1. Modified Duke criteria for infective endocarditis: Need 2 major criteria, or 1 major and 3 minor, or 5 minor.
Major criteria: 
- 2+ blood cx drawn 12 hrs apart, or 3 cx (2 of which are drawn 1 hr apart) of organisms that classically cause endocarditis (strep viridians, strep bovis, HACEK, enterococcus and s.aureus without other source)
- Echo findings: oscillating mass on valve, abscess, new valve regurg, dehiscence of part of prosthetic valve.
Minor criteria: 
- Fever > 38
- Heart valve dx, IVDU
- Vascular phenomena: arterial emboli, intracranial hemorrhages, pulmonary emboli, conjunctival hemorrhages, janeway lesions
- Immune phenomena: glomerulonephritis (immune complex deposition), rheumatoid factor (IgM against IgG), olser nodes, roth spot (immune complex mediated vasculitis leading to hemorrhages in retina)
- Blood cx findings that don't quite meet major criteria
2. Staph endocarditis: 
- Penicillins and b-lactams are the best drugs.
- In the rare incidence when it's susceptible to penicillin, use pencillin
- MSSA: use nafcillin, oxacillin, or cefazolin. Adding gent for the first 3-5 days may speed up clearance of bacteremia. Vanc is slower than these drugs, and clinda has a high failure rate in vivo (maybe because its bacteriostatic against many strains of s.aureus). Linezolid is +/- in efficacy.
- Use vanc for pen allergic people.
3. Endocarditis of prosthetic valve:
- Treat with rifampin, gent, and something to cover staph-- Naf/ox/cefazolin for MSSA or vanc for MRSA.
4. Anti-pseduomonals:
- Third gen cephalosporins: ceftazidime (no MRSA coverage), cefoperazone (has a side chain which can inhibit vitamin-K activity and cause a disulfram like reaction)
- Ag: tobra, gent, amikacin
5. Diabetic foot ulcers
- If a metal probe hits bone, 90% PPV for osteomyelitis
- Need bone bx to find the deep organisms that are responsible for the infection-- superficial ulcer organisms often do not correlate with the deep organisms.
6. Spine osteomyelitis
- If blood cx are negative, will need CT-guided needle biopsy.
7. Aplastic anemia
- Cell lines down but cell maturation normal, BM <20% cellularity
- 50% of the time no identifiable cause, 50%: drugs, chemicals, viral, collagen vascular, thymoma
- Workup: withdraw all potential causative agents, CT chest to r/o thymoma
- Interferon-activated T-cells targeting hematopoietic stem cells implicated in pathogenesis, immunosuppressives sometimes effective
8. ITP
- Platelets low, but white count normal
- May have associated hemolytic anemia, or iron-deficiency anemia from bleeding.
9. B12 deficiency:
- Serum homocysteine and MMA levels will elevate before B12 levels drop
- In folate deficiency, only homocysteine will be high.
10. Indications to screen for coagulopathy before surgery: 
- Personal or family history of bleeding
- Heavy alcoholism: alcohol partially inhibits platelets, reduces fibrinogen/factor VII/wWF levels, activates tPA -- this is perhaps responsible for the decreased risk of cardiovascular disease seen with mild or significant alcohol consumption. {source} The truth is that raging alcoholics don't get heart disease-- they die young of liver disease, or cancer, or accidents, or any of the other comorbidities of alcoholism, but they don't die of cardiovascular disease.
- Liver disease
- Malnutrition
- Anticoagulation
- For the purposes of exams, people without the above risk factors do not need a PT/PTT/INR before surgery.

