Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
62 Cards in this Set
- Front
- Back
|
What are the cystolic hepatocellular enzymes and what are they specific for?
|
AST: less specific for liver disease (may be elevated with other conditions (MI))
ALT: produced within cells of liver and elevated with liver damage (most sensitive marker) LDH |
|
|
What are some substances that are normally excreted in bile?
And what does an elevation of any of these mean? |
serum bilirubin
urine bilirubin serum bile acids Liver disease |
|
|
What are some plasma membrance enzymes?
And what does an elevation of any of these mean? |
serum Alk phosphatase
serum GGT Serum 5'nucleotidase elevation means liver disease |
|
|
What proteins made in the liver are excreted into the blood?
|
serum albumin (decrease=liver disease)
prothrombin time (factors V,VII,X,prothrombin, fibrinogen) elevation = liver disease |
|
|
What does hepatocytes metabolize?
|
serum ammonia (increase=liver disease)
aminopyrine breath test (decrease=liver disease) galactose elimination (decrease=liver disease) |
|
|
Inflammation, a form of hepatic injury, has what type of pattern of hepatic injury?
|
Acute or chronic inflammatory cells destroy antigen-expressing hepatocytes by cytotoxic lymphocytes
Granulomas abscesses |
|
|
What would cause granulomas?
|
foreign bodies, organisms, drugs
|
|
|
What does degeneration of the liver look like?
|
swelling and edema of hepatocytes
Accumulation of specific material: -retained bile pigments -iron -copper -viral particles |
|
|
What causes necrosis in the liver?
|
virtually any significant insult to the liver
|
|
|
What are councilman bodies from?
|
apoptosis of liver cells from toxic or immunologic causes
|
|
|
What are different patterns of necrosis?
|
focal: scattered through parenchyma
Zonal: ex:centrilobular necrosis submassive massive |
|
|
When can liver regeneration occur?
|
It can occur with all liver diseases except for most fulminant diseases
|
|
|
What could hepatocyte proliferation result in?
|
thickend hepatocyte cords or swirls of immature tubular structures
|
|
|
What is fibrosis a result of? And what results if fibrosis continues?
|
response of inflammation or direct toxic insult
continuing fibrosis subdivides liver into nodules of regenerating hepatocytes surrounded by scar tissue |
|
|
When could you get unconjugated hyperbilirubinemia?
|
-excess production of bilirubin
-reduced hepatic uptake -impaired bilirubin conjugation |
|
|
What results in bilirubin overproduction?
|
-excessive hemolysis of RBCs
-resorption of major hemorrhages -ineffective erythropoisesis in bone marrow |
|
|
What causes reduced hepatic uptake of bilirubin?
|
-drug inteference with membrane carrier systems
-gilbert's syndrome |
|
|
What causes impaired bilirubin conjugation?
|
physiologic jaundice in the newborn:
-breast milk jaundice caused by B-glucuronidase in breast milk genetic deficiences of UGT activity diffuse hepatocellular disease |
|
|
Is crigler-najar syndrome type I or type II more severe? Why?
|
Type I: fatal, complete lack of UGT
|
|
|
When does jaundice occur with conjugated hyperbilirubinemia? And what is it associated with?
|
when 50% of serum bilirubin is conjugated
Associated with cholestasis, decreased excretion of bilirubin glucuronides and deficiency in canalicular membrane transporters |
|
|
What are some inherited causes of predominately conjugated hyperbilirubinemia with jaundice?
|
Dubin-Johnson syndrome
Rotor Syndrome |
|
|
What are some indications of Dubin-johnson syndrome?
|
It is autosomal recessive causing defective canalicular secretion of bilirubin conjugates
Liver is brown most pts are asymptomatic, but jaundiced Normal life expectancy pigment inclusions with histology |
|
|
What are some indications of rotor syndrome?
|
autosomal recessive
poorly characterized asymptomatic conjugated hyperbilirubinemia decreased hepatic uptake and storage decreased biliary storage |
|
|
What could cause cholestasis?
|
hepatocellular dysfunction
biliary obstruction |
|
|
What are some symptoms of cholestasis?
|
jaundice
pruritis from retention of bile acids OR xanthomas elevated serum Alk phos |
|
|
Where does bile pigment acculumate with cholestasis and what does that obstruction cause?
|
acculumates within hepatic parenchyma and causes dilated bile canaliculi and degenerated hepatocytes:
portal tract distention bile duct proliferation edema periductal neutrophils necrotic parenchymal foci (may form bile lakes) |
|
|
What happens if there prolonged obstruction?
|
portal tract fibrosis and cirrhosis
|
|
|
What is the histology of cholestasis?
|
enlarged hepatocytes
dilated canalicular spaces apoptotic cells kuppfer cells bile ductular proliferation edema, bile pigment retention neutrophilic inflammation and surrounding swollen hepatocytes undergoing degeneration. |
|
|
What is the treatment options for intrahepatic cholestasis?
|
liver transplant
|
|
|
What are the treatment options for extrahepatic cholestasis?
|
surgery to remove obstruction may be possible
|
|
|
When is someone considered to be in hepatic failure? And what is the overall mortality?
|
when there is loss of more than 80-90% of hepatic function.
Mortality = 70-95% |
|
|
What are some clincial features of hepatic failure and cirrhosis?
|
jaudice/cholestasis
hypoaalbuminemia, hypoglycemia and hyperammonemia increased serum levels of hepatic enzymes:alanine coagulopathy (elevated PT) DIC gynecomastia, testicular atrophy, palmar erythema, spider angiomas of skin fetor hepaticus hepatic encephalopathy, hepatorenal syndrome, coma massive hepatic necrosis |
|
|
Why does gynecomastia and testicular atrophy occur?
|
inability of liver to metabolize estrogen
|
|
|
What does hepatic encephalopathy mean?
|
life-threatening disorder of nervous system where there is edema and astrocytic reaction.
