1. Chest pain: pivotal questions for diagnosis: 
- acuity of onset
- pleuritic vs non-pleuritic
2. Differential: 
- Skin: zoster
- Breast: fibroadenoma, gynecomastia
- MSK: costochondritis, precordial catch syndrome, pec muscle strain, rib fracture, spine spondylosis (C4 to T6), myositis
- Esophagus: spasm, GERD, tear/rupture, cancer, medication-esophagitis (K-dur, tetracycline, bisphosphonates)
- GI: peptic ulcers, liver abscess (any abscess under diaphragm), pancreatitis, GB disease,
- Lung: PE, pneumonia (viral/bacterial infection of parenchyma or pleura), cancer (of pleura or parenchyma), pHTN, serositis of pleura
- Cardiac: MI, pericarditis, myocarditis
- Mediastinum: lymphoma, thymoma
- Aorta: AAA, dissection
- Psych
3. Stable angina with normal coronaries
- LVH
- Bad anemia
- Aortic stenosis (more O2 demand, increased diastolic filling pressure that compresses coronaries and compromises perfusion) (source)
- Tachycardia
- Heart failure (filling pressures)
4. Atypical presentations of stable angina
- Atypical triggers: cold weather, emotional stress, large meals
- Atypical symptoms: dyspnea, nausea/indigestion, pain elsewhere (jaw, neck, teeth, back, abdomen), palpitations, syncope, weakness/fatigue
- In women, they tend to describe the pain as more "burning" or "tender"
5. Risk factors for CAD
- Age > 55 (men), >65 (women)
- Chronic diseases (HTN, DM, etc), smoking, fam hx of CAD at <55 men and <65 women
- Bad lipids
- Hyperhomocysteinemia (causes endothelial damage)
- Elevated CRP
- Plasma fibrinogen
- Microalbuminemia
6. Likelihood of CAD
- Sx: substernal location, precipitated by exercise, relieved by rest
-0/3 sx = asymptomatic, 1/3 sx = nonanginal, 2/3 atypical angina, 3/3 typical angina

Overall prevalence of CAD at autopsy = asymptomatic 

7. Initial workup

- Lipids/A1c/glucose: tells you about risk factor diseases

- Hemoglobin/TSH: tells you alternate causes of angina 

- Resting EKG: look for current/past ischemia/infarction

- Cardiac enzymes

8. Stress test

- Purpose: diagnose CAD, determine whether they should get meds only, stent or CABG

- How it works: induce ischemia (exercise, dobutamine, adenosine, dipyridamole), detect ischemia (EKG, echo, nuclear imaging) 

- When not to get it: when you're so sure that they have CAD that you can go straight to cath, or they aren't a candidate for stent or CABG anyways 

9. When to get the more expensive imaging stress tests 

- Abnormal resting EKG

- High risk patients (where you need a high NPV to definitively rule it out) 

