Lecture 7.2 MJ slides Flashcards
List the 3 manifestations of alcoholic liver disease, and how common each is
1) Hepatic steatohepatitis (90-100%)
2) Alcoholic hepatitis (10-35%)
3) Cirrhosis (8-20%)
Hepatic steatohepatitis (90-100%) (Alcoholic Liver Disease):
1) What increases?
2) What decreases?
3) What is the net effect?
1) ↑ lipid biosynthesis
2) ↓ the assembly and secretions of lipoproteins
3) Accumulation of intracellular lipids
Alcoholic hepatitis (10-35%; Alcoholic Liver Disease)
1) Acetaldehyde (metabolite of ETOH) disrupts _____________ and _____________ function.
2) ETOH affects what two things?
3) What damages membranes and proteins?
1) cytoskeleton and membrane function
2) Mitochondrial function + membrane fluidity
3) ROS (generated during oxidation of ETOH)
Cirrhosis (Alcoholic Liver Disease) (8-20%):
1) When does it typically occur?
2) What can make it happen faster?
3) What % of alcoholics have this factor that accelerates towards cirrhosis?
1) Usually after 10 years
2) Can be expedited w/ concurrent Hep C infection
3) 30% of alcoholics have Hep C
Nonalcoholic Fatty Liver Disease (NAFLD) is associated with what 4 things?
1) Metabolic syndrome
2) Obesity
3) Type 2 diabetes
4) Dyslipidemia and/or hypertension
Nonalcoholic Fatty Liver Disease (NAFLD)
1) NAFLD may show all the changes associated with alcoholic liver disease, including what?
2) The features of _____________ often are less prominent than they are in alcohol-related injury.
-Give some examples
1) Steatosis, nonalcoholic steatohepatitis (NASH), and cirrhosis
2) steatohepatitis
-hepatocyte ballooning, Mallory-Denk bodies, and neutrophilic infiltration
What pediatric condition is increasingly being recognized as the obesity epidemic spreads to pediatric age groups, but its histologic pattern differs somewhat from that seen in adults?
Pediatric NAFLD (Nonalcoholic Fatty Liver Disease)
1) What lab is decreased with Wilson disease?
2) What 2 labs are increased? Include sensitivity/ specificity
1) ↓ serum ceruloplasmin
2) ↑ hepatic copper content (most sensitive)
↑ urinary excretion of copper (most specific)
1) Normal α1AT inhibits what?
2) Describe the pathogenesis & inheritance of α1-Anti-Trypsin Disease
3) How can it cause lung injury?
4) How can it cause liver injury?
not sure how much of this slide we need to know
1) Proteases released by neutrophils
2) Autosomal recessive caused by mutations that lead to misfolding of α1AT > ↓ levels of circulating α1-anti-trypsin
2) Pulmonary emphysema b/c destructive protease not inhibited
3) Hepatocellular build up of misfolded α1AT
1) What is Charcot’s Triad?
2) What condition is it indicative of?
1) RUQ pain + Jaundice + Fever
2) Cholangitis
α1-Anti-Trypsin Disease:
What are the 3 clinical manifestations?
not sure how much of this slide we need to know
1) Newborns: neonatal hepatitis w/ cholestatic jaundice
2) Adolescents: attacks of hepatitis w/ apparent recovery, which may lead to failure or cirrhosis
3) Adults: may be “silent” until cirrhosis is discovered
Neonatal Cholestasis:
1) What is it?
2) What are the 2 major causative conditions?
1) Prolonged conjugated hyperbilirubinemia [in neonates]
2) Biliary atresia + Neonatal hepatitis
1) “Complete of partial obstruction of the extrahepatic biliary tree (occurs in first 3 months)” describes what?
2) What is Neonatal hepatitis a cluster of?
1) Biliary atresia
2) Disorders that could be toxic, metabolic, or infectious
________________ carcinoma has the highest mortality rate secondary to diagnosis at advance stage
Pancreatic
Cirrhosis Causes: What is the mnemonic to remember these? What are they?
VW’s Happen
Virus (hepatitis)
Wilson’s
Hemochromatosis
Alpha-1
PSC
PBC
Etoh
NASH
Cholesterol stones: List at least 4 groups who are at risk for these
1) Advancing age (>40)
2) Female
3) Pregnancy
4) Obesity
5) Gallbladder stasis
6) Dyslipidemia syndromes
7) Rapid WL
Besides cholesterol stones, what’s another type of stone that’s found in different conditions & in a different demographic?
Pigment stones (biliary infection, GI disorders, asian more than western and more rural)
What are 2 things to remember for Cholangitis? Describe/ define each
1) Charcot’s Triad: RUQ pain, Jaundice, Fever
2) Reynold’s Pentad (even worse): Hypotension + AMS
Acute pancreatitis:
1) What are the Sx like?
2) What are 5 causes/ risk factors?
1) Symptoms range: focal edema → widespread hemorrhagic necrosis
2) Alcoholism, hyperlipoproteinemia, gallstones, iatrogenic surgery, or endoscopic problems w. dye injection
What is the pathogenesis of acute pancreatitis? (i.e. what causes it after the initial factors are in place?)
Autodigestion of the pancreas by inappropriately activated pancreatic enzymes
Alcoholism, hyperlipoproteinemia, gallstones, iatrogenic surgery, and endoscopic problems w. dye injection can all cause what?
Acute pancreatitis
1) 3rd leading cause of cancer deaths in US is what?
2) What are the first 2 causes of cancer deaths?
1) Pancreatic carcinoma
-(aka infiltrating ductal carcinoma)
2) Lung & colon
What is the pathogenesis of pancreatic carcinoma?
1) Probably arise from pre-cursor lesions (Pancreatic intraepithelial neoplasia (PanINs))
2) Developed by mutation of 1 oncogene and 3 tumor suppressor genes