosal or muscular layer involvement especially need some form of maintenance therapy. Various steroid sparing agents (eg, sodium cromoglycate—a stabilizer of mast cell membranes, ketotifen—an antihistamine, and montelukast—a selective, competitive leukotriene receptor antagonist) have been proposed, centering around an allergic hypothesis with mixed results. Dietary modifications may be attempted with limited benefit if specific food allergens are identified by skin or blood testing. Antibiotics or anti-parasitic agents are not effective. Surgical treatment is limited to those patients with small bowel obstruction or perforation.

The patient was discovered to have human immunodeficiency virus (HIV) infection in the setting of evaluation for this lymphoma. HIV-associated lymphomas occur with low CD4 counts and are usually either large B-cell or Burkitt type lymphomas, but Hodgkin, plasmablastic, and primary effusion lymphomas may also occur. Lymphomas may also occur concomitantly with Kaposi sarcoma, or active herpes virus or Epstein-Barr virus co-infections. Highly active antiretroviral therapies (HAART) has changed the natural history of the disease, but malignant lymphoma is still the most common neoplasia and cause of cancer-related death in this population.

D-lactic acidosis (D-LA) is an intestinal bacterial dysbiosis with increased intestinal colonization of D-lactate producing bacteria, including Lactobacillus species (as opposed to L-lactate by humans), as a result of intestinal carbohydrate malabsorption and increased bacterial fermentation producing D-lactate. This causes an encephalopathy consisting of confusion, delirium, ataxia, slurred speech, loss of memory, and cognitive decline. It is usually a result of short bowel syndrome (SBS), but has also been reported with other severe malabsorptive syndromes, bariatric surgery (such as jejuno-ileal bypass), and colonic atonia.

Interestingly, the neurological manifestations of D-LA are independent of gastrointestinal symptoms, and other factors beyond the acidosis contribute to the neurological derangement as elevated serum D-lactate has been detected in asymptomatic patients. A complex interaction between microbe-gut-brain occurs, which includes D-LA enhanced intestinal permeability, bacterial translocation, and systemic inflammation mediated by TNF-α. This affects the brain by enhanced entero-cephalic circulation, and dysregulation of enteric and central nervous system pathways.

In this case the known SBS, poor dietary habits and use of probiotics, which are mostly of the Lactobacillus species, caused the D-LA. Probiotics should not be used for therapy. Serum or urine D-lactate with normal L-lactate may help the diagnosis. Patients with SBS may be diagnosed with psychiatric or substance abuse disorders before being diagnosed with D-LA, so a level of suspicion is necessary in high risk patients.

Treatment includes restriction of oral intake, fluids, and parenteral nutrition, and an adaptive diet.

Dumping syndrome has early and late manifestations. Given that the stomach no longer functions as a reservoir, particularly if high-osmolarity foods are ingested (such as soda or processed carbohydrates), this results in an osmotic overload in the proximal small intestine. Fluid enters and distends the lumen, there is a vagal reaction, and the levels of several gastrointestinal hormones (ie, peptide YY, vasoactive intestinal polypeptide, and neurotensin) rise. Patients experience upper abdominal cramping and distension, tachycardia, nausea, and occasionally syncope. During the second phase, the presence of excess carbohydrates in the jejunum results in hyperinsulinemia resulting in hypoglycemia. Patients may experience fatigue, perspiration, palpitations, fatigue, tremor, and syncope.

The initial approach to therapy is to modify diet by recommending multiple small meals each day and to avoid rapidly absorbed carbohydrates. Most patients respond to these measures to minimize the sudden influx of hyperosmolar material into the proximal gut. Guar gum and pectin may increase the viscosity of intake and may delay gastric intake. Acarbose interferes with carbohydrate metabolism and may mask later manifestations of dumping. Somatostatin can be used to delay gastric and small bowel motility as well as release of implicated gastrointestinal hormones and insulin.

Recently an endoscopic technique using endoscopic suturing, argon plasma coagulation, and fibrin glue injection to tighten the gastrojejunostomy has had favorable results.

The European Society of Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) guidelines for celiac disease recommend that biopsy samples should be obtained from the second and/or third portion of the duodenum (at least four specimens) and from the duodenal bulb (at least one to two samples from the 9 o’clock and 12 o’clock positions in the duodenal bulb). In some celiac disease patients with duodenal sparing, enteroscopy with jejunal biopsies may provide the answer.

Brunner gland hamartomas are uncommon submucosal tumors, comprising 5-10% of all small bowel tumors and are mostly asymptomatic, but may present with gastrointestinal bleeding or anemia, obstruction or intussusception, or vague symptoms, such as dyspepsia. The overgrowth of mature differentiated cells is believed to occur as a response to increased duodenal acid exposure; thus, over 70% occur proximally. They are usually single and may extend distally into duodenum on a stalk. Biopsies of overlying mucosa usually show normal results. Endoscopic ultrasound demonstrates a hyperechoic submucosal lesion, which may contain cystic spaces, as in this case. Most are amenable to endoscopic resection as demonstrated in the images. An endoloop was placed on the polyp stalk before polypectomy to decrease the risk of post-resection hemorrhage, and the endoloop was clipped to the gastric wall to better expose the lesion (see Figure 4). Other investigators have used clips to facilitate polyp resection.

. VCE small-bowel transit times are variable, but studies have shown that lesions seen on VCE within the first 66% to 75% of total small-bowel transit time (which excludes the gastric transit time and the colon) are more likely to be found performing an antegrade device-assisted enteroscopy (DAE). For lesions within the last 25% to 33% of the VCE total small-bowel transit time, retrograde device-assisted enteroscopy should be attempted. The active bleeding was seen in the last 25% of VCE small-bowel transit time, so a retrograde device-assisted enteroscopy should be performed.

The yield of repeat VCE is highest (50% to 75%) when done in the setting of overt bleeding causing a drop in hemoglobin, and within two weeks of an initial overt bleeding episode. While the individual yield of VCE and device-assisted enteroscopy (DAE) are comparable, VCE is more widely available and may enhance the yield of DAE when performed first; it can help determine if an antegrade or retrograde DAE should be attempted, and DAE can be avoided if the VCE is negative as the yield will be low.

Patients with continuous flow left ventricular assist devices (LVAD) can present with bleeding as a consequence of an acquired von Willebrand factor deficiency due to degradation from sheer stress of the device on the factor, but it is still not clear why some patients develop this condition or why some experience hemorrhage, but others do not. Pulsatile flow LVAD may be associated with a lower rate of gastrointestinal (GI) bleeding. A meta-analysis of 1,697 patients on continuous flow LVAD described a 23% prevalence of GI bleeding. Older age and elevated creatinine were risk factors. An escalating incidence of GI bleeding was described in another study using the Nationwide Inpatient Sample database, where age over 65 was associated with a 20.5 times greater odds for GI bleeding in patients with LVAD suggesting that age is a significant risk factor.

Sero-negative celiac disease was suspected based on histology, but the differential diagnosis of the findings is broad, and includes food allergies, eosinophilic gastroenteritis, peptic duodenitis, post viral enteropathy, Crohn’s disease, small-intestinal bacterial overgrowth, tropical and collagenous sprue, autoimmune enteropathy, giardasis, human immunodeficiency virus enteropathy, tuberculosis, radiation enteritis, Zollinger–Ellison syndrome, Whipple disease, intestinal lymphoma, alpha-chain disease, graft-versus-host disease, hypogammaglobulinemia, and severe malnutrition.

Medications that can mimic celiac disease in presentation and histology include mycophenolate mofetil, methotrexate, azathioprine, and olmesartan (and possibly others in the same family). The enteropathy has been described even years after being on the medication. Diarrhea is a common side-effect effect of most medications, but the extreme clinical presentation in this case points towards olmesartan-associated enteropathy as the cause. Olmesartan is an angiotensin II receptor antagonist that can cause a clinically significant enteropathy and the etiology remains unknown. Sometimes the whole bowel can be involved, and severe malnutrition and muscle wasting have been described. The diagnosis may lag for years, so clinical suspicion is necessary. A high prevalence of the presence of HLA-DQ2 and HLA-DQ8 has been found in olmesartan induced enteropathy suggesting a permissive effect of these genetic variants and confuses the diagnosis with celiac disease. Stopping the offending medication results in rapid clinical improvement.

At least 20% of patients with LVAD develop chronic anemia and gastrointestinal (GI) bleeding despite a therapeutic INR, and thrombosis occurs in up to 6% when anticoagulation is stopped.

The etiology of the bleeding, which can occur outside the GI tract, is due to an acquired von Willebrand factor (vWf) deficiency as a result of protein denaturation and loss of function because of the sheer stress of the assist device itself. Interestingly, pulsatile flow LVAD cause less damage to vWf compared to continuous flow devices, so a change to the pulsatile LVAD may decrease gastrointestinal bleeding.

Aberrant blood flow through mucosal and submucosal vessels in the intestine promotes the formation of angiodysplasia which hemorrhage due to a combination of vWf deficiency, sheer pressure on the blood vessel wall, intestinal motility, and possibly food bolus friction. Remarkably, anticoagulation appears to play a small role because modifications to the anticoagulation regimen have little effect on the incidence or recurrence of GI bleeding associated with LVAD. The GI bleeding resolves after cardiac transplantation.

Thalidomide suppresses tumor necrosis factor and angiogenesis and has been used successfully to treat GIAD associated with LVAD. Side effects preclude the therapeutic dose of 200 mg/day in over 50% of patients, and a recent case series indicated strict exclusion criteria for thalidomide use, including thromboembolic disease without anti-coagulation, major wounds, symptomatic autonomic neuropathy, peripheral neuropathy, bradycardia, and concurrent radiotherapy which further limits general use.

LVAD-associated GI bleeding is unlikely to present in a patient of child-bearing age, but reproduction precautions need to be discussed, including males. In the United States to prescribe thalidomide the prescriber and the pharmacy have to be certified through the THALOMID Risk Evaluation and Mitigation Strategy (REMS).

This patient continues to experience GI bleeding despite endoscopic therapy and is suffering congestive heart failure exacerbations with resuscitation efforts. Previous endoscopies, enteroscopies, and the recent video capsule endoscopy confirm that the GIAD are located proximally. Rebleed rates from GIAD is between 30% to over 50% after endoscopic therapy, and in this patient with symptomatic anemia who tolerates resuscitation poorly, failure of endoscopic treatment should be recognized, and alternate therapy should be used. Introducing thalidomide at this stage of the disease is a reasonable next step. Case series have shown immediate and long-term benefits reducing rebleed rates and blood transfusions, even at lower therapeutic doses of 100 mg/day, especially when iron is co-administered. There is almost immediate recurrence of GIAD bleeding when thalidomide is discontinued. Octreotide, and more recently lanreotide, have been used with success, but the need for daily injections and cost limit their use. Comparison trials of medical therapy for GIAD are needed.

The combination of obstructive symptoms and anemia with negative routine endoscopies should raise the suspicion of small-bowel diaphragm disease. This is a rare disease that is believed to occur as a complication of NSAID-induced enteropathy, which leads to the formation of diaphragms which cause lumen narrowing, and diaphragm like structures (Figure 4), mucosal ulceration, hypertrophy and fibrosis of the mucosal layer (Figure 5).

A high level of suspicion is necessary because diagnostic tests including small bowel imaging are frequently inconclusive. Surgery or endoscopy can be diagnostic and therapeutic. Histology, as described above, is characteristic of the disease, and confirms the diagnosis. Given the severe back pain and history of peptic disease, it is likely that this patient is taking over-the-counter NSAIDs on a regular basis. It is important to elicit the history of NSAID use as part of the history, especially in patients with anemia, gastrointestinal bleeding, and obstruction. Actually, NSAID use may not even be active when the disease is diagnosed.

The clinical presentation is highly suspicious for post-transplant lymphoproliferative disease (PTLD), and the endoscopic images are representative. PTLD are a heterogenous group of disorders ranging from reactive-polyclonal hyperplasia to aggressive non-Hodgkin’s lymphomas. Incidence is 1%-3% of solid organ transplants, with variable mortality from 0 to 60% depending on response to changes in the immune suppression and to chemotherapy including rituximab. 90% are related to infection with Epstein-Barr virus (EBV). Often, a prodrome of fever and upper respiratory infection symptoms precede development of PTLD and represents primary infection or reactivation with EBV.

Risk factors include:
• First year after transplant.
• EBV seronegative patients, especially when younger.
• Organ transplant from EBV seropositive donors to naïve recipients.
• Type of immunosuppression. The incidence has increased with the introduction of tacrolimus-based therapy.
Symptoms include fever, malaise, tonsillar enlargement, and lymphadenopathy. Gastrointestinal (GI) tract involvement occurs in 55% and includes abdominal pain, vomiting, diarrhea, and GI bleeding. PTLD may also involve the central nervous system, bone marrow, kidneys, liver, lungs, and spleen. Surgery, conventional chemotherapy, and radiation have also been used. The role of antiviral to prevent PTLD is not clear.

capsule miss rate for neoplasms is around 19%, which is in part due to poor bowel preparation that can happen in about 10% to 15% of studies, regardless of the preparation regimen. In a long-term follow-up study of patients with obscure GI bleeding and who had non-diagnostic video capsule endoscopy (VCE), a second look VCE identified lesions in a subgroup of patients in whom occult GI bleeding changed to overt GI bleeding or there was a drop in hemoglobin > 4 g/dL. For patients with overt bleeding or persistent anemia and negative tests, repeating VCE, enteroscopy, or (in selected cases of life-threatening hemorrhage) intra-operative enteroscopy should be pursued until a source is identified.

Endoscopic biopsy may assist in differentiating GAVE from other etiologies such as PHG, particularly when fibrin thrombi are seen within dilated capillaries. Most cases of GAVE are idiopathic, although there are associations with cirrhosis and systemic sclerosis. GAVE occurs more often in elderly women (> 70 years), and the typical clinical presentation is that of chronic GI bleeding, iron-deficiency anemia, and hemoccult positive stool.

Bleeding secondary to GAVE can be effectively treated by endoscopic therapy. Options include argon plasma coagulation (APC), mono or bipolar thermal therapy, radiofrequency ablation, and endoscopic band ligation. Most reports are retrospective studies and there are no randomized controlled trials comparing these techniques. Most experts endorse the use of APC due to ease of treating a more diffuse area and radiofrequency ablation for cases refractory to APC.

Antrectomy is rarely necessary (0.4% of cases), but should be considered for patients who fail endoscopic therapy. Reduction of portal pressure (eg, by the use of propranolol or TIPS) has not demonstrated to be of benefit in treating bleeding secondary to GAVE. Treatment outcomes appear to be similar in patients with or without cirrhosis.

In general, gastric cancer re-bleeding can be controlled with endoscopic therapy; dual endoscopic therapy being superior to monotherapy. In cases of refractory advanced gastric cancer bleeding, external beam radiotherapy is an effective modality for treatment.

Patients typically follow consumption of multiple, small meals that are low-fat and low-residue. A small particle-size diet improves symptoms of gastroparesis in diabetic gastroparesis. Liquids may be more beneficial than solids in gastroparetic patients.

Gastrointestinal bleeding in the setting of a known pseudocyst and/or necrotizing pancreatitis can occur from any of the following:
• Bleeding through a small vessel from the pseudocyst wall (intracystic bleeding).
• Extravasated blood leaking into the peritoneal cavity or pancreatic duct.
• Pseudoaneurysm formation and subsequent rupture into the pseudocyst itself or an adjacent structure, such as the pancreatic duct, peritoneal, or directly into the surrounding hollow viscera.

indications for emergent endoscopy include:
• Esophageal food impaction with complete obstruction
• Sharp-pointed objects stuck in the esophagus.
Indications for urgent endoscopy within 24 hours include:
• Esophageal food impaction without complete obstruction
• Sharp-pointed objects within the stomach or duodenum
• Large objects that cannot pass beyond the pylorus, typically objects that are greater than 6 cm in length
• Magnets in the stomach or duodenum
• Objects lodged in the esophagus that are not sharp

The use of the Doppler endoscopic probe (DEP) for detecting arterial flow was first described in 1982 and its use in predicting the risk of rebleeding and successful endoscopic treatment has been shown in several prospective studies. The DEP is typically passed through the channel of an endoscope and the tip of the probe is then applied to the base of an ulcer or any stigmata of recent bleeding. A positive DEP signal is defined as a repetitive and similar visual spiking waveform or audible signal indicative of pulsatile blood flow. A negative DEP signal post-therapy has been associated with effective hemostasis, while a persistent positive DEP signal post-therapy has been associated with higher rates of rebleeding.