- Previous stent/cabg

10. When to go to the cath lab

- Stress test showing severe ischemia or ischemia at low stress

- Stress test with uncertain diagnosis

- Disabling symptoms despite treatment

- Clinical heart failure 

1. Febrile neutropenia
- Defined as T>38 for 1 hour or any T>38.3 + ANC <1500
- Mild neutropenia (ANC <1500)
- Moderate neutropenia (ANC <1000) - susceptibility to infection increases
- Severe (ANC <500) - lose ability to control endogenous flora, risk of death markedly increased
2. Management
- Mild: outpatient antibiotics
- Moderate/severe neutropenic fever: hospitalization with IV antibiotics
- If someone is really sick (ANC <100, shock vitals, invasive fungal infection, uncontrolled primary disease, pneumonia) consider adding G-CSF
3. Antibiotic choice 
- In chemotherapy patients: most common site of mucositis is GI tract, most frequently involved = GNR (pseudomonas), however more and more it's shifting to gram+ infections.
- Given this, recommend monotherapy with anti-psedudomonal b-lactam (zosyn, mero, cefepime)
- If there is evidence of pneumonia, sepsis, soft-tissue infection or line infection, shock vitals, severe mucositis, history of resistant staph/strep infections, recent fluroquinolone prophylaxis, add vanc
- If there is evidence of necrotizing mucositis, or abscess assoc with GI tract (periodontal, perirectal), intrabdominal or pelvic infection, typhlitis (necrotizing neutropenic colitis) or anaerobic bacteremia, add flagyl
- If neutropenic fever persists despite broad spectrum antibiotic therapy, add antifungals
4. Peripheral arterial disease. 
- PAD with intermittent claudication have 20% 5-year risk of nonfatal MI/stroke and 15-30% 5-year risk of death due to cardiovascular causes.
- PAD with critical limb ischemia have a 25% 1-year risk of cardiovascular death
- PAD with intermittent claudication - at 5 years, 70-80% will have stable symptoms, 10-20% progress to worsening claudication, 1-2% progress to critical limb ischemia with rest pain, nonhealing ulcers, and tissue gangrene that may lead to amputation.
5. Mortality and Cardiovascular Risk Across the Ankle-Arm Index Spectrum {Circulation}
Methods and Results— We examined total and cardiovascular mortality and cardiovascular events across the AAI spectrum among 5748 participants in the Cardiovascular Health Study (CHS). The mean age of the sample population was 73±6 years, and the sample included 3289 women (57%) and 883 blacks (15%). The median duration of follow-up was 11.1 (0.1 to 12) years for mortality and 9.6 (0.1 to 12.1) years for cardiovascular events. There were 2311 deaths (953 of which were cardiovascular) and 1491 cardiovascular events during follow-up. After adjustment for potential confounders, AAI measurements ≤0.60 (hazard ratio [HR] 1.82, 95% CI 1.42 to 2.32), 0.61 to 0.7 (HR 2.08, 95% CI 1.61 to 2.69), 0.71 to 0.8 (HR 1.80, 95% CI 1.44 to 2.26), 0.81 to 0.9 (HR 1.73 95% CI 1.43 to 2.11), 0.91 to 1.0 (HR 1.40, 95% CI 1.20 to 1.63), and >1.40 (HR 1.57, 95% CI 1.07 to 2.31) were associated with higher mortality risk from all causes compared with the referent group (AAI 1.11 to 1.20). The pattern was similar for cardiovascular mortality. For cardiovascular events, risk was higher at all AAI levels <1 but not for AAI levels >1.4 (HR 1.00, 95% CI 0.57 to 1.74). The association of a high AAI with mortality was stronger in men than in women and in younger than in older cohort members.
6. Stent vs tPA for MI
- Stents have better outcomes
- Door to balloon time (stent) goal <90 mins
- Door to needle time (tPA) goal <30 mins
7. Bacillary angiomatosis
- Typically caused by bartonella henselae and bartonella quntana
- Generally affects immunosuppressed patients (AIDS, liquid cancers, chemo, transplant)
- Systemic symptoms-- malaise, fever, weight loss, abdominal pain.
- Lesions (large, pedunculated exophytic papule with collarette of scale) appear on the skin and in the viscera, and are extremely prone to hemorrhage when biopsied
- Dx is with tissue biopsy -  microscopic ID of organisms and angiomatous histology
- Tx with antibiotics
8. Diarrhea in AIDS patients 
- CD4 < 180 - tend to have a more persistent course with parasitic infections.
- Oocysts on modified acid fast stain - cryptosporidum parum or isospora belli, however crypto is much more common
- MAI, usually assoc with lung infections in immunocompetent patients with chronic lung dx, can cause disseminated disease and invade intestinal epithelium in people who are very immune compromised and caused malabsorption.
- Spores in the stool- microsporidia organisms like enterocytozoon bieneusi and encephalitozoon intestinalis, very rare, can cause diarrhea in immunocompetent and severe/persistent diarrhea/malnutrition in immunocompromised.

9. Strep bovis

- S. gallolyticus (S. bovis type 1) is one of the 4 major species of group D strep and is associated with a significantly increased risk of colorectal cancer and endocarditis compared to S. Bovis type II. 

10. Drugs and toxins that cause liver injury

- Drugs that cause direct toxic effects (dose dependent, short latent periods: tylenol, carbon tetrachloride (CCl4), tetracycline, amanita phalloides

- Drugs that cause idiosyncratic reactions (not dose dependent, variable latent periods): isoniazid, chlorpromazine, halothane, antiretrovirals 

- Drugs that cause cholestatic liver damage: anabolic steroids, erythromycin, chlorpromazine, nitrofurantoin 

- Drugs that cause fatty liver: antiretrovirals, tetracycline, valproate 

- Drugs that cause hepatitis (histology: hepatic cell necrosis, panlobular mononuclear infiltration): isoniazid, halothane, phenytoin, alpha-methyldopa. 

