UW CIRROSIS Flashcards
2 indicators of liver function in cirrhosis?
Impaired biosynthetic capacity (elevated PT; hypoalbuminemia)
Impaired transport and metabolic capacity (elevated bilirubin)
2 indicators of liver injury in cirrhosis?
Markers of hepatocyte injury (asp and alan aminotransferazes)
Markers of cholestasis (elevated alkaline phosphatase; elevated gama-glutamyl transpeptidase)
Impaired biosynthetic capacity (2)
elevated PT
hypoalbuminemia
Impaired transport and metabolic capacity?
elevated bilirubin
Markers of hepatocyte injury?2
elevated asp (SGOT) and alan (SGPT) aminotransferazes; usually SGOT>SGPT
What other laboratory abnormalities can be detected in cirrhosis?
trombocytopenia (due to splenic sequestration of platelets)
Markers of cholestasis?
elevated alkaline phosphatase; elevated gama-glutamyl transpeptidase)
elevated PT; hypoalbuminemia. What marker?
Impaired biosynthetic capacity
elevated bilirubin
Impaired transport and metabolic capacity
elevated asp (SGOT) and alan (SGPT) aminotransferazes; usually SGOT>SGPT? Markers of what?
Markers of hepatocyte injury
elevated alkaline phosphatase; elevated gama-glutamyl transpeptidase). Markers of what?
Markers of cholestasis
Alcohol-associated hepatic injury evolves through the stages of …….. (reversible), ………..(reversible), and ….. (irreversible).
Alcohol-associated hepatic injury evolves through the stages of steatosis (reversible), hepatitis (reversible), and cirrhosis (irreversible).
Alcohol-associated hepatic injury. Steatosis revers or non?
reversible
Alcohol-associated hepatic injury. Hepatitis revers or non?
reversible
Alcohol-associated hepatic injury. Cirrhosis revers or non?
irreversible
Hepatocyte injury causes a release of intracellular enzymes and an increase in …..
serum transaminases
biliary injury is reflected by increases in …….2
alkaline phosphatase and gamma-glutamyl transpeptidase (GGT)
What lab studies are indicative of ongoing hepatobiliary injury?
increase in serum transaminases;
increases in alkaline phosphatase and gamma-glutamyl transpeptidase (GGT).
a key determinant of prognosis in patients with cirrhosis?
liver’s functional reserve
what are indicators of the liver’s biosynthetic function?
Serum albumin levels and prothrombin time (PT)
3 signs of inadequate liver function?
- Hypoalbuminemia;
- elevated bilirubin levels;
- prolonged PT
serum bilirubin level reflects …..
ability to transport and metabolize organic anions
does elevation of transaminases reflect liver function?
Transaminase elevations do not reflect liver function and do not predict outcomes; these enzymes can be transiently elevated by a number of self-limited processes.
in alcohol-associated liver disease which aminotransferases are more elevated?
aspartate aminotransferase (AST) is classically elevated to more than 2 times the level of alanine aminotransferase
fibrinogen level in infection?
increased synthesis
fibrinogen level in inflammation?
increased synthesis
fibrinogen level in liver failure?
decreased synthesis
increase of gamma-glutamyl transpeptidase (GGT) is more specific for liver or biliary injury?
biliary
why occurs thrombocytopenia develops with chronic alcohol use? 2
due to both direct toxic effects of alcohol on the bone marrow as well as splenic sequestration of platelets.
!!The bleeding time is a measure of platelet function (not liver synthetic function) and is often prolonged in severe alcohol-related liver disease, although with a fair degree of variance.
.
2 histologic components seen in hepatic cirrosis?
diffuse hepatic fibrosis with replacement of the normal lobular architecture by fibrous-lined regenerative parenchymal nodules
normal lobular architecture in cirrosis is replaced by …..
fibrous-lined regenerative parenchymal nodules.
The most common causes of cirrhosis include ……
chronic viral hepatitis (eg, hepatitis B and C)
alcohol,
hemochromatosis,
nonalcoholic fatty liver disease.
when in cirrhosis develops portal hypertension, if so?
develops in advanced cirrhosis
Fat infiltration (ie, hepatic steatosis, visible as clear vacuoles within the parenchyma) is commonly seen in ………
both alcohol-induced fatty liver disease and NAFLD.
in response to chronic injury what cells are acticated?
stellate (Ito) cells
what do stellate (Ito) cells once are activated?
In response to chronic injury, stellate (Ito) cells are activated and transform into myofibroblasts capable of proliferating, promoting chemotaxis, and producing collagen in large quantities. This leads to progressive scar formation and cirrhosis.
Clinical presentation of cirrhosis?
Jaundice, scleral icterus, spider angiomas, and elevated liver enzymes.
What stain is used to detect collagen in cirrhosis?
Collagen stains blue with Masson trichrome stain.
Primary cells involved in hepatic fibrosis?
Stellate (Ito) cells
Hepatic steatosis is a nonspecific condition characterized by ….
