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D&T test 7- GI > Class: Liver path > Flashcards

Class: Liver path Flashcards

1
Q

Portal triad is made up of?

A

bile duct, Portal vein, hepatic artery

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2
Q

How are lobular and acinar liver units different by what is at their center?

A

lobular: Portal vein at center
acinus: Central vein at center

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3
Q

acinus/lobule which is structural which is functional

A 
lobule = structure
acinus = functional
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4
Q

In a liver bx, what ix poorest px:

  1. focal necrosis
  2. fatty degeneration
  3. lymphocytic infiltration
  4. Bridging fibrosis
  5. Single cell necrosis
A

bridging fibrosis

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5
Q

What is the mildest form of injury in the liver?

A

Hydropic degeneration or swelling

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6
Q

WHat organelles does Hydropic degeneration affect and what is the pathogenesis of injury?

A

lack of adequate energy supply (ATP) inhibits the activity of the ATP-pump that maintains water homeostasis across the cell membrane . This leads to intracellular water retention (swelling).

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7
Q

The next step in hepatocellular injury after hydropic degeneration is due to a further inability to do what? and results in an increased level of one thing and a decrease in another?

A

inability to produce ATP–>
increased Triglycerides
decreased lipoprotein synthesis

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8
Q

WHt is the result of fatty degeneration (aka fatty metamorphosis) is a progression from one pathilogical state to another. Nme those 2 states

A 
retained lipids (from lack of lipoprotein synth) are packaged into vesicals:
early = microvesicular steatosis
later/chronic = macrovesicular steatosis
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9
Q

What are 3 etiologies of microvesicular steatosis

A

Reye’s syndrome (inborn error of ASA mtb)
Pregnancy
tetracycline

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10
Q

What are 3 etiologies of macrovesicular steatosis?

A

Alcohol
Diabets
Obesity

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11
Q

Which can be life threatening via hepatic failure, micro- or macrovesicular steatosis?

A

micro

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12
Q

WHat is the pathogenesis of steatohepatitis

A

in macrovesicular steatosis, some cells rupture and die –> inflammatory reaction = steatohepatitis

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13
Q

What are the 4 types of hepatocellular necrosis and the progession from mild to severe

A
  1. single cell necrosis
  2. Focal necrosis
  3. zonal necrosis (zones 1-3)
  4. diffuse necrosis (submassive and massive)
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14
Q

what zone of the acinus is the first to be affected by ischemia?

A

zone 3

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15
Q

what zone of the acinus is the first to be affected by viral hepatitis and ingested toxins

A

ZOne 1

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16
Q

what zone of the acinus is the first to be affected by Yellow fever

A

Zone II

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17
Q

healing by secondary intention (scar formation) occurs in the case of what two types of injury to the liver?

A

Extensive acute necrosis as well as chronic (repetitive) injury

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18
Q

healing by secondary intention (scar formation) involves activation of what cell types?

A

stellate cell, kupfer cells

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19
Q

in cirrhosis: Fibrosis is mediated by what cytokine/cell

A

Transforming Growth Factor-beta (TGF-β) acting on stellate cells

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20
Q

What is the morphological hallmark of end-stage liver disease/cirrhosis.

A

bridging fibrosis and nodular regeneration

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21
Q

How is chronic hepatits defined? as evidenced by elevated what?

A

necroinflammatory dz of liver lasting >6 months

as evidenced by high ALT (and others)

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22
Q

two ddx of cirrhotic liver? and what are they in terms of fibrosis and nodules?

A

chronic hepatic fibrosis (fibrosis wothout nodules)

partial nodular transformation (nodules without fibrosis)

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23
Q

What antigen is used to dx HBV?

A

HBVsAg

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24
Q

Presence of what 2 markers in blood indicate that you are infectious with HBV?

A

HBeAg (need an envelope to infect)

HBV DNA

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25
Q

Is HAV acute, chronic, or both

A

only acute illness- full recovery always occurs

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26
Q

What antibody marks active infx of HAV

A

Anti-virus IgM (non-specific response)

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27
Q

What antibody marks protection agaisnt or immunization against HAV

A

Anti-virus IgG

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28
Q

What Hepatitis Viruses are there vaccines fro?

A

HAV, HBV

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29
Q

HEV infection in pregant women is assc with what?