Erythromycin is the correct answer. Erythromycin (250 mg) may be infused intravenously over 20 to 30 minutes approximately 30 to 90 minutes prior to endoscopy. Multiple meta-analyses, including randomized controlled trials, evaluating administration of erythromycin prior to endoscopy for upper gastrointestinal bleeding have shown significance in improvement of gastric mucosa visualization, reduction in the length of hospital stay, and a decreased need for second-look EGD.

Sucralfate acts in an acidic environment by binding with positively charged proteins in exudates, thereby forming a viscous substance that acts as a coating to protect the gastric surface. Sucralfate may impede the mechanism of action of proton pump inhibitors (PPIs). As the name implies, proton pump inhibitors act on the hydrogen-potassium ATPase pump.

Anal manometry – rest anal pressure weak, rest normal – scleroderma
Squeeze anal pressure and resting pressure weak + weak rectal sensation MS
Squeeze anal pressure and resting pressure weak, normal sensation – pudental nerve injury

AIH – treat if ALT more than 10 x, or more than 5 x and increased immunoglobulin more than 2 or active necrosis

The colonic biopsies documented mucosal erosion, focal acute cryptitis, and patchy chronic inflammatory infiltrates with minimal architectural distortion. Histologically, there is no reliable method to distinguish segmental colitis associated with diverticular disease (SCAD) from chronic inflammatory bowel disease. Active chronic inflammation outside the distribution of diverticulosis would raise the possibility of an alternate diagnosis such as inflammatory bowel disease. The endoscopic image is notable for shallow mucosal erosions, but the pathologist did not notice mucosal necrosis suggestive of ischemic colitis.

As there was evidence for histologically confirmed inflammation, the diagnosis of symptomatic uncomplicated diverticular disease (SUDD) is incorrect. Crohn’s disease is a consideration in this case, but as the inflammatory changes are limited to the diverticular segment, this diagnosis is less likely. Microscopic colitis is not generally associated with abnormal endoscopic findings and, hence, this diagnosis is incorrect.

The tracing represents an evaluation for the recto-anal inhibitory reflex (RAIR). This is part of the standard evaluation performed during an anorectal manometry. A balloon is inflated in the rectum resulting in increased pressure along the rectal walls (arrow). If this reflex is intact, the distension should lead to relaxation of the internal anal sphincter and a decrease in intra-sphincteric pressures. In this example, there is no evidence of anal sphincter relaxation with rectal distention. An intact RAIR almost completely excludes the possibility of Hirschsprung’s disease, but a negative study indicates that Hirschsprung’s may be present. Hirchsprung’s disease develops due to a lack of migration of neural crest cells into the distal colon, consequently resulting in an aganglionic segment of the colon which fails to relax. This causes a functional obstruction. While Hirschsprung’s is usually diagnosed in infancy or early childhood, a small percentage of cases are not detected until adulthood and this is usually associated with an ultra-short segment of the rectum 2-4 cm proximal to the anal sphincter.

In contrast, juvenile polyposis syndrome (JPS) is an autosomal dominant (with incomplete penetrance) colon cancer syndrome that should be suspected when there are multiple (>5) juvenile polyps in the colon, juvenile polyps outside the colon, or a family history of JPS. JPS is a hamartomatous polyposis syndrome. The histology of JPS polyps is similar to isolated juvenile polyps but adenomatous features may also be present. Family studies suggest up to a 50% risk of GI cancer, which can present at an early age (mean age 30s). Cancer of the colon, duodenum and stomach, and pancreas are most common. Genetic mutations are identified in 40-60% and include BMPR1A, DPC4, and SMAD4, a transforming GF-Β intracellular signaling molecule. Surveillance should be performed and consists of colonoscopy every 3 years from time of symptom occurrence or in early teen years if no symptoms in patients with a family history and EGD every 2 years beginning at age 15.

This is segmental colitis associated with diverticulosis (SCAD). SCAD is characterized by inflammation in the interdiverticular mucosa without involvement of the diverticular orifices. The prevalence of SCAD ranges from 0.26-1.5%. The pathogenesis of SCAD is unclear. Mucosal prolapse, fecal stasis, and localized ischemia have all been implicated. Patients with SCAD typically present with chronic diarrhea, cramping abdominal pain primarily in the left lower quadrant, and in some cases intermittent hematochezia. Approximately one-third of patients have more than 1 symptom at the time of diagnosis. The endoscopic features of diverticular colitis can vary in severity and have been classified into 4 subtypes:

Type A (crescentic fold pattern) – Characterized by reddish round lesions ranging from 0.5-1.5 cm in diameter at the top of the colonic folds
Type B (mild to moderate ulcerative colitis-like pattern) – Characterized by loss of the submucosal vascular pattern, edema of the mucosa, hyperemia, and diffuse erosions
Type C (Crohn colitis-like pattern) – Characterized by isolated aphthous ulcers
Type D (severe ulcerative colitis-like pattern) – Characterized by loss of submucosal vascular pattern, intense hyperemia, diffuse ulcerations, and reduced caliber of colonic lumen

SCAD is usually diagnosed incidentally during the course of evaluation of chronic diarrhea and/or abdominal pain. The diagnosis of SCAD is made by the presence of inflammation on endoscopy and chronic inflammatory changes on biopsy only in an area of the colon with diverticula (usually the sigmoid colon and in some cases the descending colon) and absence of inflammation in the rectum.

The majority of patients with SCAD appear to respond to medical therapy, but approximately one-third of patients relapse within 3 years. A small percentage ultimately require surgery for diverticulosis-associated strictures causing obstruction or bleeding leading to chronic anemia. Progression to inflammatory bowel disease has been reported in some case series. The optimal treatment for diverticular colitis has not been well-defined. Initial treatment is often with antibiotics, typically ciprofloxacin 500 mg orally twice daily and metronidazole 10 mg/kg per day in 2 or 3 divided doses for 10 to 14 days. In patients who do not respond adequately, oral mesalamine started at 800 mg orally 3 times daily for 7 to 10 days should be added, and if symptoms persist in 2-4 weeks, the dose should be increased to 1,600 mg orally 3 times daily. In patients with continued symptoms despite antibiotics and mesalamine, prednisone 40 mg daily should be added for 1 week and then gradually reduced and discontinued over 6 weeks.

This case illustrates the now appreciated presentation of isolated right colon ischemia (IRCI) in which abdominal pain predominates over rectal bleeding. IRCI is more likely than any other segmental pattern of involvement to be associated with coronary artery disease, atrial fibrillation and chronic kidney disease that requires dialysis. Dialysis is likely associated with IRCI because of shifts in intravascular volume and possibly localized non-occlusive vascular disease. Indeed, in some cases of IRCI, the adjacent small intestine is also injured. Length of hospitalization, need for surgery and mortality are also greater with IRCI than any other pattern of colon ischemia, except perhaps pancolitis. In addition, because the superior mesenteric artery (SMA) supplies blood to the small intestine and the right side of the colon and because some cases of IRCI have been associated with or followed by acute mesenteric ischemia which also has a mortality exceeding 70%, imaging studies of the splanchnic vasculature are recommended. This recommendation is in contrast to our usual recommendation not to do these studies in cases of colon ischemia because at the time of presentation of non-IRCI, colon blood flow has already returned to normal and the acute clinical presentation is more a result of reperfusion injury than it is of ischemic injury. With IRCI, if vasoconstriction is found, or if an SMA embolus is discovered, intra-arterial infusion of papaverine with or without surgery has been associated with the best outcomes.

The only pattern that is said to be pathognomonic for colon ischemia, and which has a 75% histopathologic yield in making the diagnosis, is the so-called “single-stripe” sign. It typically is found in the descending colon and connotes a good prognosis. Ischemic colitis

In a cohort of patients with diverticulosis incidentally discovered during colonoscopy, the cumulative probability of diverticulitis was 4.3% over a median 6 years of follow-up when using a liberal definition, not requiring CT scan for confirmation, and only 1% when requiring CT scan or surgery to confirm the diagnosis of acute diverticulitis.

Smoking appears to be a particularly strong risk factor for perforated diverticulitis. Several medications are also associated with an increased risk of diverticulitis and diverticular bleeding, including non-steroidal anti-inflammatory drugs, steroids, and opiate analgesics, while calcium channel blockers and statins may have a protective effect. Lastly, physical inactivity and obesity are associated with an increased risk of diverticulitis and diverticular bleeding.

Diverticulitis patients, more likely to develop IBS, have health conscious issues with diet and emotional disorders

There is a risk of immediate further deterioration and death. The first step should be needle decompression of the abdomen. The abdominal wall is prepped and an angiocath hooked to a syringe partially filled with water is inserted through the abdominal wall with suction applied. When gas is aspirated, the angiocath is threaded into the peritoneal cavity and gas is allowed to escape. In severe cases, gas may have dissected into the pleural space, requiring further needle decompression of the chest cavity. Barotrauma perforations have occurred with carbon dioxide insufflation. Although barotrauma perforations are generally in the cecum or proximal colon, patients with barotrauma nearly always have a complicated sigmoid, usually from severe diverticular disease. The colonoscope passing through the narrowed and angulated sigmoid produced a temporary obstruction in which gas cannot escape backward around the instrument. If the ileocecal valve is competent, gas may be trapped in the proximal colon, resulting in distention and eventual perforation. Switching to water insufflation in all difficult sigmoid colons has been endorsed as a method of preventing barotrauma perforations.

The FIT-DNA test is 92% sensitive for CRC, 42% specific for advanced neoplasia and has 87% specificity. The FIT-DNA test is more costly than FIT, and less cost-effective than either FIT or colonoscopy. The evidence for the 3-year interval recommended for FIT-DNA comes from modeling studies, not case series or randomized controlled trials.

The second generation colon capsule measures 31.5 X 11.6 mm and is equipped with 2 cameras. It has a 172 degree angle and covers almost 360 degrees of the colon mucosa. The frame rate ranges from 4 images/second to 35 images/second and allows for improved visualization and enhanced battery life. The preparation is more challenging than that for colonoscopy and requires 2 boosters of sodium phosphate to accelerate transit through the small bowel and colon. Contraindications are similar to that of the small bowel capsule. A recent study suggests that the colon capsule can reduce unnecessary conventional colonoscopy by 71% in patients with a positive fecal occult blood test.

This history, endoscopic finding, and basophilic crystal present on histology are all consistent with sodium polystyrene sulfonate (Kayexalate) as the cause of this patient’s esophageal ulcer. Kayexalate is a cation-exchange resin used for the management of hyperkalemia, and acts in the colon to exchange sodium for potassium. The most serious gastrointestinal toxicity related to this medication is mucosal ulceration which may be transmural and sometimes fatal. This has most often been reported in the colon, but also in the small bowel, esophagus, and rarely the stomach. This adverse event had been attributed to its preparation with highly concentrated sorbitol (70%). However, there have been continued reports of similar toxicity with preparations using lower concentrations of sorbitol and those containing no sorbitol. Not surprisingly, 71% of patients with Kayexalate gastrointestinal toxicity have renal disease (chronic renal insufficiency or renal failure requiring dialysis), and another 16% have a history of solid organ transplant.

Curcumin is a phytochemical (diferuloylmethane) derived from the spice turmeric, which is common in Indian foods. Curcumin has been shown to have multiple immune effects that theoretically would be beneficial in IBD. Two small, placebo-controlled, randomized trials of curcumin supplementation at doses of 2-3 grams per day in combination with mesalamine have shown promise for patients with ulcerative colitis. These studies used pure forms of curcumin so it is important that patients purchase pure curcumin (answer C is correct)

Dysplastic lesions in the setting of inflammatory bowel disease should be described based on terminology adapted from the Paris classification. These include the presence of ulceration as well as a description of the border of the lesion. The lesion shown in the figure represents a polypoid visible dysplasia with indistinct borders. Polypoid lesions protrude from the mucosa into the lumen at least 2.5 mm. Current guidelines recommend abandoning terms such as dysplasia associated lesion or mass (DALM) and non-adenoma-like lesion.

Ustekinumab, an antibody to the p40 subunit of IL12 and IL 23, is FDA approved for the treatment of moderate to severe Crohn’s disease and has shown efficacy, anecdotally, against pyoderma gangrenosum.
Live vaccines include MMR, varicella, herpes zoster, and intranasal influenza vaccine and are usually contraindicated in patients on high-level immunosuppression, such as our patient on adalimumab.
On day 3 of hospitalization, patients with more than 8 stools a day or those with between 3 and 8 stools on day 3 as well as a CRP >45 mg/L have a high likelihood for need for colectomy (Answer B is correct). The other laboratory values are also important prognostic markers at the time of admission but are not used as predictive markers on day 3 of hospitalization (Answers A, C, and D are incorrect). UC colectomy evaluation on day 3 in hospital
The breath hydrogen curve shows a double peak and an early and marked rise in breath hydrogen typical of small intestinal bacterial overgrowth (SIBO), which is best treated with an antibiotic such as rifaximin.
Reducing FODMAP content of the diet has minimal effect on fecal water content, but can still be helpful in relieving symptoms of IBS. Although data are limited, 12 weeks of a moderate increase in exercise in patients with IBS improved many symptoms in the short and longer term.

Prophylactic antibiotics have been shown to reduce mortality in variceal bleeding but include specifically quinolones or ceftriaxone in areas with high resistance to quinolones and potentially advanced cirrhotics (answer D is incorrect). While IV octreotide has not been proven to decrease mortality in variceal bleeding, it does reduce rebleeding rates.

the use of hepatitis B vaccination for all unvaccinated adults aged 19-59 years upon diagnosis with type 1 or type 2 diabetes mellitus, in whom an increased risk for acute hepatitis B has been reported by the Centers for Disease Control and Prevention (CDC). Unvaccinated adults age 60 years or older may be vaccinated at the discretion of the treating physician after individualized assessment of risk and likelihood of mounting an adequate immune response to HBV vaccination.

MELD = 3.78×ln[serum bilirubin (mg/dL)] + 11.2×ln[INR] + 9.57×ln[serum creatinine (mg/dL)] + 6.43.

there is an association between microscopic colitis and celiac disease with a prevalence rate ranging from 2-19%. This appears to be possibly linked to the HLA-DR3-DQ2 haplotype. Thus, in an individual with rheumatoid arthritis and microscopic colitis who has failed multiple therapeutic interventions, the next most prudent option would be further evaluation for celiac disease, and serologic testing (answer E) would be the most appropriate initial test.

This patient has mycophenolate mofetil-associated gastrointestinal toxicity. GI adverse events, in particular diarrhea, are common with this medication and are the most common reason for its discontinuation. Both the colon and small bowel may be involved, and the injury to the mucosa may be due to 2 metabolites: N-(2-hydroxyethyl) morpholine and acyl-MPAG. Medications that increase the concentration of mycophenolate mofetil, such as tacrolimus and acyclovir, may worsen the toxicity. AIE autoimmune enteropathy does not have goblet or plasma cells

Esophageal varices have developed from pre-hepatic portal hypertension. Cavernous transformation occurs after decades of portal vein thrombosis. Anti-coagulation is not clinically indicated in this setting and will not resolve the thrombosis. The varices have already bled. In this situation the risk of rebleeding is significant. It is therefore reasonable to band the varices to obliteration. Beta-blockers could be prescribed. TIPS is not indicated in a patient with cavernous transformation of the portal vein.


Steinberg notes
Saturday, September 22, 2018
9:06 AM

Steinberg course

HDV can be 2 ways : same time as HBV and that is co infection
Superinfection occurs later
Rare in USA and from Greece
Check HDV once with everyone with HBV

Hepatitis E

Common in Africa, india, caribean, Mexico and south America. Self limited like A.

Phases of Infection of hepatitis

Incubation HAV 4 weeks incubation, HBV 3 months, HCV 6 weeks average HCV can be as high as 20 weeks. HCV. And also is HBV can be incubation upto 6 months also.
Prodrome phase : flu like sysmptoms, mild RUQ pain, and serology is positive and lasts 3-5 days
Icteric phase : jaundice, serology, flu like increased ALT

Variants to phases. : 25% of patient get jaundice many have anincteric phase. Icteric viral hepatitis is rare
Acute liver failure in acute phase very uncommon, less than 1% and more common if more than 40 years or if you have chronic liver disease . SO vaccinate ALL with chronic disease for hepatitis A and B. ALT is more than 10,000, bilirubin more than 10, increased INR HE, mortality is 80%
HEV in pregnantwoman ALF 1%

HCV 80% chronicitiy
HDV and HBV then chronicity is 100%
HEV chronic from immune suppression.

