Kgi 200-250

Front 1

Q200. complications of cirrhosis

Back 1

A200. portal HTN; hepatocellular failure

Front 2

Q201. 2 most common causes of cirrhosis

Back 2

A201. alcohol use; chronic hepatitis b and c

Front 3

Q202. clinical features of portal HTN

Back 3

A202. bleeding from varices - most life threatening; hemorrhoids; caput medusae

Front 4

Q203. tx of portal HTN

Back 4

A203. tips (transjugular intrahepatic portal systemic shunt) to lower portal pressure

Front 5

Q204. what is the most common type of varices from portal HTN

Back 5

A204. esophageal (90%) gastric (10%)

Front 6

Q205. acute tx of varices

Back 6

A205. hemodynamic stabilization (plus fluids); ligation/banding; endoscopy sclerotherapy; octreotide

Front 7

Q206. long-term treatment of varices

Back 7

A206. beta blocker to prevent rebleeding

Front 8

Q207. etiologies of ascites

Back 8

A207. increased portal HTN (hydrostatic pressure increased); decreased albumin concentration (decreases oncotic pressure)

Front 9

Q208. how to differentiate the causes of ascites

Back 9

A208. calculate the SAAG; if >1.1, then from portal HTN,; if <1.1, then from hypoalbumin state

Front 10

Q209. tx for ascites

Back 10

A209. bed rest, low sodium diet, and diuretics

Front 11

Q210. pathophysiology of hepatic encephalopahthy

Back 11

A210. ammonia accumulates because the liver is unable to detoxify it

Front 12

Q211. clinical presentation of hepatic encephalopathy

Back 12

A211. asterixis; fetor hepaticus

Front 13

Q212. treatment of hepatic encephalopathy

Back 13

A212. decreased protein diet; lactulose; neomycin (last resort) to decrease bacteria that produce ammonia

Front 14

Q213. pathophysiology of hepatorenal syndrome

Back 14

A213. decreased renal perfusion because RAAS gets activated from decreased BP in splanchnic circulation, so there is peripheral vasoconstriction --> poor renal perfusion

Front 15

Q214. clinical features of hepatorenal syndrome

Back 15

A214. azotemia; oliguria; hyponatremia; hypotension; low urine sodium

Front 16

Q215. tx for hepatorenal syndrome

Back 16

A215. octreotide + midodrine: palliative; liver transplant is the only cure

Front 17

Q216. pathophysiology of spontaneous bacterial peritonitis

Back 17

A216. portal HTN increases --> gut hypomotility, and bacterial overgrowth; bv become more permeable and bacteria enter mesenteric ln and then enter blood stream; ascites fluid becomes infected

Front 18

Q217. organisms usually involved with spontaneous bacterial peritonitis

Back 18

A217. usually monomicrobial (e coli, klebsiela, strep pneumo)

Front 19

Q218. dx of spontaneous bacterial peritonitis

Back 19

A218. pnml >250; ascites cx

Front 20

Q219. tx of spontaneous bacterial peritonitis

Back 20

A219. iv antibiotics

Front 21

Q220. complications of spontaneous bacterial peritonitis

Back 21

A220. hepatic abscess; hepatorenal syndrome; intestinal obstruction

Front 22

Q221. pathophysiology of Wilson’s disease

Back 22

A221. copper is normally excreted by the liver, but in Wilson’s disease, there is a ceruloplasmin deficiency (required for excretion) so cu builds up; cu accumulates in hepatocytes, causing them to die and release cu into plasma and accumulate in kidney, cornea, and brain

Front 23

Q222. clinical features of wilson's disease

Back 23

A222. hepatitis; cirrhosis; fulminant hepatic failure; kayser'-fleischer rings; extrapyramidal signs; psych disturbances (depression, neurosis, psychosis, personality changes)

Front 24

Q223. dx of wilson's disease

Back 24

A223. elevated aminotransferases; low ceruloplasmin levels; liver biopsy shows elevated cu

Front 25

Q224. tx for wilson's disease

Back 25

A224. chelating agents (penacillamidene - removes and detoxifies cu deposits); Zn (prevents dietary uptake of cu); liver transplant