- Drugs that cause fulminant liver failure: tylenol, CCl4, amanita

- Drugs that cause granulomatous liver injury: allopurinol, phenylbutazone. TB infection can also cause this. 

1. CAP
- Viruses that cause viral pneumonia - influenza A/B, para flu, adeno, rsv
- No recent exposure to serious organisms (no hospital stay within 90 days, not living in a nursing home, doesn't go to dialysis frequently) can treat as outpatient without coverage of hardcore gram negatives
- Low suspicion of resistance: can tx with z pack or doxy, if you suspect resistance can give respiratory quinolone or z pack plus cephalosporin
2. Inherited thrombophilias
- high risk mutations/deficincies : antithrombin, protein c and s deficiency, homozygous factor v or prothrombin
- low risk: heterozygous factor v
3. Anti phospholipid syndrome
- For diagnosis need both a vascular event or pregnancy morbidity and 2 positive anti phospholipid Ab tests at least 12 weeks apart
- Can occur alone or with other autoimmune disease (lupus)
4. When to screen for inherited thrombophilias: 
- first clot at age <50 without provoking factor
- family history
- recurrent clots
- unusual sites (i.e. mesentery)
5 Don't screen for inherited thrombophilias in the following
- Clots in the context of a reason (cancer, immobility, disease process known to cause clotting)
- Arterial clots, (inherited dx tend not to cause arterial clots)
- Upper limb clots (likely catheter releated) this is controversial.
6. When to anticoagulate people with inherited thrombophilias
- Asymptomatic/never had a clot: don't anticoagulate them (evidence grade 1c, unless they are going through a hyper coagulable period (surgery, pregnancy)
- History of one clot - treat as any other first clot : If provoked, 3 mos of anticoagulation, then stop. If unprovoked, give 3 mos anticoagulation, check bleeding risk, if bleed risk not high then treat forever, if bleeding risk high then stop at 3 months.
- If they clot multiple times, they've bought themselves a lifetime of coumadin.
7. What to anticoagulate with
- lovenox not tested in thrombophilia patients
- riviaroxaban/dabigatran not tested in thrombophilias
- recommend warfarin
8. Crich: (vs trach)
- Cricoid is the only complete tracheal ring; if you push the plastic against it, it's more likely to go down towards the trachea
- Lower risk of bleed as it avoids going through thyroid tissue
- Accessible in an emergency
- Its proximity to vocal cords leads to increased risk of subglottic stenosis, fibrosis over time. Should be converted to trach within 24-48 hours.
9. Trach (vs ETT)
- Usually for people who can't be off the ventilator
- People really shouldn't be on the ETT for longer than a week or so-- any longer and they should switch to trach
-  Shorter straw, less dead space
- Allow better suctioning
- More comfortable
- Decreased risk of subglottic stensois
- Allows speaking
- More secure
- These things all increase likelihood/ease of weaning vent
- If you see someone bleeding massively after they get a trach put it, they may have a tracheal-innominate fistula. If this happens, take out the trach, put your finger through the tracheostomy, and pull forward (as the vessel is usually anterior). Then put in an ETT tube with a cuff, inflate it, and go to the OR.
10. How to wean
- Weaning ETT/trial extubation: patient requires 3 things: adequate GCS to follow commands, strong cough, ability to control secretions. Deflate the cuff, see if you can hear air leak around it. If not, keep in the tube, if so, they can probably be extubated.
- Weaning trach: downsize the trach. Cap the trach to see how they do, then take it out.

1. Localization of ischemia: 
- ST elevation and q-waves are localizing. T-wave depression and ST depression are NOT localizing-- just because they are in leads of a certain distribution means nothing.
- Seeing reciprocal ST depressions in the opposite territory increases likelihood of MI, vs something like pericarditis which can have a similar clinical presentation and ST-elevation on EKG.
- Anterior: V1-V4 = LAD
- Lateral: I, aVL, V5, V6 = Lateral circumflex
- Inferior (meaning inferior part of septum): II, III, aVF = R coronary, lateral circumflex
- Posterior: see large R in V1, ST depression V1 and V2 = R coronary
2. Coronary anatomy 

- R acute marginal (labeled here as R marginal)- comes off RCA, supplies RV free wall. Thus if you clot off the RCA high enough, you will infarct out the RV as well as the posteroinferior part of the septum

- Posterior descending - comes off RCA in 80-90% of people. So inferior MIs are generally RCA infarcts. In the rest of the people, it comes off the circumflex from the LAD. 