HCV – can get trapped with cryoglobulin. However cryoglobuin can occur with ALL viral hepatitis
HAV _ stills disease, aplastic anemia , (See slide), ATN
HBV _ PAN, GN, pemphigoid, lichen planus, GB syndrome
HCV – GN, type 2 DM, PCT, B cell NHL, vasculitis and polyneuropathy
HEV – pancreatitis, GB, hemolosys, aplastic anemia

Two types of Ab are produced – preventive AB, non protective Ab – internal viral proteins, such as HBcAb, HBe Ab, anti CMV, EBV, herpes

HAV – cholestatic HAV, elevated ALP can be prolonged upto 6 months

Other HAV variants is relapsing HAV -HAV , lasts many months
Window period between HbsAg and HbsAb is few days to 6 weeks (none is positive)
Seroconversion if Hep B e Ag positive to eAb occurs with a second flare up! Can be years later, at that time Hep B IgM becomes positive again. You may mistake this as acute hep B. Check for fibrosis on liver. That will help differentiate. (hep B e Ag is now negative). This can become fulminant hepatic failure
Serconversion is not related to HBV DNA level, ALT or histology, but solely chronicity

E Ag Hep B
E Ag is in the precure region of HBV. It is not neded for replication. It is the target for immune response to inactive HBV.
E neg disease is mutation of the E gene, – the mutated protein is not picked up by the assay now. And this prevents immune response,
How you can get E neg disease
Hep B s – develop Ab and inactive HBV. Or mutated E Ag – HeE Ag neg and chronic HBV (see slide)
Immune tolerant HBV – normal ALT, high HBV DNA, and if bx done, no inflammation and no fibrosis. NO treatment is indicated. (immune tolerant state).
However, when there is HBV DNA, and ALT goes up, and there is loss of immune tolerance and this when you treat. See slide. ALT more than 2 x normal (USA guidelines uses ALT and 20,000, but it is archaic, ) Gray zone patients – discortdant between level of virus and and ALT. Immune tolerate virus level is extremely high. Not like 300,000
HCC cancer risk – Ag positive must be followed regularly. And have to be screened for liver cancer. (low risk but not zero). (80% of them ). Total HCC cases – 40% from Ag (carrier)
HCC risk goes up between 2000-20,000 range of HBV viral level.
Most cancers occur without cirrhosis
Treatment – vaccinate, A and B, For family – vaccinate close contact – IgG or HBIG for hepatitis B (household of index patient)
HBIG given to new born with vaccine

Treat HCV in mom after 3 months of birth

Baby transmission occurs if HBV DNA 200,000, then vertical transmission is 10%. Treat mom for HBV to prevent vertical transmission
HBV booster therapy needed? – 40% after the patient lose response to HBV vaccine in 10 years ( by titers). For needle stick, give booste and then document response.
Interferon therapy with HBV – for genotype A. (Caucasians and AA) 50% conversion rate.
Oral treatment for HBV – ALT normal and HBV DNA less than 400. If hep E neg, need life long therapy. Tenofovir Alafenamide is 25 mg (due to better delivery compared to Tenofovir TDF version. (this reduces less bone and renal toxicity). If you stop treatment too soon, flare up occurs.
Treat active disease or prophylaxis before any biologic and chemotherapy
HCV – Baby boomers – 45-65 birth year.
Polymerase cycle, protease cycle or replication complex cycle. For HCV drugs.
Zepatier if resistance in 1a, treat for 16 weeks. HIV infected or not, response rate is the same. Dialysis patients same cure rate
If only Hep B c Ab positive, ?? just monitor
HBV cirrhosis gets better if you treat long term
HCV, 5 years after cure – cirrhosis improves / resolves in 50% of cases
Risk of HCC goes down. Also risk of extrahepatic goes away, including lymphoma it is 0% but with C, risk is 3% for lyphoma. Similarly risk for Dm and ESRD improves with treatment for HCV.
If HBV DNA more than 200,000 treat HBV in third trimester. (see slides)

DILI – 1:5000 to 1:100,000 use of drugs. 60^ of ALF from DILI. 50% from Tylenol, other drugs 11% responsible for ALF, rest is miscellaneous causes 57% is from drugs)
Children more risk for valproic, aspirin,
Age more than 50 risk for DILI
Women more likely than men
Obesity and malnutrition are risk factors, alcohol , higher dose of meds, multiple drugs and prior DILI are other risk factors.
Genetic factors – cytochromes, drug transporters, immunologic factors, mitochondrial enzymes and cytoplasmic detox.
Tylenol is preferred analgesic in cirrhosis patient – if no alcohol. Cirrhosis and NSAID is bad increases renal failure risk
Methotrexate should not be used in cirrhosis.
Biotransformation – active metabolite can be toxic, or recognized as toxic by immune system. Usually in ER and cytochrome.
Rash, fever or eos – Dilantin, phenytoin, halothane and sulfa medications (example of allergic reaction)
DILI – intrinsic or idiosynchratic . Intrinsic – INH, amantia mushrooms and Tylenol are intrinsic hepatotoxicity. (now there are no other drugs)
Almost all other causes are idiosynchratic –
Liver has ADAPTATION – example with statin, might go up transiently, and then it is tolerated. Check liver panel montly. If less than 3 ULN ok to continue
Statin, check LFTs 3 months after starting

If LFT between 3-5x ULN – 10% develop ALF and if more than 5 timex ULN – 50% ALF (if jaundice). Hys Law
DILI – drug induced – gets better in 6 weeks. Check drugs that causes it. Turmeric causes cholestasis. When itching stops, the ALP starts declining
NSAIDS, H2 blockers, PPI, estrogens, antifungal and macrolide causes cholestasis
Fatty liver – valproic acid, steroids, tetracyclines,
Niacin – dose dependent, significant liver toxicity, can occur after many years of using niacin. (most drugs do it in 4-6 weeks of starting), fatigue, jaundice etc
INH – minor elevation is common in 20% of cases, severe liver injury in 1% of patients and 2% in age past of 50. 2 types of metabolizer – fast or slow. Slow metabolizer get toxicity
Herbal meds causing toxicity, chaparell, Chinese tea, Jamaican tea, (veno occlusive disease), cascara, germander, jin B huan ( see list), kava. And zulu medication
Methotrexate – after 2 grams or 2 years. Stages are fatty liver, portal fibrosis, bridging fibrosis and cirrhosis. No liver Elevation. (use fibroscan to monitor)
Tylenol : NAPQ is a toxic metabolite – glutathione metabolizes it. (lower in alcolism and poor nutrition) If you start NAC within 16 hours – risk of ALF is 0
If between 16-24 hours risk of liver failure is 3% and after 24 hours then the mortality is 15%^ from ALF. (anyone who comes after 24 hours, transfer to transplant center)20% death rate
Worst combination is Tylenol and ethanol.
Things that induce P450 include alcohol, anti seizure medication and rifampin (so higher Tylenol toxicity)
INH toxicity Rx – NAC reduces the risk of developing in ALL causes of DILI. Also effective in hep B and undetermined causes. AIH use steroids.


ANCA is for PSC
PBS – 50% get sicca syndrome, RA and thyroid disease and
PSC – 90% will have UC or less commonly CD
They are genetic.
If ASMA or AMA positive, genetic risk but may get it if there is a trigger
AIH – ASMA and anti LKM or anti LC1. Type 2 disease common in USA, more in France, young women, more severe and rapid.
Type 1 is ASMA and 20% are ANA neg.
15% with AIH marker neg. Diagnosed by Liver biopsy and increased fibroscan more than 7.
AIH histology – piecemeal necrosis (lymphocytes around hepatocytes). Diagnostic criteria for AIH from mayo clinic ( markers, IgG elevated, and score more than 7 certain, and more than 6 and probable AIH)
Types of presentation – Flu like, AST and ALT 500-1000, cirrhosis maybe present, ALF can occur and have symptoms. Bil is 5-15.
Less common is indolent form – 50-100, normal bili,no symptoms, mild inflammation and ALF does not occur. Third type is cryptogenic cirrhosis – normal enzymes, cirrhosis present, no inflammation is noted, and DO NOT TREAT WITH STEROIDS< markers positive,
Do not treat with steroids without doing liver biopsy.
How to treat – 60 mg for 2 weeks, and then 40 mg for 2 weeks and then 20 mg till LFT normal, then 10 mg for prolonged time – 6 months to a year. Add azathioprine or cellcept – Dr. Schiff likes cellcept. 1 or 1.5 mg/kg. Can start either at 60 or when at 20 mg. ( question – mild indolent AIH at 68, treatment is not needed).
Mild AIH – treated or untreated no change in survival.
Key word is piece meal necrosis – aggressive (my understanding)
Tacrolimus is an option with target serum 2-4 ng/ml
(uncommon renal disease at this low dose)
33% will develop cirrhosis even if normal ALT and immune suppression. (treatment slows it but does not eradicate inflammation). Stop treatment – ? trial and error
Secondary drugs ( myconphenolate mofetil (cellcept), or tacrolimus if you cant get patient off prednisone.
Dexa scan if on long term prednisone. (prednisone makes you hungry and then get weight gain occurs)

PBC : 9 types of AMA. In PBC is M2. Other subtupes are M4, M8 and M9. Positive markers in 95% cases
Bx is not necessary, elevated ALP, and AMA and biopsy. Need only 2/3.
Life expectancy worse when symptoms occur. Rx is Urso. Bile salts are toxic. (disease is from bile salt leaking out of duct in liver and then it causes damage).
Start urso early and earlier the start point, the better the outcome.
Clinical response is 40% reduction of ALP from baseline. Now the response is less than 1.67 level of ALP. If that is not achieved, second line of therapy.
ALP closer to normal – best outcome in survival
Osteoporosis is at higher risk. 2 times higher risk of fractures
Get DEXA at time of diagnosis.
Increased risk at teeth problems (lots of fluid, dental visits)
High cholesterol also occurs.

PSC : large and small duct disease. Liver biopsy for staging and MRCP. In large duct
Small duct PSC – needs liver biopsy, ALP elevated.
Scarring of portal tract, onion skin around bile duct, portal fibrosis without inflammation, (bland fibrosis). NO treatment
Even with OLT – 20 year survival is 60% meaning they develop cirrhosis
Vancomycin helps PSC – More effective in pediatric age. 125 mg a day
ERCP indicated with dominant stricture – and jaundiced
Urso does not help. High dose of colon cancer and death ( dose30 mg/kg)
Only 5% of IBD patients have PSC. Not related to severity of PSC and IBD.
Can develop even after colectomy in UC
Or can develop IBD after PSC OLT
Progressive jaundice (not intermittent) and weight loss, means possible cholangioca with tight stricture
Can check CA19-9 and CEA. 40 x CEA plus CA19-9 if more than 400 then cholangio ca

Overlap syndrome – histology that looks like PBC and titers of AIH. Treat with urso. Treat histology not markers.

Liver in Pregnancy

Normal physiology – ALP can be up, palmer erythema, spiders and even small varices. , AFP and ALP (2-4 x ULN0 can go up.
AST, ALT< GGT, PT and bili remain normal. (even with Gilberts syndrome)
GB and sludge 10% of all pregnancies. ERCP and chole usually best in 2ndr trimester
Vertical transmission of HBV – in e neg 25% and e positive 90%. HCV and HAV vertical is 1-5%
20% mortality of HEV in pregnancy.
HCV vertical is 5%. No difference if vaginal or c section. Breast feeding is safe. Treat after delivery
HBV – C section reduces vertical transmission. Breast feeding is safe if if infant gets HBIG and vaccinated. HBIG in 12 hours of birth and then vaccinate at birth
Tenofovir – during third trimester E ag positive reduces risk to infant from 80% to 7.1
And if e neg, then reduces it to 0
If HBV DNA less than 200,000 then just HBIG and vaccine to infant
If more than 200,00 then give tenofovir is safe in pregnancy, and HBIG and vaccine
If preterm labor then they are high risk like having HBV DNA more than200,000 and give tenofovir

HSV high liver enzymes bilirubin less than 3, and use acyclovoir.
Budd-chiari can occur in pregnancy. Schistosomiasis gets worse in pregnancy due to progesterone. (in Egypt)
Conditions that get worse in pregnancy include portal HTn, AIH, PBC, Wilson, liver masses, splenic artery aneurysm with cirrhosis.
Portal HTN in pregnancy – from increased volume, usually in 2 and 3 trimester. MELD more than 10 is bad. Consider prophylactic banding if large EV.
Continue immune suppression and azathioprine in AIH and urso is safe too.

PSC – premature preterm birth increased

FNH, Adenomas, hemangiomas can increase in size in pregnancy. Monitor with US.

First trimester – hyperemesis gravidarum
Second trimester – cholestasis of pregnancy
Third trimester –

Incidence of liver disease in pregnancy is 1%. Pre eclampsia is the commonest, 70%. Then HELLP

Hyperemesis Gravadarum .3 to 2 % of pregnancy- RF, nulliparity, twin pregnancy and increased BMI,DM and hypothyroid. Unconjugated bilirubin goes up, IV fluids, thiamine, and anti emetics.

Intrahepatic cholestasis of pregnancy – 1 %incidence. Genetic predisposition. Defect in bile acid transporter. Associated with leaky gut, low vitamin D and selenium levels
25-32 weeks, pruritis worse at night, normal GGT, elevated ALP, bile acids more than 40 umol or 10-100 x ULN increased fetal morbidity. AST and ALT as high as 1000. Can have steatorrhea.
Treatment is urso, cholestyramine is not recommended. Give vitamin K around birthing. High fetal mortality,still birth and prematurity. This can occur with subsequent pregnancy and can occur with use of estrogen in future.

• Toxemia, then HELLP and then AFLP
• 30% in multiple gestation
RF nulliparity, HTN, age more than 40,
Hepatic manifestations include – mild increase in ALT to liver failure in minority. RUQ pain, AST and ALT less than 10 x ULN, mild bilirubin more than 3.
Later HELLP, hepatic infarction and rupture

HELLP – can occur without hypertension. 2-12% of pregnancy, multiparity, Caucasian and age more than 35. ALT can be upto 50 x ULN. Bilirubin is less than 5. Steroids can help if less than 34 weeks of pregnancy. Can recur.

Hepatic infarction / rupture – sudden abd. Pain shock liver, fever, anemia, spiking fevers, usually right lobe

AFLP – severe microvesicular steatosis, can occur post-partum. Defect in the LCHAD. Male fetus, AST more than ALT, high wbc, jaundice less than10, coagulopathy and low fibrinogen.

Differentiate HELLP and AFLP

AFLP is not with toxemia usually, has nausea vomiting, more common.

AFLP Mx – move to ICU, prompt delivery, can recur in subsequent pregnancies,

5% fat in liver is steatosis. Large or small droplets. Fibrosis predicts liver related outcome. Microvesicular – TCN(tetracycline), valproate, antivirals, ryes, HELLP, inborn errors, AFLP
Macrovesicular – TPN, wilsons, tamoxifen, HCV type 3, amiodarone, MTx, diltiazem, tamoxifen, NAFLD, alcohol, starvation
Risk of alcohol include female gender, race, dose, duration, obesity iron overload, HCV and HBV, tobacco use, coffee is protective
Threshold for men 80 gm a day (6 pack) or for women 40-60 grams a day. (4 drinks a day)
Binge drinking steatosis. 50% of the develop steatohepatitis, and then 20-40% develop fibrosis and 10% – 20%of alcoholics will develop cirrhosis
Acute mortality in 10-20% alcoholic hepatitis. SIRS criteria (increased HR, RR, WBC and absence of fever are predicters of severe injury and death
Zieves syndrome (hemolysis plus alcohol). If ALT is more than 400 think Tylenol
Burr cell anemia.
ANI index from mayoclinic. (BMI, MCV, AST/ALT ratio, gender) (differentiate alcoholic to non alcoholic index
Electrolyte imbalances in alcohol, Mg, phosphate, K, zinc, thiamine, glucose, folate and vitamin K. Often protein malnourished
Check MELD and DF, SIRS,
STOPAH trial – steroids may not help alcoholic hepatitis. Steroids helps only with 28 days data but not more.
MELD more than 20, DF more than 32 and more than 2 SIRS use steroids
Severe alcoholic hepatitis Steroids plus NAC
Use Lille score -0.45 is cutoff at 7 days If less than 0.45 continue

Contraindication to steroid is sepsis or GI bleed. Consider pentoxifylline if you cannot use steroids can be considered
Baclofen for alcoholism 5 mg tid and taper down

40% of the US population
Insulin and adiponectin resistance. Increase in FFA, leptin and TNF alpha. Fat resolution as fibrosis regresses. Genetic predisposition : PNPL3A and TM6SF2
NAFLD less than 21 for men and 14 for women (drinks per week)
HCC in alcoholic liver disease is 2-4% /year (from NASH directly) and decompensation is 3-5%/year. Cardiovascular disease is the biggest cause of mortality in this group
Cirrhosis occurs in 1-3% patients per year from NASH to cirrhosis
Other causes for NAFLD include, TPN , short bowel, chronic inflammation, Wilson disease, HCV, hypothyroid

Consider EST in NASH patients, elevated uric acid, lipid abnormality, PCOS, OSA, vitamin D def, higher chance of polyps

Can use APRI, FIB-4, NAFLD score (neg predictive value, if neg. rules out NAFLD), fibrosure, Fibroscan

Rx for NASH, weight loss, omega 3 FA, fish oil, can help, decrease fructose, exercise 30-40 min a week, pioglitazone, GLP-1

Hepcidin controls ferroportin. Liver senses iron. If high, secrets hepcidin and this inhibits ferroprotin and less iron picked up
IL 6- decreases hepcidin gene, so less hepcidin, and more iron absorption
HFE gene – needed to internalize Tf and Fe in the cells. So if a defect in the gene, less iron in cell, liver senses less iron and then less hepcidin and body keeps absorbing iron.
Juvenile 2A and 2 B disorder. cardiomyopathy and second decade /third decadeand hypogonadism.
Ferroportin disease – anemia but also increased iron.
Secondary causes of overload of iron includes, Dysmetabolic syndromes, acerulopasminemia and atransferrinemia.

