1. Pearls about diagnosis of acute cholecystitis/cholangitis: 
-Acute-onset RUQ plus obstructed LFTs (increased alk-phos, GGT, bili): suspected choledocholithiasis.
-Workup: CBC to find leukocytosis (indicates cholangitis has set in), pancreatic enzyme levels. U/s won't reveal stones in bile ducts, but will reveal bile duct dilation (useless in someone who's had a cholecystectomy, because their CBDs can dilate to 1cm)
-If someone has symptoms/labs consistent with acute pancreatitis AND acute cholangitis/choledococystitis, ERCP is indicated.  If they only have symptoms/labs of acute pancreatitis, do not do an ERCP-- it won't help the diagnosis and will (possibly) worsen the pancreatitis. If they have pancreatitis and equivocal symptoms/labs of cholangitis, do MRCP.
-If you do an MRCP or EUS and it reveals stones, go to ERCP and remove the stone; if there are no stones, put in a CBD stent; the symptoms may be caused by abnormal sphincter of oddi spasm.
-Rectal NSAIDs (i.e. indomethacin) can reduce ERCP-induced pancreatitis; but not NSAIDs delivered by other routes.
2. Estimating risk of choledococystitis: 
Very strong predictors: you saw a bile duct stone on u/s, they have clinical cholangitis, Tbili>4
Strong predictors: common bile duct dilated to >6mm, Tbili 1.8-4
Moderate predictors: any abnormal LFTs other than bili, age>55, clinical gallstone pancreatitis
-High Risk: One very strong predictor, or both strong predictors. Estimated risk >50%, go to ERCP
-Medium risk: one strong predictor, or one moderate predictor: estimated risk 10-15%, do an EUS or MRCP first. If the MRCP is positive for stone, go to ERCP. If the MRCP is negative, but if you saw sludge or stones in the GB, schedule elective cholecystectomy later. If the MRCP is negative but the patient fails to get better, do EUS to get a better look (can do ERCP at the same time if EUS is pos)
-Low risk: no predictors. <10% risk. If you saw sludge and GB stones, schedule for surgery if they're stable for surgery. Otherwise medical stone dissolvers.
3. Acute SAH management: 
-watch Na (will often drop, incl because of ADH secretion)
-reverse all anticoagulation until the aneurysm can be clipped
-watch for increased ICP due to edema, obstruction: treat with mannitol, steroids, emergent craniotomy
4. Blood pressure & SAH: if the blood pressure goes too high, you will blow out the aneurysm and/or push more blood through an already ruptured aneurysm, worsening the bleed. If it is too low, you may not be able to have enough MAP to provide adequate cerebral perfusion pressure, esp if there is increased ICP and the brain will go ischemic.
General guidelines:
-Keep systolic <160. If you can measure CPP (i.e with EVD) and can monitor perfusion status because the patient is A&O, and thus utilize these two measures to assure adequate perfusion, then you can keep the systolic even lower, <140. If you don't have this clinical information, you don't want to risk underperfusion so go higher (esp if you suspect the reason for the loss of mental status was because of increasing ICP leading to less CPP)
-Do not use vasodilators (nitrates) to lower BP if it is high; it will worsen ICP by dilating intracerebral vessels. Use beta-blockers, ACE-I, Ca channel blockers
5. Incidence of angiographic vasospasm after SAH: 30-70%; incidence of clinically obvious vasospasm (i.e. loss of mental status) after SAH 20-30%
6. Most (90%) people with bad CF don't get pancreatitis: CFTR d508/d508 -> ductal bile inspissation in utero -> fibrotic pancreas before birth, complete fibrofatty replacement. Endocrine function is spared. The other 10% have some remaining functional exocrine pancreas and can still get pancreatitis.
7. Heterozygous d508 or other mutations (more common) don't necessarily lead to full-blown CF with lung involvement: they may present later in life as isolated pancreatitis, or isolated male infertility
8. SPINK1 is a protease inhibitor packaged with pro-pancreatic enzymes in zymogens. Mutations in it predispose to chronic pancreatitis, and may be triggered in someone who adds on risk factors (i.e. drinks heavily). N43S is the most common mutation. Caffeine triggers pancreatitis.
9. Bad chronic pancreatitis can lead to many consequences:
-Portal hypertension. Inflammation around portal vein can cause portal vein thromboses, or splenic vein thromboses.
-AV fistula. Inflammation and enzymes can erode through walls of arteries, weakening them and leading to pseduoaneurysms that eventually fistula-ize with neighbouring veins
-Duodenal compression secondary to progressive fibrosis of the region around the pancreatic head, leading to constriction of ducts, vessels, duodenum.
10. Aortic dissections: 
-A-type: aortic arch dissection, tend to dissect retrograde, can cause acute aortic regurg and heart failure, need to go to surgery immediately. Getting BP control buys you some time, you still need to go fast.
-B-type: Below the L subclavian. Only troublesome if it restricts blood flow through the renal arteries or celiac/SMA/IMA or iliacs, in which case you need to go to the OR. Otherwise just manage medically with BP control.