1. Gilbert's- Tbili will often be <3, with direct bili <0.3
Acute cholecystitis- Tbili usually <2 (cholangitis may be higher)
2. Pancreatitis:
- Parental nutrition (esp PPN) has super high infection rate. Enteral feeding if at all possible.
- Antibiotics only indicated with necrotic pancreatitis (IV contrast CT-- pancreatic tissue that doesn't enhance is necrotic)
3. Manage erosive esophagitis (thought to be 2/2 GERD) with PPI
4. Indications for endoscopy in someone with dyspepsia (i.e. "alarm signs")
- Weight loss
- Dysphagia
- Odynophagia
- Unexplained iron deficiency anemia
- Jaundice
- Age over 55 (because incidence of gastric cancer is higher)
5. Differential for multiple nodular opacities concentrated in the upper lobes on CXR
- Granulomatous infection (TB, histo, blasto)
- Localized bronchiectasis with mucous plugging (tubes can look like nodules if shot at obliquely) - ABPA, which occurs in asthmatics. CF tends to produce more distributed bronchiectasis and is an unlikely diagnosis in an older person
- Much less likely - cancer. Metastatic disease tends to be more evenly distributed and if anything concentrates in the lower lobes as there is more blood flow, and it would be unusual to have dozens of primaries.
6. Critical care learning:
http://www.aic.cuhk.edu.hk/web8/Renal.htm
7. Screening for hepatocellular carcinoma
- Abdominal u/s + aFP > 500 is diagnostic without a biopsy
- You can develop HCC in hep B without cirrhosis.
8. Primary Biliary Cirrhosis
- Occurs predominantly in women (80-90%), typically aged 40-60
- Diagnostic triad: cholestatic liver profile, +Antimitochondria antibody, liver bx
- Alk phos is often 10x normal
- Normal alk phos and negative antimitochondria ab => look for a different disease.
9. Microscopic colitis:
- Older people
- Nonbloody diarrhea
- Macroscopically normal
- Histology shows either increased intraepithelial lymphocytes (lymphocytic colitis) or increased submucosal collagen layer (collagenous colitis)
- Typical onset is 60s for collagenous, 70s for lymphocytic. Affects women more than men
10. Crohn's disease in the small bowel can present as non-bloody diarrhea.
Sunday, May 18, 2014
Friday, May 16, 2014
1. Adult Heparin gtt protocol: Initiation
- DO NOT START heparin for 24 hours after a patient gets tPA for an ischemic stroke.
- Baseline labs: PT, PTT, CBC, BMP (within 24 h of initiating therapy)
- Discontinue: other anticoagulants, aspirin > 162 mg, IM injections
2. Adult heparin gtt protocol: exclusion criteria
- Epidural catheter
- Platelets <50, PTT higher than whatever your goal PTT would be
- TTP, HIT (Not DIC - you can treat thrombotic DIC with heparin actually)
- High bleeding risk or current bleed
3. Dosing of heparin depends on body weight and indication. See chart:
4. Titration and monitoring of Heparin depends on goal PTT. Below is a sample titration algorithm:
- DO NOT START heparin for 24 hours after a patient gets tPA for an ischemic stroke.
- Baseline labs: PT, PTT, CBC, BMP (within 24 h of initiating therapy)
- Discontinue: other anticoagulants, aspirin > 162 mg, IM injections
2. Adult heparin gtt protocol: exclusion criteria
- Epidural catheter
- Platelets <50, PTT higher than whatever your goal PTT would be
- TTP, HIT (Not DIC - you can treat thrombotic DIC with heparin actually)
- High bleeding risk or current bleed
3. Dosing of heparin depends on body weight and indication. See chart:
5. Heparin titration patterns for other goal PTTs, depending on bleed risk:
6. Bridging to warfarin:
- Need to overlap 5 days AND have INR to goal
- Can start warfarin the same time you start heparin for most people
7. Goal INR and duration of anticoagulation depending on indication:
- A-fib, stroke, antiphospholipid syndrome, mechanical aortic valve: INR 2-3, FOREVER
- Antiphospholipid syndrome with multiple clots through anticoagulation, mechanical mitral valve: INR 2.5-3.5 forever
- Bioprosthetic heart valve: INR 2-3, 3 months.
- First time DVT or PE provoked by time-limited risk factors (surgery, temporary immobilization, trauma, estrogen use) - INR 2-3 for 3 months, then stop.
- First time DVT/PE that is unprovoked, INR 2-3 for 3 months, then reassess bleed risk-- if their bleed risk is high, stop; if their bleed risk is low, continue forever.
- Multiple DVT/PE: INR 2-3 for the rest of their life.
- All the above refer to proximal DVTs-- distal DVTs just get 3 months of therapy then stop.