HFE most common – 1:250 to :1-700 phenotype and genotype 1:200 to 1:300,
One copy of HFE 15% H63D and 6 % C287
C282Y both being present is the commonest phenotype (80%). Rare is S65C.
3-5% are compound heterozygous (C282and H63) less likely
Two copies of H63D does not cause phenotype
Can get pseudogout, chondrocalcinosis, dilated cardiomyopathy, dysrhythmias,
PCT – rule out HH, early arthritis or premature sexual dysfunction

Check HH if sat more than 45 or ferritin 400. (check it fasting since ferritin and saturation varies with meals)
IF age more than 40, ferritin more than 100, hepatomegaly and plt less than 200, and increased LFTs – do liver biopsy otherwise get phlebotomy directly
Once cirrhosis, morbidity and mortality is high. Alcohol less than 60 grams/week might be ok for HH ( but advise no alcohol)
Death is from HCC, cardiomyopathy, liver disease,diabetes and liver cancer

Increased ferritin – acute phase reactant, DD, ferroportin disease (type 4 if anemia), HFE negative HCC, HCV, HBV, alcohjol, NAFLD (ast less than ALT)

Ferroportin disease sat less than 45 and elevated ferritin, and anemia.

One unit removes 250 mg of Iron. Check ferritin less than 50 and HCT less around30,s avoid vitamin C shell fish,

Improving with phlebotomy is DM and cardiomyopathy and skin color. But arthropathy, cirrhosis and hypogonadism does not improve

A1AT def. Autosomal recessive. 8% with A1have liver disease. ALT does not predict liver disease
Check level first, then phenotype Pi ZZ and then PI Sz. PAS Diastase stain.
Infancy, neonatal hepatitis, hepatomegaly, mild AST and ALT
Childhood mild liver abnormality
Adults, – cirrhosis, portal HTN, liver cancer, increased risk of arterial aneursms, ulcerative neutrophilic panniculitis.
MZ phenotype carrier state – makes other liver disease like alcohol, HCV, HBV< NASH worse.

Wilsons disease

Defect in copper excretion. IN liver, kidney, brain, cornea an joint and RBC
1:30,000 gene def, but autosomal recessive. Chromosome 13.
Gene abnormality causes low copper transport protein
Diet 2-3 mg of copper a day, then goes into liver, then exported from enterocytes, and then goes to the liver and then leaves liver with ceruloplasmin.
KF ring, hemolysis causes RTA, dysthymia,
Age is NOT a reason not to check for Wilsons.
Clinical features, psych problems, movement disorder, KF ring, sun flower cataracts, drooling, seizures, hemolytic anemia, coombs ne, osteoporosis and osteoarthritis.
Can present hepatomegaly, cirrhosis, Acute liver failure, renal involvement, distal RTA and nephrotic syndrome
To diagnose low ceruloplasmin can occur but diagnosis urine copper 24 hours, more than a 100.
Hepatic copper – more than250. Serum free copper more than 200
You can stop workup if ceruloplasmin is normal and 24 hour urine copper is not needed

Copper rich foods, nuts, shellfish, chocolate, mushrooms
Rx is Trientine (chelation), decrease absorption by giving zinc.
Zinc causes metallothionine in intestinal cell. Dose 50 mg tid 30 min before meals.
Acute wilsons disease – low ALP, high bili to alk phos ratio, coombs neg anemia, coagulopathy, hypouricemia. TRANSPLANT immediately

Vascular disorders

Hepatic vein thrombosis and Budd chiari syndrome.
7 segments of the liver based on vasculature.
Segment 1 involved – budd chiari syndrome.
TIPS is usually in right hepatic vein, easier access.
See slide.
WHV pressure wedge, HVPG (hepatic portal gradient)free HV pressure no balloon inflated.

HVPG is WHV minus FHV

Portal thrombosis – bone marrow biopsy (in question) (JAK neg patient has myeloproiferative disorder, spleen enlarged)
Acute or chronic
Acute – abdominal pain, new onset ascites, lumbar pain, fever, ileus, acidosis, peritonitis and elevated AST/ALT
Not an expansile throbus (expansile thrombus – malignant)
Non enhancing Enhancing thrombus (malignant)
Coagulate for 3 months if no identifiable cause found
If plt less than 50,000 do not anticoagulate

Chronic portal vein thrombosis – non cirrhotis ( usually 85%^ eso varices, 30% gastric varices, )
No anticoagulation is NOT needed. Use anticoagulation if it reaches the superior mesenteric vein.

Tumor thrombus. Enhancing clot – do not anticoagulated.

Hepatic vein thrombosis – in young female with BCP. Anticoagulate first then think of TIPS etc.
Caudate lobe is enlarged.
Budd chiari – In Asians look for web in suprahepatic IVC
In West look for outflow obstruction at hepatic veins. Caudate lobe is enlarged and presses the IVC.
Can be acute or chronic. Presentation is transudate on fluid, and high ascites protein more than 3. Liver biopsy shows blood in liver (budd chiari or heart failure)

Other causes, similar to hypercoagulable state, including anti phospholipid, factor 5, protein c and S, oral contraeptives, myeloproliferative (Jak 2 positive or neg)

Rx is heparin, then LMWH, warfarin.
Portocaval or mesocaval shunting. TIPS ha a 9% 30 day mortality.

Urso can be tried to prevent sinusoidal obstructive syndrome with myeloablative therapy. For bone marrow cancer.
SOS (sinusoidal obstructive syndrome)

Cardiac ascites – Usually protein more than 3. Do not be aggressive with diuretics. They develop hypotension and get cardiac arrest since they are volume dependent for right ventricular failure.

Arterial disease – Shock liver. Patients with sepsis or peripheral arterial disease in history.
Usually ALT goes up, and 3 days later, bilirubin goes up. Bilirubin can take months to come to normal

Vascular diseases of Liver. HHT (hereditary hemorrhagic telangiectasia).
Recurrent eigastaxis, give iron, embolize pulmonary AVM, bevazicumab

Osler weber Rendu syndrome
Autosomal dominant.
Most of them have

NRH. (nodular regenerative hyperplasia).
Azathioprine can cause this. Normal Bx, nodules, hepatocytes rearranged into nodule. Can occur with systemic AI disease.
Portal hypertension, and no cirrhosis.

Peliosis hepatitis
From AZT, or HIV, bartonella, anabolic steroids, blood filled cavities in liver and biopsy.


IF cyst in liver is large and compresses the stomach – try unroofing cyst if aspiration helps symptoms
Wall nodularity or internal echoes then biliary cyst adenoma, needs surgery
DO not remove giant hemangioma.
Kasabach, Merritt syndrome, (MRI test of test ) centripetal enhancement
FNH – prevalence 5% in females, usually solitary, less than 5 cm

Hepatic adenoma ( tumor that lacks bile duct), associated with BCP, glycogen storage disease, PCOS, steatosis?
Risk is bleeding.
Hepatic adenomatosis – diffuse adenoma throughtout liver, needs OLT
Beta cetanin

Hepatic adenoma present after stopping BCP. Consider ablation if close to the capsule.


Cirrhosis – stage 1 to 4.
Based on varcies and ascites. See chart.
Stage 4 cirrhosis V with bleed and A. 57% mortality
Stage 3. V plus A
Stage 2. V and no A
Stage 1 no V and no A. 1% mortality

HVPG more than 10 causes ascites
50% cumulative chance of getting ascites in 10 years
50% mortality in 2 years with ascites
MAP less than 82, do not give beta blocker

Ascites – initial test get cell count protein, albumin.

Non portal HTn with SAAG less than 1.1
Heart failure pancreatic ascites, hephrortic syndrome, myxedema, tb, biliary ascites. ( see list)

Start ascites treatment with Aldactone, increase to 100 to 150/day.
Add furosemide, increase ratio 2.5:1,
Diuresisis 500 to 1 liter /day
Stp if cr more than 1.5
Na /K ratio more than 1 and weight gain, suspect non compliance.
If refractory, LVP
Use albumin, 8 gm/L
Read again
AKI if albumin not given and more than 5 liters removed, or Cr 1.5 and no peripheral edema
FFP is not needed.

DO not put TIPS if right ventricular failure

TIPS if MELD less than 18, patent portal vein, no pulm. HTN, age, less than 70, INR less than 3 and Cr less than 2.5 and no HE.

Can be done if partial PV thrombosis

Contraindications to TIPS – CHF, Pulm HTN, multiple hepatic cysts, biliary obstruction, infection etc.
Bilirubin more than 4, INR more than 5 and mELD more than 18, portal V thrombosis relative contraindication.

Occluded and fever rule out SBP

SBP 20% of cirrhotics develop it. 15% mortality, PMN more than 250, 50% of them with SBP have bacteremia
IV cefotaxmine,v/ augmentin / quinolone IV albumin on day 1 and 3 1.5 first and then 1 g/kg if Cr more than `, bili more than 4 and BUN more than30. (see chart)
Repeat paracentesis in 72 hours if no response . If PMN drops by 25% can change to oral antibiotics
Stop treatment in 7 days. Unless drug resistant organism
If no nausea, vomiting or HE, can treat SBP as out patient
(ofloxacin or cefotaxime same response rate)
Bactrim DS daily, cipro 500 daily, C
Norfloxacin if available
Cirrhosis with GI bleed ceftriaxone 1 gm daily, and then switch to norfloxacin

Primary prophylaxix not needed unless, CPT more than 9, Cr 1.2 and bili 3, sodium less than130 and low protein in fluid less than 1.5

Hepatorenal syndrome

LVP, SBP, cholangitis, nephrotoxic drugs, GI bled and over diuresis are causes
‘Type 1 rapidly progressive and doubijg of cr more than 2.5in less than2 weeks

Type 2, cr more than 1.5,
6 months survival,
norepinephrine ,
octrotide and midodrine and albumin,

Cirrhosis – AKI
Cr more than 1.5
Can be transient, persistant or progressive

Hypovolemic Hyponatremia may need IV saline
Avoid hypertonic saline,
V2 receptor antagonists do not use

Cirrhosis and beta blockers

SBP or ascites is not an indication to stop beta blocker
Stop if MAP less than 60 and refractory ascites.
Keep MAP more than 82


NO varices do not start beta blocker. 8% / year development rate of varcies
EV – start beta blocker
3 sizes small medium or large. If it occupies more than 1/3 of lumen or less

Follow up on EGD every 3 years for varices.
Large varices 25% bleed in 2 years, small 10% bleed /year, LOOK at slide

Antibiotics improve survival after varices bleed
Do not over transfuse.
Octreotide for 72 hours.
Consider early TIPS.
Do not band above 35 cm. (thin esophagus, perforates)
Here use banding plus beta blocker but not for primary prophylaxis
Early tips within 72 hours of bleed better prophylaxis
PPI in cirrhosis -Use it for 14 days after banding and then stop (stop acute ulcer post banding)
Fundic varices think of splenic vein thrombosis

Gastric varices
Rx TIPS or glue or balloon tamponade, vasoactive drugs.
If EUS available then post discharge coil and glue

Look words to differentiate GAVE and portal gastropathy. Slide

Tense ascites, high Cr, stop beta blocker (low blood pressure in the question bank)

HE classification
A in ALF
B shunting in portosystemic shunt
C cirrhosis

Level based on intellect, consciousness and neuromotor abnormality
Parkinsonism like syndrome
Seizures with high ammonia
Hepatic myelopathy
Focal deficits, tics
Involuntary movements
Babinski sign

Rx – give rifaximin, lactulose titrate to 2-3 BM/day, rule out spontaneous shunt
Correct low sodium, fiber diet, vegetable protein, elevate K to 5 or 5.5, add zinc, and ? probiotics

BCAA is controversial ( amino acid)
LOLA IV can be useful
Zinc and L carnitine

TIPS with reduction of gradient by lower below 12 is associated with HE.

If malnourished, give late night snack (fasting malnourishment overnight)
Protein intake should be 1.2 to 1.5 g/kg/day
Can use lactulose enemas if poor mentation


Onset of encephalopathy within 8 weeks and absence of pre existing liver disease

Status ventilator dependent, INR more than 2 and renal failure, Highest level for OLT

Tylenol – Cr more than 3.4, INR more than 6.5 and PH less than 7.3

Non Tylenol – INR more than 6.5, (kings criteris check)

If bilirubin normal and AST and ALT more than 1000 – Herpes toxicity, uniformly fatal

Death is from infuction, or fungal, cerebral edema, ICP monitoring

ACLF – acute on chronic liver failure

Refer if MELD more than 15, SBP, HCC,
MELD exception are hepatopulmonary or portopulmonary syndrome

If no social support, no OLT

HCC wait 6 months before OLT

Portopulmonary HTN – increased pressure just like Pulmonary HTN. Use vasodilators

Hepato pulmonary syndrome – shunt from right to left. Would look like PFO

They need echo, right heart cath.

Hepatic hydrothorax

FLuid on the right side. Ascites disappears and all fluid in the right pleura.

Early OLT complications include CMV infection, biliary leak, biliary stricture.
CMV is most common opportunistic infection. Check CMV PCR
If Donor is CMV positive then very likely reactivation
Side effects of immunosuppressive – tacrolimus causes CKI, cyclosporin high cholesterol
Cellcept causes shingles, stop drug.
Cyclosproin interacts with HCV drugs
Recurrent disease after OLT usually PSC. Less with PBC, AIH

Cancer after OLT – squamous cell of skin more than basal cell.
Colon every year after PSC OLT
Biliary stricture late complication of OLT

Neoplasm of liver

HCC survellience washes out quickly leaving capsule. Bx not needed
Barcelona criteria.
TACE, Ablation or radioembolization or SBRT
Milan criteria – 3, 3, 5
Downstaging of Milan. Shrink tumor with TACE or ablation
Goes to lung or bone

New HCC policy – wait 6 months with biologic MELD and if MELD more than 28.
AFP should drop to less than 500 with treatment

Cholangiocarcinoma – DO NOT do percutaneous bx, brushings on ERCP is ok

Cholestasis of pregnancy – first treatment is urso

Diclofenec is the most common cause of liver toxicity amongst NSAId (voltaren)
Augmentin, Azathioprine are other common drugs with DILI

Suppress hep B for upto 12 months after stopping chemotherapy

OLT contraindication

Portopulmonary pressure more than 35 is contraindication
Liver with hepatic vein cancer involvement

NASH more likely to die from cardiovascular disease – bx marker balloon degeneration

Tenofovir no resistance
Entecavir 1.5% resistance. If they fail entecavir then add tenofovir

Acute hep C – Observe for a few weeks, do not treat. High bilirubin is from immune response

MRI with enhancement during arterial phase and no washout in periphery to rule out cholangio carcinoma or atypical HCC

Charcoal for ingestion within 4 hours for Tylenol

Rumack algorithm is not used unless ALT more than a 1000 for Tylenol

After EGV eradication, repeat EGD in 3-6months.

Biliary tree

Mirizzi syndrome – dilated hepatic duct and intrahepatic duct and normal CBD

Gallstones is a risk factor for GB cancer

Pigment gallstones – risk factor is female gender, hemolysis, liver cirrhosis from splenomegaly with hypersplenism, not associated with stone(cholesterol stones occur with obesity, parity, female gender weight loss, estrogen therapy, bcp, ostreotide, DM, vagotomy, high TG and low HDL)
80% stones are cholesterol stones not pigment
Brown pigment Pigment stones , amenable to dissolution therapy, it is the primary biliary CBD stone from stasis, common in Asia and risks are stasis and infection
Question – cholecystectomy -classic biliary colic and if patient has sludge, treat like stones Go by history not labs

Sludge – US diagnosis, usually disappears spontaneously, and can cause same symptoms as stones
Features of biliary colic – severe pain, epigastric or RUQ (epigastric is more common), constant, for hours, post prandial and can be nocturnal, radiate to shoulders with N and V
Acute cholecystitis – 5-10% mortality in elderly with infection complications. Usually 90% resolve spontaneously
Lap chole 0.1% mortality
LC lap chole contraindicated with adhesions or coagulopathy
Urso can help small floating stones in 70% (floating means cholesterol, lighter), and 50%^get recurrent stones.
If inoperable cholecystostomy, GB sten
Low GB EF – no cause effect for biliary dyskinesia, lap chole no data to support is helpful. In exam, chose functional dyspepsia. 9 meta analysis – shows biliary dyskinesia does not cause colic. Predisposes to sludge and stones and chronic cholecystitis. Unclear cause of symptoms
30% of functional bowel have low EF.
Cholesterol polyp – non shadowing adherent to GB wall, less than 10 mm. GB adenomyomatosis – if 1 cm or more. If more than 1 cm – adenomyomatosisi and if less than 10 mm it is cholesterol polyp. In PSC it is adenoma if more than 8 mm. Repeat US for cholesterol polyp every 6 months to 1 year for 2 years
Adenomyomatosis -in 18% of cholecystectomy found incidental
PSC is associated with GB cancer, female gender, survival is under 10%, adenomatousous GB polyps, chronic salmonella, probable porcelain GB, pancreatic biliary anomaly

Removal of stone in remnant cystic duct with ERCP possible but has to be large cystic duct, they need surgical removal

SOD – 3 types – type 3, normal CBD. Sphincterotomy works only if elevated LFT and pain and dilated bile duct.

Choledochal cysts – common in asia Present pain, jaundice and palpable mass, surgical cyst removal due to risk of cancer. If cyst is in the duodenal wall, treatment is sphincterotomy
Often have diverticulum from bile duct, caroli syndrome – cysts in BD and renal cysts and renal tubule anomalies

Exam questions – contracted GB poor GB visualization, in obese, do not trust US, patient has CBD stones,

Predictors of CBD stone – very strong indicator Bilirubin more than 4,CBD n CT or TUS
Strong is dilated CBD more than 6 and bilirubin 1.8 to 4 (strong or very strong go to ERCP directly)
Moderate is abnormal LFT, more than 55 age, and has gallstone pancreatitis. (GUIDELINES BUT NOT ACCURATE)
In reality if you watch trending, it is not reliable for presence of CBD stone.
EUS most sensitive for stones. Exception to that morbid obesity or altered anatomy. MRCP not accurate if CBD less than 6 mm

ERCP for large CBD stone, do large balloon dilation of prior sphincterotomy (enlarge sphincterotomy) and mechanicl lithotripsy is 80% successful. Balloon dilatation match size to size of CBD. Can go from 12, 15 and 18 mm balloons.

Duct of Luschka – duct from liver to GB,
Bile leaks from cystic duct, duct of Luschka, post transplant anastomosis, post trauma, severed common hepatic duct Large bilomas need percutaneous drain.

Exam question – bile duct stricture history of lap chole, with liver atrophy. Needs MRCP first
Post op benign biliary stricture, usually occurs within 2 years of lap chole, complicated surgery in history, requires multiple stents and multiple sessions, surgical therapy is high morbidity.

Benign biliary strictures – PSC, post transplant ( can occur at anastomosis, donor duct stricture is ischemic, or SOD), post op and chronic pancreatitis.
Rare is autoimmune cholangiopathy, two types 1 is IgG4 positive and 85% of cases. Type 2 is rare.

Strictures recurrence is common with stents

Distal bile duct stricture in chronic pancreatitis – if no pancreatic calcification success rate is better. If calcification in pancreas unlikely to respond to endotherapy. ALP more than 3 x ULN and CBD more than 12 mm is when you do endotherapy.

Recurrent bile duct stricture consider FCSEM (fully covered self expanding metal stent)
FCSEM – success is 92% compared with 85% for plastic, migration is more likely 25% compared to 16% for stent, Avoid metal stents in small ducts (6 mm)

SOD – Type 1 Exam showed classic case of classic pain, dilated duct and abnormal LFT. Go straight to sphincterotomy. (manometry not needed). Best case is post chole
Most associated studied is AIDs, opiates, post transplant, chronic pancreatitis
Type 2 is biliary pain.
Type 3 pain only and functions. Now SOD is called sphincter stenosis is type 1
Type 2 is called suspected sphincter disorder
Type 3 is called functional disorder.
In class 1, SOmanometry is contraindicated. (falsely neg)
In Type 2, SOM predicts response.

How to diagnose cholangiocarcinoma – use FISH for the cytology
Presents as painless jaundice and weight loss.
Hilar cancer Klatzkin angle tumor – MRCP.
If patient is going for surgery for cancer, poor outcome with doing preop ERCP if patient is going for surgery in a week. If patient needs neoadjuvant Rx, then stent needed.

Idiopathic pancreatitis – if high SOM, 50% success rate with sphincterotmy.. MRCP with secretin is best test but not reimbursed.
EUS is good for CBD stones chronic pancreatitis and ampullary tumors
MRCP is good for divisum but not for missedstones
ERCP with manometry – has to have multiple attacks before doing it.

Pancreas Divisum – 5% of population.

Chronic pancreatitis – EUS superior to MRCP for diagnosis. EUS often overcalls CP. Changes more common in smokers hence over calls. ERCP is used for therapy not diagnosis

Pancreatic endotherapy for clearance of stones and stricture treatment. If cyst communicates with PD – pancreatic stent is treatment

Pancreatic cyst with LAMS, 30% blockage and needs repeat EGD.

ERCP related pancreatitis
Highest risk is in patients with normal pancreatogram
Death rate is 0.4% with ERCP.
If you do less than 1 sphincterotomy a week, higher complication and less success.
Balloon dilatation without sphincterotomy, high risk of pancreatitis.
To prevent indomethacin, rectal 100 mg and give IV fluid
Hold anti-coagulation for 3 days.

EUS basics
GIST comes from fourth layer ( mucosa, deep mucosa, submucosa and then fourth layer, muscle and then serosa ).
Cyst drainage needs antibiotics. ( esophageal dilatation does not need antibiotics !!)


Needs amylase and lipase 3 x ULN, findings on CT and pain. 2/3 criteria.
Readmission occurs in 1/3 cases of pancreatitis.
Alcoholic pancreatitis highest at 30’s and 40’s
True idiopathis is less than 10%.
Biliary pancreatitis – stones or sludge in 80% seen. Repeated examination after recovery detects another 10%
Alcohol more than 5 years and 4 drinks /ay. Binge does not count. Smoking affects risks also
Other causes macro and microlithiasis, missed alcohol use, medication, malignancy including IPMN, AIP, Pancreatic duct obstruction in celiac. divisum and SOD is controversial
Genetics and chronic pancreatitis.
CT not indicated for pancreatitis. More extensive evaluation if age more than 40, then rule out malignancy.
Atlanta revisions – two phases, early and late
Mild -no organ failure or local complications
Moderate – transient organ failure or pancreatic necrosis
Severe persistant complications more than 48 ours
Early more than 4 weeks
Fluid collection pseudocyst
Necrosis walled off necrosis

Critical pancreatitis – MOF and infected necrosis
Death rate 2%
However referral centers refer 20% mortality
Hospitalization 3-4 days but could be weeks to months
In 1-2 weeks renal, respiratory and circulatory problems are cause of death
In week 2-6 weeks, persistent organ failure.
Single organ failure 27-36% death and MOF 50%

Predict MOF – age more than60, comorbid conditions like renal failure, heart failure, cancer, chronic alcoholism, BMI more than 30 increases mortality 2 x.

Scoring systems – BISAP, SIRS, Ranson, Apache, Glasgow, HAPS etc.
CRP is a marker
BUN, Cr more than 1.8 and HCTmore than 44%

Fluid resuscitation
Rapid or gradual hydration – no reduction MOF, necrosis or death
Plasma expander – increased MOF, similar death
LR – impact unclear.
No clear answer on type of fluid, amount or goals

250-500 cc over first 12 to 24 hours. (RL) and goal is to decrease BUN
Beware of CHF and compartment syndrome

Nutritional support
Enteral nutrition is better compared to parenteral.
Nasojejunal versus nasoduodenal or NG. NO difference in outcome. Formula does not matter. Start early is the key. Can wait maximum 5 days

Mild AP – start oral feeding immediately if no nausea or vomiting and pain is better
Start with low fat solid diet.

Remove impacted gallstone, Urgent ERCP is not needed if no cholangitis
Predischarge lap chole though

Interstitial pancreatitis can progress to necrotizing pancreatitis
Criteria for infected necrosis
Persistent sepsis, gas in collection on CT and gram stain or culture positive

Prophylactic antibiotics no longer recommended

Management of necrotizing pancreatitis – if intervention required, endoscopic or minimally invasive approaches. Percutaneous tube drainage if septic

Antibiotics recommended are penems, quinolones, zosyn, flagyl
Suspect infection when there is drainage at day 7-10 when patient deteriorates

After AP – DM is common and EPI in 1/3 acute setting
10% if smoker develop chronic pancreatitis
20% develop recurrent AP


Abdominal pain is common but not universal
EPI – can occur without CP (Schwachman-Diamond syndrome)
Type 3c diabetes
SV thrombosis, pancreatic malignancy, SIBO, gastroparesis are other complications
Causes – alcohol, 44%, idiopathic is 29% (more in women), then genetic,
Smoking is more potent than alcohol in causing CP
Smoking and alcohol is a toxic brew
Stopping drink and alcohol slows progression
Mutations include PRSS-1 (causes pancreatitis), mutations that predispose SPINK-1, CFTR, CasR, claudins,Chymotrypsin C

AIP – IgG4 elevation is not specific. Systemic disease with salivary glands, biliary system, retroperitoneum, lungs others
Type 2. Less likely IgG4 is not elevated and is not systemic, local disease
Can mimic malignancy
MRI sausage shaped pancreas and string like pancreatic duct

Can check fecal chymotrypsin, fecal elastase, fecal fat, secretin / CCK test, serum trypsin

Mayo criteria – Maximum 16 points. Symptoms, calcification, histology, abnormal imagin, EPI and diabetes. Definite if 4 or more.

EUS scoring – Rosemont system or minimal standard terminology for CP, cysts, duct dilatation, duct irregularidy, visible side branches, hyperechoic duct walls etc
Problem is inter observer variability. However, smokers, drinkers, elderly, diabetics, obesity all can cause some of those variations

Rx involves pain management, EPI , DM
Pain is from anatomic and non anatomic causes (visceral hyperalgesia, central processing and chronic narcotic use)
Pancreatic morphology does not predict pain pattern
Enzymes – no data to show it helps. Anti oxidants mixed results, tramadol and gabapentoids can help
1 year surgical versus ercp pain control same. At 5 year surgery was superior
(Surgery was resection)
EUS guided celiac block not durable, neurolysis is not appropriate
Use only as palliation in malignancy
Surgery can be Frey (peustow plus debridement of pancreastic head) and peustow procedure and Berne procedure or Begger procedure
Peustow 40% long term relief. Others have more morbidity but long term is better relief

Diagnosis EPI

Fecal fat evaluation, fecal elastase less than 200 and serum trypsin less than 20 ng/ml
90,000 USP units lipase per meal. If you convert to IU units, then it is 30,000
Suppress acid if using non enteric coated prep
Zenpep, Pancrease, creon, viokace and pertyze. Viokace is not coated.
Primary outcome – check CFA
PERT only partially corrects CFA ( normal is more than 93%).
Diet fat – fecal fat / dietary fat is CFA
Failure occurs in bile acid def (in SIBO, bile obstruction, ileal disease), celiac disease, gastroparesis, surgery, inadequate dose
Increase incidence of Bone fractures

They lose insulin and glucagon. Type 3c diabetes.
Prone to hypoglycemia.
Can cause pancreatic cancer 4% risk, SIBO, gastroparesis, pseudocyst and CBD obstruction

Pancreatic cysts

Mucinous cysts – IPMN Can be main duct, branched duct and mixed variant
M more than F, age 6 and 7 decade, head more often, malignant potential
Communicates with duct

Mucinous cyst neoplasm (MCN), cystadenoma or carcinoma
More in women, 5 and 6 decade, body more common, ovarian like stroma, no communication with duct, calcification noted.
Malignancy risk of cancer in MCN is 6-36%, Main duct IPMN 10-90%

Serous cyst

Serous cystadenoma (SCA)
Central scar, lined by cuboidal epithelium that stains for glycogen, F more than M, 7 decade, more in body, rarely turn to cancer, unilocular

Psuedocyst – history of pancreatitis, fibrous granulation tissue, communicates with PD, and does not turn to cancer.

Cyst fluid analysis – CEA, cytology and DNA analysis
CEA if more than 192 is cut off in fluid

EUS for cyst is more than 3 cm, dilatation of main PD and solid component of cyst
International guidelines for EUS are tapering of duct, presentation with pancreatitis, non enhancing mural nodules 3 cm size

Surgical evaluation if PD more than 10 mm, obstructive jaundice, solid component of cyst

IPMN – surgery if PD more than 10 mm, cyst more than 3 cm if BD-IPMN, mural nodules
MCN – cyst more than 3 cm, symptomatic, egg shell calcification and mural nodules

IF cyst less than 10 mm check MRI every 12 months, 10-20 every 6-12 months, more than 20 mmin 3-6 months. If no change in 2 years lengthen interval.Forexam use old criteria.

Mild ileus in pancreatitis – still give jejunal feeding

HRM – Basal EGJ is 10-35 mm
EGJ relaxation is done in 10 seconds, generally 5 sec
Deglutitive EGJ relaxation – known has Integrated relaxation pressure . IRP should be lower than 15 mm or lower. Impaired relaxation if more than 15 mm
IRP – integrated relaxation pressure
Speed of peristalsis –
CFV – contractile front velocity. It is not important Chicago classification. Less than 9 is normal.
DCI – distal contractile integral – pressure x length x time. Normal is more than 450 and less than 8000
IRP more than 15
Abnormal motility does not establish clinical correlation
Achalasia 3 types (Greek word does not relax)
It is a disease of neuron, loss of neuron in myenteric plexus.
3 features, aperistalsis, incomplete relaxation and LES hypertension
Achalasia treatment attacks the LES- calcium channel blockers, nitrates
Pneumatic dilation with 30-40 mm balloons. (4% perforation in PD, mucosal tear in hellers myotomy 12%. Similar success rate. But after Rx, now scleroderma esophagus ! 25% of patients with PD need repeat dilation.
Botox injection
Classic achalasia type 1 – low amplitude less than 40 mm and high IRP.
Type 2 – achalasia with esophageal compression. There is a yellow column, in the esophagus
Type 3 spastic achalasia. Vigorous contractions in the distal esophagus and high IRP
Isobaric contour 30 mm helps diagnose type 2.

Type 1 response to treatment it is 56%
Type 3 response rate is 29%
Type 2 response rate to treatment is 96%

Achalasia Management algorithm

Low surgical risk – either PD or heller. PD start at 30, 35 and then 40 mm if needed. Young male go to 35 can skip 30 mm balloon.
Heller myotomy failure, repeat PD or myotomy
High surgical risk use botox, try nitrates or calcium channel blockers
POEM role – post POEM gerd can be a problem
Short term success is 98%
Perioperate complications incude perforation, pneumoperitoneum, pleural effusion, pneumothorax, perforation and mucosal injury
GERD occurs in 13% and abnormal reflux on pH 47% !!
POEM success drops to 78% at 2 years
Role of POEM is unclear.
Type 3 achalasia – POEM does long myotomy and could be better.
Achalasia management should be phenotype specific.
Type 3 use POEM
Type 2 PD or HM – responds best to treatment
Type 1 – PD or Hellers

Pseudo diverticulum occurs post myotomy

Nothing restores normal esophageal function
There is no cure, symptoms improve
It is a chronic disease
Will need repeat therapy should be told

Distal esophageal spasm – chest pain, spastic abnormality in esophagus.

Distal latency – locate contractile deceleration point. And start of swallow. Normal distal latency should be 4.5 sec or longer.
DES is DL less than 4.5 in more than 20% swallows.
No such thing as simultaneous. It was just rapid contractions!
Diagnsis is DL less than 4.5 or CFV more than 9 cm/sec
This can occur with spastic achalasia or DES. All have dysphagia.