Advanced loss of hepatocellular function leads to exposure of the brain to altered metabolic function:excess ammonia levels) |
|
|
What are some clincial features of hepatic encephalopathy?
|
disturbances in consciousness(behavioral abnormalities, confusion, stupor, coma, death)
electroencephalographic changes limb rigidity and hyperreflexia, seizures, asterixis |
|
|
What is hepatorenal syndrome?
|
renal failure in pts with severe liver disease--there is no intrinsic renal distrubances
|
|
|
will kidney function improve if liver function improves in hepatorenal syndrome?
|
yes
|
|
|
What is the pathophysiology of hepatorenal syndrome?
|
decreased renal perfusion pressure and GFR
renal vasoconstriction |
|
|
Is renal ability to concentrate urine retained?
|
yes.
mimics profound dehydration |
|
|
What is cirrhosis defined by?
|
1.fibrosis: generally irreversible
accompanied by reorganization of vascular architecture formation of abnormal interconnections btw inflow/outflow 2.nodules disruption of liver parenchymal architecture |
|
|
What are some causes of cirrhosis?
|
EtOH liver disease(60-70%)
cryptogenic(10-15%) viral hepatitis(10%) biliary diseases(5-10%) primary hemochromatosis(5%) wilson disease (rare) alpha -1-antitrypsin deficiency (rare) |
|
|
What is the pathogenesis of cirrhosis?
|
progressive fibrosis
interstitial collagen (types I and III) deposited in all portion of lobule capillarization of sinusoids major source of excress collagen |
|
|
What are the causes of collagen synthesis in cirrhosis?
|
1.chronic inflammatory conditions with cytokine generation
2.release of cytokines by kupffer, endothelial cells 3.disruption of normal extracellular matrix 4.direct stimulation of stellate(Ito) cells by toxins |
|
|
What are some clinical features of cirrhosis?
|
may be NONE
leads to anorexia, weight loss, weakness, osteoporosis, generalized debilitation |
|
|
When will cirrhosis cause death?
|
hepatic failure
complications of portal HTN hepatocellular carcinoma |
|
|
What is portal hypertension and what causes it?
|
increased resistnace to portal blood flow and leads to:
ascites portosystemic venous shunts congestive splenomegaly hepatic encephalopathy |
|
|
What are the characteristics of pre-hepatic portal hypertension?
|
obstructive thrombosis and narrowing of the portal vein or massive splenomegaly with shunting of blood to spleen
|
|
|
What causes intrahepatic portal hypertension?
|
cirrhosis, schistosomiasis
veno-occlusive disease massive fatty change diffuse, fibrosing granulomatous disease nodular regenerative hyperplasia |
|
|
What are characteristics of pre-hepatic portal hypertension?
|
severe right sided HF
constrictuve peridcarditis hepatic vein outflow obstruction (budd-chiari) |
|
|
How does ascites cause portal hypertension?
|
percolation of hepatic capsular and intestinal serosal lymph into peritoneal cavity
renal retention of sodium and water |
|
|
How does portosystemic venous shunts cause portal hypertension?
|
develop at principal sites for portal systemic venous bypass:
-cardioesopheal junction(may rupture, causing hematemesis and death) -rectum retroperitoneum -falciform ligament and umbilicus |
|
|
How does congestive splenomegaly contribute to portal hypertension?
|
caused by long-standing congestion and may induce hematologic abnormalities attributable to hypersplenism (anemia, thrombocytopenia)
|
|
|
What is fetor hepaticus?
|
characteristic body odor:musty or sweet and sour
related to formation of mercaptans by action of intestinal bacteria on sulfur-containing amino acids methionine and shunting of splanchnic blood from portal into systemic-cirrculation |
|
|
What are characteristics of HBV carriers?
|
may exhibit normal liver archietecture and hepatocytes
STAIN POSITIVE FOR HBsAg |
|
|
Is it possible for HCV carriers to not exhibit chronic hepatitis?
|
no, will always exhibit chronic hepatitis
|
|
|
What can mimic acute viral hepatitis?
|
drug reactions
|
|
|
What is the clinical morphology of acute viral hepatitis?
|
-liver is slightly enlarged
-necrosis of scattered hepatocytes, clumps or lobules -necrotic hepatocytes are eosinophilic and round up(councilman bodies) or swollen (ballooning degeneration) -lymphocytes present -macrophages engulf nectrotic hepatocytes -lobular disarray -bridging necrosis (more severe disease) |
|
|
What are ancillary features of acute viral hepatitis?
|
-hypertrophy and hyperplasia of kupffer cells and sinusoidal lining cells
-portal tract inflammation -hepatocellular regeneration -occasionally, cholestasis |
|
|
What are the clinical morphology of chronic hepatitis?
|
mild: chronic inflammatory infiltrate limited to portal tracts
progressive: extension of chronic inflammation from portal tracts into parenchyma bridging necrosis continued loss of hepatocytes |
|
|
What clinical features are associated with viral hepatitis?
|
spider angiomas
palmar erythema hepatosplenomegaly hepatic tenderness |
|
|
What are major causes of death with hepatitis?
|
cirrhosis
liver failure hepatic encephalopathy massive hematemesis (varices) hepatocellular carcinoma |
|
|
What is fulminant hepatitis?
|
hepatic insufficiency progressing from onset to death(or transplantation) within 2-3wks
|