8. Lovenox & heparin & antithrombin
- Both lovenox and heparin are able to bind Antithrombin, and antithrombin is capable of inhibiting thrombin (factor II) AND factor Xa. Heparin binding will accelerate activity of antithrombin against factor II/Xa by a factor of 1000.
- However lovenox, because of its shorter tail, is only able to accelerate the activity antithrombin against factor Xa. So it's much more of a Xa inhibitor than a factor II inhibitor.
- So you can check levels of both heparin and lovenox with anti-Xa levels.
9. Pharmacokinetics:
- Lovenox: Half life 3-6 hours after subQ injection.
- Lovenox: Anti-Xa levels peak 3-5 hours after dosing.
- Lovenox renally cleared, standard dose 40 for GFR>60, 30 for GFR 30-60, <30, pick a different anticoagulant, or be careful.
- Heparin: half life depends on dose! Clearance is a combination of a fast (saturable) non-linear mechanism and a slow, first-order (non-saturable) mechanism. The fast phase -- binding to endothelial cells and macrophages, where it is depolymerized. The slow phase is renal. At IV doses of <25 U/kg (i.e. when we'll almost always be using it) it's mostly degraded through the fast mechanism, and the apparent half life is 30 minutes. At IV doses of 100 U/kg, the apparent half life is 60 minutes, and at IV doses of 400 U/kg, the apparent half life increases to 150 minutes. {source: Circulation}
10. More data for heparin dosing depending on indication: {source}
- DVT/PE prophy: 5000 U sq TID
- DVT/PE tx: 80 u/kg bolus, 18 u/kg/hr drip
- Catheter patency aka Heparin lock IV: 100units/mL, enough fluid to fill lumen
- STEMI: 60 u/kg bolus (max 4000), 12 u/kg/hr drip (max 1000). goal PTT 50-70
- NSTEMI/unstable angina: 60-70 u/kg bolus (max 5000), 12-15 u/kg/hr (max 1000), goal PTT 50-70.
Thursday, May 15, 2014
1. DNA synthesis inhibitors
- Fluroquinolones: No matter what the lab susceptibility says, these drugs have NO clinically significant MRSA coverage. In fact, they make it worse-- they increase MRSA colonization because they kill off everything that isn't staph, and encourage the development of resistant strains. Cipro and levo typically cover pseudomonas, while moxi does not.
- Metronidazole: lead to DNA fragmentation
- Rifampin: has terrible, awful, horrendous drug-drug interaction. Ridiculous CYP inducer. On warfarin 7.5? Add rifampin, and you'll need 25. Outside of TB, used as a supplement/combination antibiotic with an anti-staph agent for MRSA to improve penetration -- useful in cases like osteomyelitis with hardware. Also turns all your bodily fluids orange.
2. Antibiotics that target the cell membrane:
- Colistin aka Polymyxin E. Super, super toxic as the difference between prokaryotic and eukaryotic cell membranes are not that different. Very nephrotoxic. Generally used as an inhaled neb against pseudomonas; it shouldn't have much systemic absorption (just like inhaled steroids don't have much systemic absorption) unless your lungs are really crappy.
- Polymyxin B: Useful against MDR gram negs, very similar to colistin
3. PO anti-MRSA agents:
- Doxy
- Clinda (sorta bad)
- Bactrim
- Linezolid
4. Agents that cover atypicals
- Macrolides
- Tetracycline
- Flouroquinolones
- Chloramphenicol
5. Major risk factors for pancreatic cancer:
- First degree relative with panc cancer
- Hereditary pancreatitis
- Germline mutations (BRCA1, BRCA2, Peutz-Jeghers)
- Cigarettes - most significant environmental risk factor. Dose-dependent; heavy smokers have 2-3x the risk of nonsmokers.
- Obesity, inactivity
- Nonhereditary chronic pancreatitis
- AdenoCA most common histology; overall pancreatic cancer typically occurs after 45, more common in men and AA pateints.
6. Inferior MI
- After an inferior MI, you expect hypotension. There should be compensatory tachycardia; if not, suspect concomitant SA node ischemia.
- After a R sided MI, people need tons of fluids to maintain the preload to the LV. Do not give diuretics or nitroglycerin, as you need all the pre-load you can get (LV infarct its a good idea, it pulls fluid off the R side and lungs)
- Expect +JVD and +Kussmaul's sign: increase in JVD with inspiration.
7. Stevens-Johnson syndrome:
- Aka erythema multiforme major.
- Immune complex mediated hypersensitivity
- Drugs that commonly trigger: NSAIDs, sulfonamides, phenytoin.
- Presentation: sudden onset mucocutaneous target-shaped lesions on 2 sites (usually oral/conjunctival).
