Lecture 7.2 MJ slides Flashcards

1
Q

List the 3 manifestations of alcoholic liver disease, and how common each is

A

1) Hepatic steatohepatitis (90-100%)
2) Alcoholic hepatitis (10-35%)
3) Cirrhosis (8-20%)

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2
Q

Hepatic steatohepatitis (90-100%) (Alcoholic Liver Disease):
1) What increases?
2) What decreases?
3) What is the net effect?

A

1) ↑ lipid biosynthesis
2) ↓ the assembly and secretions of lipoproteins
3) Accumulation of intracellular lipids

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3
Q

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?

A

1) cytoskeleton and membrane function
2) Mitochondrial function + membrane fluidity
3) ROS (generated during oxidation of ETOH)

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4
Q

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?

A

1) Usually after 10 years
2) Can be expedited w/ concurrent Hep C infection
3) 30% of alcoholics have Hep C

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5
Q

Nonalcoholic Fatty Liver Disease (NAFLD) is associated with what 4 things?

A

1) Metabolic syndrome
2) Obesity
3) Type 2 diabetes
4) Dyslipidemia and/or hypertension

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6
Q

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

A

1) Steatosis, nonalcoholic steatohepatitis (NASH), and cirrhosis
2) steatohepatitis
-hepatocyte ballooning, Mallory-Denk bodies, and neutrophilic infiltration

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7
Q

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?

A

Pediatric NAFLD (Nonalcoholic Fatty Liver Disease)

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8
Q

1) What lab is decreased with Wilson disease?
2) What 2 labs are increased? Include sensitivity/ specificity

A

1) ↓ serum ceruloplasmin
2) ↑ hepatic copper content (most sensitive)
↑ urinary excretion of copper (most specific)

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9
Q

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

A

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

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10
Q

1) What is Charcot’s Triad?
2) What condition is it indicative of?

A

1) RUQ pain + Jaundice + Fever
2) Cholangitis

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11
Q

α1-Anti-Trypsin Disease:
What are the 3 clinical manifestations?

not sure how much of this slide we need to know

A

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

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12
Q

Neonatal Cholestasis:
1) What is it?
2) What are the 2 major causative conditions?

A

1) Prolonged conjugated hyperbilirubinemia [in neonates]
2) Biliary atresia + Neonatal hepatitis

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13
Q

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?

A

1) Biliary atresia
2) Disorders that could be toxic, metabolic, or infectious

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14
Q

________________ carcinoma has the highest mortality rate secondary to diagnosis at advance stage

A

Pancreatic

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15
Q

Cirrhosis Causes: What is the mnemonic to remember these? What are they?

A

VW’s Happen
Virus (hepatitis)
Wilson’s
Hemochromatosis
Alpha-1
PSC
PBC
Etoh
NASH

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16
Q

Cholesterol stones: List at least 4 groups who are at risk for these

A

1) Advancing age (>40)
2) Female
3) Pregnancy
4) Obesity

5) Gallbladder stasis
6) Dyslipidemia syndromes
7) Rapid WL

17
Q

Besides cholesterol stones, what’s another type of stone that’s found in different conditions & in a different demographic?

A

Pigment stones (biliary infection, GI disorders, asian more than western and more rural)

18
Q

What are 2 things to remember for Cholangitis? Describe/ define each

A

1) Charcot’s Triad: RUQ pain, Jaundice, Fever
2) Reynold’s Pentad (even worse): Hypotension + AMS

19
Q

Acute pancreatitis:
1) What are the Sx like?
2) What are 5 causes/ risk factors?

A

1) Symptoms range: focal edema → widespread hemorrhagic necrosis
2) Alcoholism, hyperlipoproteinemia, gallstones, iatrogenic surgery, or endoscopic problems w. dye injection

20
Q

What is the pathogenesis of acute pancreatitis? (i.e. what causes it after the initial factors are in place?)

A

Autodigestion of the pancreas by inappropriately activated pancreatic enzymes

21
Q

Alcoholism, hyperlipoproteinemia, gallstones, iatrogenic surgery, and endoscopic problems w. dye injection can all cause what?

A

Acute pancreatitis

22
Q

1) 3rd leading cause of cancer deaths in US is what?
2) What are the first 2 causes of cancer deaths?

A

1) Pancreatic carcinoma
-(aka infiltrating ductal carcinoma)
2) Lung & colon

23
Q

What is the pathogenesis of pancreatic carcinoma?

A

1) Probably arise from pre-cursor lesions (Pancreatic intraepithelial neoplasia (PanINs))
2) Developed by mutation of 1 oncogene and 3 tumor suppressor genes