1. Human nasopharynx is a reservoir for neisseria meningitis; use droplet precautions.
2. PPD skin test cutoffs for TB
- 5: HIV, transplant, immunosuppressed (ie. lupus, >15mg/day of prednisone for >1mo). Close contact with TB+ person. Suspicious CXR (c/w prior TB)
- 10: Recent immigrants (<5 yrs) from high prevalence countries, IV drug users, people close to jails, homeless shelters, hospitals, kids < 4 years old, kids exposed to high risk adults, some chronic diseases (DM, renal failure, some cancers like leuk, lymph, head+neck, lung, silicosis, gastrectomy, some GI bypass procedures)
3. TB: 
- BCG vaccine induced false-positive PPDs should fade after 10 years, so anyone >10 years out should be treated like anyone else and the tests interpreted accordingly.
- Exposure in the distant past may lead to a false neg PPD; repeat testing in 1-3 weeks may reveal a positive test. Indicated in older people, people who may have had a distant exposure
- B6: 2% of people develop peripheral neuropathy on isoniazid without B6. People at esp high risk for neuropathy: diabetes, uremia, alcoholism, malnutrition, pregnancy, HIV, seizure disorders.
- Screen for latent TB before getting solid organ transplant, starting chemo, or starting TNF-a inhibitor (infliximab, adalimumab, etanercept). Any PPD >5 qualifies as + in these people (regardless of their other risk factors) and should get 6-9 months of INH + B6. You can probably start the TNF-a inh 2 months into INH therapy but this is a matter of debate.
4. Severe CAP
- Pseudomonas risk factors: bronchiectasis, recent (<1 month) steroid/broad spectrum antibiotic use, malnutrition.
- MRSA risk factors: severe, rapidly progressive course, infection during flu season, cavitary infiltrates on CXR, history of MRSA
5. Legionella
- Risk factors: smoking, DM, HIV, CKD, liquid and solid tumors.
- Often presents with high fevers, hyponatremia, GI sx,
- Urine legionella test: 70-90% sens and 99% spec for L. pneumophila serogroup 1-- doesn't detect other serogroups. Neg test does not r/o. Test will be pos day 1 of infection and remain + for weeks.
- Blood and thora cx will not grow + cultures so don't bother
6. CKD + immunity
- Uremia causes an immunocompromised state
- CKD associated with dysfunction in innate and adaptive immunity, TLR, etc
7. Erythromycin does not cover h.flu.
8. Criteria for antibiotic prophylaxis before dental procedures: 
- Prosthetic valve
- History of infective endocarditis
- Congenital heart disease that is unrepaired/not fully repaired or has been repaired within last 6 mos
- S/p heart transplant with valve disease
9. Antibiotic prophylaxis before dental procedure:
- Cover for strep viridians
- PO amox
- IV amp, cefazolin, ceftriaxone for people who can't take PO
- Clinda, azithro, clarithro for people who are pen allergic
- Take 30-60 mins before procedure
10. Injection drug user, multifocal pneumonia, heart murmur:
- Think septic emboli from tricuspid valve endocarditis
- Usually s.aureus, cover MRSA, pseudomonas until cx come back proving they're not present.

1. Cold agglutinins are usually due to infections or lymphoproliferative disorders
- Lymphoproliferative disorders: anything involving increased production of antibodies (i.e B-cell cancers), so waldenstrom's macroglobulinemia, lymphoma, CLL, multiple myeloma.
- Viral infections: CMV, EBV (60% of mono pts will have cold agglutinins, but hemolytic anemia is rare), VZV, Mumps, rubella, HIV, influenza
- Bacterial infections: legionella, e.coli, syphilis, listeria
- Parasitic infections: trypanosomes, malaria
- CANOMAD syndrome (chronic ataxic neuropathy ophthalmoplegia M-protein agglutination disialosyl antibodies): gait and upper-limb ataxia, external ophthalmoplegia, cold agglutinins, IgM paraprotein, and anti-disialosyl antibodies. Neurologic and hematologic symptoms respond to rituximab.
2. Warm agglutinins: 
- 80% of all autoimmune hemolytic anemia (AIHA).
- Always polyclonal. IgG1 and IgG3 are the most destructive, and the people with AIHA with a significant component of one or either will have a more advanced, aggressive course. The composition of Ig subtypes is unique and does not always reflect serum composition.
- Usually caused by drugs
- Drugs: cephalosporins (cefotetan most commonly, ceftriaxone next), penicillins (esp piperacillin), NSAIDs,
- Systemic autoimmune diseases: Lupus, RA
- S/p URI
- CLL
3. Acute chest
- Infarctions may lead to secondary infections, so pneumonia in a homozygous sickle cell patient may represent ACS
- Multiple infarctions -> pulmonary congestion, shunting of blood, hypoxia -> more sickling
- Treat with exchange transfusion to goal of HbA > 50% to decrease sickling.
- Hydroxyurea is good to prevent sickle crises (increases Hb F production), but is not an effective treatment in the acute setting.
4. Osteonecrosis (aka avascular necrosis) of the femoral head:
- Common in sickle cell, hypercoagulability (i.e. antiphospholipid), steroid use, gout, alcohol use, lupus, s/p trauma, gout.
- Unclear why alcohol use causes this... but there is a clear relationship. Compared to demographically matched controls, RRs of osteonecrosis of the femoral head were 3.3, 9.8, and 17.9 for current consumers of less than 400, 400-1000, and greater than or equal to 1000 ml/week of alcohol {source}
- CXR: initially will show nothing, later on may show increased density (marrow infarction -> calcification). MRI is >90% sensitive, good for detection in the early phases.
- Can use radionuclide bone scan in people who can't get MRI- although this is not as sensitive.
5. Complex regional pain syndrome/reflex sympathetic dystrophy
- pain in the extremities, swelling, local vasomotor instability (hot flashes), limited range of motion,
- local osteoporosis (bone densitometry scan)
6. Septic arthritis: 
- Always should suspect in acute onset monoarticular arthritis, but is uncommon in the absence of prosthetic hip, recent trauma/surgery, previous hip disease
7. Platelet transfusion should be avoided in consumptive processes unless there is life-threatening bleeding.
8. TTP
- ADAMTS13 normal levels: 65-133%, in fulminant TTP expect to be very low.
- More importantly, ADAMTS13 inhibitor should be positive. No inhibitor = No TTP
9. Evans syndrome: 
- Coombs+ warm AIHA + ITP
- Smear: spherocytes/microspherocytes + decreased platelets + elevated retics
- Tx like TTP: steroids and IVIg. children have a good response to steroids.
10. Thrombocytopenias: 
- Pseudothrombocytopenia: where platelets agglutinate in large clumps, occasionally to neutrophils but sometimes to other cell types. These large platelet clumps are not read by the cell counter and you get a falsely low platelet count. Repeat the test with heparin or sodium citrate (instead of EDTA).
- Gestational: occurs in 5% of pregnancies, appears in late gestation. Platelets are 70-150K. Generally no treatment.
- ITP: no findings other than low platelets. No large spleen, no adenopathy, no abnormal white or red cell morphology. Sometimes you will see giant (i.e. immature) platelets on smear.

