Flashcards in HIGH YIELD LIVER/GALLBLADDER (PATHOMA) -- Leah Deck (56):
-failure to form/ destruction of EXTRAhepatic biliary tree
-jaundice (conjugated bilirubin) --> cirrhosis
Cholelithiasis is the big word for _____.
-most common type?
1. supersaturation (cholesterol or bile)
2. decreased bile or phospholipids
**Most common type = cholesterol (90%); bile less common.
-FAT FERTILE FEMALE FORTY
What does radioLUCENT mean? OPAQUE?
(Sorry, dumb card guys, I know. But I mess these up.)
-Lucent= too "L"ight to be seen
-Opaque= seen on xray
-2 risk factors
-(clonorchiasis, ascaris lumbricoides)
-most common presentation
-until they cause..... biliary colic, cholecystitis, ascending cholangitis, gallstone ileus, gallbladder cancer
what is it?
-waxing/ waning RUQ pain caused by gallbladder contracting against a stone in the cystic duct
Common bile duct obstruction may lead to?
-acute pancreatitis/ obstructive jaundice
What is unexplained jaundice in and older person until proven otherwise?
-PANCREATIC CANCER BECAUSE THIS CAN BLOCK COMMON BILE DUCT.
-how is it different from biliary colic?
-stone in cystic duct --> dilation/ pressure ischemia/ bacterial overgrowth of the gallbladder
-more constant RUQ pain, also see that "pericolic --however you say it-- fluid" on U/S (not mentioned in pathoma) ++ fever, N/V, ^^WBC also seen (patient is SICK, not just in pain)
-risk gallbladder rupture
-classic histo findings
-classic xray finding + risk
-herniation of mucosa into muscular wall (Rokitansky Aschoff sinuses)
-porcelain gallbladder --> risk carcinoma (take it out!!)
-shrunken/ fibrotic gallbladder
-chemical irritation 2ndary to long standing cholelithiasis
-bacterial (#1 gram neg) infection of bile ducts
-SEPSIS + abdominal pain +jaundice
-more common with choledocholithiasis
Cause of gallstone ileus
-fistula between gallbladder and small bowel --> stone gets stuck in intestine --> obstruction
-major risk factor
-stones major risk
-cholecystitis in ELDERLY (DOESNT FIT THE FAT, FERTILE, ***FORTY***, FEMALE) criteria
-bilirubin level when icterus (yellow eyes) begins
-most dangerous type?
-kernicterus (DEPOSITS IN BABY'S BASAL GANGLIA.)
Describe steps of leading up to the synthesis of conjugated bilirubin in a healthy person (4)
1. reticuloendothelial macs break down RBCs
2. Heme --> protoporphyrin --> unconjugated bili
3. unconjugated bili to liver via albumin
4. unconjugated --> conjugated via **uridine glucuronyl transferase** (UGT)
How is conjugated bilirubin removed from the body?
conjugated bili --> stercobilin + urobilin
(sterco goes to stool, uro to urine)
What can overwhelm the bilirubin conjugating ability of the liver?
Two assc findings?
-hemolysis/ ineffective erythropoiesis
What causes physiologic jaundice of the newborn?
-ineffective UGT enzyme
-phototherapy makes UCB water soluble
Gilbert Syndrome & Crigler- Najjar:
-difference in presenation?
-type of jaundice?
-both effect UGT; low in gilbert but ABSENT in CN
-Gilbert- benign; transient stress induced jaundice
-CN: kernicterus + fatal
-both cause ^^UNconjugated bili *UCB*
Dubin Johnson & Rotor Syndromes
-type of jaundice
-difference in clinical presentation?
-deficient bile canalicular transport protein (AR)
-causes ^^ CB
-DUBIN causes a DARK liver; Rotor does not.
(I think of Dubin Johnson as a black man....)
-two other lab findings?
-^^ urine urobilinogen + alk phos
-pale stool, dark urine
-pruritis, xanthomas, fat malabsorption
Possible causes of obstructive jaundice:
-cancers (pancreatic v cholangiocarcinoma)
-parasites/ liver fluke
-type of ^^ bili?
-conjugated + unconjugated
-inflammation disrupts BOTH hepatocytes + bile ductules
-dark urine but low --> normal urobilinogen
-fecal/ oral variants
-types spread by blood/ sex?
