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Gastrointestinal - step > Pathology - liver > Flashcards

Pathology - liver Flashcards

1
Q

describe the histopathos in cirrhosis

A

diffuse bridging fibrosis and nodular regeneration via stella celsl that dursrupts the normal architecture of the liver.

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2
Q

what does cirrhosis increase the risk for

A

hepatocellular carcinoma

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3
Q

what cells cause the fibrosis

A

stellate cells

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4
Q

etiologies for cirrhoses

A 
OH
HepC
HepB
biliary disease
metabolic disorders
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5
Q

describe the pathophys effects of cirrhosis

A

compresses sinusoids and central bile canals

  • increased intrasinusoidal hypertension
  • decreases number of functional sinuisoids
  • increases hydrostatic pressure in the portal circulation
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6
Q

what is the result of a portosystemic shunt

A

partially alleviates portal hypertension

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7
Q

how do portosystemic shunts manifest in increased portal hypertension

A

A) esophageal varices (left gastri with esophageal)

b) caput medusa ( paraumbilica and small epigastrics)
c) anal varices (Superior rectal and middle/inferior rectals)

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8
Q

result of portal hypertension please

A 
esophageal varices - hematemesis and melena
peptic ulcer - melena
congestive splenomegaly
caput medusa
ascites
portal hypertensive gastrophaty
anorectal varices
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9
Q

effects of liver cell failure

A 
hepatic encephalopathy
scleral icterus
fetor hepaticus
spider nevi
gynecomastia
jaundice
testicular atropy
liver flapasterixis
bleeding tendency with increased PT
anaemia
dependeing pitting oedema/ankle oedema
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10
Q

how does cirrhosis show up on a CT

A

splenomegaly with also nodularity of the liver counter due to regeneration macronodules
cirrhosis: diffuse bridging fibrosis and nodular regeneration via stellate cells that disrupts liver architecture.

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11
Q

what does disruption of the urea cycle show up as in cirrhoses

A

decreased BUN and increased serum ammonium

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12
Q

what does disruption to gluconeogenesis and glycogenolysis present as in cirrhosis?

A

hypoglycemia

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13
Q

A-B balance in cirrhosis please

A

chornic respiratory alkalosis: tpxic prodcuts stimulate the respiratory centre to hyperventilated
metabolic acidosis - lactic acid build up bc cant be converted to pyruvate after the cori cycle brings lactate from other tissues

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14
Q

what happens to salt balance in cirrhosis

A

get hyponatremia due to secondary aldosteronism

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15
Q

hypoalbuminemia in cirrhosis results in

A

hypocalcemia - less carriage, no effect on free ca, just total
dependent pitting oedema

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16
Q

why do you see hypocalcemia in cirrhosis

A 
decreased Vit D 
decreased albumin (carries in blood. decrease total but no effect on free Ca...confuses my brain?)
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17
Q

list dzs where you see increased alkaline phosphatase

A 
cholestatic hepatobiliary disease
obstructive hepatobiliary disease
hepatocellular carcinoma
infiltrative disorders
bone disease
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18
Q

list diseases wher eyou see increased aminotransferase levels please

A

viral hepaitits ALT > HST

OH hepatitis AST > ALT

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19
Q

list dzs where you see increased amylase

A

actue pancreatitis

mumps

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20
Q

list dzs where you see changes in ceruloplasmin

A

decreased in Wilson disease

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21
Q

list dz where you see altered gamma-glutamyl transpeptidase

A

increased in liver and biliary disease - like AL[
NOT increased in bone disease
associated with alcohol use

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22
Q

list dzs where you see increased lipase

A

acute pancreatitis most specific marker

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23
Q

child
afebrile, quiet lethargic, sleepy
hepatomegaly
liver dysfucntion

A

reyes syndrome

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24
Q

what is reyes syndrome

A

rare
often fatal
childfood enchaphalopathy

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25
Q

discuss findins in reyes syndrome

A 
mitochondrial abnormalities
microvesicular fatty change in liver
hypoglycemia
vomiting
hematpomegaly coma
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26
Q

what is reyes syndrome associated with

A

aspirin to treat viral infection especially VZV and influenza

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27
Q

what is the MOA of reyes syndrome

A

aspirin metabolies decreased beta oxidation by reversible inhibition fo mitochondrial enzymes