- LAD - gives off septal branch that supplies the septum, and diagonal branches & obtuse marginals (labeled here as L marginals) that supply the lateral wall. 

3. When you see inverted T-waves, ST-elevations, and Q waves all at the same time on the same EKG- think resolving MI (~24 hours out). When the MI starts to resolve, T-waves start flipping back. 

4. If you suspect R side MI: 

- Put the leads on the R side of the chest, V1 in the center V6 on the lateral R. If you see ST elevation in V4, that is very characteristic of R MI. 

- Do NOT give nitroglycerin-- because the R side will be preload-dependent, if you give nitro (venodilator), blood will pool in the legs and you will have decreased preload and they will lose their pressure. 

- On the contrary, in L side MI, blood backs into the lungs as the L side fails, so venodilation will be good because it pulls blood out of the lungs. Probably still drops preload but in this case the cost-benefit is a little different. 

5. Things that mimic an MI: 

- Repolarization changes (benign early repolarization/BER) can cause ST elevation (usually concave up): common in young, healthy males. If your suspicion for MI is low, you can walk the patient. Changes in HR will often make the repolarization pattern change, often the ST elevation will disappear. If you have reason to suspect someone is actually having a STEMI, don't walk them. 

- Pericarditis: will see concomitant PR depression and ST elevation. ST elevation will often be diffuse, and there will be no reciprocal ST depressions. Also, PR elevation & ST depression in aVR are both very characteristic of pericarditis and are a rarely seen in MI or BER. 

- Dig toxicity: will cause rounded ST depression 

6. Electrolytes

- High K: peaked T, flattened P, eventually torsades 

- Low K: U-waves

- Hypercalcemia: short QT

- Hypocalcemia: long QT 

- Common causes of hypocalcemia: giant transfusions, as the citrate in the transfused blood chelates off all the Calcium. Watch out in MICU patients who get admitted for GI bleeds and get a lot of transfusions. Can also occur after parathyroidectomy. 

7. PE

- Most common EKG change? Sinus tach #trickquestion

- Can also see S1Q3T3: s-wave in I, Q wave in III, T wave inversion in III. 

8. Other EKG findings;: 

- Osborne wave: tiny peak after narrow QRS = hypothermia 

- Delta wave: WPW. Often accompanied by a short PR interval (the electrical signal bypasses) 

9. Pacemakers

- Looks like a LBB pattern, because they typically pace from RV apex

- Most modern pacemakers are dual chamber pacing and sensing; if they sense no P, they will give an atrial pace, await QRS; if they sense no QRS, they will give a ventricular pace. If they sense an intact P or QRS, they will allow the natural rhythm to occur. 

- Bi-ventricular pacemakers will have narrow-complex QRS because they are pacing bilaterally. 

10. Phosphate replenishing

- K-Phos: don't use if your K is >4.5 as it raises your K by around 0.2

- NaPhs: current national shortage. 

1. Hepatitis C 
- Peg-Interferon A + Ribavirin treatment led to undetectable HCV RNA level after treatment in 40% of  patients with genotype 1 infection and 75% of patients with genotype 2 or 3 infection.
- If they have genotype 1, trials have shown that boceprevir or telaprevir added to the above regimen can achieve higher remission rates (60s-70s) in genotype 1 patients; importantly, the people in those trials were all treatment-naive. It's unclear what the results would have been if it had been tried on people who had failed other regimens.
- Amazing Trial in NEJM found Daclatasvir plus Sofosbuvir could lead to viral remission rates of 98% in people with genotype 1 (both treatment naive and people who had failed other treatments), 92% in genotype 2 and 89% of genotype 3 patients. Of note, this study was non-blinded and did not have controls.
2. Lack of blinding/allocation concealment does not lead to biased results in studies with objectively measured outcomes. In studies with subjective outcomes, non-blinding does lead to exaggerations of effect outcomes. {BMJ} analysis of 146 meta-analyses containing 1346 randomized controlled trails.
3. Atrial enlargement 
- R atrial enlargement: large biphasic P with tall initial component on V1, Tall P "p pulmonale"  (>2.5 little boxes) in lead II
- L atrial enlargemnet: large biphasic P with wide terminal component on V2, Wide P "p mitrale" (>3 little boxes)
4. LVH 
- Ischemia can occur with increased demand (ie hypertrophy) and with decreased supply. Thus you can get an MI with patent coronaries if your hypertrophy is bad enough.
- Look for signs of ischemia in V5/V6
Some criteria:
- S of V1 + R of V5 or V6 >35 mm
- R in aVL > 11 mm
- R in 1 and S in 3 add to > 28 mm in men, > 20 mm in women.
5. Ischemia: 
- Can occur in the presence of a normal EKG - this happens most commonly with lateral wall MIs; treatment is still warranted if clinical suspicion is high enough. If an older guy with a history of multiple MIs and a medical history full of coronary equivalents comes stumbling into your ER, sweating, short of breath, telling you he has crushing substernal chest pain radiating down his left arm that feels just like his last MI, take him to the cath lab irrespective of what the EKG shows.
- Coronary angioplasty should happen as soon as possible. Door to balloon time should be <90 minutes, <60 minutes ideally. After around 18-24 hours, there is no benefit from intervention. If anything, the ischemic tissue is less elastic and more likely to be traumatized by the cath wires, leading to tamponade and perforation.
6. In ischemia, there is a predictable temporal progression of EKG findings: first you will see hyperacute T-waves:
- T-waves are tall, look like peaked T-waves, postulated to originate from localized hyperkalemia.

