Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Hepatobiliary Tract > Flashcards

Hepatobiliary Tract Flashcards

1
Q

Hepatic failure

A

80-90% function is lost
- most common cause is consequence of successive waves of injury or progressive chronic damage
Sx: jaundice, hypoalbuminemia, hyperammonemia, fetor hepaticus, hyperestrogenemia due to impaired estrogen metabolism
Complications: coagulopathy, multiple organ failure, hepatic encephalopathy which is lifethreatening disorder of CNS and neuromuscular transmission; porto-systemic shunting, loss of function, brain edema, consciousness, limb rigidity, hyperreflexia, asterixis; hepatorenal syndrome renal failure with decreased renal perfusion pressure and vasoconstriction; hepatopulmonary syndrome presenting with hypoxia caused with intrapulmonary vascular dilation

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

Acute liver failure

A

Liver illness associated with encephalopathy within 6 months of initial diagnosis
- caused by hepatic necrosis attributable to drug or toxin injury, viral hepatitis, autoimmune damage

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

Chronic liver disease

A

Most common cause of failure

- chronic hepatitis ending in cirrhosis

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

Budd-Chiari Syndrome

A

Acute thrombosis of major hepatic veins or inferior vena cava at the level of hepatic veins
Associated with: polycythemia vera, pregnancy, post-partum state, use of oral contraceptives, paroxysmal nocturnal hemoglobinuria, intra-abdominal cancers, including hepatic cancer
Sx: Acute abdominal pain (capsule can’t change fast enough with it), hepatomegaly, ascites
Path: acute and chronic passive congestion

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

Viral hepatitis causes

A

EBV, CMV and yellow fever or more commonly hep A, B, C, D, E
Morph: ground glass appearance for Hep B and C
- councilman body with acidic apoptosis acidophilic body
- damage around portal triad
- bridging necrosis with bridging fibrosis

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

Hep A virus

A

Single stranded RNA, benign self limited disease, only fulminant in pregnancy
Spread: fecal oral route
Path: antiHAV IgM in serum, IgG appears as IgM declines and persists for years

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

Hep B virus

A

Virus: circular partially double stranded DNA virus
- Dane particle with outer surface protein and lipid envelope encasing electron dense core
Disease: Subclinical nonprogressive chronic heptatitis, acute self limited hepatitis, progressive chronic disease culminating in cirrhosis, or fulminant hepatitis with massive liver necrosis, asymptomatic carrier state
Path: HBsAG appears before sx
Sx: anorexia, fever, jaundice

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

Hep C virus

A

Virus: single stranded RNA enveloped virus
Disease: cirrhosis common 20%, chronic disease in 80-85%
- carcinoma
- potentially curable

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

Hep D virus

A

Virus: defective RNA virus that can replicate and cause infection only with Hep B
- Dane like particle with HBV envelope
- delta antigen small and circular
Disease: mild to fulminant hepatitis, not chronic

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

Hep E virus

A

Spread: Fecal-oral
Virus: non-enveloped single stranded RNA virus
Disease: high rate of fulminant disease in pregnant women

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

Hep G virus

A

Nonpathogenic RNA virus

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

Hereditary hyperbilirubinemia - unconjugated hyperbilirubinemia (3)

A

Crigler-Najjar Syndrome Type I, Type II, and gilbert syndrome

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

Hereditary hyperbilirubinemia - conjugated hyperbilirubinemia (2)

A

Dubin-johnson syndrome and Rotor syndrome

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

Crigler-Najjar Type I

A

Inheritance: auto recessive
- absence of UGTIA1 causes jaundice leading to high unconjugated bilirubin
Morph: histologically normal liver
Sx: death and fatal neurologic damage without liver transplant

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

Crigler-Najjar Type II

A

Inheritance: auto dominant
- dysfunction of UGTIA1
Sx: not lethal

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

Gilbert Syndrome

A

Inheritance: auto rec
Path: 30% reduction in UGTIA1 with fluctuating unconjugated hyperbilirubinemia
- hyperbilirubinemia and jaundice may be exacerbated by infection, strenuous exercise or fasting

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

Dubin-Johnson Syndrome

A

Inheritance: auto rec
Path: defective hepatocyte secretion of bilirubin conjugates due to absent multidrug resistance protein 2 (MDR2)
- responsible for bilirubin gluronide transport
Morph: brown liver with pigment granules
Sx: jaundice but normal lifespan

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

Rotor syndrome

A

Inheritance: auto rec
Morph: defective hepatocellular bilirubin uptake or excretion
Morph: liver not pigmented
Sx: jaundice but normal lifespan