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28
Q

what is except to avoidance of aspirin in children

A

Kawasaki disease

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29
Q 
fatty liver
hypoglyecemia
vomiting
hepatomegaly
coma 
child
recent VZV or influenza
A

aspirin

reyes syndrome

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30
Q

what is hepatic steatosis

A

macrovesicular fatty change that may reversible with OH cessation

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31
Q

what causes OHic hepatitis

A

sustained, ong term consumption of OH

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32
Q

describe the histopathos of OHic hepatitis

A

swollen and necrotic hepaticyes with PMN infilriation

Mallory bodies - intracytoplasmic eosinophilc inlcuisons of damaged keratin filmaets

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33
Q

labs in OHic hepatitis

A

AST> ALT usually 1/5

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34
Q

what is OHic cirrhosis

A

final and irreversible form

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35
Q

histoatphos on OHic cirrhosis

A

micronodular, irregularly shrunken lvier with ‘‘hobnail’’ apperances
sclerosis around central vein aka zone III

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36
Q

microvesicular fatty change

A

reye syndrome

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37
Q

Mallory odies

A

OHic hepatitis

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38
Q

hobnail apperance

A

OHic cirrhosis

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39
Q

macrovesicular fatty chane

A

hepatit steatosis with OH

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40
Q

swollen and necrotic hepatocytes with lymphocytic infiltration

A

OHic hepatitis

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41
Q

drugs that can cause fatty change in the liver

A

amiodarone

methotrexate

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42
Q

drugs that can cause fibrosis in the liver

A

amiodarone
methotrexate
retinoic acid

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43
Q

what is non OHic fatty liver disease associated wtih

A

metabolic syndrome/insulin resistance

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44
Q

how does metabolic syndrome/insulin resistance cause non OHic fatty liver disease

A

increased fatty infiltration of hepatocytes – cellular ballooinign and evnetal necrosis

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45
Q

what can nonOHic fatty liver disease end up as?

A

cirrhosis and HCC

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46
Q

labs in nonOHic fatty liver dsiease

A

ALT > AST

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47
Q

cellular ballonign and necrosis

A

non OHic fatty liver disease

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48
Q

swollen and necrotic hepatocytes with PMN infiltration

A

OHic hepatitis

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49
Q

how does hepatic encephalopathy come about? pathophys time

A

cirrhosis – portosystemic shunts – decreased HN3 metabolsi – neuropsychiatric dysfuction

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50
Q

describe cxpx of hepatic encephalopathy

A

spectrum: disorientation/asterixis to difficulr arousal or coma

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51
Q 
altered mental status
somnolence
disordered sleep rhythma
asterixa
coma or death
A

hepatic encephalopathy

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52
Q

treatment of hepatic encephalopathy

A

lactulose - increased NH4 generation

rifaxamin

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53
Q

what causes decreased NH3 removal

A

renal failure
diuretics – cause alkalosis (loops and thiazides) – keep NH3 as is not excreted in H buffferint to NH4, hepatic blood flow post TPIS is bypassed

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54
Q

what causes increased HN3 production and absorption

A

dietary protein
gi bleed
constipation
infection

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55
Q

what to avoid in pts with hepatic encephaolpaty

A 
dietary protein
gi bleeds
constipation
infection
renal failure
diuretics
portosystemic shunts man made.
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56
Q

what is most common primary malignant tumor in adults

A

hepatocellular carcinoma

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57
Q

what is hepatocellular carcinoma associated with

A

cirrhosis: including HepB, HepC, Oh and non OH fatty liver disease, autoimmune diseases, hemochromatisos, alpha1 antitrypsin def and wilsons and aflatoxin

58
Q

what syndrome can hepatocellular carcinoma lead to

A

budd chiari syndrome

59
Q

describe budd chiari syndrome presentation

A

congestive liver disease: hepatomegaly, varices, abdominal pain, eventual liver failure without JVD

60
Q 
jaundice
tender hepatomegaly
ascites
polycythemia
anorexia
A

renal cell carcinoma

61
Q

how does HCC spread

A

hematogensouly

62
Q

fever
pain
increased liver size
blood in ascistes fluid

A

hepatocellular carcinoma

63
Q

how to diagnosis hepatocellular carcinoma

A

increased alpha fetoprotein
u/s
contrast CT/MRI, biopsy

64
Q

what are paraneoplastic syndromes with hepatocellular carcinoma

A

EPO
PTHrP - hypercalcemia
insulin like factor - hypoglycemia

65
Q

serum markers in hepatocellular carcinoma

A

increased alpha fetoprotein
increased ALP
increased GGT
NO AMINOTRANSFERASE DIFFS

66
Q

what is the most common benign liver tumor

A

cavrernous hemangioma

67
Q

what is typical tumor in 30-50 years old lvier

A

cavernous hemangioma

benign

68
Q

histopathos of cavernous hemangioma please

A

biopsy is contraindicated due to risk of hemorrhage bc made up of a collection fo dilated blood vessels

69
Q

what liver tumors have a risk of hemorrhage

A

caveronous hemangioma and hepatic adenoma

70
Q

what is a hepatic adenoma

A

rare

benign liver tumor that can spontaneously regress or rupture - hemorrhage

71
Q

who is like to get a hepatic adenoma

A

OCP and steroid useers

von gierke glycogen disease

72
Q

hepatic tumor associated with von gierkes?

