Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI Exam > Pathoma Liver > Flashcards

Pathoma Liver Flashcards

1
Q

jaundice

A

*yellow discoloration of the skin
*earliest sign is scleral icterus (yellow discoloration of the sclera)
*due to increased serum bilirubin, usually > 2.5 mg/dL
*arises with disturbances in bilirubin metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

normal bilirubin metabolism

A
  1. RBCs are consumed by macrophages of the reticuloendothelial system
  2. protoporphyrin (from heme) is converted to unconjugated bilirubin (UCB)
  3. albumin carries UCB to the liver
  4. uridine glucuronyl transferase (UGT) in hepatocytes conjugates bilirubin
  5. conjugated bilirubin (CB) is transferred to bile canaliculi to form bile, which is stored in the gallbladder
  6. bile is released into the small bowel to aid in digestion
  7. intestinal flora convert CB to urobilinogen, which is oxidized to stercobilin (makes stool brown) and urobilin (partially reabsorbed into blood and filtered by kidney, making urine yellow)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

causes of jaundice - overview

A

*extravascular hemolysis or ineffective erythropoiesis
*physiologic jaundice of the newborn
*Gilbert syndrome
*Crigler-Najjar syndrome
*Dubin-Johnson syndrome
*biliary tract obstruction (obstructive jaundice)
*viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

extravascular hemolysis / ineffective erythropoiesis & jaundice

A

*etiology: high levels of UCB overwhelm the conjugating ability of the liver
*lab findings: increased UCB
*clinical features:
-dark urine due to increased urine urobilinogen (UCB is not water soluble and, thus, is absent from urine)
-increased risk for pigmented bilirubin gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

physiologic jaundice of the newborn

A

*etiology: newborn liver has transiently low uridine glucuronyl transferase (UGT) activity
*lab findings: increased UCB
*clinical features:
-UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leading to neurological deficits and death
-tx is phototherapy (makes UCB water soluble)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Gilbert syndrome & jaundice

A

*etiology: mildly low uridine glucuronyl transferase (UGT) activity; autosomal recessive
*lab findings: increased UCB
*clinical features:
-jaundice during stress (e.g. severe infection)
-otherwise, not clinically significant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Crigler-Najjar syndrome & jaundice

A

*etiology: absence of uridine glucuronyl transferase (UGT)
*lab findings: increased UCB
*clinical features:
-kernicterus
-usually fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dubin-Johnson syndrome & jaundice

A

*etiology: deficiency of bilirubin canalicular transport protein; autosomal recessive
*lab findings: increased CONJUGATED bilirubin (CB)
*clinical features:
-LIVER IS DARK; otherwise, not clinically significant
-Rotor syndrome is similar, but lacks liver discoloration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

biliary tract obstruction & obstructive jaundice

A

*etiology: associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and liver fluke (anything that blocks the biliary tract)
*lab findings: increased CONJUGATED bilirubin; decreased urobilinogen; increased alkaline phosphatase
*clinical features:
-dark urine (due to bilirubinuria) and pale stool
-pruritis due to increased plasma bile acids
-hypercholesterolemia with xanthomas
-steatorrhea with malabsorption of fat-soluble vitamins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

viral hepatitis & jaundice

A

*etiology: inflammation disrupts hepatocytes and small bile ductules
*lab findings: increase in both conjugated and unconjugated bilirubin
*clinical features:
-dark urine due to increased urine bilirubin
-urine urobilinogen is normal or decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

viral hepatitis

A

*inflammation of liver parenchyma
*usually due to hepatitis virus; other causes include EBV and CMV
*hepatitis virus causes acute hepatitis, which may progress to chronic hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

acute hepatitis - clinical presentation

A

*jaundice (mixed conjugated & unconjugated bilirubin) with dark urine (due to CB)
*fever
*malaise
*nausea
*elevated liver enzymes (ALT > AST)
*sx last < 6 months

note - inflammation involves lobules of the liver and portal tracts and is characterized by apoptosis of hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

chronic hepatitis - clinical presentation

A

*symptoms last > 6 months
*inflammation predominantly involves portal tract
*risk of progression to cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hepatitis A (HAV) & Hepatitis E (HEV) - transmission

A

*fecal-oral transmission
-HAV is commonly acquired by travelers
-HEV is commonly acquired from contaminated water or undercooked seafood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hepatitis A (HAV) & Hepatitis E (HEV) - additional info