- Associated symptoms: fever, tachycardia, hypotension, altered mental status, conjunctivitis, seizures, coma.
- Supportive treatment--fluids, pain control.
- VS erythema multiforme minor, which is part of the same spectrum as SJS: sudden onset erythematous rash, target lesions, occurs after herpes simplex infection. Generally doesn't involve mucosal surfaces, systemic sx less severe.
8. DI
- Central: causes- idopathic, trauma, pituitary surgery, ischemia. If the thirst mechanism is impaired, serum Na can be > 150
- Nephrogenic causes: chronic Li use, hypercalcemia, AVPR2 mutations. Serum Na usu <150 due to intact thirst mechanism.
9. Acute acalculous cholecystitis: acute inflammation of GB without gallstones. Common in hospitalized patients with the following:
- Extensive burns
- Severe trauma
- Prolonged TPN
- Prolonged fasting
- Mechanical ventilation
Pathophys: local/general ischemia, biliary stasis, infection, external compression.
10. Someone who presents with new a-fib, think PE, not MI. Afib is commonly associated with PE but rarely with MI.
- Fluroquinolones: No matter what the lab susceptibility says, these drugs have NO clinically significant MRSA coverage. In fact, they make it worse-- they increase MRSA colonization because they kill off everything that isn't staph, and encourage the development of resistant strains. Cipro and levo typically cover pseudomonas, while moxi does not.
- Metronidazole: lead to DNA fragmentation
- Rifampin: has terrible, awful, horrendous drug-drug interaction. Ridiculous CYP inducer. On warfarin 7.5? Add rifampin, and you'll need 25. Outside of TB, used as a supplement/combination antibiotic with an anti-staph agent for MRSA to improve penetration -- useful in cases like osteomyelitis with hardware. Also turns all your bodily fluids orange.
2. Antibiotics that target the cell membrane:
- Colistin aka Polymyxin E. Super, super toxic as the difference between prokaryotic and eukaryotic cell membranes are not that different. Very nephrotoxic. Generally used as an inhaled neb against pseudomonas; it shouldn't have much systemic absorption (just like inhaled steroids don't have much systemic absorption) unless your lungs are really crappy.
- Polymyxin B: Useful against MDR gram negs, very similar to colistin
3. PO anti-MRSA agents:
- Doxy
- Clinda (sorta bad)
- Bactrim
- Linezolid
4. Agents that cover atypicals
- Macrolides
- Tetracycline
- Flouroquinolones
- Chloramphenicol
5. Major risk factors for pancreatic cancer:
- First degree relative with panc cancer
- Hereditary pancreatitis
- Germline mutations (BRCA1, BRCA2, Peutz-Jeghers)
- Cigarettes - most significant environmental risk factor. Dose-dependent; heavy smokers have 2-3x the risk of nonsmokers.
- Obesity, inactivity
- Nonhereditary chronic pancreatitis
- AdenoCA most common histology; overall pancreatic cancer typically occurs after 45, more common in men and AA pateints.
6. Inferior MI
- After an inferior MI, you expect hypotension. There should be compensatory tachycardia; if not, suspect concomitant SA node ischemia.
- After a R sided MI, people need tons of fluids to maintain the preload to the LV. Do not give diuretics or nitroglycerin, as you need all the pre-load you can get (LV infarct its a good idea, it pulls fluid off the R side and lungs)
- Expect +JVD and +Kussmaul's sign: increase in JVD with inspiration.
7. Stevens-Johnson syndrome:
- Aka erythema multiforme major.
- Immune complex mediated hypersensitivity
- Drugs that commonly trigger: NSAIDs, sulfonamides, phenytoin.
- Presentation: sudden onset mucocutaneous target-shaped lesions on 2 sites (usually oral/conjunctival).
- Associated symptoms: fever, tachycardia, hypotension, altered mental status, conjunctivitis, seizures, coma.
- Supportive treatment--fluids, pain control.
- VS erythema multiforme minor, which is part of the same spectrum as SJS: sudden onset erythematous rash, target lesions, occurs after herpes simplex infection. Generally doesn't involve mucosal surfaces, systemic sx less severe.
8. DI
- Central: causes- idopathic, trauma, pituitary surgery, ischemia. If the thirst mechanism is impaired, serum Na can be > 150
- Nephrogenic causes: chronic Li use, hypercalcemia, AVPR2 mutations. Serum Na usu <150 due to intact thirst mechanism.
9. Acute acalculous cholecystitis: acute inflammation of GB without gallstones. Common in hospitalized patients with the following:
- Extensive burns
- Severe trauma
- Prolonged TPN
- Prolonged fasting
- Mechanical ventilation
Pathophys: local/general ischemia, biliary stasis, infection, external compression.