-A/E = fecal oral (A trAvel, E sEEfood)
-D= "D"ependent in HBV, otherwise ineffective
-B/C= "B"LOOD AND "C"EX
Two Hep strains that can cause CHRONIC hep?
-B : 20% cases
-C: most all cases
Hep strain that can cause fulminant hep in pregnant women?
Ig that marks ACTIVE/NEW disease? Confers IMMUNITY?
-IgM= new/ active
Serologic markers for ACUTE HEP:
Serologic markers during "window" period?
-^^^IgM against HBcAG only.
Serologic markers following immunization against hep?
-^^ IgG against HBsAG only.
Serologic markers for resolved hep?
-^^ IgG against both HBs and HBc ag's
Serologic markers for CHRONIC hep?
What strains cause this?
-HBsAG more than 6 months
-+/- HBeAG/ HB DNA
-IgG against HBcAG
-20% hep C, ~100% hep C
Viruses that can cause hepatitis (3)
Histo of acute v chronic hep?
-acute: inflammation of TRACTS + LOBULES and hepatocyte apoptosis
-chronic: inflammation of ONLY PORTAL TRACTS + possible cirrhosis progression.
two histo features
cells that mediate?
cytokine that mediates?
-bands of fibrosis + regenerative nodules
-Ito/stellate cells, stimulated by TGF-B
Four general complications of cirrhosis
-shunts (i.e. varices)
-hepatorenal syndrome (renal failure)
Liver damaged causes decreased detox (NO MORE OF THE EFFING CYPS. I THINK I WANT CIRRHOSIS).
What is the result?
-mental status change, asterixis --> ammonia induced coma
-spider angiomatoma, gynecomastia (^^androgen --> estogen), palmar erythema
**asterixis = flapping tremor
Two main results of decreased protein synthesis by the liver?
-hypoalbuminemia --> edema
#1 cause liver disease in western world?
-Alcohol (AFLD) --> acetaldehyde mediated damage
But.... NON alcoholic fatty liver (obesity related) is quickly on the rise!
How to diagnose NAFLD?
-ALT higher than AST; AST higher with alcohol use
-diagnosis of exclusion
Alcoholic fatty liver disease
-2 histo findings
-fat in hepatocytes
-resolves with abstinence UNLESS cirrhosis is reached (occurs in 10-20%)
-effect on liver?
**Also: what causes "secondary" type?
-AR defect in iron absorption
(HFE gene mutation --> ^hepcidin --> ^ iron)
-^^ iron due to transfusions in secondary type
-H(A3)machromatosis= HLA-A3 linkage (MHC1)
-damage by free radicals
-HCC risk ^^
-treat with phlebotomy
classic symptomatic triad?
two histo findings?
-cirrhosis, DM, bronze skin
-high ferritin, serum iron and %saturation
-brown pigment in hepatocytes, prussian blue stain +
-Whats the mutation?
-Triad of symptoms
-AR mutation in ATP mediated Cu transport --> copper incorporated in ceruloplasmin
-urinary copper, low ceruloplasmin, copper in liver
-kid with neuro maifestations, cirrhosis, & kayser fleisher rings
-^^ HCC risk (just like haemachromatosis)
-treat with penicillamine chelation
Primary "biliary cirrhosis" and "sclerosing cholangitis":
in terms of location, whats the difference?
which causes ^^ risk of cholangiocarcinoma?
-biliary cirrhosis= intrhepatic ducts only
-sclerosing cholangitis= intra + EXTRAhepatic ducts ... so ^^ risk cholangiocarcinoma
Primary biliary cirrhosis:
~40 years of age, women
Primary sclerosing cholangitis:
-assc disease/ Ab
-periductal fibrosis + onion skinning
-beaded appearance on imaging
-p-ANCA, ulcerative colitis
cause + presentation
-kids: viral illness + aspirin
-liver failure, encephalopathy, hypoglycemia, can be FATAL
ONLY reason to kid aspirin to kids?
-OCPs, regresses with cessation
-OMA= benign BUT risk rupture + bleeding esp with estrogen exposure
three possible causes?
-cirrhosis, chronic hep B/C, aflatoxins (p53 mutations, think MOLDY PEANUTS!!)
What is Budd-Chiari?
-hepatic vein obstruction --> liver infarct --> hsmegaly + ascites
(can be caused by tumor compression i.e. hepatocellular carcinoma)
From where are tumor mets most commonly
-Cancer Sometimes Penetrates Benign Liver