- This is a transient effect that occurs in the beginning and lasts only ~30 minutes, so most people coming in from outside of the hospital won't show up until after this period is over, so you won't see this pattern on EKG
7. In ischemia, next you will see Symmetrical T-wave inversions. 

- Asymmetric t-wave inversions are more characteristic of strain.

- Flat or minimal T-wave inversions may be a normal variant.

- Other causes of T-wave inversions: LVH, electrolyte disturbances, digoxin, head injury 

- Neurogenic T-waves: deep, symmetric T-wave inversions in all leads, can occur in acute stroke and SAH 

8. In ischemia, finally you will see ST segment depression 

- Straight and downsloping are more likely to reflect true ischemia, while upsloping ST-depression more likely to be due to repolarization variation 

9. EKG markers of myocardial injury: ST elevation

- ST elevation indicating STEMI is usually 3-5 mm high; ST elevations that are really high (like 10mm) are characteristic of vasospasm/prinzmetal's angina. 

- Earliest sign of infarction. 

- "Tombstone" shaped ST-elevation more common in acute MI, ventricular aneurysm 

- Scooping, concave-up ST elevation more likely reflective of a benign process like benign early repolarization (BER), pericarditis. Although can still be an acute MI 

(source)

10. EKG marker of infarction: Q-waves

- Must be at least 1mm wide or 1/3 height of the R wave to be considered pathological. 

1.Hemochromatosis arthritis presents clinically like RA but radiographically like OA
- Clinically: affects MCP, wrist, hip, knee (MCP and wrist are rarely affected in OA)
- Radiographically: osteophytes and join space narrowing (not seen with RA)
2. Inclusion body myositis
- ANA negative asymmetric inflammatory myositis in a middle aged man - think this
- affects distal and proximal muscles.
- usually symmetric but asymmetric in up to 15% of cases
- chronic and insidious course
- usually do not have extramuscular/systemic manifestations or symptoms.
- almost always ANA negative
3. Polymyositis
- Weakness of proximal muscles
- Acute or subacute course
- Frequently has extramuscular manifestations
- usually ANA+
4. Joint aspirate white count
<200 : normal
200-5000: gout
5,000-50,000: pseudo gout
>50,000: septic joint until proven otherwise, start broad spectrum antibiotics
5. Fluids in sickle cell patients

This quote below is from a “consult the expert column” in the Sickle Cell Newsletter for December 2008  http://listserv.emory.edu/cgi-bin/wa?A2=ind0812&L=sicklecell&T=0&P=70  (The Sickle Cell Information Center, PO Box 109, Grady Memorial Hospital, 80 Jesse Hill Jr Drive SE, Atlanta, GA 30303). 

“evidence comes from the 60, 70, and 80s…The principle is simple and based on the biochemistry of sickle hemoglobin polymerization and physiology. The rate of hemoglobin polymerization (sickling) is strongly dependent on the concentration of hemoglobin in the solution. This is exponential with the rate changing with the 25th to 35th power of the hemoglobin concentration. This means that sickling of intact sickle cells is very dependent on the concentration of hemoglobin within the red cell (MCHC)…..