Front 26

Q225. pathophysiology of hemochromatosis

Back 26

A225. excessive Fe absorption in intestines --> Fe accumulation

Front 27

Q226. organs affected by hemochromatosis

Back 27

A226. liver; pancreas; skin; heart; joints

Front 28

Q227. clinical features of hemochromatosis

Back 28

A227. liver disease; fatigue; arthritis; abdominal pain; cardiac arrhythmias

Front 29

Q228. complications of hemochromatosis

Back 29

A228. cirrhosis; cmp; arthritis; DM; bronzing of the skin

Front 30

Q229. dx of hemochromatosis

Back 30

A229. liver biopsy required for dx

Front 31

Q230. pathogenesis of appendicitis

Back 31

A230. lumen of appendix is most commonly blocked by hyperplasia of lymphoid tissue or fecalith; obstruction --> stasis --> bacterial overgrowth and inflammation

Front 32

Q231. pathogenesis of ruptured appendix

Back 32

A231. distension of appendix can compromise blood supply and can lead to infarction or necrosis; necrosis --> perforation and peritonitis

Front 33

Q232. imaging to dx appendicitis

Back 33

A232. CT most sensitive and specific; Ultrasound

Front 34

Q233. pregnant woman with suspected appendicitis

Back 34

A233. surgery despite risk of false positive because risks are too severe

Front 35

Q234. most common site for carcinoid tumor

Back 35

A234. appendix

Front 36

Q235. location of carcinoid tumor if it is malignant

Back 36

A235. ileal tumor

Front 37

Q236. pathogenesis of acute pancreatitis

Back 37

A236. inflammation of pancreas from autodigestion of the pancreas

Front 38

Q237. causes of acute pancreatitis

Back 38

A237. GET SMASHeD; Gallstones; EtOH; Trauma; Steroids; Mumps; Autoimmune disease; Scorpion; Hypercalcemia, Hyperlipidemia; Drugs

Front 39

Q238. which is more specific in acute pancreatitis: amylase or lipase

Back 39

A238. lipase

Front 40

Q239. what is the purpose of liver function tests in acute pancreatitis

Back 40

A239. to ID cause (esp if related to gallstones)

Front 41

Q240. role of abdominal radiographs in acute pancreatitis

Back 41

A240. used to rule out other dx; calcifications suggests chronic pancreatitis; can sometimes see sentinel loop (air filled bowel in LUQ that demonstrates localized ileus)

Front 42

Q241. role of u/s in acute pancreatitis

Back 42

A241. to ID gallstones; can be used to follow pseudocyst or abscess

Front 43

Q242. which is the test of choice for dx of acute pancreatitis

Back 43

A242. ct

Front 44

Q243. indication for ERCP in acute pancreatitis

Back 44

A243. if it is from severe gallstone pancreatitis with biliary obstruction; to id uncommon causes of acute pancreatitis if disease is recurrent

Front 45

Q244. pathogenesis of pancreatic pseudocyst

Back 45

A244. localized collection of necrotic hemorrhagic material rich in pancreatic enzymes; it lacks and epithelial lining

Front 46

Q245. complications of untreated pseudocysts

Back 46

A245. rupture infection, gastric outlet obstruction, fisual, hemorrhage and pancreatic ascites

Front 47

Q246. dx of pancreatic pseudocyst

Back 47

A246. CT

Front 48

Q247. tx of pancreatic pseudocyst

Back 48

A247. <5cm, observation; >5cm, drain

Front 49

Q248. complications of acute pancreatitis

Back 49

A248. pancreatic necrosis; pancreatic pseudocyst; hemorrhagic pancreatitis; ARDS; pancreatic ascites; pleural effusion; ascending cholangitis; pancreatic abscess

Front 50

Q249. tx of acute pancreatitis

Back 50

A249. NPO; IVF; pain control

Front 51

Q250. pathogenesis of chronic pancreatitis

Back 51

A250. continuing inflammation of pancreas, with fibrotic tissue replacing pancreatic parenchyma and alteration of pancreatic ducts --> irreversible destruction of pancreas