Triglyceride accumulation within the hepatocellular cytoplasm.
triglyceride accumulation within the hepatocellular cytoplasm in what condition?
Hepatic steatosis
The pathogenesis of alcohol-induced hepatic steatosis appears related primarily to a decrease in free fatty acid oxidation secondary to excess NADH production by the 2 major alcohol metabolism enzymes, alcohol dehydrogenase and aldehyde dehydrogenase.
.
alcohol-induced hepatic steatosis.
Alcohol dehydrogenase and aldehyde dehydrogenase produce …..
excess NADH
alcohol-induced hepatic steatosis. Excess NADH leads to ……
decrease in free fatty acid oxidation
triglyceride synthesis in alcohol-induced hepatic steatosis is …….
increased
Peripheral fat (not phospholipid) catabolism is associated with alcohol-induced hepatic steatosis is …..
increased
…….. lipoprotein assembly is associated with alcohol-induced hepatic steatosis
Impaired (not enhanced)
Alteration of the hepatic NAD/NADH ratio due to alcohol consumption induces fatty liver through inhibition of gluconeogenesis and fatty acid oxidation.
.
microscopy in hepatic steatosis?
Cytoplasmic vacuoles as the lipid is dissolved during histologic processing
Portal hypertension leads to splenomegaly. Which part of spleen is expanded?
Venous congestion causes apparent expansion of the red pulp of the spleen, which is composed of blood-filled sinuses and cords lined by reticuloendothelial-type cells.
What mediates damage in alcoholic hepatitis?
acetaldehyde (metabolite of alcohol)
Mallory-Denk bodies seen in what?
Alcoholic hepatitis
hydropic swelling and ballooning degeneration of hepatocytes seen in what?
Alcoholic hepatitis
swollen hepatocytes seen?
Alcoholic hepatitis
what are mallory bodies?
hyaline inclusion bodies that contain keratin filaments and appear eosinophilic on HE staining
necrosis seen where?
Alcoholic hepatitis
presentation of alcoholic hepatitis?
painful hepatomegaly and elevated liver enzymes (AST>ALT)
what cells infiltra hepatocytes in alcoholis hepatitis?
neutrophils
neutrophilic granulocytes within hepatic tissue
Alcoholic hepatitis:
Pronounced excess formation of fibrous collagenous connective tissue
Pattern of chicken wire-like network in perivenous zones
Mechanical obstruction of the bile ducts and biliary stasis
.
skin presentation of cirrhosis?
teleangiectasias, caput medusae
breast presentation of cirrhosis?
gynecomastia (usually bilateral but can be unilateral)
abdomen presentation of cirrhosis?
ascites, firm or nodular liver, splenomegaly
genitourinary presentation of cirrhosis?
testicular atrophy
extremities presentation of cirrhosis?
palmar erythema, muehrcke and/or terry nails, dupuytren contracture, clubbing
where occurs sclerosis in alcoholic cirrhosis?
sclerosis around central vein may be seen in early disease
what changes induce portal hypertension in alcoholic cirrhosis?
regenerative nodules surrounded by fibrous bands in response to chronic liver injury –> portal hypertension and end-stage disease.
cirrhosis characterized by replacement of normal lobular architecture with regenerating nodules separated by bridging fibrous septa.
.
Fat infiltration seen in ….2
alcohol steatosis and nonalcoholic fatty liver disease.
what cells assist for Ito cells?
kupffer - they are indirectly involved in fibrogenesis, BUT ITS PRIMARY FUNCTION IS BACTERIAL PHAGOCYTOSIS AND THE CLEARANCE OF RBC
DM what liver disease?
Nonalcoholic fatty liver disease (NAFLD)
Medication (amiodarone, glucocorticoids, estrogen, antiretroviral drugs), liver damage?
Nonalcoholic fatty liver disease (NAFLD)
Parenteral nutrition, after resection of the small intestine and other gastrointestinal interventions, liver damage?
Nonalcoholic fatty liver disease (NAFLD)
Pathophysiology: ↑ Insulin resistance. Liver disease?
Nonalcoholic fatty liver disease (NAFLD)
Pathophysiology: ↑ Hepatic uptake of fatty acids. Liver disease?
Nonalcoholic fatty liver disease (NAFLD)
Pathophysiology: ↑ Triglyceride synthesis. Liver disease?
Nonalcoholic fatty liver disease (NAFLD)
Pathophysiology: ↑ Peripheral lipolysis. Liver disease?
Nonalcoholic fatty liver disease (NAFLD)
AST/ALT ratio < 1, what disease?
Nonalcoholic fatty liver disease (NAFLD)
The reversal of the AST/ALT ratio to values > 1 may indicate what?
Nonalcoholic fatty liver disease (NAFLD) progression to cirrhosis.
obesity, liver disease?
Nonalcoholic fatty liver disease (NAFLD)
cells in NAFLD?
Inflammatory infiltrates, with scattered lymphocytes, neutrophils, and Kupffer cells
complications of NAFLD?
cirrhosis, hepatocellular carcinoma
what marker is a good indicator of excessive alcohol consumption?
GGT