A

*acute hepatitis; NO chronic state
*anti-virus IgM marks active infection
*anti-virus IgG is protective (its presence indicates prior infection or immunization - HAV)
*HEV infection in pregnant women is associated with FULMINANT HEPATITIS (liver failure with massive liver necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hepatitis B (HBV) - transmission

A

*parenteral transmission (childbirth, unprotected intercourse, IV drug abuse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hepatitis B (HBV) - additional info

A

*results in acute hepatitis
*chronic disease occurs in 20% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

acute hepatitis B (HBV) labs

A

HBsAG: + (first serologic marker to rise)
HBeAG and HBV DNA: +
HBcAB: IgM
HBsAB: -

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the key marker of infection in Hep B

A

HBsAG (hep B surface antigen)

-first serologic marker to rise in acute infection
-negative in resolved infections
-positive presence > 6 months defines chronic state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

window phase of hepatitis B (HBV) labs

A

HBsAG: -
HBeAG and HBV DNA: -
HBcAB: IgM
HBsAB: -

21
Q

resolved phase of hepatitis B (HBV) labs

A

HBsAG: -
HBeAG and HBV DNA: -
HBcAB: IgG
HBsAB: IgG (protective)

22
Q

chronic phase of hepatitis B (HBV) labs

A

HBsAG: + (presence > 6 months defines chronic state)
HBeAG and HBV DNA: +/-; presence of HBeEg or HBV DNA indicates infectivity
HBcAB: IgG
HBsAB: -

23
Q

labs for someone immunized against hepatitis B (HBV)

A

HBsAG: -
HBeAG and HBV DNA: -
HBcAB: -
HBsAB: IgG (protective)

24
Q

Hepatitis C (HCV) - transmission

A

*parenteral transmission (IV drug use, unprotected intercourse, needle stick)
*risk from transfusion is almost nonexistent now, due to screening of the blood supply

25
Q

Hepatitis C (HCV) - additional info

A

*results in acute hepatitis; chronic disease occurs in most cases
*HCV-RNA test confirms infection:
-decreased RNA levels indicate recovery
-persistence indicates chronic disease

26
Q

Hepatitis D (HDV) - info

A

*dependent on HBV for infection
*SUPERINFECTION upon existing HBV is more severe than coinfection (infection with HBV & HDV at the same time)

27
Q

cirrhosis

A

*end-stage liver damage
*characterized by disruption of normal hepatic parenchyma by bands of fibrosis and regenerative nodules of hepatocytes
*fibrosis is mediated by TGF-beta from stellate cells, which lie beneath the endothelial cells that line the sinusoids

28
Q

cirrhosis - clinical features

A
  1. portal hypertension leads to:
    -ascites (fluid in the peritoneal cavity)
    -congestive splenomegaly/hepatomegaly
    -portosystemic shunts (esophageal varices, hemorrhoids, and caput medusae)
    -hepatorenal syndrome
  2. decreased detoxification leads to:
    -mental status changes, asterixis, and coma (due to increased ammonia)
    -gynecomastia, spider angiomata, and palmar erythema (due to hyperestrinism)
    -jaundice
  3. decreased protein synthesis leads to:
    -hypoalbuminema with edema
    -coagulopathy (due to decreased synthesis of clotting factors)
29
Q

alcohol-related liver disease

A

*damage to hepatic parenchyma due to consumption of alcohol
*most common cause of liver disease in the West
*3 common complications:
-fatty liver
-alcoholic hepatitis
-cirrhosis

30
Q

alcohol-related liver disease & fatty liver

A

*fatty liver is the accumulation of fat in hepatocytes
*results in a heavy, greasy liver
*resolves with abstinence from alcohol

31
Q

alcohol-related liver disease & alcoholic hepatitis

A

*chemical injury to hepatocytes
*generally seen with binge drinking
*acetylaldehyde (metabolite of alcohol) mediates damage
*characterized by swelling of hepatocytes with formation of Mallory bodies (damaged cytokeratin filaments), necrosis, and acute inflammation
*presents with PAINFUL hepatomegaly and elevated liver enzymes (AST > ALT)
*may result in death

32
Q

alcohol-related liver disease & cirrhosis

A

*cirrhosis is a complication of long-term, chronic alcohol-induced liver damage
*occurs in 10-20% of alcoholics

33
Q

non-alcoholic fatty liver disease

A

*fatty change, hepatitis, and/or cirrhosis that develops without exposure to alcohol or other known insult
*associated with obesity
*diagnosis of exclusion
*ALT > AST