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

Hepatocellular necrosis causes

A

Mushroom poisoning, aflatoxin, phosphorus, carbon tetrachloride, chloroform, benzene, cytotoxic drugs, acetaminophen, salicylates, vit A, methyldopa, phenytoin, halothane, isoniazid
Morph: framework in place

20
Q

cholestasis

A

contraceptive and anabolic steroids; estrogen replacement therapy

21
Q

cholestatic hepatitis

A

numerous antibiotics; phenothiazines

22
Q

steatosis

A

ethanol, methotrexate, corticosteroids, total parenteral nutrition

23
Q

steatohepatitis

A

amiodarone, ethanol

24
Q

fibrosis and cirrhosis

A

methotrexate, isoniazid, enalapril

25
Q

Granulomas

A

sulfonamides, phenbutyzone, etc

26
Q

Vascular lesions

A

high dose chemotherapy, bush teas, oral contraceptives, numerous other agents, anabolic steroids, tamoxifen

27
Q

Neoplasms

A

oral contraceptives, anabolic steroids, thorotrast, vinyl chloride

28
Q

Alcoholic liver disease

A

Leading cause of liver pathology
Morph: hepatic steatosis (fatty liver): microvesicular lipid droplets within hepatocytes with moderate or chronic alcohol intake
–> chronic turns to macrovesicular lipid droplets displacing nucleus, liver enlarged, soft, greasy, yellow
–> sx: hepatomegaly
- alcoholic hepatitis: ballooning degeneration and hepatocyte necrosis with mallory body formation neutrophilic reaction
–> sx: malaise, anorexia, tender hepatomegaly
–> injury from acetaldehyde, induction of CYP450, impaired metabolism of methionine, alcohol caloric food source, alcohol mediated release of bacterial endotoxin
- alcoholic cirrhosis: irreversible, fatty and enlarged to brown, shrunken, and nonfatty
Path: women, AA

29
Q

Cirrhosis

A

Diffuse process of fibrosis and nodular regeneration with variable degree of disorganization of the lobular architecture
Cause: alcohol abuse, viral hepatitis, non-alcoholic steatohepatitis with biliary disease and hemochromatosis less frequent
Morph: bridging fibrosis linking portal tracts, parenchymal nodules, disruption of hepatic parenchymal architecture
Path: hepatocyte death, extracellular matrix deposition and vascular reorganization
- collagen in space of disse
- proliferation and activation of hepatic stellate cells
- proinflammatory cytokines, cytokines, disruption of ECM, direct toxin stimulation
Sx: anorexia, weight loss, weakness, debilitation
- progressive liver failure, portal HTN, hepatocellular CA

30
Q

Primary biliary cirrhosis

A

Strong evidence for autoimmune pathogenesis
Assoc: ulcerative colitis, systemic sclerosis, RA
Path: antibodies of anti-mito antibodies, anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (SMA)
Morph: dense portal tract inflammation with focal noncaseating granulomas with bile duct destruction and generalized cholestasis
- obstruction leads to progressive secondary upstream damage, with ductular proliferation
- at end stage, PBC is indistinguishable from other forms of cirrhosis
Sx: pruritus, hepatomegaly, jaundice, xanthomas –> progression to cirrhosis, variceal bleeding and ecephalopathy

31
Q

Primary sclerosing cholangitis

A

Chronic cholestatic disease distinguished by inflammation and obliterative fibrosis of extrahepatic and intrahepatic biliary tree
- beading of contrast material
- autoimmune
Assoc: ulcerative colitis
Morph: periductular inflammation and onion skin fibrosis with progressive atrophy
Sx: weight loss, ascites, variceal bleeding, encephalopathy
- increased incidence of chronic pancreatitis and hepatocellular carcinoma

32
Q

Extrahepatic cholestasis

A

Bile duct obstruction by stone, stricture, carcinoma
- congenital biliary atresia
- acute and chronic pancreatitis
Morph: centrilobular cholestasis, cytoplasmic and canalicular
- edema and inflammation in portal triads
- minimal hepatocellular alteration except for feathery degeneration adjacent to severe cholestasis
- dilation and proliferation of bile ducts
- bile thrombi in dilated ducts
- extravasation of bile, bile lakes, bile infarcts
- bridging portal fibrosis and cirrhosis
- suppurative cholangitis and cholangiolitis

33
Q

Portal hypertension

A

Splenomegaly with or without hypersplenism

  • development of porto-systemic venous anastamoses
  • ascites typically aggravated by hypoalbuminemia
34
Q