1. DKA: most common cause of death is the thing that precipitated the DKA.
- If someone has abdominal pain, look for the source, don't just chalk it up to DKA. People typically only get abdominal pain from DKA if their bicarb is <10. Even if it's less than that, there's still other things that can cause it.
- Get lactate - if its high look for the source.
2. Symptom approach to dyspnea:
- Dyspnea + fever : pna, pna, pna, PE, COPD/Asthma with infection, endocarditis,
- Dyspnea and pleuritic chest pain: pna, PE (Ultrasound for UE DVT is not as sensitive because the large UE veins go behind the clavicle bones)
- Dyspnea  + nonpleuritic chest pain: Angina,
- Dyspnea with nothing else: look for highest yield diseases: heart failure, pna, asthma, copd, PE
3. Meds that directly cause edema:
- Direct vasodilators, like hydralazine.
- Dihydropuridine Ca channel blockers (peripherally acting)
- Glitazones: 1/3 of patients who use get significant edema (now only pyoglitazone is used)
- Steroids
- Estrogen.
- Don't forget that anemia is always on the differential for edema!
5. Primary Nephrotic syndrome (i.e. idiopathic)
- FSGS (33%)
- Membranous (33%) 5-20% of adults with this have cancer
- Minimal change (15%) - can occur in adults.
6. Secondary causes of nephrotic
- DM
- lupus
- infections (hep b, c, hiv, syphillis, malaria)
- amyloid
- MM
- CAncer
- Meds - NSAIDs, ACE, tamoxifen, lithium, heroin.
7. Types of nephropathy
- Hypertensive nephropathy- modest proteinuria,
- DM nephropathy- more significant proteinuria (Nephrotic- pr/cr ratio > 3-3.5)
8. Types of pulmonary hypertension 
- PAH (3%) idiopathic, genetic, drug/toxin, 2/2 - connective tissue dx, HIV, portal hypertension, congenital heart dx, chronic hemolytic anemia, schistosomiasis
-  PVH (66%): heart failure. 83% of ppl with diastolic HF have PH.
- PH 2/2 hypoxia: COPD (50% hae PH), ILD (1/3 have PH), OSA, high altitude.
- Chronic PE (<2%)
- Misc causes of PH: myeloproliferative, sarcoid,
9. Diagnosing Cirrhosis
- Plt <110 LR+ 9.8
- Plt > 160 LR 0.29
- Alb <3.5 or elevated INR: LR+ 5
- MRI - LR ~5
10. SBP
- 10-30% in hospitalized patients
- Usu GN, and s.pneumo
- 25-75% abdominal pain
- Indication for paracentesis: active GI bleed, labs suggestive of infection, new renal problems, change in clinical status,
- Paracentesis with single organism, >250 polys = diagnostic of SBP
- Paracentesis with polymicrobial - secondary BP (i.e. perforated viscous)