10. Someone who presents with new a-fib, think PE, not MI. Afib is commonly associated with PE but rarely with MI.
Wednesday, May 14, 2014
1. Bactericidal antibiotics
- Cell wall synthesis inhibitors (b-lactams, glycopeptides like vanc, lipopetides like dapto)
- Cell membrane integrating agents (polymyxin, colistin)
- DNA synthesis inhibitors (fluroquinolones, metronidazole, rifampin)
- Aminoglycosides
2. All other agents are bacterostatic
- All protein synthesis inhibitors other than aminoglycosides (tetracyclines, clinda, linezolid, macrolides, chloramphenicol, dalfo/quino)
- Folic acid synth inh (like bactrim)
3. Protein synthesis inhibitors (30s)
- Aminoglycosides: tobra typically has better coverage of psuedomonas than gent. Never use AG as single-agent therapy against pseudomonas, they rapidly develop resistance.
- Tetracyclines
4. Protein synthesis inhibitors (50s)
- Supposedly the large subunit ribosomes of eukaryotes and prokaryotes bear more resemblance than the smaller subunits, so theoretically these guys have more cross-interaction with human ribosomes and thus more side effects.
- Clinda - MRSA coverage, but crappy MRSA coverage... pick another agent if you're really worried.
- Macrolides - all lengthen QT, including azithro. Erythro is not used as an antibiotic anymore, its used more as a pro-motility agent in GI studies like EGD. It lengthens your QT, has tons of interactions, and (obvi) causes bad diarrhea.
- Linezolid: since its bacteriostatic, don't use it as the main treatment for sepsis, particularly in people who are immunocompromised, neutropenic. Static agents are only good in people with good enough immune systems to mop up the paralyzed bacteria. Linezolid has excellent CNS penetration, one of the few PO treatments vs MRSA (along with doxy, bactrim, clinda)
- Chloramphenicol - great drug, terrible side effects. aplastic anemia
- Synercid (dalfopristin/quinopristin) - last resort agent for VRE (e. faeciUM, fecalIS is often susceptible to amp). 50% of those who use this drug will report peripheral neuropathy, really bad pain. Seriously this is a last-resort drug, after you've tried ceftaroline/dapto
5. Cell wall synthesis inhibitors- B-lactams
- Penicillins, aminopenicillins, antipsuedomonal penicillins: cross-reactivity between these agents are high because they have very similar structures (i.e. aminopen = pen + animo group, etc). Empiric addition of amp to meningitis tx to cover for listeria is indicated in those <1-2 months and > 50 years
- Cephalosporins: 1st gen have 5% cross-reactivity with penicillin allergies, 4th gen have 1% cross-reactivity. So in someone who is pen-allergic, pick a higher-generation cef.
- Carbapenems: up to 40% reported cross-reactivity with penicillins. In clinical practice, its closer to 10%
- Monobactams (aztreonam): No cas reports of cross-reactivity, very different structure.
6. Cell wall synthesis inhibitors- Glycopeptides
- Vanc: can be used to cover resistant strep in meningitis. Even when taken PO, there is some measured systemic absorption (diffuse colitis, compromised barrier). The liquid formulation = IV formulation in a cup, tastes really bad. You can get the IV formulation in capsules but they cost a few thousand dollars. Add cherry syrup if you're nice.
- Televancin: new, supposedly better than vanc, butits the same as vanc.
7. Cell wall synthesis inhibitors- Lipopeptides.
- Daptomycin: pokes holes in cell walls, they leak K and die
- Dapto has TERRIBLE CNS and lung penetration (can't get through surfactant). To get through, you have to push the dose really high.
8. On cephalosporins
- Ceftaroline is the only "5th gen" cephalosporin, has MRSA coverage but no pseudomonal coverage. Used in endocarditis bacteremia, skin+soft tissue infections.
- Ceftriaxone dosing: generally 1-2 g, depending on weight. >80 kg usually needs 2g dose. Meningitis dosing-- 2g q12, always; less for skin and soft tissue infections.
9. Folic Acid synthesis inhibitors:
- TMP & SMX are bacteriostatic individually but bacteriocidal together in bactrim.
- Notorious for horrible interactions with warfarin (way worse than cipro): If you're giving someone on coumadin bactrim, plan on halving the dose of your coumadin.
- Bactrim can also cause hyperkalemia through a pseduo-RTA, and it can cause a creatinine bump as it inhibits creatine secretion in the tubule without impacting renal filtration.
- Bactrim can also cause aplastic anemia.
10. In someone with febrile neutropenia or someone with sepsis, you always want empiric double coverage of pseudomonas. Nothing kills people faster than GNR bacteremia- e.coli and pseudomonas.