A

Extremely dangerous- fulminant hepatitis: liver failure with massive liver necrosis

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30
Q

WHat marker is used to determine infx/recovery/chronic form of HCV? (only one marker)

A

HCV-RNA: if present = infx
if declining = recovery
if persistent = chronic

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31
Q

If you don’t have this marker, then you have the chronic form of HBV? ***

A

Absent IgG Anti-HBsAB

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32
Q

**recovery from HBV is indicated by what?

A

negaqtive for HBsAg

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33
Q

What are the 3 progressions from Chronic hepatitis with HBV

A

Recovery: negative HBsAg
Healthy carrier state: +HBsAg, -HBeAg
Cirrhosis: (might lead to hepatocellular CA

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34
Q

IgG anti-HCV and IgM anti-HCV indicate what?

A

only past infx - not protective

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35
Q

WHat indicates Chronic disease in HCV

A

HCV RNA

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36
Q

HDV can only infect with what help?

A

Needs HBV surface antigen for it’s viral coat

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37
Q

What is more severe: HDV co-infection with HBV or superinfection upon existing HBV

A

superinfection upon existing HBV

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38
Q

What does each represent in terms of infx:
IgG anti-delta virus
IgM anti-delta virus

A

IgG anti-delta virus = chronic superinfx

IgM anti-delta virus = recent infx of either kind

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39
Q

What are the 2 mechanisms of drug toxicity? and how is injury mediated in each?

A 
direct = toxic metabolite of drug causes injury
indirect = toxic metabolite acts as an antigen and the immune response invokes injury
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40
Q

bile duct obstruction (cholestasis) leads to high levels of what? (2)

A

ALP, gamma-glutamyl transpeptidase

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41
Q

what disease state is a mallory body chc of?***

A

Alchoholic hepatitis

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42
Q

What is a mallory body?

A

damaged cytokeratin filaments in heptocytes

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43
Q

What are the liver enzyme derangments seen in Alchoholic hepatitis? why this?

A

AST > ALT

AST is in mitochondria and EtOH is toxic to mitochindria

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44
Q

What is EtOH metabolized into (3)

A

Acetic acid plus NADH, H+

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45
Q

EtOH metabolism results in what 3 changes

A 
hypoglycemia (via GNG prevention)
Triglyceride syntyhesis (fatty liver)
lactic acidosis
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46
Q

What are the 3 patterns of liver damage in Alcohol-related liver disease

A
  1. Fatty liver disease
  2. Alcoholic hepatitis
  3. Cirrhosis
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47
Q

Is fatty liver reversible?

A

yes

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48
Q

What mediates the damage in alcoholic hepatitis?

A

Acetaldehyde

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49
Q

What are 4 histological changes chc of alcoholic hepatitis

A
  1. Mallory bodies**
  2. swelling of hepatocytes
  3. necrosis
  4. acute inflammation (neutrophils)
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50
Q

How does alcoholic hepatitis present (2)

A
  1. painful hepatomegaly

2. AST > ALT

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51
Q

what type of change is seen in Fatty liver (aka hepatic steatosis): macro- or microvesicular

A

macrovesicualr

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52
Q

What causes primary hemochromatosis? (gene, chromo, and AA replacement)

A

HFE gene, chromo 6, C282Y = cysteine replaced by Tyrosine at AA 282

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53
Q

What causes secondary hemochromatosis (in what circumstance)

A

multiple transfusions - as in Beta-thallasemia major

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54
Q

What mediates tissue damage in Hemochromatosis

A

Iron generates free radical via Fenton reaction

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55
Q

What stain distinguishes Fe from lipofuscin (and color of Fe)

A

Prussian Blue stain = Fe is blue

56
Q

what genetic defect (gene and affected function) causes Wilson disease?

A

recessive mutation in (ATP7B gene) ATP-mediated hepatocyte copper transport

57
Q

What is the pathogenesis of Wilson’s disease

A

lack of excretion of Cu into bile–> buildup in liver, brain, cornea. Cu –> free radical generation and dmg

58
Q

How does Wilson’s disease present: age

A

as a kid or at least < 40

59
Q

How does Wilson’s disease present: 3 system/organ manifestations

A
  1. Cirrhosis
  2. Neurological manifestations (behavior, dementia, chorea)
  3. Kayser-Fleisher rings in cornea
60
Q

4 sequelae of portal HTN seen in cirrhosis

A
  1. Ascites
  2. Congestive splenomegaly
  3. poto-systemic shunts (varices, caput medusae, etc)
  4. hepatorenal syndrome (renal failure)
61
Q

What changes are seen in the hand in cirrhosis (2)

A

asterixis (tremor when extended)

palmar erythema

62
Q

What causes the coma seen in cirrhosis

A

buildup of NH3 (liver normally mtbolozes it- it is toxic to brain)

63
Q

decreased protein synthesis in cirrhosis –> what 2 things

A
  1. hypoalbuminemia –> edema

2. Coagulopathy (lack of vitamin K and others)

64
Q

Which: PT or PTT is followed in cirrhosis

A

like warfarin - PT (even though lack of vitamin K knocks out 2, 7, 9, 10

65
Q

What cuases non-alcoholic fatty liver?