Wilson disease

A

Inheritance: auto rec mutations in ATP7B gene coding canalicular copper transporting ATPase; copper absorption and delivery to liver is normal, copper excretion into bile reduced
- copper accumulates in liver which results in hepatic injury through ROS generation
Morph: liver damage mild to severe, fatty change, acute and chronic hepatitis with mallory bodies, cirrhosis, and massive necrosis
- eye lesions called kayser fleischer rings involved (green-brown copper at corneal limbus)
Sx: acute and chronic liver disease before age 40
- parkinsonism
Dx: increased hepatic copper content and increased urinary excretion

35
Q

Alpha1-antitrypsin deficiency

A

Inheritance: auto rec with low levels of protease inhibitor, emphysema and hepatic disease
Path: synthesized by hepatocytes, most common genotype is PiMM, most common disease is PiZZ
- glutamate to lysine
- triggers autophagy, mito dysfunction and proinflammatory NF-kB causing damage
Morph: PAS positive cytoplasmic globules in periportal hepatocytes
- cholestasis to hepatitis to cirrhosis
Sx: jaundice, acute hepatitis or cirrhosis
- hepatocellular CA develops in PiZZ adults
- smoking worsens lung damage

36
Q

Focal nodular hyperplasia

A
  • one or more nodules
  • central stellate fibrous scar
  • scattered bile ducts
  • normal hepatocytes
  • bleeding unusual
    Age: middle aged adults
37
Q

Nodular regenerative hyperplasia

A
  • nodular transformation of liver without fibrosis
  • consequence of intrahepatic blood flow
  • occurs in transplants or vasculitis
38
Q

Cavernous hemangiomas

A

Most common benign liver tumors

- blood vessel tumor

39
Q

Hepatic adenoma

A

Benign hepatocyte neoplasms

  • common in young women associatedw tih oral contraceptives
  • beta-catenin and HNFIalpha associated
  • sheets of hepatocytes containing arteries and veins
  • portal tracts with bile ducts are absent
  • remove because could hemorrhage or be carcinomatous
  • tendency to bleed
40
Q

Hepatocellular CA

A

Most common primary liver cancer
- associated with HBV infection
Path: background of chronic liver disease
- viral, chronic alcholism, NASH and food
- less common: hemochromatosis, tyrosinemia, alpha1 antitrypsin deficiency
Morph: solitary mass, multifocal nodules, diffusely infiltrative cancer with liver enlargement in cirrhosis
- fibrolamellar CA single cirrhous hard tumor in 20-40 year olds without chronic liver disease
Sx: RUQ pain, weight loss, elevated alpha-fetoprotein

41
Q

Hepatoblastoma

A

Most common liver tumor of early childhood
Morph: activation of Wnt/beta catenin pathway
- associated with familial polyposis
- epithelial type immitates liver
- mixed has foci of mesenchymal differentiation including osteoid, cartilage, striated muscle

42
Q

Cholangiocarcinoma

A

intra and extrahepatic biliary tree
- majority perihilar
Path: most without risk antecedent
- associated with PSC, fibropoycystic lesions, HCV infection
- opisthorchis sinensis
Morph: single large mass or multifocal nodules
- pale

43
Q

Cholelithiasis

A

Substance: majority cholesterol stones, some calcium bilirubinate, some calcium carbonate
Risk: increased hepatic cholesterol uptake or synthesis
- native americans, industrialized countries, female, age, estrogen, obesity, hypercholesterolemia, rapid weight loss, GB stasis
Path: cholesterol - bile supersaturated with cholesterol
pigment - unconjugated bilirubin from hemolysis conditions
–> also with opisthorchis sinensis, E coli, ascaris lumbricoides
Morph: chole stones from GB –> hard pale and yellow
bilistones –> black color or brown
Sx: asymptomatic
- spasmodic colicky pain from passing stones in bile ducts
- infl leads to cholecystitis or cholangitis or gallstone ileus

44
Q

Strawberry GB

A

fat, fertile, forty, female, flatulent

45
Q

Cholecystitis

A

Path: chemical irritation by bile and calculi, bacterial infection, pancreatic reflux
- could be from ischemia from sepsis with hypotension
Morph: enlarged tense bright red green-black gallbladder
Age: 5th - 6th decade, female
Sx: RUQ pain, fever, anorexia, taycardia, diaphoresis, N/V

46
Q

Chronic cholecystitis

A

repeated bouts of low grade cholecystitis
- gallstones can be present
morph: fibrosis or enlarged
Sx: repated colicky epigastric or RUQ pain
Complications: bacterial superinfection, GB perforation, abscess formation or peritonitis

47
Q

CA of GB

A

Gender: women
Age: older than 70
Assoc: gallstones, chronic GB inflammation is a risk
Morph: infiltrating with GB thickening and induration or exophytic growing into lumen as irregular cauliflower like mass
- adenocarcinoma most common
Sx: same as cholelithiasis

Pathology (12 decks)

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