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.