         There are many other very important considerations. Almost all adults and most children with sickle cell anemia have renal tubular damage which prevents them from retaining free water. They cannot concentrate their urine so the loose large volumes of free water in the kidneys every day. The kidneys handle sodium normally and because of the anemia, they then to hold on to sodium they take in. When the patient becomes ill, they often decrease their intake of fluids and become free water dehydrated which greatly increases the sickling of their red cells and the potential for complications...sodium level will be 145 or higher when they come in crisis and 130 to 135 is ideal for reducing sickling without side effects.

             [a possible complication of normal saline?]  The third problem is the misconception about blood volume. Normal saline is used is a rehydrating solution because most dehydrated patients have reduced blood volume. Because of the chronic life-long anemia, the blood volume in sickle cell patients is normal or increased. This has been measured but the studies are old.  Administration of normal saline is potentially very dangerous in sickle cell patients during complications. Their plasma volume is increased, they have high cardiac demand from the anemia, and we are administering opiates that decrease cardiac output. Sodium will be retained and normal saline may precipitate heart failure.

             Very young children and individuals with Hb SC and Sbeta thalassemia may have less renal damage and be better able to retain water. Individuals with renal disease also may become hyponatremic with D5W. The best solutions for them are d5w ¼ normal or 1/3 normal saline.  I feel the best approach is to use one of the three and monitor the serum sodium, rather than to give a physiologically inappropriate replacement fluid (normal saline).

            There is no large clinical trial that directly addresses the issue.  The first reference is Guy et al In vitro and In vivo effect of hypotonic saline on the sickle phenomenon. Amer J Med Sci 266:267-277, 1973. It is also addressed indirectly in the article by Rosa et al in New Engl J Med 303:1138-1143, 1980. I don't think there will be further studies because people either believe the dogma and would consider it unimportant and unethical or such a small benefit off low cost so it is not important enough to spend the money required to test the hypothesis. There are recent attempts to capitalize on this effect by chronically decreasing the MCHC: chlotrimazole, Magnesium, and others. The studies on this are in process…"

    James Eckman, MD and Lewis Hsu, MD PhD

6. Coag negative staph

-Considered low virulence organisms
-Coagulase binds prothrombin and forms staphylothrombin, which is capable of cleaving fibrinogen to fibrin (just like thrmobin...) This fibrin coats the bacteria and makes them resistant to phagocytosis, which is why they are believed to be more virulent.
7. Staph hemolyticus: 
-Coag negative staph (CONS)
-More virulent than other CONS, perhaps because they make hemolysin (hemolysins are able to lyse RBCs to gain iron, often a rate-limiting nutrient for bacterial growth. An in vitro study of e.coli a-hemolysin from the early 1980s was shown to cripple leukocytes, significantly reducing phagocytosis and chemotaxis). http://www.ncbi.nlm.nih.gov/pmc/articles/PMC347633/
-Can cause meningitis, cellulitis, prosthetic joint infections, bacteremia, and rarely, endocarditis (http://www.ncbi.nlm.nih.gov/pubmed?cmd=retrieve&list_uids=17141458&dopt=abstract).
-Known for their remarkable resistance patterns-- commonly R to methicillin, clindamycin, cephalosporins, macrolides, tetracyclines, sulfonamides, fluroquinolones, and even glycopeptide antibiotics (vanc, teicoplanin), which most staph bacteria are susceptible to.
-From a Japanese group that sequenced the entire genome: "A comparative analysis of the genomes of S.haemolyticus, S.aureus, and S.epidermidis elucidated differences in their biological and genetic characteristics and pathogenic potentials. We identified as many as 82 insertion sequences in the S.haemolyticus chromosome that probably mediated frequent genomic rearrangements, resulting in phenotypic diversification of the strain. Such rearrangements could have brought genomic plasticity to this species and contributed to its acquisition of antibiotic resistance." Takeuchi F et al, Whole-genome sequencing of staphylococcus haemolyticus uncovers the extreme plasticity of its genome and the evolution of human-colonizing staphylococcal species. J Bacteriol. 2005 Nov;187(21):7292-308.
 8. Interstitial lung disease DDx: 
- Idiopathic
- Sarcoid
- Pneumonitis (birdkeeper's lung, etc)
- Occupational: beryllium, coal dust,
- Rheum: mixed connective tissue disease!! (hence why people need regular PFTs after this diagnosis) scleroderma
9. Other facts about ILD: 
- Hear fine rales on exam "velco rales"
- Aspergillus balls can grow in the spaces left over after honeycombing
10. Basal Bolus insulin > sliding scale 
Umpierrez GE, et al Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes (RABBIT 2 trial). Diabetes Care. 2007 Sep;30(9):2181-6.
RESEARCH DESIGN AND METHODS:
We conducted a prospective, multicenter, randomized trial to compare the efficacy and safety of a basal-bolus insulin regimen with that of sliding-scale regular insulin (SSI) in patients with type 2 diabetes. A total of 130 insulin-naive patients were randomized to receive glargine and glulisine (n = 65) or a standard SSI protocol (n = 65). Glargine was given once daily and glulisine before meals at a starting dose of 0.4 units x kg(-1) x day(-1) for blood glucose 140-200 mg/dl or 0.5 units x kg(-1) x day(-1) for blood glucose 201-400 mg/dl. SSI was given four times per day for blood glucose >140 mg/dl.
RESULTS:
The mean admission blood glucose was 229 +/- 6 mg/dl and A1C 8.8 +/- 2%. A blood glucose target of <140 mg/dl was achieved in 66% of patients in the glargine and glulisine group and in 38% of those in the SSI group. The mean daily blood glucose between groups ranged from 23 to 58 mg/dl, with an overall blood glucose difference of 27 mg/dl (P < 0.01). Despite increasing insulin doses, 14% of patients treated with SSI remained with blood glucose >240 mg/dl. There were no differences in the rate of hypoglycemia or length of hospital stay.
CONCLUSIONS:
Treatment with insulin glargine and glulisine resulted in significant improvement in glycemic control compared with that achieved with the use of SSI alone. Our study indicates that a basal-bolus insulin regimen is preferred over SSI in the management of non-critically ill, hospitalized patients with type 2 diabetes.

