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DT4 Exam 3 > Liver > Flashcards

Liver Flashcards

1
Q

blood supply liver

A

2/3 portal vein

1/3 hepatic artery

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2
Q

liver functions

A 
metabolism
synthesis
catabolism 
storage
excretion
blood reservoir
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3
Q

serum transaminases

A

present in hepatocytes
involved in amino acid metabolism
elevated in hepatic injury

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4
Q

alkaline phosphatase

A

removes PO4
borders bile canaliculi cells
also found in placenta and bone
elevated in cholestatic disorders

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5
Q

gamma glutamyl transpeptidase

A

enzyme in bile canaliculus
involved in glutathione metabolism, drug detoxification
most sensitive indicator
elevated with ALP=hepatobiliary disease

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6
Q

albumin

A

produced in liver
maintains normal oncotic pressure
decreased in liver disease-does not correlate to severity of disease

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7
Q

causes of acute hepatitis

A 
viruses
excessive alcohol consumption
acetaminophen overdose 
response to medications 
autoimmune
metabolic disorders
circulatory disorders
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8
Q

clinical manifestations acute hepatitis

A 
acute encephalopathy
coagulopathy
acute renal failure
gastrointestinal bleeding 
infection, sepsis
respiratory failure
cardiovascular collapse
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9
Q

outcomes acute hepatitis

A

resolve spontaneously
proceed to acute liver failure
develop into chronic hepatitis

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10
Q

regenerative power of liver

A

mature hepatocytes divide even in presence of confluent necrosis or chronic injury
can regenerate from 25% but need normal framework

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11
Q

acute hepatic failure

A

80-90% reduction of liver functional capacity-either diminished cell number of impaired function

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12
Q

decompensated acute hepatic failure

A

from compensated chronic disease with sudden flare of activity

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13
Q

pathology acute hepatic failure

A

acute massive hepatic necrosis
non-necrotic liver failure
chronic liver disease/cirrhosis

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14
Q

hepatic encephalopathy

A

neuropsychiatric abnormalities
altered metabolism-shunting of blood from portal to systemic circulation, bypassing liver
hyperammonemia leading to rigidity, hyperreflexia, behavioral changes

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15
Q

microvesicular steatosis

A

seen in fatty liver of pregnancy, toxic reaction to tetracycline, valproate

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16
Q

laboratory findings acute liver failure

A

elevated AST, ALT
hypoalbuminemia
hyperammonemia

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17
Q

hepatorenal syndrome

A

decreased renal perfusion in cirrhotic patients

portal HTN leading to vasodilation and renal vasoconstriction

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18
Q

hepatopulmonary syndrome

A

pulmonary vasodilation causing ventilation-perfusion mismatch
hypoxia, SOB

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19
Q

non-necrotic liver failure

A

acute fatty liver of pregnancy

Reye syndrome

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20
Q

cause of acute fatty liver of pregnancy

A

microvesicular steatosis

due to abnormal fatty acid metabolism-accumulation of toxic products from placenta and fetus in mother

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21
Q

clinical manifestations acute fatty liver of pregnancy

A

malaise, N/V, RUQ pain, jaundice, fever, pruritus

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22
Q

treatment acute fatty liver of pregnancy

A

supportive care, fluids, delivery of baby

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23
Q

Reye syndrome

A

acute metabolic encephalopathy in babies following acute viral illness and aspirin intake
abnormal fatty acid and carnitine metabolism

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24
Q

liver biopsy Reye syndrome

A

microvesicular steatosis

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25
Q

clinical manifestation Reye syndrome

A

acute encephalopathy
pernicious vomiting
evidence of dysfunctional liver

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26
Q

etiologies chronic liver disease

A 
non-alcoholic fatty liver disease
hep C, B
hereditary hemochromatosis
alcoholic liver disease 
A1AT deficiency 
Wilson disease
PBC, PSC
autoimmune hepatitis
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27
Q

appearance of cirrhosis

A

fibrosis with delicate bands or broad scars surrounding multiple adjacent regenerative lobules
portal-portal, portal-central, central-central fibrosis

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28
Q

regenerative nodules

A

<3mm micro, >3mm macro

regeneration of liver cells in canals of Hering (progenitors of parenchymal and bile duct cells)

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29
Q

role of stellate cell in cirrhosis

A

stimulated by reactive oxygen species, growth factors, TNF, IL-1
become myofibroblast like to produce smooth muscle actin and GFAP