34
Q

hemochromatosis - overview

A

*excess body iron leading to deposition in tissues (hemosiderosis) and organ damage (hemochromatosis)
*tissue damage is mediated by generation of FREE RADICALS

35
Q

primary hemochromatosis - etiology

A

*due to autosomal recessive defect in iron absorption
*due to mutation in HFE gene, usually C282Y mutation

note - secondary hemochromatosis is from chronic transfusions

36
Q

hemochromatosis - clinical presentation

A

*presents in late adulthood
*classic triad = cirrhosis, secondary diabetes mellitus, & bronze skin
*other findings: dilated cardiomyopathy, cardiac arrhythmias, and gonadal dysfunction (due to testicular atrophy)
*increased risk of hepatocellular carcinoma

37
Q

hemochromatosis - lab findings

A

*increased ferritin
*decreased TIBC
*increased serum iron
*increased percent saturation

38
Q

hemochromatosis - biopsy

A

*liver biopsy reveals accumulation of brown pigment in hepatocytes
*Prussian blue stain distinguishes iron (blue) from lipofuscin
*lipofuscin in a brown pigment that is a by-product from the turnover of peroxidized lipids; commonly present in hepatocytes

39
Q

hemochromatosis - treatment

A

phlebotomy (remove red cells, decreasing the iron load)

40
Q

Wilson disease - etiology

A

*autosomal recessive defect (ATP7B gene) in ATP-mediated hepatocyte copper transport
*results in lack of copper transport into bile and lack of copper incorporation into ceruloplasmin
*copper builds up in hepatocytes, leaks int serum, and deposits in tissues
*copper-mediated production of hydroxyl free radicals leads to tissue damage

41
Q

Wilson disease - clinical presentation

A

*presents in childhood with:
-cirrhosis
-neurologic manifestations (behavioral changes, dementia, chorea, and Parkinsonian sx due to deposition of copper in basal ganglia)
-Kayser-Fleisher rings in cornea
*increased risk of hepatocellular carcinoma
*labs show increased urinary copper, decreased serum ceruloplasmin, and increased copper on liver biopsy
*tx = D-penicillamine (chelates copper)

42
Q

primary biliary cholangitis

A

*autoimmune granulomatous destruction of intrahepatic bile ducts
*classically arises in women (avg age of 40)
*associated with other autoimmune diseases
*etiology unknown; ANTIMITOCHONDRIAL ANTIBODY is present
*presents with features of obstructive jaundice
*cirrhosis is a late complication
*tx with ursodeoxycholic acid

43
Q

primary sclerosing cholangitis

A

*inflammation and fibrosis of intrahepatic and extrahepatic bile ducts
*periductal fibrosis with an “onion-skin” appearance
*uninvolved regions are dilated, resulting in a “beaded” appearance on contrast imaging
*etiology unknown, but associated with ulcerative colitis; p-ANCA is often positive
*presents with obstructive jaundice (cirrhosis is a late complication)
*increased risk for cholangiocarcinoma

44
Q

Reye syndrome

A

*fulminant liver failure and encephalopathy in children with viral illness who take aspirin
*likely related to mitochondrial damage of hepatocytes
*presents with hypoglycemia, elevated liver enzymes, and nausea with vomiting
*may progress to coma & death

45
Q

hepatic adenoma

A

*benign tumor of hepatocytes
*associated with oral contraceptive use; regresses upon cessation of drug
*risk of rupture, and intraperitoneal hemorrhage, especially during pregnancy (tumors are subcapsular and grow with exposure to estrogen)

46
Q

hepatocellular carcinoma - risk factors

A

*chronic hepatitis (e.g. HBV and HCV)
*cirrhosis (alcohol, non-alcoholic fatty liver disease, etc)
*aflatoxins derived from Aspergillus (induce p53 mutations)

47
Q

hepatocellular carcinoma

A

*malignant tumor of hepatocytes
*often detected late because symptoms are masked by cirrhosis; poor prognosis
*serum tumor marker = alpha-fetoprotein

48
Q

hepatocellular carcinoma & Budd-Chiari

A

*increased risk for Budd-Chiari syndrome:
-liver infarction secondary to hepatic vein obstruction
-presents with painful hepatomegaly and ascites

49
Q

metastasis to liver

A

*more common than primary tumors
*most common sources include colon, pancreas, lung, and breast carcinomas
*results in multiple nodules in the liver
*clinically may be detected as hepatomegaly with a nodular free edge of the liver

GI Exam (54 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions