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Conferences and Medical Updates

Journal articles

 

 

Machine generated alternative text: Back to Outlook 07:40 medscape.com * 95% Exocrine Pancreatic Insufficiency: Seen but Not Recognized? David A. Johnson, MD I Disclosures May 21, 2014 PANCREATIC INSUFFICIENCY: POSSIBLE CA-- -- USES What causes this? Pancreatic Insufficiency: Possible Causes • Chronic pancreatitis (most common) • Alcoholism • Smoking • Surgery • Pancreatic obstruction • Cystic fibrosis • Autoimmune related • Crohn's disease • Celiac disease (Enlarge Slide) The differential when you approach a patient with chronic pancreatic insufficiency includes chronic pancreatitis, clearly the most common cause. We see pancreatic insufficiency in patients who are alcoholic and particularly in smokers, but a variety of things can aggravate this risk as well, such as surgical changes or anything that obstructs the pancreatic duct. In younger people, cystic fibrosis is a common cause of chronic pancreatitis and pancreatic insufficiency. A variety of autoimmune-related causes are increasingly recognized, including autoimmune pancreatitis and lgG4- related consequences. Even Crohn's disease can have an

 

Machine generated alternative text: Back to Outlook 07:42 medscape.com * 95% c What are the clinical presentations of pancreatic insufficiency? Clinical Presentations • Malnourishment and steatorrhea - Floating stools • Malabsorption of fat-soluble vitamins - Vitamin A: Night blindness - Vitamin D: Metabolic bone disease - Vitamin K: Abnormal coagulation • Impaired biotin absorption - Seizures (Enlarge Slide) There are several possible presentations. The classic presentation is patients who come in with malnourishment and steatorrhea, the foamy, fatty stools that float in the toilet bowl water. Anything that aggravates malabsorption can cause the patient to have symptoms. Malabsorption of the fat-soluble vitamins (A, D, E, and K) can lead to night blindness, metabolic bone disease, abnormal coagulation profiles, and neurologic dysfunction. We have seen impaired biotin absorption in a patient with seizures that was related to chronic pancreatic insufficiency. A variety of things must be considered when you expand the _net and think about Dancreatic insufficiencv

 

Machine generated alternative text: Back to Outlook 07:42 medscape.com David A. Johnson, MD I Disclosures May 21, 2014 MAKING THE DIAGNOSIS How do you make the diagnosis? Making the Diagnosis • "Tube test"; no longer practical • Diagnosis made on clinical basis combined with blood test or fecal elastase - Serum trypsin level 20 gg/L - Fecal elastase level 200 gg/g stool • Ductal anatomy evaluation - Endoscopic ultrasound (also parenchymal evaluation) - MRCP; does not show calcium, so if looking for calcific change, CT may be better - ERCP best, but risk for complications (Enlarge Slide) When I was a fellow, we did what were called "tube tests," which was when we induced secretions by secretin or CCK and collected the pancreatic juice and analyzed it for quantitative amounts of the secretions. It's not a practical test anymore. For the most part, we make the diagnosis on a clinical basis, combined with either blood tests (a serum trypsin level less than 20 pg/L) or fecal elastase, which is a test that I use more frequently. A fecal elastase less than 200 pg/g of stool is the typical standard for thinking about pancreatic insufficiency. It is also important to make some type of structural assessment, such as the endoscopic ultrasound, although I don't personally use it. It does not expose patients to radiation and gives you a nice parenchymal evaluation, as well as ductal anatomy.

 

Machine generated alternative text: Back to Outlook 07:44 medscape.com * 94% meal. The idea is to better balance the enzyme exposure throughout the meal. It is the contact time that allows the best absorptive capability. Dosing of Pancreatic Lipase Pancreatic lipase is dosed in units. The pancreas normally secretes up to 900,000 units of lipase with a meal, and you only need 10%. The starting dose for the standard patient is 500 units/kg/dose, and this dose can be upregulated to approximately 2500 units/kg/dose. Dosing of Pancreatic Lipase • Starting dose: 500 units/kg/dose • Can increase to 2500 units/kg/dose • 6000 units/kg/dose in children associated with fibrosing colonopathy • If no response to treatment: - Check compliance - Consider celiac disease or bacterial overgrowth (Enlarge Slide) In pediatric patients, high doses (6000 units/kg/dose) have been associated with a complication known as fibrosing colonopathy. Be careful if you are increasing the dose. If you are not getting the response that you think you should have, make sure that you have good compliance, but also think about other things. Think about celiac disease and bacterial overgrowth, which also may be seen in patients with exocrine insufficiency.

 

 

 

LONDON — The investigational non-steroidal mineralcorticoid receptor antagonist finerenone worked as well as eplerenone (Inspra) with a possible mortality advantage over the older drug in heart failure, the phase II ARTS-HF trial suggested.

Reductions in NT-proBNP of more than 30% from baseline to day 90, the study’s primary endpoint, occurred in 37.2% of eplerenone-treated patients compared with 30.9% to 38.8% of finerenone-treated patients across doses tested (P not significant), Gerasimos Filippatos, MD, of Athens University Hospital Attikon in Greece, and colleagues found.

 

 

 

 

The U.S. Food and Drug Administration approved Tesaro Inc’s oral drug rolapitant (Varubi) for treatment for chemotherapy-induced nausea and vomiting in adults, the company said on Wednesday.

 

 

 

Machine generated alternative text: OAT&T 06:49 a dcri.org 'lajor Bleeding Risk in Atrial Fibrillation TSh4, Jack E. Anse115, Peter R. Kowey6, Kenneth W. Mahaffey7, D. Petersonl of Medicine, Boston, MA; 4Mayo Clinic, Rochester, MN: 5Hofstra North Shore/LlJ School of Medicine, I Scientific Affairs, Raritan, NJ; 91JCLA Division of Cardiology, Los Angeles, CA RESULTS Table 3. Major bleeding rates by ORBIT score in ORBIT-AF and ROCKET-AF populations. Bleeds per Patients-Y 1.7 2.3 2.9 4.7 6.8 9.0 12.3 14.9 4.0 ROCKET-AF ORBIT Patient-years Of Bleeds per 100 Major Bleeds 37 79 90 123 130 74 36 12 581 ORBIT-AF Patient-years Of Follow-Up 2154 3426 3131 1901 822 293 80 2154 Score 2 3 4 5 6 7 Any score Major Bleeds 87 213 185 142 95 40 7 3 772 Follow-Up 4892 7661 4989 2512 1213 403 79 19 21769 Patients-year 1.8 2.8 3.7 5.7 7.8 9.9 8.9 15.5 3.5 CONCLUSIONS The ORBIT bleeding score is a novel, u friendly score to estimate major bleeding among patients with AF The simple ORBIT score exhibits similar discrimination compared with the full continuous model in the ORBIT AF and ROCKET AF study cohorts The ORBIT, HAS-BLED, and ATRIA sco each had lower discrimination and calibra the ROCKET AF trial population, likely du more restrictive trial inclusion criteria and of available information on all score components Table 4. C-statistics (95% confidence intervals) for score performance by study cohort ROCKET-AF Cohort 0.63 (0.61, 0.65) 0.62 (0.60, 064) 0.59 (0.57, 0.61) 0.60 (0.58, 0.62) Score Full continuous model ORBIT score HAS-BLED score ATRIA score ORBIT-AF Cohort 0.69 (0.67, 0.72) 0.67 (0.64, 0 69) 0.64 (0.62, 0.67) 0.66 (0.63, 0 68) ACKNOWLEDGMENTS AND FUNDING The authors would like to thank the staff and participants of the ORBIT-AF registry for their important contributions to this vwrk. The ORBIT Registry is funded by a research grant from Janssen Scientific Affairs, LLC. Disclosures: ECO, LET, and DNS: None. DES: Research Significant; Johnson and Johnson, Consultant/Advisory Board: Bayer, Boehringer Ingelheim, Bristol-Myers Squibb, Johnson and Johnson, Daiichi Sankyo. GCF: Consultant/Advisory Board: Ortho McNeil, PRK: Consultant/Advisory Board: Modest: Boehringer Ingelheim. Bristol Squibb, Johnson & Johnson. Portola, Merck, Sanofi, Daiichi Sankyo. EMH: Consultant/Advisory Board: Bayer. Boehringer Ingelheim, BMS Sankyo. Johnson & Johnson. Pfizer. Research grants from: Bristol-Myers Squibb. Ortho-McNeil-Janssen. Speaker fees for: Boehringer Ing Bristol-Myers Squibb. BEG: Consultant/Advisory board: Ortho-McNeil Janssen; Merck, Boston Scientific, St. Jude Medical, Inc. JEA: cons advisory board for Bristol Myers Squibb, Pfizer, Janssen, Boehringer Ingelheim, and Daiichi Sankyo; equity interest in Perospher_ KWM: re support from AstraZeneca, Amgen, Bayer, Boehringer-lngleheim, Bristol-Myers-Squibb, Daiichi Sankyo, Eli Lilly, GlaxoSmithKline, Johnso Johnson, Merck, Novartis, Portola, POZEN, Schenng-Plough, and The Medicines Company, and consulting agreements with Amgen, Astr Glaxo SmithKline, Johnson & Johnson, and Merck; PC is an employee of Janssen; JPP: research support from Boston Scientific and Ja consultancies to Forest Laboratories, Janssen, and Medtronic, EDP: research support from Eli Lilly & Cornpany and Janssen r_TJ

 

Machine generated alternative text: OAT&T 06:49 R dcri.org The ORBIT Bleeding Score: A Simple Emily C. O'Brien1, DaJuanicia N. Simoni, Daniel E. Singer2, Laine E. Tho Paul Chang8, Gregg C. Clinical Research Institute, Durham, NC 2Harvard Medical School and Massachusetts General Hospi Hempstead, NY; 6Jefferson Medical College, Wynnewood, PA; 7Stanford University ND important sion making re based on shown may require g scores in 'k score nformation ijor bleeding el and simple sing data on 1 patients 10 are taking le ORBIT eding models ORBIT-AF egist :ion's largest "ith AF who yoviders, •logists nth intervals cludes ion METHODS • Starting Population: N: 10, 132 patients with baseline data enrolled at 176 sites • Exclusion Criteria: - Patients not on anticoagulation (warfarin or dabigatran) at baseline (N:2419) - Patients without follow-up data (N:302) • Final Population: enrolled at 173 sites • Primary Outcome: - Major bleeding defined by (International Society on Thrombosis and Haemostasis (ISTH) criteria) • Statistical Analysis: Candidate variables for the predictive model were chosen based on existing evidence and clinical relevance Backwards selection with a stay criterion of P«O.05 was used to build the full model Five predictors were retained in the simple risk score based on individual F-statistics, with point values assigned to each predictor according to its strength of association with major bleeding Calibration and discrimination (C-index) were evaluated in both ORBIT-AF and ROCKET-AF cohorts for the ORBIT full model, ORBIT, HAS- BLED and ATRIA scores ORBIT Bleeding Risk Score Components Table 1. Baseline characteristi during followup. Variable Age in years (median) IQR Male gender White race Anemia/Abnormal hgb/hct Hypertension Diabetes Current smoker Gl bleed Prior stroke CHF Antiplatelet therapy eGFR«60 mg/dL CHADS-VASC, median (IQR) ATRIA bleeding score, median (IQR) Table 2. Association between O Variable Older age Renal Insufficiency Bleeding history Insufficient hemoglobin/ hematocrit/anemia Treatment with antiplatelets Letter O R B Component Older Age fr74 years) Renal Insufficiency Bleeding History Insufficient Hgb/HCT/Anemia Treatment with Antiplatelet Points 2 2

 

 

 

 

Voluven hydroxyl ethyl starch

Glycerin solution – 10 % glycerol plus 5 % fructose mixed in normal saline – indigo carmine

Methyl cellulose – hydroxyl propyl methyl cellulose

 

You can take solid indigo carmine and make solution

Methylene blue is ok.  5 drops in 250 cc bag

 

Coaggraaper with soft coag.

 

Ovesco clip

 

Sergey :  6%  hetastarch in 0.9%  saline with 1-2 cc methylene blue

 

 

 

 

 

 

 

 

Mgromski@iupui.edu

 

 

 

Machine generated alternative text: 2.7 million Americans are infected with HCV of which approximately 10% are genotype 3. In a clinical trial, 152 treatment-naive and treatment-experienced participants with chronic HCV genotype 3 infection received Daklinza 60 mg plus sofosbuvir 400 mg once daily for 12 weeks, and were monitored for 24 weeks post treatment; 98% of the treatment-naive participants with no cirrhosis of the liver (and 58% of the treatment-naive participants with cirrhosis) achieved a sustained virologic response. Among the participants who were treatment experienced, 92% with no cirrhosis of the liver and 69% with cirrhosis achieved sustained virologic response.

 

 

 

Machine generated alternative text: • •000 AT&T 21:06 750/0 —3, with the idea that the phenomenon occurs only in inflamed tissues. The islet-associated hyaluronan buildup eventually crescendoed and began tapering off, analogous to the investigators' observations in recent-onset versus long-established Type 1 diabetes cases in their earlier study of human tissue. Preventing hyaluronan buildup Il We wondered what would happen if we prevented that buildup, Bollyky said. "And we knew a drug that does that. The drug was hymecromone, or 4-methylumbelliferone (4- MU for short). Prescribed in many European and Asian countries for painful, gallstone- associated spasms and sold by about 60 companies worldwide for research purposes, 4- MU inhibits hyaluronan synthesis. It is inexpensive, can be given orally and, over four decades of use, has what Bollyky described as an extremely boring safety profile". a very low rate of associated adverse events. I'ltls even approved in Europe for kids, he said. (The Food and Drug Administration has not licensed 4-MU for any indication in the United States.) In the mice used in the study, as in people,

 

 

 

The recommended workup for an adrenal incidentaloma is

 

Hormonal evaluation . The evaluation in apparently asymptomatic patients has been debated. Even in asymptomatic patients, the European Network for the Study of Adrenal Tumors (ENSAT) recommends performing the following tests to determine the secretory activity of the tumor: fasting blood glucose, serum potassium, cortisol, corticotropin (ACTH), 24-hour urinary free cortisol, fasting serum cortisol at 8 AM following a 1 mg dose of dexamethasone at bedtime, adrenal androgens (dehydroepiandrosterone-sulfate [DHEA-S], androstenedione, testosterone, 17-OH progesterone), and serum estradiol in men and postmenopausal women [76].

 

Adrenal carcinomas are typically inefficient steroid producers, but they secrete excessive amounts of adrenal steroid precursors due to decreased expression of several steroidogenic enzymes (which also results in diminished cortisol production). Even in patients with adrenal carcinomas who presumably did not produce excess steroids, more sensitive methods such as gas chromatography/mass spectrometry identify increased urinary metabolites of several steroids and precursors of androgens (pregnenediol, pregnenetriol, androsterone, etiocholanolone) or glucocorticoids (17-hydroxyproesterone, tetrahydro-11-deoxycortisol, cortisol, 6-hydroxy-cortisol, tetrahydrocortisol, and a-cortol); this is different from cortisol secreting adenomas which produce cortisol, but little androgens [77]. Low serum aldosterone concentrations, but normal or high serum or urinary concentrations of aldosterone precursors (ie, deoxycorticosterone, 18-hydroxydeoxycorticosterone, corticosterone, and 18-hydroxycorticosterone, tetrahydro-11-deoxycorticosterone (THDOC), and 5 alpha-THDOC) are found in most adrenal carcinomas, but not in adrenal adenomas [77,78].

 

The European Network for the Study of Adrenal Tumors (ENSAT) also recommends that plasma metanephrines or urinary metanephrines and catecholamines be obtained in all patients to exclude pheochromocytoma, and that plasma aldosterone and renin be obtained in patients with hypertension and/or hypokalemia (see “Establishing the cause of Cushing’s syndrome” and “Adrenal hyperandrogenism” and “Pathophysiology and clinical features of primary aldosteronism” and “The adrenal incidentaloma”). Hormonal evaluation may help in establishing the adrenal origin of the tumor and provide tumor markers that can be useful during follow-up to estimate the presence of residual tumor or tumor recurrence after surgery.

 

 

 

Naloxegol – 25 mg

GFR > 60, cyp34a, can cross bbb

Contraindicated with biaxin, ketoconazole

 

 

 

 

MLH1, MSH2, MSH6, PMS2 testing – 95% sensitive

If MLH1 def, BRAF and MLH1 promoter sequence hypermethylation studies.  If either is positive no further studies needed

If PMS2, MSH2, MSH6 def pt or MLH1 def patients with neg BRAF and hypermethylation, germline genetic testing is done.

 

 

 

 

 

 

 

 

 

 

Machine generated alternative text: LJSgr DIAGNOSTIC More biomarkers than any other IBD diagnostic test to help support your diagnosis and your prognostic assessment Marker ASCA (lgA & lgG) DNAse PANCA anti-OmpC anti-CBir1 anti-Fla-X anti-A4-Fla2 Multiple markers Marker ATG16L1 ECMI NKX2-3 STAT3 VEGF ICAM/VCAM CRP SAA Description Antibodies against yeast Saccharomyces cerevisiae' Autoantibodies against neutrophil granules? Antibody against Escherichia coli outer membrane porinn Antibody against flagellin proteirF Antibody against flagellin protein from Clostridium bacteriaB Presence of 2 or more markersl Description Diagnostic Association Prognostic Value CDIO IBDI Associated with small bowel. fibrostenosis, internal perforating disease. and surgeoøu Associated with UC-like disease and pouchitisffiO Associated with internal perforating disease and surgery3•9J2 Associated with small bowel, fibrostenosis, internal perforating disease, and pouchitiss» Associated with small bowel and fibrostenosiss Increasing number and magnitude associated with faster progress and complicated disease12•i3 Diagnostic Association CDIS I BDt4 Gene related to autophagy and intestinal bacterial handling/housekeepingi4 Epithelial barrier gene that affects intestinal permeability'S Gene critical to normal gut development'* Gene necessary for signaling of immune response'4 Growth factor that mediates angiogenesis due to inflammation and injuryw Adhesion molecule that promotes recruitment of inflammatory cells17 Acute phase reactant to inflammation18 Protein that mediates intestinal inflammation19 S. MS. S. aneti,:. rd markers Siferentate non-IBC), Crest , S and 2 Corav; See-ctc•s Zss cf disease-aisociated immurs 3. Tyry•.-, SR. C.J Yana €t el. to a unique 4. Prometheus -ee S c: 'f type J 6. ana In 7. The genet's. Prometheus B. Schee$a- r. v,t.ceS. cf to r•ANCA 'AB. h a 10. A M. e-.tr, 12 S L. Cie PROMETHEI 17. *eets P. •n : 2007-:est1YGs-GE8 18.

Fecal calprotectin

 

 

 

Make a Super Hidden Folder in Windows Without any Extra Software

 

Almost anyone knows how to make a “hidden” folder in Windows, but then again almost anyone knows how to make explorer show hidden folders. Let’s take a look at how to make a folder so hidden, only you will know its there. Anyone that has used Windows for a while knows that they can right-click on a file or folder and edit its properties, more so its attributes to make it a so called “hidden” file or folder. The problem is that just as many people know you can show files and folders that have the “hidden” attribute by simply changing a radio button under the folder view options. The easiest way to make a real hidden file or folder is to mark it as an important operating system file, that way Windows wont display it even if explorer is set to display hidden files and folders…

 

 

 

<<04_2_ignjatovic.pdf>>

 

 

 

 

<<ajg2012417x3.ppt>>

 

 

 

 

<<Pit Pattern.pdf>>

 

 

 

 

The approval of patiromer for oral suspension (Veltassa, Relypsa) comes after the phase-2 

study showed that daily administration of the potassium-binding agent safely controlled hyperkalemia over 1 year in patients with type-2 diabetes and hypertension with or without heart failure (HF). They had entered with mild-to-moderate hyperkalemia secondary to treatment with renin-angiotensin-aldosterone system (RAAS)-inhibiting drugs.

 

 

 

 

 

Machine generated alternative text: o AT&T Wi-Fi 11:42 @ O * 790/0 —J, the IvaglJingtmt Vogt Into consideration all the relevant data, Including the substantial epidemiological data showing a positive association between consumption of red meat and colorectal cancer and the strong mechanistic evidence," according to a statement posted by the group on the Web site of the Lancet journal. The panel also cited studies suggesting that eating an additional 100 grams of red meat per day raises the risk of colorectal cancer by 17 percent; eating an extra 50 grams of processed meat daily raises the risk by 18 percent, according to the research cited. The research into a possible link between eating red meat and cancer has been the subject of scientific debate for decades, with colorectal cancer being a long- standing area of concern. But by concluding that processed meat causes cancer, and that red meat "probably" causes cancer, the WHO findings go well beyond the tentative associations that some other groups have reported. Keep Reading vv p' CISION:. HOW'S YOUR Find Cisws BRAND'S HEALTH?

 

 

 

 

Sarcina ventriculi gastroparesis

 

 

 

Dragapv@medicine.ufl.edu

 

ESD.  CONFERENCE

 

Dr Aihara.  Boston

 

IT 2 – 3 or 9 to 6

 

Dual – 6 to 3

 

Two types of dual.  Smaller one for colon.  1.5 mm

 

Gastric is 2.0

 

 

 

Bleeding in rectum

Hemostatic sponge for rectum

Forced coag for bleeding

Marking soft coag

Coag- use ef 5 80w for gastric ESD

Ef 5 50w for colon

epinephrine 1:100,000

Gonak 45ml+ saline 50ml

 

 

 

 

Make room, cholesterol. A new disease marker is entering the medical lexicon: suPAR, or soluble urokinase-type plasminogen activator receptor. A study in the New England Journal of Medicine shows that suPAR, a circulating protein measured by a simple blood test, can reliably predict a person’s chances of developing chronic kidney disease as much as five years before this common killer starts causing damage.

 

The New England Journal of Medicine article appears in Online First, November 5, 2015 to coincide with the American Society of Nephrology’s Kidney Week meeting. It will also appear in the printed issue of the journal on November 12.

 

 

 

 

 

 

 

The number needed to treat to prevent a heart attack for patients with a DAPT score of 2 or higher is 34 and the number needed to harm (to cause bleeding) is 272, Yeh said. When the score is less than 2, the number needed to treat to prevent ischemia is 153 and the number needed to harm is 64.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

SAN FRANCISCO — Eight weeks of therapy with grazoprevir and elbasvir may be effective in patients with low fibrosis scores, according to findings presented at The Liver Meeting 2015.

 

 

 

Tedizolid phosphate is a second-generation oxazolidinone antibiotic that offers enhanced antimicrobial potency and low rates of bacterial resistance.

 Available in both IV and oral forms, tedizolid exhibits bacteriostatic activity by binding the 50S subunit of the bacterial ribosome, resulting in inhibition of bacterial protein synthesis.

 The recommended dosage is 200 mg once daily for 6 days,

 which may offer increased convenience and compliance when compared to twice daily linezolid.

 

 

 

 

 

THE RIGHT WAY OF ADMINISTERING BLOOD PRODUCTS (

)

 

[ from “THE CLINICAL — — USE OF BLOOD: HAND BOOK , World Health Organization & Blood Transfusion Safety , GENEVA ]

 

Prefer a larger cannula: A doubling of the diameter of the cannula increases the flow rate of most fluids by a factor of 16.

 

In case of Whole blood, red cells, plasma and cryoprecipitate

>Use a new, sterile blood administration set containing an integral 170–200 micron filter

 

>Change the set at least 12-hourly during blood component infusion

>In a very warm climate, change the set more frequently and usually after every four units of blood, if given within a 12-hour period

 

In case of Platelet concentrates

 

>Use a fresh blood administration set or platelet transfusion set, primed with saline.

 

WARMING BLOOD:

 

>There is no evidence that warming blood is beneficial to the patient when infusion is slow.

 

>At infusion rates greater than 100 ml/minute, cold blood may be a contributing factor in cardiac arrest. However, keeping the patient warm is probably more important than warming the infused blood.

 

>Warmed blood is most commonly required in: [1]Large volume rapid transfusions:

   -Adults: greater than 50 ml/kg/hour      -Children: greater than 15 ml/kg/hour

[2]Exchange transfusion in infants  [3]Patients with clinically significant cold agglutinins.

 

>Blood SHOULD ONLY BE WARMED in a blood warmer. Blood warmers should have a visible thermometer and an audible warning alarm and should be properly maintained.

 

>Blood should never be warmed in a bowl of hot water as this could lead to haemolysis of the red cells which could be life-threatening.

 

Severe reactions most commonly present during the first 15 minutes of a transfusion. All patients and, in particular, unconscious patients should be monitored during this period and for the first 15 minutes of each subsequent unit.

 

The transfusion of each unit of the blood or blood component should be completed within four hours of the pack being punctured. If a unit is not completed within four hours, discontinue its use and dispose of the remainder through the clinical waste system.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

<<gastroparesis-diet.pdf>>

 

 

 

 

 esophagus patients. There are case reports of proton pump inhibitor induced gastric neuroendocrine tumours and adenocarcinomas as consequences of these effects. In pernicious anemia and chronic gastritis, clinicians should be aware of potential increased risk of gastric neuroendocrine tumour development with chronic proton pump inhibitor use in these patients. Eradication status of Helicobacter pylori prior to commencing long term proton pump inhibitor therapy should be established to reduce the risk of severe atrophic gastritis and development of gastric dysplasia.

 

 

 

<<26341719.pdf>>

 

 

 

 

 

 

 

 

Fluoroquinolone labeling currently has warnings about the risks for tendonitis, tendon rupture, central nervous system effects, peripheral neuropathy, myasthenia gravis exacerbation, QT prolongation and Torsades de Pointes, phototoxicity, and hypersensitivity. But panel members called for stronger wording, with some suggesting the risks be called out with a black box warning.

 

 

 

Cardiac resync therapy with Defibrillator helps morbidity mortality in HF ( CRT-D)

 

 

 

 

 

 

 

 

 

 

 

Phase 2.  Ghrelin agonist drug

 

 

 

VIberzi is contraindicated with SOD spasm, alcoholism or drink more than 3 drinks a day or pancreatitis or cirrhosis Child’s C or severe constipation or mechanical obstruction

It is the first and only mixed opioid receptor modulator.  It binds to kappa, mu and delta.  It stimulates kappa and mu and blocks delta which is antagonistic.

Overall, it then modifies GI motility and slows down contraction of smooth muscle.It also decreases the activity of afferent neuron of the gut.

This causes decreased visceral hypersensitivity.

It does not get absorbed and only binds to mucosal receptors in the gut.  Give with food?

Bristol stool scale : Pain scale was 6.1 and stool consistency was 6.2 (max is 7 diarrhea)

The trial was 52 weeks and more than 1200 patients and the primary end point was improvement in pain, diarrhea at 12 weeks.

Composite responder ( improved pain and diarrhea )

Benefit was 30 and 33% in the 12 and 24 months compared to 16 and 20% in placebo

SOD occurs in patients with s/p chole. SOD occurs in 0.2% of s/p lap chole.  

Pancreatitis occurred in 6 out of 3000 patients.

Side effect profile otherwise similar to placebo (except constipation 1-2% had to stop it). 1 % at 75 mg and 2% at 100 mg

It can cause euphoria (0.2%)and feeling drunk (0.1%).  Since it can activate mu receptor it is labeled as Schedule IV.

75 mg dose for patients with child’s A or B cirrhosis, s/p chole patients, those unable to tolerate 100 mg bid dose or they are on gemfibrozil or cyclosporine. (Similar to lomotil)  

OATP1B1 receptor ((drugs are Rifampicin, Rifamycin SV, Clarithromycin, erythromycin, roxithromycin, telithromycin indinavir, saquinavir, ritonavir, Cyclosporine, gemfibrozil) (organic anion transporting polypeptide)

It increases absorption of Viberzi.

40% increase in Crestor level

Developed by same scientist from J and J that developed loperamide.  

10%  delta (compared to placebo) of patients who did not respond to loperamide responded to Viberzi.

Agonist for mu, antagonist to delta and unknown to kappa.  Passes BBB.  Eat it with meal to decrease absorption

Avoid in lap chole : because they may have SOD.  

Child’s A and B, use reduced dose and Child’s C contraindicated.

Most of the events of constipation occurred in first 2 weeks (50%)

P value for primary endpoint.  Confidence interval for secondary endpoint.

SOD issues occurred in 0.2% at 75 mg dose and 0.8% in 100 mg dose.  All resolved after stopping medication.

1 pt with SOD got abnormal LFT, one got pancreatitis. The other 5 pancreatitis had sludge or had alcohol.

 

 

Discontinuation rate of Viberzi is 8%

 

 

 

Combination of leucine, meteor in and sildenafil for NAFLD : accelerated trial.  Measured with proton-density-fat fraction on MRI.  NuSirt pharmaceutical

 

 

 

 

 

 

 

 

 

 

Use bottled water or  teaspoon of apple sauce

Open capsule.  Drug is coating beads.  So if beads remain it’s ok !

 

 

 

Rifaximin EIR 800 bid for moderately active crohns

 

 

 

 

 

KALK German area

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Markers at 25 and 15

Inflate balloon with water 5 cc, aspirated to get rid of air, empty air from syringe and then reinflate ballon to fit cap.  

Use cap

 

 

 

 

Among 10 patients who developed inflammation of the ileoanal anastomosis, or J-pouch, all reported clinical improvements in stool frequency, and symptomatic relief typically was observed within 2 to 3 weeks after treatment with serum-derived bovine immunoglobulin/protein isolate (SBI), according to 

, of South Nassau Communities Hospital in Oceanside, N.Y.

 

The product, also known as 

 is derived from bovine plasma that has been USDA approved and contains immunoglobulins (primarily IgG), albumin, and other proteins. Pouchitis is not currently included in the labeling for EnteraGam.

 

 

 

 

 

 

 

Anastrozole/ tamoxifen for HR + which is better ?

 

Denosumab for post menopausal women breast cancer.  Cancer prevention plus osteoporosis prevention

 

 

 

Subset of pbc pt do poorly

Correlated with bilirubin and Alk phos elevation

OCA start at 5 mg and titration at 3 or 6 months to 10 mg.  Continue Urso ?

Fibrates help pruritis.

Benzafibrate

Then   

 

 

 

 

 

 

An isolated report from a single center suggested that a purple or crimson discoloration of both anterior tonsillar pillars (crimson crescents) in the absence of pharyngitis is might be a marker in patients with CFS. The cause of crimson crescents is unknown, but they are common in patients with CFS. However, crimson crescents are not specific for CFS, 

 

 

 

 

 

 

Fibroblast growth factor 21 suppresses carbohydrate and alcohol craving.  It is produced by the liver

 

 

 

Hopkins bandits shark shutdown

 

 

 

Taken together, our findings suggest it is possible that migraine is a neurologic disorder of ‘minor’ sphingolipid dysmetabolism,” they conclude. “Further research, validating the ceramide and sphingomyelin associations with migraine, as well as research examining mechanisms for these associations, may advance our understanding of migraine pathophysiology and open possibilities of the identification of novel migraine biomarkers and targeted drug therapies directed against sphingolipid pathways.”

 

 

 

 In analysis of data from a phase 2 study of the effects of glycerol phenylbutyrate in patients with cirrhosis, we found that fasting levels of NH3 in blood can identify patients at risk for HE-related morbidity. Patients with HE might benefit from NH3-lowering therapy. 

 

 

 

Recticare lidocaine

Either wipes or jelly

 

 

 

ELAFIBRINOR   

OCA MAY NOT EIRK

 

 

 

CDX2.  For stage 2. If absent aggressive cancer  

 

 

 

Gene marker in future

Right now pro calcitonin level

 

 

 

including exercise, healthy diet, stopping smoking, or moderating alcohol intake if indicated. This little extra time is appreciated by the patients and goes beyond treating patients as if guidelines were a cookbook. 

 

 

 

AIMS65 scoring system for survival.  Older are rockall and Glasgow blatchford score

 

Age more than 65, bp less than 90, change in mental status, INR more than 1.5, albumin less than 3.

One point each.

0

0,3% || 1

1,2% || 2

5,3% || 3

10,3% || 4

16,5% || 5

24,5%

 

 

 

 

 

 

ESKAPE pathogens – Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species – named for their ability to resist the effects of antibiotics. 

 

 

 

 

 

 

 

 

 

Unit is Sv which is seivert 1 Sv is 100 rem.

CT of abd and pelvis is 10-20mSv (this is like 3-7 years of radiation exposure from natural environment)

 

 

 

Machine generated alternative text: AT&T Wi-Fi 20:40 dailymail.co.uk @ o * 490/013 6 pSv: Typical radiation from a dentist's X-ray 10 pSv: Average daily natural radiation 40 pSv: Radiation from flying from New York to Los Angeles 100 pSv: Radiation from a 10-hour flight across the North Atlantic 2,100 pSv: Annual radiation of a typical person in Europe 3,000 pSv: Radiation from a mammogram 3,600 pSv: Average annual radiation of a US citizen 50,000 pSv: Maximum allowable yearly occupational dose in the US 100,000 pSv: Lowest yearly dose linked to increased risk of cancer 2,000,000 pSv: Severe and potentially fatal It can measure all the relevant types of radiation, in particular neutron radiation produced in the atmosphere. Using the TrackYourDose app, users enter the details of the airports they are flying from and to and the date they are travelling.

 

 

 

Machine generated alternative text: AT&T Wi-Fi 20:42 a en.m.wikipedia.org @ o * 470/0 The sievert is of fundamental importance in dosimetry and radiation protection, and is named after Rolf Maximilian Sievert, a Swedish medical physicist renowned for work on radiation dosage measurement and research into the biological effects of radiation. One sievert carries with it a 5.5% [3] chance of eventually developing cancer. One sievert equals 100 rem. The rem is an older, non-Sl unit of measurement. To enable a comprehensive view of the sievert this article deals with the definition of the sievert as an Sl unit, summarises the recommendations of the ICRU and ICRP on how the sievert is calculated, includes a guide to the effects of ionizing radiation as measured in sieverts, and gives examples of approximate figures of dose uptake in certain situations. Definition External dose quantities Calculating protection dose quantities

 

 

 

Approved for 1, 4

 

 

 

Soft coag. 80 watts effect 5. For marking

 

Forced coag. 50 watts.  Effect 2. ( 3-1-1)

Effect-duration-interval)

 

Endocut   3-1-1 50 watts effect 3.  Or 3-2-1 or 3-3-1

 

Increase cutting duration for larger duration

 

Let cautery do the cutting

 

 

Dry cut :  50 watts effect 2

 

Submucosal dissection. : endocut or drycut. Less used is swift coag

 

Forced coag.  25 watts effect 2. For  pedunculated polyp

 

EMR. Endocut.  Q.  3effect duration 1 and 3 interval

Upside down. Take lower part first. Must close in 1 cm.  And check mobility   Only polyp should move and not wall

 

Submucosal  dissection : Stomach Dual knife Forced coag Effect 2 Watts 40.  For esophagus and colon Effect 1 watts 40

 

Effect is voltage.  Higher the number the higher the voltage

 

IT 2 knife in stomach : Effect 2, watts 50-6 0

 

Machine generated alternative text: Generally Accepted Starting Points ERBE USA VIO 300 D gram A M.ri COAG S ENDOCUTQE3-Oi4t fORCEO E 2 ORY CUT E2 FORCED n FORCED E 2 SOFT COAGOW E S SO" COAG mw E S ENOOCUT Q FORGO SOW E SOFT E S ORY cur E2 ENOOCUT Q FORCED SOW n FORCED E 2 COAG S son COAG E S ENOOCUT Q SORGO SOW 2 COAG E DRY cur E2 ENDOW r Q 0-01. FORGO E 2 COAG SOW E S COAG S ENOOCUTQE3.Oi4t 'ORCW SOW E 2 COAG OW E s cur E2 (or to Q 001-11 FORCED E2 FORCEO row E 2 SOFT COAGOW E s Use more or less electrode with touch to hcrease / decrease sir of - rture tk•irg LOhg area hc.rease Le. 112 from i to 2 (or 3) to •gist dean and corsBtent altlrg. a ruch twrnal sve•d tap EfOO cur or D cur too aureøw to 2SW E 2 ORY Cur for Ferrostatk dissectbn. If na I due to surface •ea. hcrease to IWW Svgems use simiar to DRY cur. VORCEO COAG abo uæd dissectim of matomy. too drco to 2 SW E2.

 

Fold convergence, mucosal bleb are sign of fibrosis under polyp.  Also when snare is around polyp you should be able to lift it  otherwise fibrosis

 

Endocut effect is the blend.  Goes from 1-4. Higher the number more coag.   For EMR use effect 2  less coag. You decrease the thermal injury by squeezing tightly before cautery

Forced coag – deep injury.  So prefer soft coag.

Soft coag by Doug Rex – effect 5, watts 80 blue pedal

Hot forceps avulsion technique – use endocut i( letter ) effect 3 cut duration 1 interval 3. Advantage over q lowers voltage setting  313

Underwater technique –  use pure autocut effect 5 max watt 80

APC for flat lesion –  power 30 flow 0.8 to 1 liter flow

 

 

 

 

Can cause :intracranial calcifications, ventriculomegaly, and neuronal migration disorders (lissencephaly and pachygyria). Other anomalies included congenital contractures and clubfoot, microcephaly

Babies check eyes and hearing 6 months  

 Testing  3 tests  PCR, IgM, PRNT

reverse transcriptase-polymerase chain reaction (RT-PCR) on infant serum. Serology assays can also be used to detect Zika virus-specific IgM and neutralizing antibodies. Plaque-reduction neutralization testing (PRNT) can also be performed to measure virus-specific neutralizing antibodies and differentiate from other flaviviruses.

 

 

 

Like the more well-known 

 causes symptoms like fever, rash, headache, and neck pain, and as the disease progresses it can cause arthritis. Unlike the original strain, though, 

 can also cause vomiting and nausea. The initial bacteria was also characterized by a rash that looked like a bull’s eye, but an infection with 

 can cause a more widespread rash on the body.

 

 

 

 

 

 

 — Several medications can delay gastric emptying. These include [

]:

Narcotics (affecting mu opiate receptors alone or combined with inhibition of norepinephrine reuptake [eg,

and

, respectively]) [

]

Alpha-2-adrenergic agonists (eg,

)

Tricyclic antidepressants [

]

Calcium channel blockers

Dopamine agonists

Muscarinic cholinergic receptor antagonists

[

]

Glucagon-like peptide (GLP)-1 agonists and amylin analogues [

]

Phenothiazines [

]

(but not

, which is derived from macrolide molecule like

, and does not inhibit gastric emptying)

 

 

 

 

 

Machine generated alternative text: Rapid Diagnostic Methods for Nosocomial Pneumonia MALDI-TOF: rapid diagnostic test for pneumonia — Identifies bacteria, fungi, and mycobacteria isolated from cultures of sputum or BAL specimens in clinical microbiology laboratories Fast, accurate, and helps to rule out infection Does not identify resistance genes Facilitates antimicrobial stewardship by allowing clinicians to target the precise pathogen, and in some cases narrow the spectrum of antimicrobial coverage • Shorter duration of therapy • Reduced resistance by de-escalating antibiotic therapy for gram-positive organisms Singhal N, et al. Front Microbiol. 2015;6:1-16.

 

Machine generated alternative text: Use of Procalcitonin in Reducing Duration of Antibiotic Therapy Observational, historical control study to assess the impact of using PCT levels Procalcitonin correlates with bacterial load and responds very quickly to reduction in bacterial load Increased confidence in decision to stop antibiotics when level decreases significantly • Findings Duration of antibiotic use decreased by 3.3 days (P =.0238) Hospital LOS decreased by 4.3 days (P =.029) Rate of readmission to hospital decreased by 16% (P =.055) 30-day readmission for infection to hospital decreased by 24% (P = .001) Bishop BM, et al. Ann Pharmacother. 2014;48:577-583.

 

 

 

 

 

 

 

 

Larger virus. Like a prokaryote

Get infected by virophage  ( eg zamilon phage virus)

Have CRISPR immunity that destroys the phage virus. ( areas of DNA that mimic phage DNA and destroy it )

 

 

 

 

 

Telmisartan is an angiotensin receptor blocker that could be used as a weapon against NAFLD by increasing insulin sensitivity (and decreasing hepatic fat accumulation), and suppressing hepatic fibrogenesis. It is also reported to be effective in mild to moderate hypertension, and improves insulin sensitivity to type 2 diabetes mellitus, as well as cholesterol and triglyceride levels.

 

 

 

Keytruda and Opdivo

 

 

 

Machine generated alternative text: Harvard Health Publications HARVARD MEDICAL SCHOOL Trusted advice for a healthier life V CART FREE HEALTHBEATSIGNUP SHOP SIGN What can we help you find? HEART HEALTH MIND & MOOD PAIN STAYING HEALTHY CANCER DISEASES & CONDITIONS MEN'S HEALTH WOMEN'S HEALTH Glycemic index and glycemic load for 100+ foods Ghycemic ndex and glycemc load offer Information about how foods affect blood sugar and nsulln. The lower a food's glycemc index or glycemc load, the less t affects blood sugar and nsulln levels. Here IS a list of the glycemic ridex and glycemic load for more than 100 common foods. FOOD BAKERY PRODUCTS AND BREADS Banana cake, made wth sugar Banana cake, made wthout sugar Sponge cake, plan Vanilla cake made from packet mix wth vanilla frosting (Betty Crocker) Apple, made wth sugar Apple, made wthout sugar Waffles, Aunt Jemma@ (Quaker Oats) Bagel, whte, frozen Baguette, whte, plan Coarse barley bread, 75-80% kernels, average Hamburger bun Kaiser roll Pumpernickel bread 50% cracked wheat kernel bread Whte wheat flour bread Wonderå$ bread, average Whole wheat bread, average 100% Whole Grain@ bread (Natural Ovens) Pta bread, whte Corn tortilla Wheat tortilla BEVERAGES Coca Cola@, average Fanta@, orange soft drnk Lucozade@, ongnal (sparkhng glucose drink) Apple JUIce, unsweetened, average Cranberry Juice cocktail (Ocean Spray@) Gatorade Orange JUIce, unsweetened Tomato juice, canned BREAKFAST CEREALS AND RELATED PRODUCTS All-Bran@, average Coco Pops@, average Cornflakes@, average Cream of Wheat@ (Nabisco) Cream of Wheat@, Instant (Nabisco) Grapenuts, average Muesli, average Oatmeal, average Instant oatmeal, average Puffed wheat, average Rasn Bran@ (Kellogg's) Special K@ (Kellogg's) GRAINS Pearled barley, average Sweet corn on the cob, average Couscous, average Qunoa Whte rice, average Quick cooking whte basmati Brown rice, average Converted, whte rice (Uncle Ben's@) Whole wheat kernels, average Bulgur, average COOKIES AND CRACKERS Graham crackers Vanilla wafers Shortbread Rice cakes, average Rye crisps, average Soda crackers DAIRY PRODUCTS AND ALTERNATIVES Ice cream, regular Ice cream, premium Milk, full fat Milk, skim Reduced-fat yogurt wth frut, average FRUITS Apple, average Banana, ripe Dates, dried Grapefrut Grapes, average Orange, average Peach, average Peach, canned lght syrup Pear, average Pear, canned In pear juice Prunes, ptted Rasns Watermelon BEANS AND NUTS Baked beans, average Blackeye peas, average Black beans Chickpeas, average Chickpeas, canned n brine Navy beans, average Kidney beans, average Lentils, average Soy beans, average Cashews, sated Peanuts, average PASTA and NOODLES Fettucni, average Glycemic index Serving (glucose = 100) size 47 55 46 42 44 48 76 72 95 34 61 73 56 58 71 73 71 51 68 52 30 63 68 95ı10 44 68 78 50 38 55 77 93 66 74 75 66 55 83 80 61 69 28 60 65 53 89 67 50 38 30 48 74 77 64 82 64 74 57 38 41 32 33 39 62 42 25 59 40 42 40 38 43 29 64 72 40 33 30 10 38 31 29 29 15 27 7 32 (grams) 60 60 63 111 60 60 35 70 30 30 30 30 30 30 30 30 30 30 30 50 50 250 mL 250 mL 250 mL 250 mL 250 mL 250 mL 250 mL 250 mL 30 30 30 250 250 30 30 250 250 30 30 30 150 150 150 150 150 150 150 150 50 150 25 25 25 25 25 25 50 50 250mL 250 mL 200 120 120 60 120 120 120 120 120 120 120 60 60 120 150 150 150 150 150 150 150 150 150 50 50 180 Glycemic load per serving 14 12 17 24 13 9 10 25 15 7 9 12 7 12 10 10 9 7 10 12 8 16 23 40 30 24 12 12 4 12 20 23 17 22 16 16 13 30 17 12 14 12 20 9 13 43 28 16 14 11 12 14 14 10 17 11 12 6 3 5 4 11 6 16 18 3 11 4 5 5 4 5 10 28 4 6 10 7 3 9 9 7 5 3 0 15 Sign Up Now For HEALTHbeat our FREE E-Newsletter Get health information and advice from the experts at Harvard Medical School. E-mail Address First Name (Optional) Sign Up Now Best-selling Reports Walking for Health Stretching: 35 exercises to improve flexibility and reduce pain Improving Sleep: A guide to a good night's rest HARVARD MEDICAL SCHOOL Now and Zen: How mindfulness can change your brain & improve your health uesday. March 8 oo - 7:30 pm ET Register Related Topics Diseases & Conditions Diabetes Heatthy Eating Nutrition Ask Harvard Med School COPD Breathing Exercises Dr. Howard LeWne Add mindfulness to your day in only 10-15 minutes Here are 4 ways to add mindfulness to you schedule, each way only takes 10-15 minutes of your time: paying attention tn any tension or Relax at the end Of the day with a guided meditation. Take a break to check in with your breathing. •Remember consistency is key Related Articles How often should you get your bbod

 

Machine generated alternative text: Macaroni, average Macaroni and Cheese (Kraft) Spaghetti, whte, boiled, average Spaghetti, whte, boiled 20 min, average Spaghetti, wholemeal, boiled, average SNACK FOODS Corn chps, plan, sated, average Frut Roll-Ups@ M & M's@, peanut Microwave popcorn, plan, Potato chps, average Pretzels, oven-baked Snickers Bar@ VEGETABLES Green peas, average Carrots, average Parsnps average Baked russet potato, average Boiled white potato, average Instant mashed potato, average Sweet potato, average Y am, average MISCELLANEOUS Hummus (chickpea salad dp) Chicken nuggets, frozen, reheated In microwave oven 5 mn Pizza, plain baked dough, served wth parmesan cheese and tomato sauce Pizza, Super Supreme (Pizza Hut) Honey, average 47 64 46 58 42 42 99 33 55 51 83 51 51 35 52 111 82 87 70 54 6 46 80 36 61 180 180 180 180 180 50 30 30 20 50 30 60 80 80 80 150 150 150 150 150 30 100 100 100 25 23 32 22 26 17 11 24 6 6 12 16 18 4 2 4 33 21 17 22 20 0 7 22 9 12 The complete ist of the glycemc ndex and glycemc load for more than 1,000 foods can be found n the article "International tables of glycemc Index and glycemic load values: 2008" by Fiona S. Atkinson, Kaye Foster-Powell, and Jenne C. Brand-Miller n the December 2008 ssue of Diabetes Care, Vol. 31, number 12, pages 2281-2283. February 3, 2015 Updated: August 27, 2015 Share this page: Pmt ths page: Harvard Health Publications Home Sign up for HEALTHbeat Subscribe Special Health Reports Subscriptions Customer Service About us Licensing/permissions Privacy Policy C 2010 - 2016 Harvard University. All rights reserved.

 

 

 

 

 

 

acoustic radiation force impulse was more accurate for detecting hepatitis C virus infection positivity in liver transplant recipients vs. Fibrotest, according to published findings.

 

 

 

 

 

 

Gattex – 0.5 mg /kg

Usual pt is TPN Or frequent dehydration from diarrhea

 

Contraindications

Polyps or colon cancer or other cancers

Reduce doses of opiates

Increased absorption of fluid so can cause CHF

It is GLP 2 agonist with single ALA with Gly

Monitor LFT

Colonoscopy 6 months before starting

SQ injection

Respiratory infection, nausea, bloating, hypersensitivity , abd pain

Sleep disturbance, atoms complication

 

 

 

 

Hydroxy ethyl starch plus methylene blue injection

Right squeeze first

EMR

Use Endo cut

 

Margins use tip of snare with soft coag

 

SPS use  serrated polyposis syndrome

Do annual colonoscopy

If more than 5 lesions or more than 2 cm every 3-6 cm

 

Use serrated squeeze

Serrated polyp have more fat   Some people squeeze, open a little and then squeeze again. This lets muscularis pop up

 

 

 

 

 

“We found that the Westernized diet did increase fatty liver, but we saw that the broccoli protected against it,” she said. “Broccoli stopped too much uptake of fat into the liver by decreasing the uptake and increasing the output of lipid from the liver.”

 

Previous research conducted by Dr Jeffery found that chopping or steaming broccoli was the best way to enhance the availability of sulforaphane, broccoli’s anticancer compound.

 

 

 

 

 

The tests measured two proteins nicknamed GFAP and UCH-L1, which are present in brain cells. In a head injury, the proteins can leak into the bloodstream, Papa said.

 

Do blood test for upto 1 week after concussion

 

 

 

CURB65.   Confusion, uremia, respiration, blood pressure and age.  Score to admit

 

 

 

Machine generated alternative text: News & Perspective: Muitspeciaity COMMENTARY Artificial Sweeteners: A Wolf in Sheep's Clothing? David Johnson, MD Disclosures March 22, NOT SO SWEET? Hello. Pm Dr David Johnson, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia I recently attended a conference at the Weizmann Institute of Science in Rehovot, Israel, and wanted to highlight some particularly fascinating information about noncaloric artificial sweeteners. In use for over a century now, there are six commercially available artificial sweeteners in the United States. They are commonly used in a variety of foods, processed sodas, and other products that we routinely see on the shelf and ingest perhaps every day. Artificial sweeteners are frequently recommended to patients With predabetes, diabetes, and obesity because they are noncaloric and don't have an absorbable sugar. Are they really good for us? The data on glycemic control in patients with diabetes or obesity are quite mixed. What I want to share with you today IS why some of these artificial sweeteners are really not good and, in fact, may be bad for you. A FASCINATING SERIES OF EXPERIMENTS Let's look at a fascinating series of experiments from the Weizmann Institute of First, they took mice and gave them three artificial sweeteners: saccharin, sucralose (which is Splenda@), and aspartame. (These are the three most commonly used artificial sweeteners, but there are also three others.) They compared mice that were fed these sweeteners With mice that had routine chow feeds and glucose or sucrose, which are both absorbable sugars. At the end of the 4-week experiment, there was a profound effect on the glycemic control of the mice that were being fed the noncalonc artificial sweeteners; they had signficant dysregulation of their glycemic control. Saccharin had the most pronounced effect, so they did another experment using a lower dose of saccharin, which showed the same type of glycemc worsening in the mice. Was this effect related to the microbiome? We know that sugars are potentially fermentable; noncaloric sugars can be presented to the gastrointestinal tract, and the microbiome can take advantage of them. The microbiome can convert them to things that may be fermented and then upregulate certain pathways by themselves, through degradation products, or they may have a prebloüc effect. In a preblotlc effect, the ingested substance may actually be toxic due to the metabolic waste products that the bacteria generate and may knock off some other bacteria or may favor some of the bad bacteria, creating what we call intestinal dysblosis_ In the artificial sweetener model, the investigators at the Weizmann Institute of Science took the mice with artificial sweetener-induced glycemic intolerance and gave them antibiotics for 4 weeks. They were able to show that the antibiotics reversed this effect on glycemic Intolerance. So, antibiotics directed at bacteria would actually correct glycemic control to normal. This suggests that the microflora were pan and parcel to this, f not the crux of the problem They took this a step further and looked at some of the metabolic consequences, including what we call metagenomics, where pathways are upregulated by some of these bacterial changes. What they found was that there is a host of pathway upregulations_ One pathway upregulation, in particular, among the saccharin-fed mice was an Increase In the glycan degradation pathway. This is a pathway that has been strongly associated—not only In mice but also in humans—with diabetes and obesity. In addition to the glycan degradation pathway, other pathways In the saccharin-fed mice were upregulated, such as pathways that enhanced starch, sucrose, fructose, and mannose metabolism and folate, glycerolipld, and fatty acid biosynthesis. In contrast, the mice that didn't receive the saccharin didn't have these effects. These metagenomc upregulaüons are all well recognized as pathways that are expressed and enhanced in diabetes and obesity. What they demonstrated when they looked at the microbiome and the bacteria genomic profiling were increases in bacteria belonging to the Bacteroides genus and Clostridiales order and decreases In Lactobacillus reuteri among the saccharin-fed mice. Again, we can see that not only IS there a dysblosls, but there is a pattern that is reproducible across these studies. Findings Relevant in Humans Too Next, they tested these findings in humans, using a database with nutritional profiling in a large number of patients, With ongoing data collection_lll They &ntified 381 nondabetics in their database with about 44% males. They looked at associations with glycemic control and ingestion of noncaloric artificial sweeteners. They had a very dynamic way to look at dietary recall With a validated dietary history questionnaire. When they looked at this and correct

 

 

 

 

 

 

“Now the microbiome is another element in this equation—it’s not just diabetes, high blood pressure and obesity,” Iadecola notes. “There are also other factors which we need to know in order to tailor treatment.” The study suggests that such treatment may involve antibiotics, probiotics, dietary changes or other interventions that would change the gut’s microbiota to be supportive of regulatory T cells and reduce delta gamma T cells. For example, patients undergoing heart surgery, many of whom end up suffering a stroke, might go on a special preemptive diet, he says.

 

 

 

In the study of nearly 3,000 patients, researchers from the Intermountain Medical Center Heart Institute in Salt Lake City discovered that the presence of high levels of the biomarker glycoprotein acetylation, or GlycA, was associated with an increased risk of 

 or stroke.

 

 

 

LOS ANGELES (CBS News) – Drinking coffee may cut your risk of colon cancer by as much as 50 percent, a new study suggests.

 

The more you drink, the more you may reduce your risk – and it makes no difference whether the coffee is regular or decaf, researchers said.

 

“The protective effect is not caffeine, per se, but probably a lot of other antioxidant ingredients in the coffee that are released in the roasting process,” said senior researcher Dr. Gad Rennert. He is director of the Clalit National Israeli Cancer Control Center in Haifa, Israel.

 

 

 

 

 

 

 

 

 

 

 

Machine generated alternative text: NEWS MEOICAL Browse: Q Drugs O Health MENU O News Bariatric arterial embolization safe, effective in sustaining weight loss in severely obese people Posted in: Medical Procedure News Medical Research News Medical Condition News Healthcare News Published on April 4, 2016 at 3:11 PM Findings from the early phase of a clinical trial led by Johns Hopkins investigators indicates that a new, minimally invasive weight loss treatment known as banatnc anerial embolizatlon is safe and effective In sustaining weight loss in severely obese people. The data, although preliminary, show the procedure seems to initiate weight loss, dramatic hunger reduction and lower évels of ghrelin, one of the man hormones Involved in controlling hunger. The results Will be presented at the Society of Interventional Radiology's 2016 Annual Scientfic Meeting In Vancouver, British Columbia, on Sunday, April 3. "Obesity is a highly prevalent, detrimental and costly disease in the L.I_S_ and abroad," says Clifford Weiss M.D. associate professor of radiology and radiological science and director of interventional radiology research at the Johns Hopkins University School of Medicine. "The interventions currently available to treat this condition are behavioral modifications, diet and exercise, medications, and invasive surgery. We're excited about the possibility of adding baratrlc anenal embolizatlon as another tool for health care providers to offer patients In the effort to curb this epidemic." Johns Hopkins researchers, along with former Johns Hopkins faculty member Aravlnd Arepally, designed the Bariatric Embolizatlon of Afterles for the Treatment of Obesity (BEAT Obesity) pilot clinical trial. The trial Included a multidisciplinary team of weight loss physicians, physiologists, hormone specialists, gastroenterologists, registered dieticians, psychologists and surgeons. As pan of this trial, Weiss and his team enrolled seven mostly female participants (SIX women) ages 31 to 59 who were severely obese but otherwise healthy. Participants had a body mass Index (BMI) ranging from 40 to 50, far above the obesity threshold ével of a BMI of 30. Participants were enrolled at the Johns Hopkins Weight Management Center. Investigators tracked the subjects' weight loss, ghrelin levels, hunger and satiety assessments, and adverse events at one, three and six months. Each participant was educated on ways to implement critical Ifestyle and diet changes before and after the procedure. Participants then underwent a banatrlc aneral embolizatlon, an mage-guided procedure that involves the in]ectlon of microscopic beads through a small catheter Inserted In a tiny nick in the skin of the groin or wrist The beads are targeted to a portion of the stomach known as the fundus, which produces the vast majority of the body's ghrelln_ The beads decrease blood flow, limiting the secretion of ghreln, thereby minimizing hunger and Initiating weight loss, researchers hypothesize. In these seven patients, bariatric embolization was safe, with no major adverse events reported. All patients demonstrated weight loss and dramatic hunger reduction levels after the procedure. Ghrelln levels also trended down. Following bariatric anerial embolization, participants had an average excess weight loss of 5.9 percent, 9.5 percent and 133 percent at one, three and SIX months, respectively. Excess weight loss IS the percentage of pounds lost above the patient's deal body weight. Participants reported an average 81 percent, 59 percent and 26 percent decrease in hunger/appetlte score at two weeks, one month and three months, respectively. Appetite and satiety questionnaires assessed a participant's perceived sensation of hunger throughout the day. They were completed for SIX consecutive days prior to the procedure and for six consecutive days prior to each follow-up Visit. Participants also had an average 17.5 percent decrease In ghreln évels at three months. "These early results demonstrate that bariatric afterial embolization is safe and appears to be effective In helping patients lose a significant amount of weight in the shon and Intermediate term," says Weiss. "Compared to a surgical gastric bypass procedure, baratric anerial embolizatlon IS significantly less invasive and has a much shorter recovery time." Weiss cautions this research IS still in its early stages. Now that the safety of this procedure has been demonstrated he says, more clinical trials are needed to evaluate larger numbers of patients to determine the treatment's efficacy and durability over time. Additional research Will also have to be done to explore the potential cost savings of this procedure. Weiss says there is not enough data to determine this yet "As this study expands and includes more patients both at Johns Hopkins, and now at Mount Sinai Health System in New York, we will be able to gain more Insight into the effectiveness