1. "dizziness" means one of 4 things
- Vertigo : world is spinning
- Pre syncope: feeling like you're gonna pass out
- Dysequilibrium: feeling like you're gonna fall down
- Ill defined lightheadedness
2. When people can't describe it, look for clues that its neurological or cardiac- ie.. look for other neurological or cardiac symptoms.
3. Vertigo:
- Peripheral: BPPV, labyrinthitis
- Central: posterior fossa. Cranial nerves, gait, cerebellar coordination
4. History for vertigo:
- BPPV is often positional, but just b/c its positional doesn't mean its BPPV-- central can be too
- Length of vertigo: BPPV (minutes), menieres (hours), vestibular neuritis (days), cerebellar stroke/central lesions (days). If they have a lot of risk factors for stroke and vertigo and no other neuro sx or findings,
5. Tests for central vs peripheral:
- skewed deviation: have them follow your finger up, if their eyes become disconjugate = think brainstem lesion
- head thrust test: distinguish vestibular neuritis from cerebellar stroke in someone who has had vertigo for days.
- If those are both negative, pretty good sensitivity for r/o central lesion.
6. History: rule out central lesion
- CN: diplopia, weakness, slurred speech
- Cb: ataxia, coordination
- Headache: r/o posterior fossa bleed
- History of cancer, anticoagulation
7. Nystagmus:
- Benign (i.e. peripheral, labyrinthitis): unidirectional, a few beats, fatigues with repeated exam, only happens on one side (i.e. to the left, nystagmus in one direction, to the R, nothing)
- Malignant: bidirectional, vertical,
8. Symptom approach to abdominal pain:
- Abdominal pain + peritonitis: call surgery
- Abdominal pain + jaunidce: biliary or hepatic
- Abdominal pain + significant distention: air or fluid.
- Abdominal pain + unexplained hypotension (i.e. no n/v/d, no sepsis, no GI bleed): intra-abdominal hemorrhage.
9. Any exertional pain from mouth to belly-- think angina. Even if its in a weird place like uvula.
10. Bowel perfusion: 
Ischemic colitis: splenic flexure, hypoperfusion. Typically spares the rectum because of the dual blood supply.
Chronic mesenteric ischemia - usually 2 vessel dx (celiac and sma)

1. Transient loss of consciousness - seizure vs trauma vs hypoglycemia vs drugs/alcohol vs stroke/TIA vs syncope
2. Syncope: vasovagal/reflex vs orthostatics vs cardiac
- Vasovagal: ask about pain, anxiety. Pathogenesis: Heart squeezes down until there's no volume left, brain sees that they need to slow down to fill better, tells vagus nerve to brady and peripheral vessels to vasodilate
- Orthostatics: orthostatic BP. Pathogenesis: dehydration, autonomic instability (old people-- can't mount tachycardic response), diabetes (peripheral neuropathy)
- Cardiac: ask about cardiac dx, risk factors for cardiac dx. In someone with a history of heart disease, you have to rule out NSVT as the cause. In someone young and healthy, still get an EKG because if they have a congenital QT prolongation or if they are on a drug that can prolong QT (macrolide, quinolone) they can go into torsades.
3. When to not blow it off as just vasovagal/orthostatic: 
- Occurs lying down (by definition you can't be orthostatic)
- Occurs during exercise

- Any history of heart disease

4. Syncopal convulsions: couple of twitches after syncope is common-- no postictal phase tells you its not a true seizure. 