- Zosyn, tobra, cefepime, Imipenem (all bactericidal)
- Add vanc if you're worried about MRSA
- Add anaerobic coverage if someone has bad mucositis and you think it may be the source.
- Cell wall synthesis inhibitors (b-lactams, glycopeptides like vanc, lipopetides like dapto)
- Cell membrane integrating agents (polymyxin, colistin)
- DNA synthesis inhibitors (fluroquinolones, metronidazole, rifampin)
- Aminoglycosides
2. All other agents are bacterostatic
- All protein synthesis inhibitors other than aminoglycosides (tetracyclines, clinda, linezolid, macrolides, chloramphenicol, dalfo/quino)
- Folic acid synth inh (like bactrim)
3. Protein synthesis inhibitors (30s)
- Aminoglycosides: tobra typically has better coverage of psuedomonas than gent. Never use AG as single-agent therapy against pseudomonas, they rapidly develop resistance.
- Tetracyclines
4. Protein synthesis inhibitors (50s)
- Supposedly the large subunit ribosomes of eukaryotes and prokaryotes bear more resemblance than the smaller subunits, so theoretically these guys have more cross-interaction with human ribosomes and thus more side effects.
- Clinda - MRSA coverage, but crappy MRSA coverage... pick another agent if you're really worried.
- Macrolides - all lengthen QT, including azithro. Erythro is not used as an antibiotic anymore, its used more as a pro-motility agent in GI studies like EGD. It lengthens your QT, has tons of interactions, and (obvi) causes bad diarrhea.
- Linezolid: since its bacteriostatic, don't use it as the main treatment for sepsis, particularly in people who are immunocompromised, neutropenic. Static agents are only good in people with good enough immune systems to mop up the paralyzed bacteria. Linezolid has excellent CNS penetration, one of the few PO treatments vs MRSA (along with doxy, bactrim, clinda)
- Chloramphenicol - great drug, terrible side effects. aplastic anemia
- Synercid (dalfopristin/quinopristin) - last resort agent for VRE (e. faeciUM, fecalIS is often susceptible to amp). 50% of those who use this drug will report peripheral neuropathy, really bad pain. Seriously this is a last-resort drug, after you've tried ceftaroline/dapto
5. Cell wall synthesis inhibitors- B-lactams
- Penicillins, aminopenicillins, antipsuedomonal penicillins: cross-reactivity between these agents are high because they have very similar structures (i.e. aminopen = pen + animo group, etc). Empiric addition of amp to meningitis tx to cover for listeria is indicated in those <1-2 months and > 50 years
- Cephalosporins: 1st gen have 5% cross-reactivity with penicillin allergies, 4th gen have 1% cross-reactivity. So in someone who is pen-allergic, pick a higher-generation cef.
- Carbapenems: up to 40% reported cross-reactivity with penicillins. In clinical practice, its closer to 10%
- Monobactams (aztreonam): No cas reports of cross-reactivity, very different structure.
6. Cell wall synthesis inhibitors- Glycopeptides
- Vanc: can be used to cover resistant strep in meningitis. Even when taken PO, there is some measured systemic absorption (diffuse colitis, compromised barrier). The liquid formulation = IV formulation in a cup, tastes really bad. You can get the IV formulation in capsules but they cost a few thousand dollars. Add cherry syrup if you're nice.
- Televancin: new, supposedly better than vanc, butits the same as vanc.
7. Cell wall synthesis inhibitors- Lipopeptides.
- Daptomycin: pokes holes in cell walls, they leak K and die
- Dapto has TERRIBLE CNS and lung penetration (can't get through surfactant). To get through, you have to push the dose really high.
8. On cephalosporins
- Ceftaroline is the only "5th gen" cephalosporin, has MRSA coverage but no pseudomonal coverage. Used in endocarditis bacteremia, skin+soft tissue infections.
- Ceftriaxone dosing: generally 1-2 g, depending on weight. >80 kg usually needs 2g dose. Meningitis dosing-- 2g q12, always; less for skin and soft tissue infections.
9. Folic Acid synthesis inhibitors:
- TMP & SMX are bacteriostatic individually but bacteriocidal together in bactrim.
- Notorious for horrible interactions with warfarin (way worse than cipro): If you're giving someone on coumadin bactrim, plan on halving the dose of your coumadin.
- Bactrim can also cause hyperkalemia through a pseduo-RTA, and it can cause a creatinine bump as it inhibits creatine secretion in the tubule without impacting renal filtration.
- Bactrim can also cause aplastic anemia.
10. In someone with febrile neutropenia or someone with sepsis, you always want empiric double coverage of pseudomonas. Nothing kills people faster than GNR bacteremia- e.coli and pseudomonas.