 

 

 

 

 

n this first stage of research the team developed the blood analysis in 26 patients with NAFLD. The test detects chemical changes on tiny amounts of “cell-free” DNA that are released into the blood when 

 are injured. Changes in DNA methylation at genes like PPARγ that controls scar formation are then used to stratify patients by fibrosis severity.

Senior author Dr Jelena Mann of Newcastle University’s Institute for Cellular Medicine added: “This is the first time that a DNA methylation ‘signature’ from the blood has been shown to match the severity of a 

.

 

 

 

researchers at the Dana-Farber Cancer Institute and the Broad Institute of MIT and Harvard report on their findings from a new study, which found that colorectal cancers festooned with tumor-related proteins called neoantigens were likely to be saturated with disease-fighting white blood cells, mainly lymphocytes.

 

. Patients whose tumors had high numbers of neoantigens also survived longer than those with lower neoantigen loads.”

 

 

 

 

 

 

 

 

Machine generated alternative text: < Back-to-WhatsApp o. of Pages 12 nal lumen Akkermansia Bifidobacterium 08:19 a researchgate.net ARTICLE IN PR P.D. Cani et al. / Diabetes & Metabolism xxx (2 Dorea 3 Collinsella Prevotella O R. gnavus/torques CO o o 0 00 o F.prausnitzii Roseburia O O O O nal epithelium ?? Lactobacillus ?? Bacteroides ?? Proteobacteria O O O O 3 Mucus degradation O O Altered EndocannabinoiC System tone Adipocytes between gut microbiota and host. Obesity and type 2 diabetes (T2D) are associ; genera and decreases in others (arrow direction indicates either increased or d esity and T2D, depending on the study (indicated by question marks). Increased otoxaemia, triggering inflammation, macrophage infiltration of adipose tissue an

 

Machine generated alternative text: < Back-to-WhatsApp 08:19 a researchgate.net 4 of 13 m IN PRESS • et al. / Diabetes & Metabolism xxx (2014) xxx—xxx o Gut microbes lla lla Is/torques O O O CO o o o o 0 00 oo O LPS O Gut Permeability o O O 3 Mucus degradation O O O O Altered Endocannabinoid System tone Adipocytes Inflammation Liver and type 2 diabetes (T2D) are associated with changes in the composition of g lirection indicates either increased or decreased abundance). Some bacteria are p dicated by question marks). Increased mucus degradation is associated with incrc ophage infiltration of adipose tissue and insulin resistance (adapted from Delzem

 

Machine generated alternative text: < Back-to-WhatsApp 08:20 a researchgate.net orma y acl Itate energy Int e an stor- 3). As eCB levels in tissues are tightly between synthesis and degradation, dys- rol can lead to pathological conditions such ig. 3). Indeed, the eCB system is severely hich may result in increased eCB levels le brain, liver, adipose tissue and skeletal Teased levels of enzymes and receptors in the stomach, kidneys and heart (Fig. 3) etal y omas e w o oun up-regulated by HFD, while ABHD6-/- mic DIO. These data suggest that the eCB syster a central role in the control of body weight a regulation. eCBs have also been implicated in the de and insulin resistance, as CBI-/- mice do not bances associated with DIO. The first studies mice and pharmacological inhibition of CB I in press as: Cani PD, et al. Glucose metabolism: Focus on gut microbiota, the endocannabinoid ), http://dx.doi.org/l().1016/j.diabet.2014.()2.()()4 Pages 12 PANCREAS MUSCLE ARTICLE IN PRESS P.D. Cani et al. / Diabetes & Metabolism xxx (2014) xxx—xxx LIVER Insulin release and signaling P-cell function CBI Lipid storage Insulin sensitivity ADIPOSE TISSUE Glucose uptake Insulin sensitivity Adipogenesis Glucose uptake Insulin sensitivity GASTROINTESTINAL TRACT AND GUT MICROBIOTA Gut barrier function Gut permeability Metabolic endotoxemia 'inoid (eCB) system and metabolism. This system plays a central role in the regulation of glucose homoeostasi s. CBI receptor activation induces gut permeability. Gut microbiota composition is associated with intestinal eCB n DIO mice [49,501 and more muscle glu- The role of eCBs in the control of glucose 'een reported by several studies showing the 3CB system in pancreatic islets in rodents and t is still not clear whether CBI receptor acti- insulin signalling pathways or, more directly, under physiological conditions and exace erance under HFD challenge, highlightin the eCB system in controlling glucose ho CB2 receptor has also been implicated in sis, as CB2 receptor activation improves rats receiving a glucose load, mimickin

 

 

 

This article has pictures that explains it succinctly

 

Basically, there are CB ( cannabinoid receptors ) in the brain and gut. Two types. They are very lipophilic. Certain gut bacteria up regulate it and some down regulate it.

When certain gut bacteria bind to it, it decreases mucos production , increase intestinal cell permeability and that leads to translocation of pro inflammatory systemic conditions. Moreover , other things that happen are GLP receptors get stimulated and this affects the glucose metabolism locally and then systematic to lead to T2D. This is at gut level, pancreas, liver and skeletal muscle

At central level, it increases sense of odor and craving of food

 

There are on the other hand certain gut bacteria that do the exact opposite! This there is a balance that is needed. When people get gastric bypass even the gut microbiota changes

 

Hope that is not over simplified but it is a primer 101

 

Bhavin Dave

 

 

 

 

ECR is performed in the setting of clinically obvious associated high-risk features (polyposis, IBD, synchronous/metachronous cancers) but not in isolated/sporadic CRC. However, attention must be paid to patients with seemingly lower risk characteristics (isolated CRC, no polyposis), as LS can still be present. In addition, the presumed sporadic group requires further study as metachronous CRC risk in early-onset sporadic CRC has not been well-defined, and some may harbor undefined/undiagnosed hereditary conditions. Abnormal MSI (LS risk) is not associated with ECR; abnormal MSI results often return postoperatively after segmental resection has already occurred, which is a contributing factor.

Extended colon resection versus local resection

 

 

 

Heart disease, cancer, liver disease and obesity  / metabolic syndrome

 

 

 

When patients with lean-NAFLD and overweight patients were divided according to waist circumference, lean-NAFLD with higher waist circumference had greater prevalence of metabolic syndrome, carotid plaques and significant fibrosis compared with patients who were overweight or had obesity.

 

 

Soy is of two types.  Fermented and non fermented.  Non fermented has phytic acid and lecithin which some people is chelating and toxic.  Fermented soy has iso flavin which is beneficial.   

So not straightforward.  

 

 

 

Reduced total cortical volume and temporal lobe cortical thickness and greater lateral ventricle and inferior lateral ventricle volumes were seen in the AC

 participants relative to the AC

 participants.

 

Weschler Memory Scale–Revised Logical Memory Immediate Recall 

 

For elderly patients above 70

 

 

This was part of  Alzheimer’s Disease Neuroimaging Initiative (ADNI) and the Indiana Memory and Aging Study (IMAS).  Published in JAMA neurology

 

 

 

 

 

 

Machine generated alternative text:

Scientists may have found the ultimate sports enhancing drug – dark chocolate.

Cyclists who snacked on the sweet treat were able to go faster and further.

It that thought that epicatechin, a plant chemical particularly abundant in dark chocolate, gives the body a boost by widening the blood vessels.

Is that thought that epicatechin, a plant chemical particularly abundant in dark chocolate, gives the body a boost by widening the blood vessels.

Is that thought that epicatechin, a plant chemical particularly abundant in dark chocolate, gives the body a boost by widening the blood vessels.

Same with beet root but milder

 

 

 

Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans.” Individuals “who carried Porphyromonas gingivalis had an overall 59 percent greater risk of developing pancreatic cancer, and those who carried Aggregatibacter actinomycetemcomitans were at least 50 percent more likely overall to develop the disease.” 

 

 

Three or more alcoholic drinks per day every day increases risk of stomach cancer. A standard drink is 12 ounces of beer, 5 ounces of wine or 1.5 ounces of distilled spirits, according to the U.S. National Institutes of Health.

 

• For every 1.8 ounces of processed meat eaten every day – the equivalent of one hot dog or two slices of bologna – the risk of cancer in the lower stomach rises by 18 percent.

 

• Every five-unit increase in body mass index – BMI, a ratio of weight to height – causes a 23 percent increased risk of cancer in the upper stomach.

 

 

 

Machine generated alternative text: Back to Outlook 10:37 Medscape reference.medscape.com 2 of 22 Heparinoids Vitamin K antagonists Platelet inhibitors The anticoagulant agents in current use may be divided into the following classes: r Xa inhibitors Heparinoids — Heparin, enoxaparin, dalteparin, tinzaparin Vitamin K antagonists — Warfarin Platelet inhibitors — Aspirin, clopidogrel, ticagrelor, dipyridamole, eptifibatide, tirofiban, prasugrel Direct thrombin inhibitors — Dabigatran, lepirudin, desirudin, argatroban Direct factor Xa inhibitors — Rivaroxaban, apixaban, edoxaban Indirect factor Xa inhibitors — Fondaparinux Image courtesy of Medscape. Swipe to next slide Diagnosis and OTC treatment of migraine » VISIT THE MIGRAINE CENTER

 

Machine generated alternative text: Back to Outlook 10:42 reference.medscape.com Medscape Intrinsic Pathway: Surface Contact Xll Xlla 4 of 22 Coagulation Pathway Vila Xla Extrinsic Pathw Tissue Damag + Vil Tissue Factor IXa v Ill Dlrect F-act00(ä h nonoc Drect mromblrn lnNbRor Prothrombin (Il) Thrombin (lla) Foncapannux (+ antitnromoln) Low-molecular-weight heparin (+ antltnromt)ln) Fibrinogen (l) Untacuonated nepann (+ antltnromt)ln) Vurrun K antagonM Fibrin (la) Clot As indicated by the modified representation of the clotting cascade shown in the slide, numerous factors can be affected by these commonly used medications, some of which (eg, heparin and warfarin) work to block the action of multiple clotting factors. Not shown in the slide is the effect of antiplatelet medications whose action on platelets further impedes clot formation. Most providers have cared for patients who are simultaneously receiving both antiplatelet drugs and anticoagulant drugs. A biologic therapy for moderate to severe plaque Pso HEAR EXPERT PERSPECTIVES USA-EDRM-105545

 

Machine generated alternative text: Back to Outlook 10:42 Medscape reference.medscape.com 5 of 22 Fibrinolysis • Comprehensive chemistry panel • Hematology panel • Coagulation studies (P T, activated partial thromboplastin time [aPTT], and INR) Additionally, either rotational thromboelastoplasty (ROT EM) or thromboelastography (TEG), if available (shown), can prove beneficial in determining clot strength and the need for specific clotting factors. Cotton et al, in a letter to the New England Journal of Medicine, reported that in a small group of injured patients who were taking dabigatran, the results of conventional coagulation studies were normal but the results of rapid TEG (rTEG) were markedly abnormal.[4] Some caution should be exercised, however, with regard to the reliability of routine coagulation studies for the purpose of determining the degree of anticoagulation in patients taking NOACs. The NOACs have effects on standard anticoagulation assays that limit the assays' ability to quantify the agents' anticoagulant activity. [5] Image courtesy of Medscape. Swipe to next slide Help for your adult patients with chronic moderate to severe plaque Pso See before-and-after photos USA-EDRM-105520

 

Machine generated alternative text: Back to Outlook 10:43 Medscape reference.medscape.com 7 of 22 Reversing Anticoagulant Effects of Heparinoids Reversal of the heparinoids is achieved through intravenous (IV) administration of protamine.[7] The primary laboratory study is the aPTT, which is elevated in the presence of heparin-induced coagulopathy. Dosing is as follows: • Heparin neutralization — Give 1.0-1.5 mg of protamine per 100 units of heparin (total dose not to exceed 50 mg) • Dalteparin or tinzaparin overdose — Give 1 mg of protamine per 100 units of dalteparin or tinzaparin; if the aPTT is prolonged 4 hours after protamine overdose, administer 0.5 mg per 100 units of dalteparin or tinzaparin • Enoxaparin overdose — Give 1 mg of protamine per 1 mg of enoxaparin if the overdose was within 8 hours; if the overdose occurred more than 8 hours previously or if bleeding continues after 4 hours from the first dose, give 0.5 mg of protamine per 1 mg of enoxaparin Image courtesy of Medscape. A biologic for moderate to severe plaque Pso Hear expert perspectives USA-EDRM-105542

 

Machine generated alternative text: Back to Outlook 10:43 Medscape reference.medscape.com 9 of 22 inhibition induced by this class of agents is irreversible, and platelets that have been affected will remain so for at least 7 days.[8] Accordingly, patients who present with inability to clot as a consequence of irreversible platelet inhibition will require the administration of donor platelets in order to achieve platelet aggregation and clot propagation.[9] Donor platelets have a short lifespan. Because of this, repeat administrations every 3 or 4 days may be required to improve clot formation. In addition to platelet administration, desmopressin (the synthetic analogue of vasopressin) will increase factor Vlll and tissue plasminogen activator levels and shorten the aPTT. Platelet aggregation is improved when desmopressin is given in the presence of clopidogrel and aspirin; however, there is a realistic concern about arterial vasospasm in the presence of desmopressin that must be taken into account, especially in patients receiving this class of medications. Ticagrelor, a P2Y12 inhibitor, reduces platelet aggregation by 700/0110]; administration of platelets will partially reverse the platelet inhibition. Image courtesy of Ami Images I Science Source. Swipe to next slide A biologic for moderate to severe plaque Pso Hear expert perspectives USA-EDRM-105542

 

Machine generated alternative text: Back to Outlook 10:44 Medscape reference.medscape.com 10 of 22 and desirudin are all administered IV and thus are limited to use within a healthcare facility. Nevertheless, one can imagine a scenario wherein a hospitalized patient receiving one of these medications sustains a fall and begins to bleed internally, externally, or both. In the case of the parenteral medications, administration of the drug should be stopped immediately, and coagulation, hematologic, and appropriate radiologic studies should be performed to assess for hidden hemorrhage. PCC, which contains clotting factors Il, Vll, IX, and X along with proteins C and S, has not been shown to be beneficial in reversing the effects of dabigatran. At present, dabigatran is the only NOAC with an FDA-approved reversal agent—namely, idarucizumab. Idarucizumab is an injectable monoclonal antibody fragment, given in a dose of 5 g IV. The package insert recommends using the ecarin clotting time (ECT) and the aPTT to evaluate for excessive anticoagulation.[ll] However, the ECT is not routinely available, and other references indicate that routine clotting tests are unreliable for many if not all of the NOACs.[5] Dialysis, if available, may be used to remove as much as 60% of the drug in serum. Image courtesy of Medscape / Sam Shlomo Spaeth. Experts discuss an important milestone in dermatology USA-EDRM-105546 SEE VIDEO

 

Machine generated alternative text: Back to Outlook 10:44 reference.medscape.com Medscape Intrinsic Pathway: Surface Contact Xlla 11 of 22 Direct Xa inhibitors Rivaroxaban Apixaban Edoxa ban Extrinsic Pathwa Tissue Damag Currently, no antidotes are available for reversing the direct factor Xa inhibitors rivaroxaban, apixaban, and edoxaban. As with all oral or parenteral agents, the medication should be stopped immediately and resuscitation efforts initiated. Although FFP is not specifically indicated for bleeding as a result of NOACs, it may be used as part of a massive transfusion protocol. PCC (if available, unactivated four-factor; otherwise, three-factor) should be given if there is imminent life-threatening bleeding. Additionally, 1 g of tranexamic acid may be administered IV, followed by 1 g over 8 hours. Rivaroxaban and apixaban are highly protein-bound and therefore are not dialyzable. Unfortunately, there are no established standards of care for the treatment of major or life-threatening bleeding in patients taking direct factor Xa inhibitors. The clinician must address individual patients and specific circumstances of bleeding on a case-by-case basis. Image courtesy of Medscape / Sam Shlomo Spaeth. View efficacy and safety data of a biologic for moderate to severe plaque Pso Examine data USA-EDRM-105520

 

 

 

 

Machine generated alternative text: < Drugs and Disease Burning Mouth Syndrome Author: Vincent D Eusterman, MD, DDS; Chief Editor: Arlen D Meyers, MD, MBA more... upcatec: Jun 22, 2015 Background Burning mouth syndrome (BMS) is an idiopathic condition characterized by a continuous burning sensation of the mucosa of the mouth, typically involving the tongue, with or without extension to the lips and oral mucosa. Classically, burning mouth syndrome (BMS) is accompanied by gustatory disturbances (dysgeusia, parageusia) and subjective xerostomia_ By definition, no macroscopic alterations in oral mucosa are apparent. Burning mouth syndrome (BMS) occurs most frequently, but not exclusively, in peri-menopausal and postmenopausal women. See the following illustration. A 29-year-old female presents with tongue irritation. A diagnosis of benign migratory glossitis (geographic tongue) is made by the appearance. The portions ofthe tongue with atrophic filiform papilla are symptomatic to acidic foods. View Media Gallery Burning mouth syndrome (BMS) is a clinical diagnosis made via the exclusion of all other causes. No universally accepted diagnostic criteria, laboratory tests, imaging studies or other modalities definitively diagnose or exclude burning mouth syndrome (BMS). Various attempts to classify burning mouth syndrome (BMS) based on etiology and symptoms have been made. In a classification by etiology or cause, idiopathic burning mouth syndrome (BMS) is considered 'brimary BMS" (or 'true BMS"), whereas "secondary BMS" has an identifiable cause. For the purposes of this article, we will use these terms. Another classification of burning mouth syndrome (BMS) is based on symptoms, stratifying cases into 3 types, as • Type 1 burning mouth syndrome (BMS): Patients have no symptoms upon waking, with progression throughout the day. Nighttime symptoms are variable. Nutritional deficiency and diabetes may produce a similar pattern. • Type 2 burning mouth syndrome (BMS): Patients have continuous symptoms throughout the day and are frequently asymptomatic at night. This type is associated with chronic anxiety. • Type 3 burning mouth syndrome (BMS): Patients have intermittent symptoms throughout the day and symptom-free days. Food allergy is suggested as a potential mechanism. Burning mouth syndrome (BMS) is likely more than one disease process, and the etiology may be multifactorial_ The ambiguous definition of burning mouth syndrome (BMS) makes evaluation of prognosis and treatment difficult. Anatomy and Physiology The oral cavity is comprised of mucosa, glands, muscle, teeth and sensory receptors. The sensory capabilities of the oral cavity include pain, temperature, proprioception, light touch, vibration, and taste. Efferent innervation supplies muscles of mastication, the tongue, and autonomic reflexes. Below is an overview of the neuroanatomy, with particular paragraphs highlighting the most relevant elements. Somatosensory innervation Somatosensory innervation is provided by the maxillary (V2) and mandibular (V3) branches of the trigeminal nerve and the glossopharyngeal nerve The V2 branch supplies the following: • Hard and soft palate • Mucosa of the maxillary vestibule • Upper lip • Maxillary teeth • Maxillary periodontal ligaments • Maxillary gingiva The V3 branch supplies the following: • Buccal mucosa • Anterior buo thirds of the tongue (lingual branch) • Mandibular teeth • Mandibular periodontal ligaments • Mandibular gingiva • Anterior mandibular vestibule • Lower lip The glossopharyngeal nerve innervates the following: • Posterior third of the tongue • Posterior wall of the pharynx Pertinent to burning mouth syndrome (BMS), the lingual branch of the mandibular nerve (V3) supplies the anterior buo-thirds of the tongue. It has superficial and deep fibers, which have small receptive fields and low thresholds, creating a highly sensitive sensory field. Pain and temperature in the mouth are sensed by both simple free nerve endings and by more organized nonmyelinated endings. Sensory innervation of the periodontal ligaments provides proprioceptive information about pressure on the teeth and oral stereognosis (perceiving the form of an object) as well as jaw opening and salivation reflexes. In general, the anterior and midline portions of the oral cavity tend to be more sensitive than the posterior and lateral aspects to discriminatory touch and warm temperatures. Cold temperatures are perceived more uniformly throughout the mouth. Trigeminal neuroanatomy The trigeminal nerve enters the brainstem at the pons and bifurcates in the principal sensory nucleus. There, the different types of fibers in the trigeminal nerve follow different courses, as follows: • Discriminatory tactile fibers synapse in the principal sensory nucleus, cross midline, and ascend in the medial lemniscus to the ventroposterior medial nucleus of the thalamus (VPM)_ • Afferent proprioc

 

Machine generated alternative text: Burning mouth syndrome (BMS) has been associated with oral parafunctional habits such as bruxism, clenching, and tongue thrusting. The bruxism and clenching are increased with anxiety, which is also associated With burning mouth syndrome (BMS). Although psychogenesis is no longer regarded as the primary cause, it may exacerbate symptoms. Whether burning mouth syndrome (BMS) has a neurologic abnormality in common with parafunctional behaviors has yet to be adequately investigated. Epidemiology Good epidemiologic data documenting incidence and prevalence of burning mouth syndrome (BMS) are lacking. Statistical values vary widely and are likely affected by variable definitions of burning mouth syndrome (BMS). The overall prevalence is roughly 4% [11] Women are 3-7 times more likely than men of a similar age to experience burning mouth syndrome (BMS) 12] Burning mouth syndrome (BMS) is rarely observed in patients younger than 30 years of age and prevalence may increase from 3- to 12- fold with increasing No racial or ethnic predilections have been repotted. BMS is associated with a higher incidence of Gl and urogenital disease, the significance of which is still History History is the cornerstone of Although burning mouth syndrome (BMS) is a diagnosis of exclusion, several elements are supportive: • Bilateral mouth discomfort (burning/pain) • Pain deep in the oral mucosa • Symptoms present for at least 4-6 months • Xerostomia • Dysgeusia • Symptoms that are nearly constant throughout the day • No clear precipitating factors • Alleviated or aggravated by drinking/eating • Mood or personality disruptions The absence of any of the above symptoms does not exclude a diagnosis of burning mouth syndrome (BMS). See the image shown below. A 55-year-old female with tongue burning for f 5 months. The history for cancer risk factors was negative Examination failed to reveal any systemic or local causes. Diagnosis of burning mouth syndrome (BMS) was made, and the patent received no medical treatment except for serial examinations. View Media Gallery Classically, 3 major symptoms are associated with burning mouth syndrome (BMS): pain, dysgeusia, and xerostomia_ These occur nearly continuously for at least 4-6 months. The complete triad (pain, dysgeusia, xerostomia) is most commonly found in peri-menopausal and postmenopausal women, while other populations may have fewer symptoms. Pain Pain is typically the major symptom. The pain is described as burning, scalding, tingling, or numbness. It is bilateral, typically involving the anterior buo thirds of the tongue or tip. The hard palate mucosa and lips may also be involved. The buccal mucosa and floor of the mouth are atypical sites. In patients with dentures, alveolar ridges/gingiva are common sites. Involvement of the throat may be suggestive of allergy or gastroesophageal reflux disease (GERD)_ The pain may be mild to severe. It may be constant or worse at the end of the day with no pain on waking. It may or may not interfere with sleep, typically it does not. Food and drink may or may not exacerbate symptoms. Hot, acidic or spicy foods typically aggravate pain in patients who report worsening of symptoms with Speaking may also exacerbate pain in select individuals. Dysgeusia Dysgeusia is present in up to 70% of cases and may take the form either of a persistent taste in the mouth or altered perception of tastes. Dysgeusic tastes may be bitter, metallic, or mixed. Alterations may take the form of decreased perception of sweetness or intensified sensation of sweet or sour flavors. Xerostomia Xerostomia is a symptom in up to 64% of patients. Patients may not volunteer symptoms of xerostomia but affirm it on direct questioning. Xerostomia in burning mouth syndrome (BMS) is unlikely to be objectively confirmed by quantitative tests of salivary function. Some evidence suggests differences in salivary composition;cg, 10] however, this relationship to symptoms of pain or dysgeusia is not clear. Other associated symptoms and conditions Burning mouth syndrome (BMS) may be associated with various other nonspecific symptoms_[16, 1 7] Elicit information about bruxism or clenching, which may cause headache, ear, temporomandibular joint pain, or myofascial pain in masticatory, neck, shoulder, and suprahyoid muscles that can be associated with burning mouth syndrome (BMS). Patients may not be aware of these parafunctional behaviors, but bruxism can be observed by family members during sleep, particularly if it is loud. The patient may also notice clenching if made aware. Other signs of bruxism include worn tooth enamel, tooth sensitivity, or superficial ulceration of buccal mucosa. Tongue thrusting in patients with burning mouth syndrome (BMS) may be identified by having the patient swallow a liquid while smiling; leakage through the teeth is suggestive. Patients or family members may also report pucker

 

Machine generated alternative text: Proposed Etiologies No consensus exists regarding a definitive cause. Rather, burning mouth syndrome (BMS) appears to be multifactorial in origin. Many of the currently proposed etiologies describe secondary, rather than primary burning mouth syndrome (BMS). Endocrine Menopause, whether surgical or physiological, is associated with a higher prevalence of burning mouth syndrome (BMS), and, while the mechanism is unclear, hormonal alterations in oral mucosa have been suggested as a cause. Estrogen has documented effects on oral mucosa, and deprivation may lead to atrophic changes thereby altering stimulation of the nerve endings within the Alternatively, atrophic epithelia may be more prone to inflammation. Peripheral neuropathy secondary to diabetes mellitus is a cause of secondary burning mouth syndrome Immunologic An immunologic mechanism for burning mouth syndrome (BMS) has been suggested by the observation of elevated serum ESR and salivary lgA in burning mouth syndrome (BMS) patients compared with , 22] Allergies are infrequently identified in patients with burning mouth syndrome (BMS) but have been suggested as a cause of Type 3 burning mouth syndrome (intermittent symptoms). However, typically they are associated with signs of mucosal irritation. Suggested irritants include dental materials such as mercury (present in amalgam), methyl methacrylate, cobalt chloride, zinc and benzoyl peroxide_[23] Components of lotions such as petrolatum cadmium sulfate, octyl gallate, benzoic acid, and propylene glycol have been implicated. Food allergens include peanuts, chestnuts, cinnamon, and sorbic Nicotinic acid has also been suggested. Nutritional Deficiencies of B vitamins 1 , 2, 6, and 12, as well as zinc[24] , folate and iron, have been suggested as causes of secondary burning mouth syndrome (BMS), either from direct neurologic damage or in relation to anemia. Neuropsychiatric Anxiety, if present, is usually considered an exacerbating factor, rather than a cause of the chronic pain picture of burning mouth syndrome Cases of spontaneous resolution of symptoms after positive life events have been reported. Patients with burning mouth syndrome (BMS) may also have increased salivary cortisol relative to controls, indicative of higher levels of A proportion of patients have anxiety centered around concerns of cancer, or At this point, the nature of the association bebueen burning mouth syndrome (BMS) and anxiety is not clear. Endogenous or reactive depression has been implicated; however, depression is strongly associated with Whether depression is directly connected to burning mouth syndrome (BMS) is unclear. Serotonin deficiency has been suggested as a possible mechanism for sensory alterations in burning mouth syndrome (BMS) because of its role in the descending inhibition of pain. In addition to serotonin, alterations in dopamine transmission and nigrostriatal pathway abnormalities have been suggested as a root cause for the Whether parafunctional habits relate to dopamine transmission is unclear. Infectious Oral infection has been explored, and a few microbes have been identified to be potentially more prevalent in burning mouth syndrome (BMS) patients without visible mucosal lesions: Candida, Enterobacter, Fusospirochetals, Helicobacter pylori, and Klebsiella. Of note, candidal infections may not always produce visible Iatrogenic Various cases of drug-associated burning mouth syndrome (BMS) have been reported. ACE inhibitors and angiotensin receptor blockers are perhaps the most commonly noted in case 30. 31] This may be the product of an inflammatory reaction generated by increases in bradykinin (similar to the mechanism by which angioedema may result). The mechanism as it relates to burning mouth symptoms has not been determined, but kallikrein, a molecule active in the kinin pathway, may be increased in the saliva of burning mouth syndrome (BMS) patients, resulting in increased Other drugs that have been repotted are the antiretrovirals nevirapine and efavirenz[32, 33] No clear mechanism has been proposed. L-thyroxines have also been implicated in burning mouth syndrome (BMS), although whether the medication itself or the underlying hypothyroidism is the cause is Topirimate, a common treatment for trigeminal neuralgia, has been reported to cause BMS-Iike Burning mouth syndrome (BMS) symptoms have been noted in patients with dental Local trauma (particularly in patients with parafunctional habits) has been proposed as a mechanism of secondary burning mouth syndrome (BMS). As mentioned above in Immunologic etiologies, contact dermatitis due to materials used in prostheses may also be a mechanism. Allergic A study by Lynde et al suggested that in some patients with burning mouth syndrome, contact allergy may play a role in the condition. Of 132 patients with burning mouth syndrome who underwent patch testing, 89 (67%) demons

 

 

 

 

 

 

 

 

 

Machine generated alternative text:

 

 

 

 

 

 

Steatosis predicted C-IMT better than diabetes or dyslipidemia, and steatosis independently predicted C-IMT (P=0.002) and FRS (P <0.001) after adjustment for the metabolic syndrome and cardiovascular risk factors, Pais and colleagues reported.

 

In the 1,872 patients with a follow-up ultrasound, C-IMT increased in patients with steatosis, from 0.60 ± 0.13 mm to 0.66 ± 0.14 mm (P=0.001), but C-IMT did not change in patients who remained free of steatosis.

 

(Carotid intima media thickness).  Did not do biopsies though. Cannot differentiate between NASH and NAFLD.  From France,  Journal of Hepatology

 

 

 

 

 

 

 

 

“Results of these studies showed that a single, one-time infusion of the antitoxin bezlotoxumab given with standard of care 

antibiotic treatment significantly reduced the recurrence of 

infection compared to standard of care alone, and demonstrated this benefit over a 12-week period,” said Dr. Mark Wilcox, Leeds Teaching Hospitals and University of Leeds, U.K., and a lead investigator for the studies. “These results were also demonstrated in patient subgroups known to be at high risk for 

recurrence.”

 

 

 

Relamorelin (RM-131, Motus) is a ghrelin agonist being developed for treating patients with diabetic gastroparesis or GI functional disorders, which works by stimulating GI motility in these patients, according to a press release. The FDA has granted fast track review status to relamorelin for the indication of diabetic gastroparesis, and phase 2a clinical trials in diabetic gastroparesis and 

 have already been completed.

 

 

 

Hcv drug interactions

 

 

 

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Anti mullerian hormone

 

 

 

Ozanimod is a modulator of the sphingosine-1-phosphate subtype 1 (S1P1) and S1P5 receptors. Agonists of S1P1 interfere with the migration of B and T lymphocytes from secondary lymphoid tissues, so the lymphocytes are unable to track to the sites of inflammation. Its mechanism is thus similar to 

 

 

In addition, clinical responses at that time point were seen in 57% of the 1-mg group and in 54% of the 0.5-mg group, compared with 37% of the placebo group (

=0.02 and 

=0.06, respectively), the investigators reported in the May 5 

.

 

 

*Sea hero quest*. How good are you at it?

Have your patients play it!  Poor scores?

*dementia* is a possibility

 

 

 

The antibody, researchers believe, only recognizes the structurally different part of CFH protein that they believe is only found in tumor cells. It then impacts tumor growth by disabling the protective CPH layer and destroying cancer cells. They don’t necessarily want the antibody to kill all the tumor cells, though, Patz noted.

 

 

 

 

 

Clostridium difficile infections, according to a case-control study presented at the European Society of Clinical Microbiology and Infectious Diseases annual congress. Tigecycline effected a 76% clinical cure rate, compared with 53% for the combination regimen of intravenous metronidazole and oral vancomycin, Dr. Baltin Gergely Szabo reported.

 

 

 

44% chance of infection after abd or perianal infection

 

 

 

NAFLD and fibrosis will be dosed with either 400 mg of aramchol (Galmed) — a conjugate of cholic acid and arachidic acid — vitamin D, 400 mg of aramchol plus vitamin D or placebo for 24 weeks, followed by a 4-week follow-up period.

 

 

*Impella* was approved for *pVAD   Tandem* is another one.  Both are used for CHF   

*Mirca* is a leadless pacing device.  A good option for pediatrics

MRI safe pacemakers about to be released

*TAVR*curiously causes renal flow by high urine flow nephritis  small study

 

 

 

Researchers found that while the H2 blockers had no effect on vascular aging, chronic use of the PPIs indeed impaired the lysosomes, preventing them from generating acid.

 

“We also saw the telomeres shortening – they’re on the tips of chromosomes and like our biological clock,” Cooke added. “Those vascular cells couldn’t proliferate or divide as well, and that’s necessary for repairing a wound in the vessel.”