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64 Cards in this Set

  • Front
  • Back
complications of cirrhosis
portal htn
hepatocellular failure
2 most common causes of cirrhosis
alcohol use
chronic hepatitis b and c
clinical features of portal htn
bleeding from varices - most life threatening

hemorrhoids
caput medusae
tx of portal htn
tips (transjugular intrahepatic portal systemic shunt) to lower portal pressure
what is the most common type of varices from portal htn
esophageal (90%) gastric (10%)
acute tx of varices
hemodynamic stabilization (plus fluids)
ligation/banding
endoscopy sclerotherapy
octreotide
long-term treatment of varices
beta blocker to prevent rebleeding
etiologies of ascites
increased portal htn (hydrostatic pressure increased)
decreased albumin concentration (decreases oncotic pressure)
how to differentiate the causes of ascites
calculate the saag
if >1.1, then from portal htn, if <1.1, then from hypoalbumin state
tx for ascites
bed rest, low sodium diet, and diuretics
pathophys of hepatic encephalopahthy
ammonia accumulates b/c the liver is unable to detoxify it
clinical presentation of hepatic encephalopathy
asterixis
fetor hepaticus
treatment of hepatic encephalopathy
decreased protein diet
lactulose
neomycin (last resort) to decrease bacteria that produce ammonia
pathophys of hepatorenal syndrome
decreased renal perfusion b/c RAAS gets activated from decreased bp in splanchnic circulation, so there is peripheral vasoconstriction --> poor renal perfusion
clinical features of hepatorenal syndrome
azotemia
oliguria
hyponatremia
hypotension
low urine sodium
tx for hepatorenal syndrome
octreotide + midodrine: palliative
liver transplant is the only cure
pathophysiology of spontaneous bacterial peritonitis
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
organisms usually involved with spontaneous bacterial peritonitis
usually monomicrobial (e coli, klebsiela, strep pneumo)
dx of spontaneous bacterial peritonitis
pnml >250
ascites cx
tx of spontaneous bacterial peritonitis
iv abx
complications of spontaneous bacterial peritonitis
hepatic abscess
hepatorenal syndrome
intestinal obx
pathophys of wilson's disease
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
clinical features of wilson's disease
hepatitis
cirrhosis
fulminant hepatic failure
kayser'-fleischer rings
extrapyramidal signs
psych disturbances (depression, neurosis, psychosis, personality changes)
dx of wilson's disease
elevated aminotransferases
low ceruloplasmin levels
liver bx shows elevated cu
tx for wilson's disease
chelating agents (penacillamidene - removes and detoxifies cu deposits)
zn (prevents dietary uptake of cu)
liver transplant
pathophys of hemochromatosis
excessive fe absorption in intestines --> fe accumulation
organs affected by hemochromatosis
liver
pancreas
skin
heart
joints
clinical features of hemochromatosis
liver dz
fatigue
arthritis
abdominal pain
cardiac arrhythmias
complications of hemochromatosis
cirrhossi
cmp
arthritis
dm
bronzing of the skin
dx of hemochromatosis
liver bx required for dx
pathogenesis of appendicitis
lumen of appendix is most commonly blocked by hyperplasia of lymphoid tissue or fecalith

obx --> stasis --> bacterial overgrowth and inflammation
pathogenesis of ruptured appendix
distension of appendix can compromise blood supply and can lead to infarction or necrosis
necrosis --> perforation and peritonitis
imaging to dx appendicitis
ct most sensitive and secific
u/s
pregnant woman with suspected appendicitis
surgery despite risk of false positive b/c risks are too severe
most common site for carcinoid tumor
appendix
location of carcinoid tumor if it is malignant
ileal tumor
pathogenesis of acute pancreatitis
inflammation of pancreas from autodigestion of the pancreas
causes of acute pancreatitis
GET SMASHeD
Gallstones
EtOH
Trauma

Steroids
Mumps
Autoimmune dz
Scorpion
Hypercalcemia, Hyperlipidemia
Drugs
which is more specific in acute pancreatitis: amylase or lipase
lipase
what is the purpose of lfts in acute pancreatitis
to ID cause (esp if related to gallstones)
role of abdominal radiographs in acute pancreatitis
used to r/o other dx
calcifications suggests chronic pancreatitis
can sometimes see sentinel loop (air filled bowel in LUQ that demonstrates localized ileus)
role of u/s in acute pancreatitis
to ID gallstones
can be used to follow pseudocyst or abscess
which is the test of choice for dx of acute pancreatitis
ct
indication for ercp in acute pancreatitis
if it is from severe gallstone pancreatitis with biliary obx
to id uncommon causes of acute pancreatitis if dz is recurrent
pathogenesis of pancreatic pseudocyst
localized collection of necrotic hemorrhagic material rich in pancreatic enzymes

it lacks and epithelial lining
complications of untreated pseudocysts
rupture infx, gastric outlet obx, fisual, hemorrhage and pancreatic ascites
dx of pancreatic pseudocyst
ct
tx of pancreatic pseudocyst
<5cm, observation
>5cm, drain
complications of acute pancreatitis
pancreatic necrosis
pancreatic pseudocyst
hemorrhagic pancreatitis
ARDS
pancreatic ascites
pleural effusion
ascending cholangitis
pancreatic abscess
tx of acute pancreatitis
npo
ivf
pain control
pathogenesis of chronic pancreatitis
continuing inflammation of pancreas, with fibrotic tissue replacing pancreatic parenchyma and alteration of pancreatic ducts --> irreversible destruction of pancreas
most common cause of chronic pancreatitis
chronic alcoholism
presentation of chronic pancreatitis
chronic epigastric pain + calcifications on plain abdominal films

steatorrhea, DM, and pancreatic calcifications
serum and amylase levels in chronic pancreatitis
not elevated
appearance of chronic pancreatitis on ct
calcifications and pseudocysts an be seen
appearance of chronic pancreatitis on ercp
chain of lakes appearance from areas of stricture and duct dilation throughout the pancreatic ducts
complications of chronic pancreatitis
dm
narcotic addiction
malabsorption/steatorrhea
pseudocyst formation
pancreatic ductal dilation
b12 malabsorption
pancreatic carcinoma
non surgical tx for chronic pancreatitis
narcotics for pain
npo
pancreatic enzymes + h2 blockers
insulin
alcohol abstinence
frequent small low-fat meals
surgical tx for chronic pancreatitis
pancreaticojejunostomy (drains the pancreatic ducts to decompress dilated ducts)
pancreatic resection
most common location for pancreatic cancer
pancreatic head
risk factors for pancreatic cancer
cigarette smoking (most common)
chronic pancreatitis
dm
heavy etoh use
exposure to benzidine and b-naphthylamine
purpose of h2 blockers + pancreatic enzymes in chronic pancreatitis
pancreatic enzymes inhibit cck release and decrease pancreatic secretion after meals
h2 blockers inhibit gastric acid secretion, preventing degradation of pancreatic enzyme supplements by gastric acid
test for dx pancreatic ca
ct
ercp
tumor markers for pancreatic ca
ca 19-9
CEA