1. Hypoammonemia

Path of ammonia - (associated illnesses)
- Ammonia made by gut enterocytes from glutamine or bacteria that metabolize nitrogen products like ingested protein, urea.
- Travel from portal vein to liver (portosystemic shunt)
- Metabolized in liver to urea (liver failure like Reyes, cirrhosis, inborn urea cycle disorders like citrullinemia or ornithine transcarbalymase deficiency)
- Urea is transported to kidneys and excreted (renal failure, distal renal tubular acidosis)
Other causes of hyperammonemia
- Organic acidemia/aciduria - disorders of amino acid metabolism (ie branched chain amino acids) leading to accumulation of organic acids in the blood and urine. Clinically manifest with high gap anion acidosis, ketoacidosis, pancytopenia (possibly these amino products inhibit hematological cell maturation) and hyperammonemia because coenzyme A derivatives accumulate and inhibit carbamyl phosphate synthase.
- Drugs- salicylates, antiepileptics (Depakote!!, carbamazepine, topamax), transexamic acid, some chemo agents (5-FU, rituximab)
- Pregnancy
2. Acute liver failure:
-Defined as INR >1.5 + any hepatic encephalopathy
-Fulminant: development of encephalopathy within 8 weeks of onset of hepatic sx
-Subfulminant: development after 8 but before 26 weeks.
3. DDx fulminant hepatic failure:
-Viral: Hepatidities, CMV, EBV, VZV, HSV, hemorrhagic fevers (ebola, marburg, lassa), adenovirus
-Drugs: Tylenol, hypersensitivity drug reactions, Isoniazid, weight-loss drugs (oxyelite pro)
-Toxins: Alcohol, Amanita, B.cereus toxin
-Vascular: Budd-Chiari, Ischemia of any cause, HELLP
-Metabolic: Wilsons, Reyes, Eclampsia, acute fatty liver of pregnancy, congenital enzymatic diseases (galactosemia, fructose intolerance, tyrosinemia)
-Miscellaneous: cancer (breast, small cell, lymphoma, myeloma, melanoma), autoimmune hepatitis
4. Transaminases & diagnosing liver disease 
<100: think hemochromatosis, chronic hep B/C, fatty liver
100-300: NASH, alcoholic hepatitis, autoimmune
>1000: toxins, acute hepatitis, autoimmune, ischemia
5. Figuring out timing of liver failure: 
- PT/INR half life of a few days, albumin has a half life of 21 days
- Albumin is low- are they malnourished or are they in liver failure? Look at factors, including factor VIII. It's not made in the liver, if its low you have malnutrition.
- Someone who appears well is more likely to have acute liver failure, someone with stigmata of cirrhosis (palmar erythema, spider veins, ascites)
6. Wilsons disease: 
-1:30,000-1:100,000
-Usually affects people aged 5-35, although can be older or younger; depends on penetrance.
-Children tend to present with more hepatic disease (jaundice, hepatosplenomegaly)
-Adults tend to present with more neuropsych disease (dysarthria, tremors, parkinsoninan sx, dementia)
-98% of people with neurological symptoms will have kayser-fleischer rings, however you need a slit-lamp exam as this is not always seen with a normal exam.
-In a study comparing wilsons disease to other causes of acute liver failure, the following were found to be most predictive of Wilsons: low Hb, low AST/ALT, very high urine copper, low serum ceruloplasmin (however this is an acute phase reactant)
-Labs: Alk phos is not that high-- it can be normal or sub-normal (Alk Phos/Tbili ratio <4), AST/ALT ratio >2
-Coombs-negative hemolytic anemia is also characteristic
-Thrombocytopenia from splenomegaly
7. Treatment for wilsons disease: 