A

hepatic adenoma

73
Q

abdominal pain and shock

A

rupture of a hepatic adenoma

74
Q

what is an angiosarcoma

A

maligi tumor of epithelial origin

75
Q

rf for angiosarcoma

A

vinyl chlorid
arsenic
torium dioxide in radiocontrast

76
Q

vinyl chloride
arsenic
thorium dioxide/radiocontrast

A

angiosarcoma of liver

77
Q

what mets show up in the liver

A

git, breas, lung

78
Q

what is most common place to find mets

A

lvier
git
breast
lugn

79
Q 
hepatomegaly
varices
abdominal pain
eventual liver failure
no JVD
A

budd chiari syndrome

80
Q

what causes budd chiari cyndrome

A

thrombosis or compression of the hepatic veins with centrilobular congestion and necrosis ie congestive liver disease

81
Q

what is associated with budd chiari syndrome

A 
NO JVD REMEMBE OR ELSE RIGHT HEART FAILURE
hypercoaguable states
polycythemia vera
postpartum state
HCC
82
Q

what are these risk factors for: hypercoagbaule state, polycythemia vera, postpartum state, HCC

A

budd chiari

83
Q

gross appearance of lvier in congestive liver disease

A

nutmeg: centrilobular congestion and necrosis of liver

mottled apperance

84
Q

what is most common cause of budd chiari?

A

polycythemia veraq

85
Q

enlarged painful liver
portal hypertension
splenomegaly
ascites

A

congestive liver disease
RHF if JVD
budd chiari if not

86
Q

pathophys of alpha1 AT def

A

misfolded gene product protein aggregates in hepatocellular ER - red cytogranules

87
Q

what is inheritance pattern of alpha 1 anti trypsin def

A

codominant AD

88
Q

what is the normal allele for A1AT?

A

MM

89
Q

what is worst allele for A1AT?

A

ZZ

90
Q

how does alpha1 antitrypsin manifest?

A

at lungs - panacinar emphysema

at liver - cirrhosis

91
Q

what is the most common cause of cirrhosis in children

A

alpha1 anti trypsin deficieincy

92
Q

what causes jaundice

A

tis abnormal yellowing of skin and or sclera due to bilirubin deposition

93
Q

when does jaundice occur

A

in the face of increased production ofdefective metabolism of bilirubin – when reach levels of > 2.5 mg/dL

94
Q

what causes unconjugated/indirect hyperbilirubinemia

A

physiologic neonatal jaundice
gilbert
crigler-najjar
hemolytic anaemia

95
Q

what causes conjugated/direct hyperbilirubinemia

A

biliary tract obstruction: gall stones, cholangiocarcionma, pancreatic or liver cancer, liver fluke
bilary tract disease: primary sclerosing cholangitis, primary biliary cholangitis
excretion defects: dubin Johnson and rotor syndrome

96
Q

what are biliary tract obstructive causes that lead to conjugated/direct hyperbilirubinema

A 
gall stones
cholangiocarcionma
pancreatic cancer
lvier cancer
liver cluke (chlonoarchis sinusis)
97
Q

what are bilary tract diseases that can cause conjugated/direct hyperbilirubinema

A

primary sclerosing cholangitis

primary biliary cholangitis

98
Q

what causes mixed indirect/direct hyperbilirubinemia?

A

hepatitis

cirrhosis

99
Q

pathophys of physiologic neonatal jaundice please

A

immaute UDP glucuronosyltransferase – unconjugated hyperbilirubinemia – jaundlse and kernicterus

100
Q

what is kernicterus

A

deposition of water insoluble unconjugated bilirubin the the brain particularly at the basal ganglia

101
Q

basal ganglia deposition of liver messing up

A

Wilson - copper

kernicterus - unconjugated bilirubin

102
Q

how to treat physiologic neonatal jaundice

A

phototherapy

103
Q

asymptomatic or mild jaundice with increased unconjugated bilirubin without overt hemolysis

A

gilbert syndrome

104
Q

clincali consequences of gilbert syndrome

A

none hurrah

105
Q

pathophys of gilbert syndrome

A

mildly decreased UDP-glucuronosyltransferase conjucation
AND
impaired bilirubin uptake

106
Q

what makes bilirubin increased in gilberts

A

fasting and stress

107
Q

what is the pathophys of crigler najjar type I?