- Zosyn, tobra, cefepime, Imipenem (all bactericidal)
- Add vanc if you're worried about MRSA
- Add anaerobic coverage if someone has bad mucositis and you think it may be the source.
Tuesday, May 13, 2014
1. Dysentery
- Culture and treat with appropriate antibiotics
Typical organisms:
- Campy
- Salmonella
- E.coli (STEC- makes shiga toxin, EIEC - similar to shigella)
- Shigella
- C.Diff
2. Campy
- Often has prodrome, flu like illness
- Azithro
3. Salmonella
- Turtles, reptiles
- Cipro
4. STEC e.coli (O157-H7) aka EHEC
- No fever, only bloody diarrhea, a lot of abdominal pain
- Cecal/colonic wall thickening - Can present clinically like appendicitis
- Don't treat, just let it run its course-- In kids, the data seems to show that the ones who get antibiotics are more likely to get HUS
5. Shigella
- Tends to be more L sided.
- Cipro
6. C.Diff
- There exists community acquired C.diff
- If someone comes in w bloody diarrhea, send c.diff toxin as well
- PPIs/NSAIDs are also linked-- PPIs are almost as closely linked as antibiotics
7. Community antibiotic-associated minor diarrhea without blood
- stop the antibiotics
- Likely just a consequence of changing bowel flora, give probiotics
- In community, odds of C.diff in sb on antibiotics with diarrhea ~15%
8. Giardia
- Recreational water facilities
- Treat empirically with flagyl, as it's notoriously hard to find/culture from the stool.
9. Algorithm for diagnosing diarrhea:
10. Types of E.Coli:
- STEC : shiga-toxin producing e-coli (O157-H7) formerly known as EHEC and many others
- ETEC : enterotoxigenic e.coli - watery, traveler's
- EPEC : enteropathogenic e.coli- watery diarrhea in adults and kids
- EIEC : enteroinvasive, bloody diarrhea with tenesmus, similar to Shigella
- EAEC : enteroaggregative - a different cause of traveler's diarrhea
Monday, May 12, 2014
1. Viral gastroenteritis
- Thunderclap onset
- Upper tract sx before lower tract sx
- Treat with IV LR since he's probably losing a lot of electrolytes
- Overwhelming likely to be norovirus
- Any nausea- zofran, compazine, metaclopromide, can give as suppository
- Warn patients about transient lactose intolerance since these viruses will strip your brush border - then people will drink milk and get bloating and diarrhea and come back to you thinking its recurred
- Course: 24 hrs of sx, then 24 hours of feeling weak, better
- Antidiarrheal meds fine, except dystentery and suspicion for c.diff. If you suspect bacterial gastro (fever, look sick) maybe hold off in case it turns into dysentery
2. Diarrhea
- Noninfectious - no f, abd pain, constitutional sx (less severe, longer lasting)
- Gastroenteritits - n/v, watery diarrhea, entire bowel affected
- Dysentery: grossly bloody stool, colon inflammation, tenesmus. Has to be grossly bloody-- anyone with bad viral gasteroenteritis will have heme+ stool
3. Common causes of food poisoning:
- Thunderclap onset
- Upper tract sx before lower tract sx
- Treat with IV LR since he's probably losing a lot of electrolytes
- Overwhelming likely to be norovirus
- Any nausea- zofran, compazine, metaclopromide, can give as suppository
- Warn patients about transient lactose intolerance since these viruses will strip your brush border - then people will drink milk and get bloating and diarrhea and come back to you thinking its recurred
- Course: 24 hrs of sx, then 24 hours of feeling weak, better
- Antidiarrheal meds fine, except dystentery and suspicion for c.diff. If you suspect bacterial gastro (fever, look sick) maybe hold off in case it turns into dysentery
2. Diarrhea
- Noninfectious - no f, abd pain, constitutional sx (less severe, longer lasting)
- Gastroenteritits - n/v, watery diarrhea, entire bowel affected
- Dysentery: grossly bloody stool, colon inflammation, tenesmus. Has to be grossly bloody-- anyone with bad viral gasteroenteritis will have heme+ stool
3. Common causes of food poisoning:
4. Bacterial gastroenteritis
- Campy
- Salomonella
- EPEC
- Shigella (more likely to cause gastroenteritis than dysentery; and even with d)
- C.diff
- More likely to be bacterial if its slightly longer (3-6 days), while <24-48 hours you think viral, toxin.
5. When to culture
- People you think it'll make a difference in treatment,
- Public health move - outbreak tracking.