-Fulminant Wilsons (defined as fulminant hepatic failure at first presentation, INR>2, hemolytic anemia or neuropsych symptoms): Transplant. You can try to bridge to transplant with plasma exchange or dialysis. Survival after transplant for wilsons is excellent- - 88% at 1 year, 80% at 5 years, kids do even better than adults.
-Decompensated Wilsons (defined as acute on chronic, no hemolytic anemia or neuropsych sx): may respond to chelation therapy
-Early Wilsons (few symptoms): chelation agents.
8. Chelation agents: 
-Trientine is now used as first-line by most hepatologists; it doesn't work quite as well as D-penicillamine but it has so many fewer side effects that it's preferred
-D-penicilliamine is second line despite its effectiveness because of its significant side effects- nephrotic syndrome & aplastic anemia (requiring regular CBC/BMP) and patients feel really bad
-Dimercaprol (not used anymore)
9. Transfusion strategies for acute upper gastrointestinal bleeding {RCT, NEJM, n=921}
Villanueva C et al, N Engl J Med. 2013 Jan 3;368(1):11-21.
METHODS:
We enrolled 921 patients with severe acute upper gastrointestinal bleeding and randomly assigned 461 of them to a restrictive strategy (transfusion when the hemoglobin level fell below 7 g per deciliter) and 460 to a liberal strategy (transfusion when the hemoglobin fell below 9 g per deciliter). Randomization was stratified according to the presence or absence of liver cirrhosis.
RESULTS:
A total of 225 patients assigned to the restrictive strategy (51%), as compared with 61 assigned to the liberal strategy (14%), did not receive transfusions (P<0.001) [corrected].The probability of survival at 6 weeks was higher in the restrictive-strategy group than in the liberal-strategy group (95% vs. 91%; hazard ratio for death with restrictive strategy, 0.55; 95% confidence interval [CI], 0.33 to 0.92; P=0.02). Further bleeding occurred in 10% of the patients in the restrictive-strategy group as compared with 16% of the patients in the liberal-strategy group (P=0.01), and adverse events occurred in 40% as compared with 48% (P=0.02). The probability of survival was slightly higher with the restrictive strategy than with the liberal strategy in the subgroup of patients who had bleeding associated with a peptic ulcer (hazard ratio, 0.70; 95% CI, 0.26 to 1.25) and was significantly higher in the subgroup of patients with cirrhosis and Child-Pugh class A or B disease (hazard ratio, 0.30; 95% CI, 0.11 to 0.85), but not in those with cirrhosis and Child-Pugh class C disease (hazard ratio, 1.04; 95% CI, 0.45 to 2.37). Within the first 5 days, the portal-pressure gradient increased significantly in patients assigned to the liberal strategy (P=0.03) but not in those assigned to the restrictive strategy.
CONCLUSIONS:
As compared with a liberal transfusion strategy, a restrictive strategy significantly improved outcomes in patients with acute upper gastrointestinal bleeding.
- Potentially due to increased portal pressure through varices with the blood transfusions/volume.
- Octreotide
10. Advice from rounds 
- B-blockers and surgery: if someone is on a b-blocker, they should definitely stay on it. There is some data that optimizing people to a HR of 60s to 70s may lead to better outcomes.
- Lovenox is better than heparin in people with cancer
- Sgarbossa's criteria: identifying ischemia in the context of LBBB.
- Most common cause of INR spikes: chronic CHF (2/2 liver congestion), diarrhea (loss of gut flora), those 2 are much more common than warfarin o/d's
- In bleeding peptic ulcers, people should be on a nexium drip for 72 hours and then BID PO dosing afterwards.