Nutcracker esophagus – now known has Jackhammer esophagus
More than 20% peristalsis more than DCI of 8000

Rx for hypercontractile disorder –
Still uncertain. Rule out EoE. EoE occurs with all of the disorders. PPI, then pepper mint oit, ca channel, nitrates, Viagra, TCA, or botox

Scleroderma – hypocontraction. Fibrosis and vascular obliteration of esophageal muscle
Can occur in other collagen vascular disorders, GERD, diabetes, myloid.
HRM for ineffective esophageal motility
DCI less than 100 is failed peristalsis
DCI between 100 to 450 is weak peristalsis
More than 50% should show weak peristalsis

Fragmented peristalsis – DCI is more than 450, but more than 5 cm fragmented. Not sure what to do

IRP if high – and no peristalsis is achalasia
EGJ outflow obstruction IRP more than 15 but some peristalsis noted.

Minor peristalsis disorder – ineffective esophageal motility and fragmented peristalsis.

Opoid induced esophageal dysfunction
Impair LES relaxation, hper contraction, spasm, simultaneous contration (elevated CFV)
Opoids can mimick type 3 achalasia, jackhammer, DES. Rx stop opoid.

Esophageal pain – can be from chemorecdepters, mechanoreceptors, and longitudinal muscle contraction and distension
Must exclude thoracic, heart and pancreaticobiliary disorders
Use therapeutic PPI bid.


Basal cell hyperplasia and papillary hyperplasia occurs with reflux –
There is T lymphocyte increase individually
Cytokines increase with bile and acid, then T cells and then hyperplasia
Cytokines causes the damage not the acid

Most patients with LPR do not have reflux
pH monitoring does not reliably diagnose it
Laryngoscope signs of LPR are non specific. No gold standard

TLESR – lasts more than 10 seconds, inhibited by GABAb receptors.
HH causes more TLESRs (gas distension), impaired esophageal clearance
Hp protects GERD.
Inverse relation of Hp and Barretts and cancer.
Do not routinely check Hp.

Obesity contributes to GERD and barretts. – by increased reflux, and directly by insulin resistance and creased insulin like GF , increased leptin and low adiponectin

EGD to be done with patients with alarm symptoms,
Persistence of symptoms with 4-8 weeks of twice a daily PPI
Routine reflux EGD not needed

H2 blockers for mild reflux.
Tolerance develops frequently

PPI decreases clearance of methotrexate.
First line therapy for severe GERD. Aciphex is least dependent on CYP2C19
Healing symptoms on PPI it is 60% effective but esophagitis healing is 90%
Risks of PPI – Gastrin levels rise with PPI and ? risk of gastric cancer
Risk of SBP, C diff, enteric infection, pneumonia
Interferes with B 12, iron, Calcium, Mg, increased risk of fracture
Decreased efficacy of Plavix.
Risk of nephritis,chronic renal disease, colitis, food allergy, sprue, MI, stroke, dementia
Gives association not cause and effect.
Weak association does not preclude causality, and can be important. Probably will not be resolved.

False alarms and pseudo-epidemics Obs and guynecol 2012 . Get article, Grimes D.A

Erosive esophagitis – needs long term PPI. Reduce HH, approximate diaphragmatic crura, fundoplication and restore intra-abdominal esophagus
Choose patient carefully. Complications can be severe.
Do not use it for cancer prevention
Many patients need PPI again ! after surgery

Surgery Reflux recurrence at 5 years is 17.7%, recurrence more common in older age, female, comorbidity
AGA – no indication for endoscopic surgery for reflux
TIF maybe good for regurgitation. Long term data is disappointing
LINX – 11% had dysphagia and 6 patients needed it removed.
30 % have reflux esophagitis and NERD in 70%
NETD is more difficult to treat

Combined Impedance and pH monitoring.

Symptom reflux correlation
4 possibilities, reflux with symptoms
Symptoms but no reflux
Reflux and no symptoms
No symptom and no reflux
Symptom index – greater than 50% is positive.
SAP – symptom association probability index.
Divide 24 hours in 2 min, increments.
SAP more than 95% is significant.
Symptom index and SAP do not always agree
After PPI reflux continues but it is mostly non acid reflux.

Heartburn after PPI is from

Non GERD esophageal disorder – EoE, achalasia, causes heartburn sensation
Extra esophageal from bile or cardiac disease
Reflux related – despite PPI still have reflux or may have reflux from non acid reflux or reflux hypersensitivity.
Functional reflux.

Twice daily PPI – only 7% have abnormal acid reflux or 1% in extra esophageal reflux symptoms

MII-pH – if symptoms continue 50% of them will have either persistence of acid in 11% and 40% non acid reflux

Baclofen can help in NERD.
Neuromodulators for TCA, SSRI, SNRI may block pain

Bile reflux – aluminum hydroxide.

Barretts esophagus

Hostile place – constantly has acid, nitric oxide, Nitrosocompounds and reactive oxygen

GEJ – proximal extent of gastric fold
Cardiac mucosa, what looks like barretts but no goblets cells. Cardiac mucosa can be metaplastic, can show markers like intestinal differentiation like villin, cdx 2
Frequently found next to adenoca, and risk for cancer is there. The DNA is similar to intestinal metaplasia.
Cardiac mucosa cancer risk is minimal.

On EGD look for nodules in Barretts.
Estimate of cancer in Barretts is 0.25% per patient per year

RF for barretts, age above 50, chronic GERD, male, Caucasians, central obesity, smoking, family hx of barretts or eso cancer

Screening of general population for barretts in GERD not indicated.
Could be considered screening for barretts if 2 or more risk factors. ACG guidelines screening not indicated in women.

Survellience every 3 to 5 years. Repeat EGD not needed in 1 year of index Barretts diagnosis.
Endoscopic eradication needed in patients with HGD
Endoscopic treatment is only indicated if restricted to mucosa. T1a can be cured but T1b means invaded to submucosa with 10% of them have LN involvement.

Must do LN staging even in T1a ( 1-2% LN involvement) or HGD
EMR is a staging and therapeutic.

Rx for ablating barretts – RF is the procedure of choice. RFA prevents cancer in HGD. RFA in LGD decreases risk to HGD in 25%.

RFA side effects – 8.8% adverse events – 6% stricture, 1% bleeding and 0.6% perforation.

Endoscopic eradication can be for LGD, HGD
EMR – should be offered initially and then RFA done to remaining mucosa
After RFA – 25% neoplasia and metaplasia recurs in 50% of cases.
RFA should not be used if there is no dysplasia.
After eradication of Barretts restricted to mucosa, repeat EGD in 3 months


Eos 3:1 male to female ratio. Occurs all throughout the world. Dysphagia, food impaction, reflux and upper abd. Pain
EREFS – exudates, rings, edema (pallor) and furrows and strictures. Score is 0-9. More than 2 is sensitive
Esophagus appears normal in 10% of cases
Need more than 15 Eos, eos microabscesses, basal zone hyperplasia, dilated intercellular spaces similar to reflux, and subepithelial fibrosis
50% have atopic history (rhinitis, asthma, atopic dermatitis)
15% have food anaphylaxis.
Oral immunotherapy can cause EoE in 3%
Dramatic response to elemental diet.

Why is EoE only in esophagus ? Th1 and Th2 differentiation. Antigen, activate immune system, activates TH 1 or TH2 cells ( T helper )
Th2 cytokine stimulates Eotaxin-3 specific for eos chemoattractant,
Cascade, food allergen, Th2 response, IL5,(eos production) IL13 and IL4 (eos chemoattractant)

Overlap with GERD and EoE
Gerd causes mild eosinophilia less than 7 Eos
Eos can lead to GERD and GERD can lead to Eos.

Could be from subclinical GERD, or have antigen driven eos or PPI have anti inflammatory effect
Omeprazole blocks EoE2-T cytokines

PPI-REE is a term should be abandoned.

Elemental diet has high success rate. Direct elimination from skin testing has 46% percent response rate
Empiric using 6 or 8 food elimination
Topical steroids for EoE, fluticasone, oral viscous budesonide

2018 EoE management – exclude non EoE disorders like vasculitis, connective tissue disease, crohns etc.
Topical steroids for 6-8 weeks or PPI or elimination diets are 3 strategies Can use either.
If you use steroids, check annual plasma ACTH and serum cortisol
Elimination diet is the best option
EoE is more likely to tear mucosa and chest pain for several days but not at higher risk of perforation
Commonest food trigger is milk

Eso Strictures
EoE, schatzki caustic, peptic radiation etc
Eso stricture should be dilated to 13 mm.
If 15 mm modified diet
If more than 18 -mm usually tolerate regular diet.
All dilators are equal in safety or efficacy

First dilator should be the size of the esophagus strictured
Rule of 3 for bougie dilation increments of 1mm
For balloon don’t dilate more than 3 mm.
Repeat dilations in 1-4 weeks.
Schatzkis ring is abrupt dilation needed. Use 18mm of TTS or 50F dilator

Gastritis / Gastropathy

Acute reactive gastropathy – bland, medication or toxin ingestion
Chronic gastritis – diffuse antral, diffuse corporal atrophic gastritis, multifocal atrophic gastritis

Hp infection
Commonest cause of gastritis
Infection is life long
Asymptomatic , PUD (1 in 7), atrophic gastritis , gastric adeno ca and Gastric MALT
50% of the world has it.
By 10 years of age, in developing world you get the infection
Secrets urease that neutralizes the acid
Attaches to the epithelium
Gastric secretion is modified to survive
Evades host immune response
Do not treat if Ab is positive. Need more proof
Check if patient has ITP or unexplained iron def.
Check if patient has non ulcer dyspepsia
Chronic NSAID use consider Hp evaluation
Or low dose ASA users

Evaluate using fecal antigen, UBT, biopsy, histology or culture
Histology is gold standard
PPI and previous antibiotic gives fecal antigen or UBT wrong
Failure to eradicate ( resistance to flagyl or biaxin). PPI can overcome flagyl resistance
Resistance clarithromycin is more than 15%
Poor compliance is bad, change regimen
Smoking makes it difficult to eradicate
Cipro resitance is 31%, flagyl is 20%
Rare resistance to amoxicillin, tetra or rifabutin
If biaxin resistance eradication is 18% and if not resistant then i88% response rate
Look at slide for allergy and MCL exposure
Doxicycline and tetracycline are NOT interchangeable
Go to ACG clinical guidelines for HP

Gastric mucosal diseases

AI gastritis (PA)
Infectious, lymphocytic, eosinophilic, granulomatous
Hypertrophic fold syndromes

AIG – autoimmune metaplastic atrophic gastritis
Less than 10% of gastritis, antral sparing, elevated gastrin, achlorhydria, decreased pepsinogen 1, parietal cell antibodies and B 12 def, Hp can be positive and adenoca is real risk but low.

Infections in stomachs, Hp, syphilis, TB, candida, histo, aspergillosis, giardiasis,crypto, strongyloidiasis

Lymphocytic gastritis, – nodular, giant folds, volcano lesion, occult bleeding, and associated with sprue.

Eos gastritis – all layer, needs steroids and peripheral eosinophilia

Granulomas are TB, sarcoidosis, Crohns and idiopathic

Hypertrophic fold syndromes
Menetriers, Hp can mimic menetriers, \
Children can get it from CMV, amyloidosisi, ZES, gastric lymphoma, lymphocytic gastritis

NSAID gastropathy – 30% of them get mucosal lesions and 4% can get ulcer, gastric outlet obstruction,

Cox 1 reduced blood flow
Cox 2 reduced angiogenesis
Cox 1 is the reason for side effects.
80% of NSAID complications are asymptomatic

IF patient on anticoagulation steroids or prior beed must always be on PPI, (h2 blockers don’t work) and as we get older we make less cox 1. So higher risk at 70’s age

Avoid using aspirin – causes problems.

Cox2 inhibitor – do not increase risk of UGI bleed. Even low dose aspirin consider prophylaxis

Dyspepsia 3% of population Primarily it is FD (functional dyspepsia) 70%. Fullness, early satiation, epigastric pain, epigastric burning
FD evaluate with EGD if more than 55 years. (new guidelines uses the age of 60)
If less than 60, check Hp.

Gastric evaluation
Sydney System – 3 bites from antrum and 2 from body
OLGA (operative link for gastric intestinal metaplasia assessment). OLGIM
4 stages of intestinal metaplasia
Stages 3 or 4 need surveillance at intervals

Gastric polyps

Hyperplastic polyps
Adenomatous polyps

FGP occur with PPI, and if hundreds of FGP and then think of FAP and observe
Hyperplastic polyps from high gastrin, atropic gastritis and remove large polyps

Remove large hyperplastic polyps.

Gastric cancer risk intestinal versus diffuse, Hp, AIG
Hereditary diffuse gastric cancer (Mauris in New Zealand)
Epidemic and Japan and South America and latin America and asia
Inversely associated with economic status

Risk factors are more than 50, MAG, intestinal metaplasia, incomplete IM, relatives and smokers

Intestinal metaplasia – 11% cancer risk, survelliance in FH or Asian
Pernicious anemia 1-3% cancer risk
Post gastrectomy 1 to 9%. Usually 15 years later.
NBI – to detect premalignant lesions
Hp has odds ratio of 2.26 for gastric cancer
Interleukin polymorphisms and gastric cancer – IL1B3IT polymorphism. The family members with polymorphism and had atrophic relatives – high chance of gastritic cancer
Risks that increase risk include smoking, high salt, decreased vitamin C, nitroso compounds

Diffuse type gastric cancer – linnitis plastica, missed on endoscopy, role of UGI is there, Hp is risk, Krukenberg tumor . Hereditary causes E-cadherin 1 and negative genetic testing does not exclude hereditary diffuse abnormality

E cadherin 1 mutations. First in NZ, autosomal dominant, At age 80 everyone has a problem, prophylactic gastrectomy with hereditary diffuse gastric cancer

Also do survelliance with PG syndrome, FAP lynch, Juvenile polyposis, CVID

GISTS – mesenchymal tumors, positive for c-KIT, , interstitial cell of cajal,
Malignancy of GIST is 30%,based on core biopsy mitotic lesion and size
Reuires surgery.
Tyrosine kinase inhibitor is 50% effective,

Gastric carcinoids – 3 types
Type 1 – high gastrin. Atrophic gastritis
Type 2 high gastrin antral predominant, G cell ZE syndrome
Type 3 normal gastrin
Always check serum gastrin

GI bleed

Aspirin is the most important risk factors
Mortality is 10% !!
High mortality if more than 60, transfusion of more than 6 units, shock, and other comorbidity, high INR, low blood pressure, erratic mental status
25% of upper GI bleed you wont find cause
Rebleed after hemostasis is 20^%
Forrest classification for bleed on ulcer
Flat spot 10% rebleed, adherent clot 22% bleed, visible vessel 45% and 55%if actively rebleed
Second look for rebleed
Data on hemospray is not there
Octreotide reduces gastric output and helps ulcers too
If bleed from ulcer, and primary CV prevention, do not restart ASA. If secondary aspirin use, then start it in 1-7 days of bleed. Start before they go home.
Duodenal angioectasia – CREST, radiation PSS, aging. Can be hereditary
Dieulafoys – submucosal artery large. Can use a band also
Portal hypertensive gastropathy – snake skin appearance
Stress ulcer bleed – Current incidence is 1.5% in ICU. Use of PPI depends on how sick the patient is. Biggest risks are coagulopathy and respiratory failure, hypotension, sepsis
Cimetidine at 37.5mg /hour infusion can prevent stress ulcer.