- <10% of all stool cx are +, <1% of stool O+P are positive
6. Prevention of traveler's diarrhea
- Pepto bismol before meals decreases risk of traveler's diarrhea 30%
- Prophylactic antibiotics - immunocompromised, IBD (gastroenteritis can cause IBD flare), high-stakes trip or high-risk area
- Stop PPIs
- Cipro or azithro +/- flagyl. Rifamaxin (not absorbed systemically)
- Ice, mixed drinks, refilled bottled water
- "the only way to clean lettuce is with a blowtorch"
- Any food heated for a prolonged time (unless fried before you)
- Fruit
- Table top sauces - Annals of internal medicine cultured tabletop sauces (guadelajara - 2/3 of table sauces grew out enteropathogenic organisms, 15% in houston)
7. Antibiotics for cholera
- doxy, cipro, azithro. {source}
8. Diarrhea course:
- 2 weeks acute, 6 weeks subacute, >6 weeks chronic
9. Differential Non-infectious diarrhea (no fever, chills, abd pain)
Medications and other ingestible substances (some with osmotic effect)
- Sorbitol (gum, mints, pill fillers- this is a big one for people taking mega-vitamins)
- Mannitol
- Fructose (fruits, soft drinks)
- Fiber (bran, fruits, vegetables)
- Lactulose
- Magnesium-containing medications
Nutritional supplements
- Antacids
- Laxatives
Malabsorption
- Lactose intolerance (skim milk worst-- fat makes it better)
- Pancreatitis (often chronic- look for people with alcohol hx, calcified pancreas)
Medications causing diarrhea through nonosmotic means
- Metformin
- Antibiotics
- Colchicine
- Digoxin
- Selective serotonin reuptake inhibitor antidepressants
IBS
10. IBS treatment
- High fiber diets
- Finding + avoiding trigger foods
- If people are constipation vs diarrhea predominant, you treat accordingly
Friday, May 9, 2014
1. Differential for acute recurrent hypoglycemia with hypotension requiring constant blouses of fluid and D50
- exogenous insulin/hypoglycemic drugs
- fulminant liver failure
- sepsis
- adrenal insufficiency (loss of all leads to hypotension , would expect higher K, lower Na. Loss of cortisol leads to hypoglycemia) diagnose with ACTH stim test
2. Types of adrenal insufficiency-
Primary (aka Addison's) - failure of adrenals to respond to ACTH -
Secondary - failure of pituitary to produce ACTH, adrenals are fine
Tertiary- failure of hypothalamus to produce CRH
3. ACTH stim test
- Rules out primary AI
- Doesn't rule out secondary or tertiary AI, obviously, because in those cases the adrenals are able to respond fine to ACTH
- Give 100 mcg ACTH, measure cortisol levels at 0, 30, 60 mins, cortisol should be >21
4. Addison's leads to everything crashing and burning (BP, electrolytes), while secondary adrenal insufficiency can present with only hypotension with no electrolyte abnormalities
Causes:
- autoimmune
- infectious (TB, disseminated fungal, syphillis)- suspect in international people
- hemorrhage (Waterhouse-Friderichsen)
- mets (lung, breast, melanoma, stomach/colon rarer)
- drugs (Azoles, etomidate inhibit cortisol biosynthesis; other drugs that are cyp-inducers like phenytoin, barbituates, rifampin will accelerate hepatic degradation of cortisol) These drugs, esp latter category, rarely cause AI in healthy people but may tip someone with poor adrenal reserve over the edge.
5. Treatment
- Replace glucocorticoids and mineralcorticoids
- Hydrocortisone (20 mg in the AM, 10 mg at 3 PM to mimic diurnal variation). Varies per person-- some people will get cushings from these doses and will need reduced dose.
- Florinef (0.1 mg qD) to replace mineralcorticoids
- Acute - High dose hydrocortisone 50-100 mg IV push q8 until symptoms resolve. Will cover both gluco and mineralcorticoids
6. Autoimmune polyglanduar sx type 2
- includes Schmitts and carpenters syndrome
- all have Addison's, most present with thyroid, some have type 1 DM too. Some will present with minor autoimmune conditions too (alopecia, seroneg arthritis, etc)
7. DDx for obesity, gynecomastia, galactorrhea
- how to differentiate breast tissue from adipose deposits in anterior chest - adipose is compressible, breast tissue is not
- prolactin causes galactorrhea, obesity (peripheral estrogen conversion) leads to gynecomastia
- drugs (spirinolactone, ketoconazole) - most common
- idiopathic
- cirrhosis
Rarer-
- hypogonadism
- testicular cancer that makes b-hcg
- hyperthyroid
- CKD
8. Any prolactin > 200 is a tumor
- Treat with dopamine agonist (carbegoline, dostanex, one tablet twice a week). Should see prolactin decrease in 24 hours, will see tumor shrinking in a week.