A

absent UDY-glucuronosyltransferase

108
Q

jaundice
kernicterus
increased unconjugaster bilirubin
early in life

A

crigler najjar syndrome type I

109
Q

prognosis of crigler najjar type I

A

fatal in a few years of life

110
Q

how to treat crigler najjar type Ii

A

less severe

tx with phenobarbital to increase liver enzyme synthesis

111
Q

how dose phenobarbital work

A

increase enzyme synthesis for treatment of crigler najjar type II

112
Q

grossly black liver

benign

A

dubin Johnson syndrome

113
Q

pathophsy of dubin johnson

A

defective excretion

hyperconjugated bilirubinemia

114
Q

what is roto syndrome

A

similar to dubin Johnson
hyper conjugated bilirubinemia
no black liver

115
Q

what syndrome involved impaired uptake of bilirubin

A

gilberts

NOT crigler najjar

116
Q

what is Wilson disease aka?

A

hepatolenticular degeneration

117
Q

what causes Wilson disease

A

inadequate hepatic copper excretion and failure of coppuer to enter circulation and cerloplasmin

118
Q

where do levels of coppu increased in Wilson diseas at first

A

liver

119
Q

where do levels of copper increase in Wilson disease later on

A 
after liver spews it out
blood
eyes
kidney
brain
red blood cells
joints
120
Q

type of inheritance wilsons

A

chromosome 13
AR
ATP7B

121
Q

how is copper normally dealt with in the liver?

A

excreted into bile via a hepatcoyte copper transporting ATPase that gets messed with an ATP7B mutation

122
Q

blood levels in wilsons

A

low cu at fist

low cerylplasmin

123
Q

describe effects of cu in organs

A

eyes - deposition in cornea - Kayser-Fleishcher rings
liver: cirrhosis - HCC
kidneys - fanconi syndrome
joints : dysarthria
brain: putamen - parkinsonism, subthalamic nuclei - hemiballismus and dementia
blood: hemolytic anaemia

124
Q 
asterixis
dementia
hemiballismus
parkinsonism
HCC
fanconi syndrome
hemolytic aneamia
dysarthria
KF rings
A

Wilson disease

125
Q

how do you treat Wilson disease

A

penicillamine
trientine
oral zinc - inhibits absorption in intestine

126
Q

what is hemochromatosis

A

the inherited cause of hemochromatosis - deposition of hemosiderine in tissues

127
Q

what is the classic presenting triad of hemochromatosis

A

cirrhosis
DM
skin pigmentation

128
Q

what are consequences of hemachromatosis

A

heart failure (restrictive)
testicular atrophy
increased risk of HCC

129
Q

what are causes of hemochromatosis

A

primary - AR of HFE, C282Y, H63D in HFE gene with HLA-A3

secondary - chronic transfusion therapy ie beta thalassemia major

130
Q

blood work for hemochromatosis please

A

increased ferritin
increased fe
decreased TIBC
increased transferrin saturation

131
Q

how do you id iron on a biopsy

A

Prussian blue stain

132
Q

how much body iron is enough to set off detectors at airport

A

50 g - can happen in hemochromatosis

133
Q

HLA association with hemochromatosis

A

HLA-A3

134
Q

HLA-A3

A

hemochromatosis

135
Q

why is onset of hemochromatosis slower in women than men

A

meennsseesss

136
Q

how do you treat hemochromatosis

A

phlebotomy

chelation with deferasirox, deferoxamine and deferiprone (oral)

137
Q

typical nationality with hemochromatosis

A

northern European descent

138
Q

list the organs affected in hemochromatosis

A 
liver
pancreas
heart
joints
skin
brain - pituitary
139
Q

list the organs affected in wilsons

A 
liver
eyes
joints
blood
brain - bg
kidney
140
Q

list the effects on organs by hemochromatosis

A

liver - cirrhosis - HCC
heart - restrictive cardiomyoatphy
brain - pit - infertility (decreased levels of Lh and FSH)
pancrease - DM I
skin - bronze - melanine production increased
joints - degenerative arthritis

141
Q

list organs in Wilson vrs hemochromatosis and both

A

both: liver, joints, brain,
Wilson: eyes, kidney, rbc
hemochromatosis: heart, pancreas, skin

Gastrointestinal - step (10 decks)

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