5. Orthostatics:

- Postural increase in pulse > 30 (97% sens, 98% spec, LR+ 48, LR- 0.03)
- Supine HR > 100 (12% sens, 96% spec, LR+ 3, LR - 0.9)
- Supine hypotension <95 (33% sens, 97% spec, LR+ 11.0, LR- 0.7)
6. EP techinques to work up arrhythmia 
- Measure H-V interval (see how long a signal takes to get thru his-purkinje to check for AV node block)
- Overdrive pace SA node, then stop, see how long it takes the node to recover (longer in sick sinus syndrome).
7. WPW: afib is dangerous, because there's no block through the AV node-- you conduct thru your accessory pathway, and you can pace the ventricle to a rate of 200s-300s.
8. Hypothyroidism: 
- Diagnosis: TSH- LR- <0.01, LR +99
- Elevated TSH + low T4 is overt hypothyroid
- Elevated TSH + normal/high T4 is subclinical hypothyroidism.
- Indications for synthroid: symptoms, TSH > 10 (high risk of progression from subclinical to overt hypoT),
9. Bactrim does not cover strep
10. Skin infections
- Cellulitis: systemic symptoms (ie. fever) are rare except in bacteremia or nec fasc, so when you see them, get worried. Without abscess, usu strep, with abscess, think staph
- Erysipelas - usually strep, clear demarcated border, usually superficial, often with fever (i.e. not a worrisome sign)

1. Drugs that amplify warfarin: 
- Tylenol, NSAIDs
- Phenytoin
- The standard CYP inhibitors
- Omeprazole
- Antibiotics
- Amiodarone
- Synthroid
- Foods: cranberry juice, ginkgo, vitamin E.
2. Drugs that dampen warfarin: 
- The standard CYP inducers (st.johns wort, rifampin, carbamazepine etc)
- Foods rich in vitamin K (leafy greens)
- Ginseng
- OCPs
3. Lupus 
- Cyclophosphamide is indicated in the management of lupus when there are significant renal or CNS symptoms
- For lupus nephritis, this small trial (n=80s) found that cyclophosphamide was superior to azathioprine in terms of measured Cr at 5 year f/u and incidence of HZV infection.
4. Miscellaneous drug side effects:
- Cochlear dysfunction: platinum chemo agents, aminoglycosides, lasix
- Optic neuritis: ethambutol, hydroxychloroquine/plaquenil (tx malaria, lupus, RA, sjogrens)
- Peripheral neuropathy: vincristine, isoniazid, phenytoin, heavy metals, chronic alcoholism
- Digital vasospasm/raynauds: beta-blockers, ergot
- Thyroid dysfunction: lithium (also causes tremor, nephro DI, teratogen), amiodarone (also makes you blue)
- Crystal arthritis/gout: cyclosporine
- Acute pancreatitis: steroids
5. Bronchiectasis
- Signs: COPD sx + copious sputum (>100ml/day), hemoptysis, cough + sputum most days of the week, rhinosinusitis, fevers, sx resolve with antibiotics
- Causes: post-infectious (aspergillus, viral, TB), congenital (CF, a1-antitrypsin), immunodeficiency (hypogammaglobulinemia), obstruction (ie. cancer), toxins, systemic rheum (RA, sjogrens)
- Dx with high-res CT; bronch them if its focal to look for tumor, genetic/immune/autoimmune testing if its diffuse.
6. Guillain-Barre
- Assoc with respiratory and GI infection (often campy)
- Sx: symmetric ascending muscle weakness with absent/low deep tendon reflexes, bulbar sx (dysarthria/dysphasia), facial nerve palsy, mild sensory symptoms, autonomic dysfunction. 2/3 c/o severe back or LE pain.
- Dx: LP with elevated protein, normal white count
- Treat with plasmapharesis, IvIg (steroids do not help)
7. Nephrotic syndrome
- Abnormal lipid metabolism (elevated LDL, low HDL)
- Hypercoagulability (affects vv>aa, esp renal vv)
- Increased risk of MI/stroke (because of the above 2)
- Can cause hyperparathyroidism 2/2 loss of vitamin D in the urine
8. Giant cell/temporal arteritis:
- Affects branches of the aorta-- aortic aneurysm is a possible complication. Patients should be followed with serial chest x-rays
9. Toxic shock syndrome
- High fevers T > 38.9 (102)
- Overlapping macular erythematous rash (looks like sunburn)
- Shock vitals
- Multiorgan involvement:
GI (v/d)
Renal (Cr>1-2x upper limit of normal)
Heme (platelets <100K)
MSK (severe myalgias, CK up)
Liver (ast/alt/t-bili >2x ULN)
Mucous membrane hyperemia
CNS (AMS without focal signs)
- +/- leukocytosis: bands usually up, platelets usually down.
- Toxic shock toxin = superantigen, T-cell activation
- Tx with antistaph antibiotics
10. Post infectious glomerulonephritis
- IgA nephropathy: few days (<5) after URI. Nl complement.
- Post strep: GN occurs 10 days after strep pharyngitis, 21 days for strep impetigo. Complement low.