- Titrate meds to prolactin <10 for a year, then re-image, if tumor is still present, go on half dose and see if the tumor comes back, if it does you need lifelong tx
- Dopamine agnoists can cause cardiac valve thickening/abnormalities so you need a baseline echo before staring treatment
- Lipids, insulin resistance improve with treatment - some literature about using dopamine agonist to treat diabetes, as prolactin may be implicated in metabolic syndrome
9. FOBT
- Screening test
- False positives can be caused by recent ingestion of red meat (Hb in meat will light up the test), trauma during rectal exam. Thus patient should not be eating red meat before the test
- If someone is going to be admitted for GI bleed, it should be significant-- ie visible on the glove as either red or black. If blood is not grossly visible, the bleed is not serious enough to require admission. Thus don't do an FOBT in the ER
10. Melena
- Is midnight black, tarry/sticky, and has a strange/bad odor different from typical stool
- Not just dark, otherwise normal appearing stool.
- Things that can cause dark-appearing stool: pepto bismol, milk of magnesia, iron supplements
- exogenous insulin/hypoglycemic drugs
- fulminant liver failure
- sepsis
- adrenal insufficiency (loss of all leads to hypotension , would expect higher K, lower Na. Loss of cortisol leads to hypoglycemia) diagnose with ACTH stim test
2. Types of adrenal insufficiency-
Primary (aka Addison's) - failure of adrenals to respond to ACTH -
Secondary - failure of pituitary to produce ACTH, adrenals are fine
Tertiary- failure of hypothalamus to produce CRH
3. ACTH stim test
- Rules out primary AI
- Doesn't rule out secondary or tertiary AI, obviously, because in those cases the adrenals are able to respond fine to ACTH
- Give 100 mcg ACTH, measure cortisol levels at 0, 30, 60 mins, cortisol should be >21
4. Addison's leads to everything crashing and burning (BP, electrolytes), while secondary adrenal insufficiency can present with only hypotension with no electrolyte abnormalities
Causes:
- autoimmune
- infectious (TB, disseminated fungal, syphillis)- suspect in international people
- hemorrhage (Waterhouse-Friderichsen)
- mets (lung, breast, melanoma, stomach/colon rarer)
- drugs (Azoles, etomidate inhibit cortisol biosynthesis; other drugs that are cyp-inducers like phenytoin, barbituates, rifampin will accelerate hepatic degradation of cortisol) These drugs, esp latter category, rarely cause AI in healthy people but may tip someone with poor adrenal reserve over the edge.
5. Treatment
- Replace glucocorticoids and mineralcorticoids
- Hydrocortisone (20 mg in the AM, 10 mg at 3 PM to mimic diurnal variation). Varies per person-- some people will get cushings from these doses and will need reduced dose.
- Florinef (0.1 mg qD) to replace mineralcorticoids
- Acute - High dose hydrocortisone 50-100 mg IV push q8 until symptoms resolve. Will cover both gluco and mineralcorticoids
6. Autoimmune polyglanduar sx type 2
- includes Schmitts and carpenters syndrome
- all have Addison's, most present with thyroid, some have type 1 DM too. Some will present with minor autoimmune conditions too (alopecia, seroneg arthritis, etc)
7. DDx for obesity, gynecomastia, galactorrhea
- how to differentiate breast tissue from adipose deposits in anterior chest - adipose is compressible, breast tissue is not
- prolactin causes galactorrhea, obesity (peripheral estrogen conversion) leads to gynecomastia
- drugs (spirinolactone, ketoconazole) - most common
- idiopathic
- cirrhosis
Rarer-
- hypogonadism
- testicular cancer that makes b-hcg
- hyperthyroid
- CKD
8. Any prolactin > 200 is a tumor
- Treat with dopamine agonist (carbegoline, dostanex, one tablet twice a week). Should see prolactin decrease in 24 hours, will see tumor shrinking in a week.
- Titrate meds to prolactin <10 for a year, then re-image, if tumor is still present, go on half dose and see if the tumor comes back, if it does you need lifelong tx
- Dopamine agnoists can cause cardiac valve thickening/abnormalities so you need a baseline echo before staring treatment
- Lipids, insulin resistance improve with treatment - some literature about using dopamine agonist to treat diabetes, as prolactin may be implicated in metabolic syndrome
9. FOBT
- Screening test
- False positives can be caused by recent ingestion of red meat (Hb in meat will light up the test), trauma during rectal exam. Thus patient should not be eating red meat before the test
- If someone is going to be admitted for GI bleed, it should be significant-- ie visible on the glove as either red or black. If blood is not grossly visible, the bleed is not serious enough to require admission. Thus don't do an FOBT in the ER
10. Melena
- Is midnight black, tarry/sticky, and has a strange/bad odor different from typical stool
- Not just dark, otherwise normal appearing stool.
- Things that can cause dark-appearing stool: pepto bismol, milk of magnesia, iron supplements
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