A

metabolic syndrome (insulin resistnace)/obesity –> necrosis of hepatocytes

66
Q

What are the liver enzyme levels in non-alcoholic fatty liver?

A

ALT > AST

67
Q

what is the earliest sign of jaundice

A

scleral icterus

68
Q

Where does UCB come from

A
  1. RBCs are consumed by reticuloendothelial macrophages
  2. Hb is broken down into Heme and globin
  3. Heme is broken down into Fe and protoporphyrin
  4. protoporphyrin in converted into UCB
69
Q

What enzyme conjugates UCB into CB

A

uridine glucuronyl transferase

70
Q

Where does urobilinogen come from

A

intestinal bacteria convert CB into urobilinogen

71
Q

What causes jaundice

A

increased bilirubin

72
Q

what causes conjugated hyperbilirubinermia (1)

A

biliary tract obstruction

73
Q

What is increased in Dubin-Johnson and Rotor syndromes?

A

Conjugated bilirubin (in blood)

74
Q

What cuases both Dubin-Johnson and Rotor syndromes?

A

defective transport of bilirubin to the cannaliculi (thus the bile) causing CB to build up in blood

75
Q

What is the difference between Dubin-Johnson and Rotor syndromes?

A

Dubin JOhnson has a super dark liver that has no clinical significance

76
Q

What is elevated in Crigler-Najjar and Gilbert syndromes?

A

both show elevated UCB

77
Q

What is the mechanism in Crigler-Najjar and Gilbert syndromes? (one is slightly different than the other)

A

Crigler-Najjar: absent uridine glucuronyl transferase Gilbert syndrome: low uridine glucuronyl transferase activity

78
Q

How do Crigler-Najjar and Gilbert syndromes present

A

Crigler-Najjar: kernicterus and death

Gilbert syndromes: jaundice with infx/stress, otherwise not significant

79
Q

What is kernicterus

A

UCB deposition in the brain, particularly the basal ganglia–> neurological deficits and death

80
Q

What is tx for kernicterus in newborn?

A

Treatment is phototherapy

81
Q

What is the MOA of phototherapy in kernicterus tx of newborn****?

A

it does not conjugate bilirubin

it makes UCB water soluble, allowing it to be excreted in urine

82
Q

What is pathology of Primary biliary cirrhosis

A

autoimmune granulomatous destruction of bile ducts in liver

83
Q

**what serum marker is present in Primary biliary cirrhosis

A

Anti-mitochondrial Ab

84
Q

How does Primary biliary cirrhosis?

A

with features of obstructive jaundice

85
Q

Primary sclerosing cholangitis: what is it

A

onion-skin fibrosis of both intra- and extra-hepatic bile ducts

86
Q

What is the classic appearance of Primary sclerosing cholangitis on contrast imaging?

A

beaded appearance with alternating strictures and dilations of bile ducts

87
Q

**What are 2 associations of Primary sclerosing cholangitis?

A

ulcerative colitis

p-ANCA +

88
Q

what are the 2 pathological events in Reye’s syndrome

A

Fulminant liver failure and encephalopathy

89
Q

though etiology is unclear for Reye’s, what is ti likely related to?

A

mitochondrial damage of hepatocytes

90
Q

How does Reyes present? (type of liver change- micro/macro)

A

microvascualr change (the severe kind)

91
Q

What is hepatic adenoma associated with?

A

Oral contraceptive use

92
Q

What is a possible coomplication of hepatic adenoma

A

tumor may rupture –> intraperitoneal bleeding

93
Q

What 2 viruses are risk factors for hepatocellular CA

A

HBV, HCV

94
Q

what are 3 risk factors for hepatocellular CA***

A
  1. chronic hepatitis
  2. cirrhosis
  3. aflatoxins from aspergillus**
95
Q

How do aflatoxins from aspergillus cause hepatocellular CA

A

they induce p53 mutations

96
Q

what is the serum marke for hepatocellular CA

A

AFP

97
Q

what can hepatocellular CA lead to

A

Budd-Chiari syndrome

98
Q

What is Budd-Chiari syndrome

A

liver infarction dt hepatic vein obstruction

99
Q

How does Budd-Chiari syndrome preswet (2)

A

ascites, painful heptomegaly

100
Q

what is the pathology in acute pancreatitis

A

autodigestion of the pancreas by it’s own enzymes

101
Q

**What is the first enzyme activated in acute pancreatitis?

A

trypsin–> activation fo the others

102
Q

what are the 2 types of necrosis that result from acute pancreatitis

A 
liquefactive hemorrhagic necrosis (of pancreas)
fat necrosis (of peripancreatic fat)
103
Q

2 MC causes of acute pancreatitis?

A

alcohol and gallstones

104
Q

Clinical presentatin of acute pancreatitis (2)

A

epigastric pain radiating to back, elevated serum lipase (and amylase- though this comes from mouth too)

105
Q

4 complications from acute pancreatitis

A
  1. Pseudocyst formation
  2. pancreatic abscess
  3. Shock
  4. DIC/ARDS
106
Q

what are 3 cuases of chronic pancreatitis

A
  1. recurring acute pancreatitis
  2. alcohol
  3. Cystic fibrosis
107
Q

Chronic pancreatitis also shows epigastric pain radiating to back (like acute). What is different about it’s CP? (2)

A
  1. lipase and amylase are not elevated (bc most of pancreas has been destroyed)
  2. calcification is seen on imaging (“chain of lakes” pattern)
108
Q

Chronic pancreatitis may lead to what 2 conditions

A

secondary diabetes mellitus

pancreatic carcinoma

109
Q

what tumor marker is seen in pancreatic carcinoma

A

CA 19-9

110
Q

What part of the pancreas gives rise to pancreatic CA

A

ducts

111
Q

2 major risk factors for pancreatic CA

A

smoking and chronic pancreatitis

112
Q

CP of pancreatic CA (4)

A

pain radiating to back
weightloss (malabsorption)
Trousseau syndrome
Obstructive jaundice

113
Q

What is Trousseau syndrome -

A

redness and tenderness on palpation of extremeties

114
Q

What are the 2 signs of obstructive jaundice (besides the obvious yellowing)

A

pale stools

palpable gallbladder

115
Q

WHat is surigical procedure called that treats Pancreatic CA

A

Whipple procedure

116
Q

3 cuases of cholelithiasis (gall stones)**

A
  1. increased cholesterol or bilirubin
  2. decreased bile acids (aka salts)*****
  3. stasis (of glalbladder)
117
Q

2 types of gall stones and their color (which is MC)

A

MC = cholesterol - yellow

bilirubin (aka pigment stones) = black

118
Q

Which type of stone is radiolucent? opaque

A 
cholesterol = radiolucent
bilirubin = opaque
119
Q

4 risk factors for gall stones

A

Female
Forty
Fat
Fertile (pregnant)

120
Q

Why does being pregant/Fertile increase chance of gall stones? and MOA

A
  1. estrogen –> increased activity of HMG CoA reductase –> increased cholesterol synthesis
121
Q

How does Crohn’s disease increase risk of gall stones

A

damage to terminal ileum –> decreased uptake of bile salts/acids

122
Q

What is a major risk factor for increased bilirubin stones

A

chronic extravascular hemolysis

123
Q

What is biliary colic

A

waxing and waning RUQ pain

124
Q

What is the etiology of biliary colic

A

gall bladder is contracting agaisnt a stone lodged in cystic duct

125
Q

What is acute choilecystitis

A

inflammation of the gall bladder wall usually from stone at neck of GB

126
Q

what causes acute cholecystitis

A

usually dt stone at neck of GB

127
Q

How does acute cholecystitis present? (2)

A

with RUQ pain that raditates to scapula

increased ALP

128
Q

What is pathogenesis of gallstones causing a ileocecal valve obstruction (aka gallstone ileus)?

A

a fistula occurs between the GB and the GI tract which allows gallstones to travel into the intestines and lodge in the ileocecal valve

129
Q

What causes chronic cholecystitis

A

chemical irritation of GB dt longstanding cholelithiasis

130
Q

what is the chc histo finding in chronic cholecystitis*****

A

rokitansky-aschoff sinus: herniation of GB mucosa into the muscular wall

131
Q

What is a chc late complication of chronic cholecystitis?

A

porcelain gallbladder

132
Q

What is tx for porcelain gallbladder and why

A

cholecystectomy - dt high rate of carcinoma progression

133
Q

What is the cause of ascending cholangitis

A

bacterial infx of bile ducts dt stone obstruction (stops normally clearing flow of bile which allows bact to grow)

134
Q

What is the major risk factor for GB carcinoma

A

stones (especially with porcelain GB)

135
Q

What cell does GB CA arise from and what type of cancer is it

A

adenocarcinoma arising form glandular epithelium that lines the GB wall

D&T test 7- GI (14 decks)

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