Bleeding of obscure origin –
Obscure – overt or obscure occult.
Amyloidosis can cause SB bleed, Meckels. AVM is commonest.
MDCT enteroclysis is becoming popular.
DBE complete evaluation in 44% cases

Mutation of APC gene (adenomatous polyposis coli), Chromosome 5q 21
Polyps appear at 15 and rectal bleeding at 33,average age of colon cancer at 39, Death is at age 42.
Osteomas, CHRPE, skin fibromas, lipomas epidermoid cysts, thyroid cancer, small bowel tumor, ampullary tumor, hepatoblastoma, angiofibroma
CHRPE melanocytes in deeper layers of the retina
Microadenoma of the the polyp
Screen at 12 years, then q 2 years at age 25 and then every 3 years after 35.
Screening test of choice is APC gene testing. Start at age 10-12, pretest genetic counseling
Check affected individual first. Must match completely.
Rx colectomy. – 3 options – total proctocolectomy
Option 2, leave rectum and ileorectal anastomosis
Proctococolectomy with ileoanal pull through
At 15 ileoanal pull through is recommended
They need EGD due to duodenal cancer. (second most common), annual thyroid evaluation
Desmoid tumor in abd occurs in 2% of cases
Attenuated FAP
5’ and 3’ gene mutations.
Present with <100 polyps on right side, CRC at 51 not 39. Heterogenous phenotype 6% of FAP
Genotype all pedigrees.
Colectomy in AFAP
MUTYH gene,
Looks like attenuated FAP, recessive inheritance, MAP-MUTYH associated polyposis. Base gene repair issue
Can have gastric polyps and duodenal adeno, but don’t have extra colonic FAP but have increased breast, ovarian, urinary and skin cancer

Crails syndrome (turcots formerly). APC mutation , polyposisi and medulloblastoma
Turcots syndrome – MMR mutation, oligopolyposis, glioblastoma a form of LYNCH syndrome. MMR mismatch mutation

PJ syndrome, Autosomal dominant, mucocutaneous pigmentation, hamartomatous polyps, GI and non GI cancers, lips fingers and above eye lashes. Usually in SB, then colon, stomach. Never in esophagus. 1-20 polyps
STK gene mutation (serine tyrosine k mutation gene)
PJS survival is about 60%, diverges with normal normal at 10 years due to intessusception and death. Then second time life span diverges at 30 due to cancder. 90% of them die from cancder, including breast,colon, pancreas, stomach, ovary, lung Rare tumors Sertoli cell tumors of testes, ovarian cysadenomas, granulosa cell tumors, sex cord tumors with annular tubules, adenoma malignum of cervix. (missed on pap smears). Mx is remove polyps more than 5 mm from stomach and colon. SB polyps removed with laparotomy and enteroscopy.
Survellience with SB imaging, EUS, MRI, mamm, TVUltrasound/Gyn cancer, testicular cancer, MRI of pancreas.EGD and colon

Juvenile polyposis
Autosomal dominant, distinctive juvenile polyps, in colon,39% cancer. Gastric and pancreatic cancer also a risk. Had edema of the mucosa, cysts in the cryps on histology. SMAD4 gene 16% and BMPR1a gene in 24% of cases. (50% show germline mutation, and in 50%^ no mutation seen
Survellance at age 12.

Cowden disease

Ganglioneuroma of polyp in colon. Skin lesions

Bannayan – Riley – Rubvalcaba syndrome
Penile pigmentation, macrocephaly, juvenile polyps

Colorectal cancer

141,000 cases a year in USA and 52,000 deaths a year.
80% of cases are sporadic. 3-5% is lynch, 1% is FAP, and less than 1% if MAP
Strong risk factors, age, country of birth, family hx, ureterosigmoidostomy are at high risk, FAP, MAP , LS, serrated polyposis RR more than 4
Moderate risk – red meat, prevous ca, pelvic radiation, ovarian ca at young age, dermatomyositis, IBSD, strep bovis, acromegaly
Modest. Cholecystectomy is risk factor
If both parents have colon cancer, 30 x risk of colon cancer

Protective, fruits and vegetables, exercise, NSAIDs, folate, high calcium, selenium, fiber, statins

SSA – large and flat. More like hyperplastic polyp.

No polyps or less than 1 cm hyperplastic polyp in sigmoid or rectum 10 years
More than 10 adenomas, repeat in less than 3 years.
Villous adenoma or polyp more than 1 cm adenoma, repeat in 3 years

Must do FIT annually in Tier 1.
Tier 2, FIT-fecal DNA ever 3 yers virtual colon every 5 years
Tier 3 capsule colon every 5 years

FIT – immunological test for Human Hb. Single sample. Annually
Sto0l DNA single test, every 3 years, and FIT is included
Septin 9 serum test for cancer CRC causes methylated septin 9 gene.
FIT and stool DNA – sensitivity is good for cancer but low for advanced adenoma.

Advanced adenoma in first degree less than 60 or in 2 individuals colon every 5 years
CRC beyond 60 average risk colon cancer
UC every 8 years if pancolitis and left sided after 15 years

Lynch syndrome
Autosomal dominant, MMR (mismatch repair protein), multiple primary malignancy.
Amsterdam criteria – one person less than 50 with cancer, 2 generations affected, 3 or more people affected.. in lynch, most tumors are on the right side. Mean age of diagnosis is 44 years and for sporadic mean age is 68.
Lifetime risk is 80% of colon cancer, high risk of endometrial, ovarian, uretral, stomach, small and hepatobiliary
Survellience done every 1-2 years at age of 20 or 2-5 years before youngest family if index is less than 25.
Women TAH and SBO .
Cause is MSH2, MLH1, PMS2, mSH6
Can do MSI testing of the cancer
BRAF testing in tumor or MLH1 promoter hypermethylation testing is done if MSI is positive
Lynch – if cancer, do proctocolectomy.
Familial Colorectal cancer type x
Meet Amsterdam criteria, but neg for MSI. No risk of other types of cancer

MSI testing is done on advanced adenoma and cancer
IF SSA less than 1 repeat colon in 5 years
If multiple SSA 1 year
If SSA more than 1 cm, 3 years repeat colon

If lynch start screening at 20 irrespective of index case. Breast cancer is not a risk factor

SSA – WHO criteriam 2 SSA more than 1 cm and total of 5 sSA, it is called serrated polyposis. No other extra colonic cancers, not a PTEN, and 5% of serrated polyposis have siblings or inherited disease

If sub cm adenoma repeat in 5-10 years


Functional dyspepsia – Buspirone helps FD.

Relationship with nausea, vomiting or pain in gastric emptying relationship is unclear
Causes of gastroparesis
Idiopathic is 36% and diabetics 29%, Upper GI surgery 13%, parkinsons 8%, collagen tissue disordedr 5%, CIIP 4% and eating disorders in 6%
Drugs that make it abnormal – beta agonists, anticholinergics, TCA, opiates, PPI, lithium, tobacco,antihistamin, dexfenfluramine, dopamine agonists phenothiazines.

Upper limit of normal for gastric emptying – 4 hour emptying should be less than 10%. But to diagnose gastroparesis should be more than 20% retention at 4 hours. Obesity causes 10-20% at 4 hours ? Uniquely American

Diet modifications
Reduced fiber, small meals, reduce fat, liquid calorie supplementation.
Prokinetic agents – neostigmine, emycin, domperidone, reglan, proculopride, relamorelin
Emycin – stimulates MMC, 3mg/kg every 8 hours, 125 mg every 4 hours,does not help nausea
Reglan – dopamine 2 antagonist, and 5 HT agonist, 5-20 mg qid
Boxed warning include TD, Parkinson type syndrome, hyperprolactinemia, 30% experience side effects. DO not use longer than 3 months.
Start with Erythromycin first and then reglan
Domperidone – effective, peripheral D2 antagonist only, no side effects of relgan, 10 to 30 mg qid. Improved symptoms in 64%, 60% emptying, reduced hospital admission. Not approved for FDA.
Relamorelin – ghrelin receptor. Reduces vomiting, best dose twice a day, poor correlation between improved GE and symptom.
Botox for gastroparesis – sham studies show it does not work.

Gastric pacemaker does not pace stomach, and does not improve emptying and improves nausea and vomiting from unclear mechanisms
Improvement is only in diabetics with nausea and vomiting. Does not help pain. Non diabetics do not benefit

Complete gastrectomy – high post op symptoms continue Do not consider

Cyclic vomiting syndrome – symptom free in between, gastric emptying is normal. 2 types cannabinoid hyperemesis – compulsive hot water bathing, poor response to TCA,
Non cannabinoid vomiting- migraine headachs, anxiety, depression, no hot water and responds to TCAs

Small bowel motility
VIP and NO inhibits motility. Substance P, serotonin stimulates motility
CIIP – myopathy from familial, collagen, amyloid. And hisrschprungs, Chagas and paraneoplastic syndrome
Megaduodenum in Scleroderma. ANNA 1 and ANNA 2 in paraneoplastic in small cell ca of lung.
SS – SIBO and malabsorption

Fat in diet stimulates colon motility. Carbohydrates and protein has no effect on colon motility

Anorectal motility

Anal manometry cannot evaluate the puborectalis muscle. It evaluates sensation, internal and external sphincter

Overflow incontinence
Obstipation, megarectum, blunting of rectal sensation, more common in dementia, children, elderly,

Reservoir incontinence
Bowel compliance is low from surgery. Needs flex sig. Occurs in IBD, radiation, and rectal surgery. Reduce dietary fiber, loperamide and Lomotil, treat inflammation

Internal sphincter incontinence – Scleroderma, sphincterotomy for anal fissure, middle aged to adults. Low digital tone,
Rx – Cotton pledget is inserted. Referral is not needed

Pudendal Neuropathy

Manometric patterns are –

Only IAS weakness – scleroderma
EAS trauma – squeeze pressure is abnormal
Peripheral nerve damage – squeeze and puborectalis is weaks
Central nerve damage in MS – sensation, plus PRM plus squeeze is abnormal

Fecal incontinence eg in diabetics, pudendal nerve damage, anal sphincter damange

Biofeedback is better than kegals.

Surgical sphincter repair low long term efficacy

Sacral nerve stimulators – effective

Defecation abnormalities

Defect in expulsion, dyssenergia of mucles and failure to relax in Hirschsprungs
Rectal balloon distension should lead to IAS relaxation.

Hirschsprungs Must confirm with rectal biopsy

Balloon expulsion test – should occur in 60 seconds, usually less than 30 seconds

Dyssenergia – narrowing of the anorectal angle on straining. (should widen on straining)

2 types –
Type 1 – both anal and PRM contract
Type 2 EAS contracts and no contraction with PRM

Diltiazem only helps IAS. Best treatment for dyssenergia is biofeedback
Laxatives only helps 20% of patients


Causes drugs, iron, aluminum, opiates, calcium blockrs, 5 HT3 antagonists

Bulking agents
Nonabsorbable substances
Secretory drugs

Bisacodyl can be used every other day.
Safety in pregnancy. – Lactulose. PEG is class c but is used.
Senna stimulates prostaglandin and cause uterine contraction Theoretical
Transit test – x ray 5 days later. If markers still present, Slow transit
Some studies take x rays 7 days later. ( no markers between day 4 to 7). Hinton or Metcalf technique. Metcalf more than 68 is abnormal
Colon intertia – slow transit of proximal colon. Neuropathic disorder. Abnormality of myenteric plexus. Misoprostol and PEG is a good combination in this condition. Others don’t work
Colchicine does not work
Before surgery, defecography is needed.
Refractory constipation
Start with balloon expulsion and and anal manometry and then if normal go to colon transit.
If both expulsion and manometry abnormal – go to biofeedback

Don’t do subtotal colectomy for abdominal pain, no evidence of CIIP, normal anorectal function.

Chronic megacolon and megarectum
More common in psychotic disorder, parkinsons,
Chronic megacolon is a failed colon. Not to be treated as constipation
Low fiber diet, 8 oz water enema twice a week, small doses of PEG
At times exclusion and diversion surgery.

Stimulant laxatives increase propulsion
Opoids blocks VIP release. So there is more segmenting contractions and decreased flow
3 drugs for OIC – Me-naltrexone (works on all 3 receptors) , naloxegol only on mu and naldemedine only on mu
Hypothalamus stimulates CRF with stress, which increases ACTH and CRF directly stimulates colon motility.
Check FCP, CRP, stool c and s and can consider colon if poor response to rx.
No perfect breath taste for SIBO
Lactulose breath test – Hydrogen and methane produced by gut bacteria. 2 criteria – increase in 20 ppm in either 180 min or 90 min. If increased I 90 min, use rifaximin?
Normal bacteria in cecum raises Hydrogen. So it could be rapid SB transit also
Same for glucose or galactose breath test.
Desipramine 10-100 mg/day
Patient physician relationship is most effective
Eluxadoline – viberzi
Desipramine 12.5 mg/day does not have the same side effects like amitriptyline .
Can switch TCA
Can use TCA or SNRI (Cymbalta, Effexor)
5 HT drugs – Zofran and Alosetron – both helps diarrhea. (5HT3)
5HT4 for constipation prucalopride.
Cognitive behavioral therapy is very effective


VEOIBD. Very early younger than 2, probably all genetic
Fastest growth of IBD is in asia specific regions. Japan, Hong Kong
12/100,000 for CD and 25/100000 for UC
Age 15-30. Most IBD is NOT jewish.
Most don’t have a family history!! Most young have IBS.
So within 10 years of coming to western – their incidence of IBD is like they lived here
In IBD bx, mucin decreased, surface less damage, crypt abscess, no edema.
Pancolitis is 18%, distal 44%, and left sided is 36%. Distal progresses to pancolitis
High risk for colectomy are C diff in IBD, CMV, steroid requiring, extensive, deep ulcers,age less than 40, high CRP, history of hospitalization
CD – 50% relapse even with latest treatment. Overall 60% require surgery. And half need hospitalization.
High risk CD is age younger than 30, extensive anatomic involvement, perianal disease, deep ulcers, prior surgery and stricture or fistula
Smoking is a high risk but was not part of the criteria for high risk

After surgery, strong recommendation to do endoscopy in 6 months
No rule for post op CD mesalamine. Use anti TNF after surgery or thiopurines.

Role of FCP
FCP approved for diarrhea
Stress does not increase FCP.

Overlap of IBS and IBD.

IBD genome
If one parent has IBD child has 5% chance
If brother or sister, then risk is 30%
NOD2 is a genetic variation but it is minor.

Crohns of just ileum does not increase colon cancer risk
Men do worse with IBD
Missing a dose for a few days for UC does not cause a flare up

Phenotype of UC with rectal sparing is rare.
The UC patients who get it after they quit smoking. Those pateints get better if they start smoking
CARD15 is crohns gene and in those pouchitis


Not good for diagnosis. More common with leaky gut

ASCA (part of leaky gut also)
pANCA. More common in UC and crohns colitis

pANCA neg more likely to respond to infliximab. Positive patients similar to placebo
pANCA is associated with higher chance of pouchitis


Must check TPMT and reactive thiopurine.
TDM reactive monitoring. Meaning if treatment fails. Proactive where patient is doing well is not indicated

Thiopurine metabolite testing routine testing not indicated for quiescent IBD.

ASCA in CD – more common in Crohns and more likely to be positive in fistulizing disease

Management of IBD

Tight control in IBD to get a target CRP or FCP or Hb to assess control. Do serial adjustment of therapy till optimal is achieved. In crohns disease, less hospitalization and better control
Medications :

Can cause renal problems. Must give appropriate dose.
3% are 5 ASA intolerant. They get worse with treatment within a few days. Then stop the medicine. Dose reduction in deep remission is ok do colon before you drop dose for mucosal healing
Combined oral and rectal 5 ASA for distal UC 90% response
Check Cr before starting mesalamine
Sulfasalazine affects fertility

3 types of of budesonide
EC budesonide
Budesonide foam.
Mild or moderate crohns use budesonide
Vitamin D check annually in IBD
IBD patients may have a receptor vitamin D receptor mutation
Don’t taper too long – waiting for maintenance to take effect. 2 months reasonable. 40 mg for 2 weeks can stop without tapering. (example)

Lymphoma is from Imuran not anti TNF
Imuran causes higher viral infection
Genotype is not needed for TPMT. Activity is more important
Low TPMT is in 0.33% and 11% have intermediate activity
Intermediate activity do better with Imuran
Split or bedtime dose for nausea predominant
Pancreatitis is genetic determined
15% of people get shunted to the 6 MMP pathway and not 6 TG pathway so more likely to get toxic
NUDT15 asian mutation causing leukopenia for Asians. (including Indian)
May also be true for Europeans in a minority
True allergy with second day of therapy – fever! Stop medication.
Early crohns – AZA was not effective.
Lymphoma risk – NHL. More often EBV positive. Highest lymphoma risk is in Imuran who develop EBV acute infection on AZA.
Stopping AZA brings risk of lymphoma back to normal
Lymphoma risk occurs after years of use. Does not occur in first 2 years. T cell lymphoma occurs in combination therapy and not reported with methotrexate and does not occur in first 2 years either
Basal cell cancer with AZA is unclear
Allopurinol rescue – changes pathway to 6TG and MMR pathway goes away. Reduce the dose to 50%. Works great in 3 weeks. Especially good if patient has abnormal LFT

Methotrexate induction for CD remission is 25 mg IM or SQ weekly
It maintains sperm integrity.
Cant use in young women due to teratogenicity.
It does not work in UC
15 mg methotrexate oral once a week or in combo with anti TNF
Premedicate with Zofran 30 min if using 25 mg a day
Folic acid 1-2mg/day. Take methotrexate on weekends
Rash, nausea, mucositis, diarrhea, hypersensitivity pneumonitis, increased liver panel, hepatic fibrosis, BM suppression

3 classes of biologics

Anti TNF – Swapping change class. Cycling in same class
Better in combination
Half the time patient lose response in 1 year.
If mucosal healing occurs less likely to go to colectomy in UC
Loss of response is from Ab only in minority of cases.
Side effects, – maybe higher risk of melanoma. Slightly higher risk of lymphoma with TNF alone
No higher risk of solid tumors with anti TNF
Stopping anti TNF – male, low Hb, high CRP, high FCP, or WBC more than 6. Relapse rate is high 44%
CRP and FCP go high up before getting symptoms
CD recurrence after surgery is first endoscopic.
Rutgeerts score – Normal is 0
1 is less than 5 apthous
2 more than 5 apthous ulcers
3 ulcerations
4 severe ulcer and abnormal intervening area
FCP less than 100 no need to do post op endoscopy?

Infliximab 1/3 get remission from single dose and clinical response in 2/3 cases with one dose

Nasopharyngitis can occur.
Does not go to CNS
Check for TB and HBV
Use in older patients and other immune problems

Stelara (Ustikinumab)

Great if patient has CD and psoriasis
Elemental diet in CD

C diff and IBD
Rising incidence
Bad outcome, need colectomy often and higher death rate
Consider hospitalization
Do not escalate treatment of IBD but continue present treatment if both C diff and IBD
Recurrent – offer FMT


DD includes C diff,CMV, CD, ischemia, Irritable pouch syndrome, NSAID use,
DNA sensitivie pANCA more likely to get pouchitis
Probiotics only helps in antibiotics naïve patients
Probiotics to be given after surgery prevents pouchitis

Bamboo spine in UC
EN fix bowel and ENgets better
Pyoderma gangrenosum – Triggered by trauma to skin. Not fixed by IBD control
Anti TNF psoriasis or pustular changes in feet and palms. Usually long term use. Change them to ustekinumab. Prior answer use topical cream
UC long term, commonest extraintestinal is low back pain
Annual colonoscopy if PSC – high risk of colon cancer

Vaccinate for meningococcal , Tdap and HPV in young patients / pediatric

FCP goes up in people taking NSAIDs
Pregnancy does not cause FCP to go up


Commonest lethal is C diff
Second is norovirus
Most lethal is listeria but rare 17% mortality
Commonest cause if green leafy vegetables
LTCF – is usually from virus, fecal oral and from fomites, re useable grocery bag, no long term immunity. Lactase if first to be lost
Norovirus is most common. 70,000 a year hospitalization. Air spread likely, 20% world wide.
Incubation 12-24 hours, 10 virus enough, lasts less than 72 hours, contagious for 3 weeks
Rotavirus- most common in children ¼ million die, oral vaccines available, alcohol handgel does not prevent transmission.
ORT – change in formula, lower osmolarity, less glucse and salt. Rice cereal instead of glucose. Recipe ½ cup rice cereal ,
Dilute apple juice helps ORS
Saltines, or pretzels and mineral water
Salty yogurt drinks, Chicken broths
Sports drink does not work
Severe diarrhea use azithromycin over cipro. Mild rifaximin
BSS for prophylaxis

Cyclospora – exotic fruit plate. Raspberries from Guatemala. Could be giardia crypto, cystoisosporiasis
Giardia antigen is the test. Hypogammaglobulinemia Usually recurrent case cause
Cryptosporidia Treat with Nitazonximide, watery borne
Blasto. Hominis is a pathogen and does not always need treatment. But can be treated
Rx would be nitazoxanide. 600 mg bid x 3 days

Strongyloides -death after heart transplant. Ivermectin tablets per NGtube
Check before transplant now.
Look for eos in peripheral smear. Use stool and serology to diagnose. 85-100 serology sensitivity. Can have auto infection. Risk is HIV, HTLV1, high dose steroids

Colon pathogens, Campy, salmonella, Shigela, shiga toxin

CMV – watery diarrhea becomes bloody. Ileo colits. Rx with emycin, tcn or cipro (increasing resistance). Most common cause of GB syndrome

Salmonella – gastroenteritis, bacteremia, 1% carriers, 10% with complications. Hemoglobinpathies more likely to get it. Risk from reptiles , eggs, peanut butter, spinach, raw almonds, aquatic frogs, mangos Mild cases do not treat.
But bacteremia in 2-4% esp if older, or less than 1 year, immune suppressed, artificial joints or grafts

Shigella – watery diarrhea, bloody, azithro better than cipro

STEC – shigella like toxin. (e coli). Mimics child birth pain. May have fever. Right colon similar to ischemic colitis. Shigella and Stec can lead to HUS

HUS – higher rates in non -0157. 22% . O157 and shiga toxin. Antibiotics and antimotility is contraindicated.

Yersinia enterocolitica and Y pseudotuberculosis
Ileitis and mesenteric adenitis. Granulomatous appendicitis. Reactive arthritis 2-3 weeks later, middle age man with diarrhea and arthritis.
Usually do not treat.

Reiters arthrisi or reactive arthritis, Yersenia shigella, salmonella and

Vibrio species
Shellfish colon invasion, lasts 1 day, self limited.,
More common in low acid, immunosuppression and chronic liver disease and diabetes

Listeria monocytogenes – unpasteurized cheese, watery diarrhea, headaches, fever, bacteremia Pregnant women and diabetes

E histolytica – 90% are asymptomatic carriers. 10%coliits. Treat carriers. Stool antigen is best.
Cecal ulcer in asymptomatic could be E histolytica

Albendazole for whip worm. Trichuris trichuria. Tropics and US, livesin colon, may cause chronic diarrhea, dysentery.

Bloody diarrhea in US – check stool culture

Fish tuna or mahi can lead to skin rashes. From Scombroid in infection. Candevelop diarrhea, respiratory distress, blured vision

Cigautera fish poisoning. Can be fatal

HSV distal proctitis

C diff

3-7% of c diff positive are carriers
Don’t check for cure. Can stay positive for a month
Severe c diff, WBC more than 15K low albumin and distended abd

Poor prognosis if lactate more than 5, WBC more than 20, low BP, age more than 75
3 more recurrences – vancomycin 125 qid for 10 days and then 125 mg every 3 days for 10 more doses. Pulse therapy
Kefir can help. ( drink)

Diverticulitis risk factors are smoking, obesity, NSAIDS, steroids/opiates (higher risk of perforation. Mesalamine to prevent recurrence not indicated. Surgery is not indicated after 2 episodes

Juvenile polyp does not need workup. Usually left side, can occur at any age. If more than 5 polyps or family history of juvenile polyposis then juvenile polypsis syndrome. Then do genetic testing. Autosomal dominant and hamartamatous polyp outside colon

Rectal cancer follow up at 1 year is with flex sig.
Transanal excition requires flex sig in 3-6 months or EUS for the first 2-3 years

10% collagenous colitis in normal colon. Meds include NSAIDs, ARB, celiac disease, thyroid disease associations

Renal dialysis on PD – give antibiotic prophylaxis. Other places where antibiotics is needed, CBD obstruction, cirrhosis with bleeding, pancreatic cyst drainage, chronic PD by ID guidelines.

Anterior cutaneous nerve entrapment – Localized pain near surgical site. Treat lidocaine injection. Press on the site and have patient sit up. If lidocaine works then give him 20-40 mg of a long acting steroid.

Intessusception – target lesion, more common in children IC valve intesussception is usually adenoca, infectious causes are other cause.

SRUS – anterior wall, classic histology, often not solitary and not often ulcerated and not always just in rectum.

Lower GI bleed – do EGD only if low pressure. Red color on rectal with clot, favors lower source

OEC – opiate exacerbated constipation . Use lubiprostone

Inadequate prep, repeat colon in 1 year.

LGV incidence is increasing. 3 types, primary secondary or tertiary. Diagnosis is based on serology. Rx doxycycline 100 mg bid for 21 days. Alternatives are azithromycin

Sore throat and RLQ pain – Yersinia Treat with Bactrim, doxy, quinolones and aminoglycosides
Treat elderly diabetes, health care and child care workers,

Isolated colonic ischemia – IN the right side usually. Presents as abdominal pain,Usually with a fib, . Diagnose with CTA, . Supportive care. Can be mesenteric artery embolism or thrombosis or mesenteric vein thrombosis

Palatal torus. Bony extrusion of hard palate. Incidental finding

Look up serrated polyposis syndrome

Perforation in EGD – use water soluble media to diagnose

PEG insertion – upto 15% mortality 30 day all cause. Prophylactic antibiotics.

Methhemoglobinemia Rx IV methylene blue. Cyanosis but normal PaO2. Fe plsu2 is now Fe plus 3

Post bleed on warfarin. Use unfractionated heparin. UFH. Safe to do if INR is less than 2.5

Andexxa for factor 10 reversal
Praxbind for dabigatran thrombin inhibitor

Lactase def : more than 75% in Africa, Asian and Mediterranean.
Onset I late childhood or early adult life
Secondary occurs with diffuse small bowel disease
Convergence evolution – genetic variation of lactase

Carbohydrate diarrhea
Sorbitol, mannitol, fructose, sucrasae isomaltase def, FODMAP

Secretory diarrhea
Cholera toxin E coli, staph toxi, HIV and rotavirus
Hormonal – VIP, calcitonin, gastrin, serotonin, prostaglandins

Ideal ORS – 90 mmol sodium and carbohydrate of 111 mmol. That’s why apple juice, ginger all have too much sugar and low sodium. Chicken broth has too much salt. These things are not absorbed with too much sugar
Osmolar gap is
pH is more than 6, reducing substance is negative, osmotic gap is normal (less than 50), and sodium is more than 70. Fasting moderate reduction of diarrhea.

FCP is elevated in inflammatory diarrhea.

Steatorrhea – Fecal fat more than 8 gm/24 hours, fat ADEK vitamin malabsorption, pancreatic, biliary or Small intesting SI
(SIBO – degradation of bile salts leading to steatorrhea)

iBS-D. (intolerance to carbs, bacterial, sprue and drugs are the DD)

PI-IBS-D. can be life long!

Whipples disease – Tropheryma whipplei. All with organism don’t have disease
Joint pain, GI involvement, CNS, lymphoreticular and heart involvement. Can be fatal
DD by SB bx.
Ceftriaxone IV x 2 weeks and then Bactrim long term 1 year

Travelers diarrhea
PI, persistent infection like giardia, ameba, salmonella, Yersinia, SIBO, c diff, tropical sprue, unmasked of celiac and IBD

Diabetic diarrhea
Rule out celiac and SIBO and pancreatic insufficiency
Metformin related
1-5% of diabetics
Probably ANS dysfunction, often have neuopathy and microvascular eye complications
Often rapid intestinal transit.
Glucose control does not help
10-15% will have steatorrhea also
RX can include octreotide, clonidine, questran and Lomotil

Post cholecystectomy diarrhea
Can be significant is 10-15%
More common in women from reporting
Unknown mechanism
May respond to bile salt binding

Tropical sprue
Usually after 4 weeks,
Acquired in India, Caribbean, SE asia
Enteropathy on bx
Herald acute infection then chronic
B 12, folate and vitamin D,
Low Albumin
Rx folate and tetracycline for 3-6 months

Celiac disease
1% in USA
1:100 cases
But only diagnosed 15% cases
Commones age of diagnosis is 45
Constipation can be presentation in children
Diagnosis ttg-IgA is 72 PPV, IgA EMA 83 PPV,IgG anti DGP 68 PPV (if IgA low)
Do genetic testing if lack of response and disparity between labs
If patient on gluten free diet – do HLA Dq2 or dq 8 testing

Olmesartan induced enteropathy.

Refractory celiac
Type 1. Usually responds, and needs enteric coated budesonide
Type 2 Characterized by abnormal T cell lymphocyte on Sb bx. 50% mortality

Lymphoma and NHL and HL both are higher
SB adenoca

Seronegative celiac
2% of celiacs are seronegative

Short bowel syndrome
Colon present avoid oxalate
SB less than 50 cm with colon
SB less than 100 cm without colon
Less than 100 cm bile salt diarrhea
More than 100 cm TI removed Fatty acid diarrhea
Bile re cycles about 6-8 times a day. Bile acid excretion only 0.5 gram a day and total pool is 4 grams a day

SIBO – b 12 def, bloating, fat malabsorption, protein loss from enteropathy
Prebiotic, probiotic or antibiotic therapy (cyclical courses), or continuous
Low carb, low LCT, add MCT, food supplements vitamin supplements

SIBO occurs in diabetic neuropathy, scleroderma CIIP
Lactulose breath test
Glucose hydrogen breath test is better.
Emperic therapy

Primary bile acid diarrhea – Hormonal FGF 19 def, loop feedback absent, more bile produced by liver

Colon Ischemia

Alteration in systemic circulation.
Autonomic stimulation wil decrease colon blood flow
During BM, colon blood flow decreases even more
RF – female gender, increasing age, COPD, hypertension, IBS, ASCVD, AF, constipation
Surgery aortic, ileostomy and abdominal
Medications – interferons, anti TNF – alpha, constipation meds, NSAIDS (pg depletion, less vasodilation), diuretics, cocaine, amphetamines
Coagulopathy – factor V and APCR (activated protein C)

C diff bleeding is rare 6-8% cases only
Colon ischemia – usually reversible. But rarely can cause gangrene, stricture, become chronic and fulminant

Rectal bleeding, blood diarrhea it is usually Left compared to right
Moderate pain then right compared to left
BE thumbprints
CT shows segmental wall thickening, thumbprinting.
Clinical and radiologic healing in 1-2 weeks if segmenta wall thickening
Thumbprinting – segmental colitis 24-72 hours
Colon ischemia symptoms more than 2 weeks – develop chronic symptoms, perforation or stricture
Bowel distension with air increases ischemia. MUST — USE CO2
Colonoscopy is best test to diagnose ischemia
Stop colon at the most distal area of ischemic changes
Do not biopsy gangrene
Ghost cells or infarction are pathognomonic of colonic ischemia
Isolated right colon or portal vein gas (80% mortality)or pneumatosis – poor prognosis
No role for angiography
Recurrent sepsis – eg. Gram negative rods. (subclinical injury to portions of bowel and try to locate)

Isolated right sided occurs with vasculitis also and worse prognosis
Stool mass, carcinoma, stricture, diverticulitis or hirschsprungs all predispose to colon ischemia

Look at slide for severe to moderate colon ischemia features
Moderate to severe – give broad sprectrum antibiotics

Acute mesenteric ischemia
Find cause
Abdominal pain out of proportion of physical findings.
Do CT before vascular imaging
High mortality
SMA embolus – gaseless abdomen, sudden presentation
NOMI – vasospasm occurs in MI,CHF, DD CTA, Give papaverine or Prostaglandin alprastodil
No angiography in vasopressor use or low BP.
Do not use vasopressors
With papaverine, can reduce mortality to 45% with aggressive treatment

Chronic mesenteric ischemia – usually 2/3 celiac, SMA, IMA blocked

Do doppler US of the CA and SMA -before and after meals

30% of whipples disease work in farming or in maintenance
Darkening of skin addisons, niacin def, whipples disease, hemochromatosis
Whipples disease – cns relapse is bad. Tetracycline causes CNS relapse
NO pseudomembranes on colon in 10% of cases with UC and c diff
5 ASA inhibits TPMT and gives high 6 TG level. So lower dose of Imuran needed with concomitant 5 ASA

Live vaccine is MMR

IUD rule out actinomycosis?

Porphyria – precipitated by estrogen and alcohol. Unresolved abdominal pain. Rx is glucose

Low albumin in C diff is bad prognosis. Drop in albumin is fast in C diff compared to other colits

FMF – jewish, multiple surgeries, testicular pain, albuminuria, hematuria.

Cyclical vomiting syndrome Rx amitriptyline, erythromycin, cyprohepatidine,propranolol, phenobarbital

AVM – rarely causes rectal bleeding. Usually slow drop in Hb

Celiac axis compression syndrome / Dunbar syndrome / Arcuate ligament syndrome.
Bruit that gets worse with expiration is pathological.
Full expiration shows worsening pain (right crux of diaphragm catches the celiac) (inspiration diaphgram descends and expiration does not descend)
Pain is from neuritis with constant pounding of the artery, nerve

SMA is where duodenum is compressed. Normal angle is 38 to 65. Less than 25 is abnormal. Weight loss is usual clue
Women mean age 41.
Rx weight gain, if that fails, cut ligament of trietz or gastro jejunostomy or duodenojejunostomy
EGD pulsatile expansion of duodenum