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30
Q

pathology of cirrhosis

A

loss of functional integrity
loss of sinusoidal cell fenestrations
shunt development
high pressure vessels without solute exchange

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31
Q

clinical manifestations cirrhosis

A

liver failure

portal HTN-ascites, shunts, congestive splenomegaly, hepatic encephalopathy

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32
Q

result of impaired estrogen metabolism

A

gynecomastia, spider angiomas

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33
Q

bile

A

complex fluid of bile acids and bilirubin produced by liver

flows through biliary tract into small intestine where bile acids are reabsorbed and returned to liver and re-secreted

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34
Q

functions bile

A

emulsification and micelle formation
bicarbonate for neutralizing gastric acid
eliminate cholesterol, highly protein bound organic molecules, heavy metals, lipophilic drug metabolites
protects gut from infection

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35
Q

bile salts

A

bile acids conjugated with taurine or glycine

detergents-solubilize water-insoluble lipids cholic acid, chenodeoxycholic acid

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36
Q

bilirubin

A

breakdown product of heme from spleen

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37
Q

unconjugated bilirubin

A

water insoluble bound to albumin, toxic to cells

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38
Q

conjugated bilirubin

A

water soluble, occurs in liver, nontoxic, secreted in bile ducts

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39
Q

bilirubin in the gut

A

converted to urobilinogen
excreted as stercobilinogen
reabsorbed in gut, recirculated, metabolized in liver or excreted via kidneys in urine

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40
Q

cholestasis

A

decreased bile flow accompanied by accumulation of substances normally excreted in bile (bilirubin, bile acids, cholesterol)

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41
Q

prehepatic causes jaundice

A

hemolysis

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42
Q

hepatic causes jaundice

A

hepatitis
cirrhosis
malignancy
defect in bilirubin metabolism

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43
Q

posthepatic causes jaundice

A

gallstones
tumors, strictures
compression by tumor (pancreatic head)

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44
Q

bilirubin product in feces

A

urobilinogen

due to beta glucuronidases of bacteria in gut making pyrroles and urobilinogen

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45
Q

clinical manifestation increased bilirubin

A

jaundice

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46
Q

clinical manifestation serum bile acids

A

pruritis

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47
Q

clinical manifestation malabsorption of fats

A

steatorrhea

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48
Q

malabsorption of ADK

A

hemorrhagic, clotting disorders

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49
Q

increased serum cholesterol

A

xanthomas

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50
Q

non-hepatitis viruses causing hepatitis

A

EBV
CMV
adenvirus-neonates
yellow fever

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51
Q

most common chronic

A

hep C

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52
Q

symptoms pre-icteric

A

malaise, fatigue, anorexia, nausea, fever

2 weeks post-exposure

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53
Q

symptoms icteric phase

A

jaundice, dark color, clay colored stools, hepatomegaly

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54
Q

convalescence

A

diminishing jaundice, 6-8 weeks post-exposure

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55
Q

most infectious time with hepatitis

A

last asymptomatic days of incubation period

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56
Q

laboratory signs hepatitis

A

high levels ALT, AST
hyperbilirubinemia
viral serology

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57
Q

hepatocellular damage hepatitis

A

host adaptive immune response to viral proteins

T cells cause necroinflammatory activity and apoptosis

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58
Q

transmission hep A

A

oral-fecal route
ingested through contaminated water, food
contaminated shellfish concentrates virus, can infect if undercooked

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59
Q

serology acute infection hep A

A

IgM

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60
Q

immunity against reinfection hep A

A

IgG

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61
Q

shedding hep A

A

shedding 2-3 weeks before and 1 week after jaundice

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62
Q

transmission hep B

A

vertical-childbirth
horizontal
sex/iv in low prevalence regions

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63
Q

chronic hep B

A

small % progress to cirrhosis and/or develop HCC

age at infection predicts chronicity (younger more likely)

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64
Q

early response to hep B

A

innate immune response protects

IF gamma to clear infected cells

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65
Q

most variable portion hep C

A

E2 envelope protein

new virus strains can escape neutralizing antibodies

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66
Q

anti HCV IgG and future infection

A

does not protect due to high rate of chronicity

also mutated strain

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67
Q

incubation period HCV

A

4-26 weeks

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68
Q

laboratory HCV

A

HCV RNA in blood 1-3 weeks

elevated AST and ALT

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69
Q

treatment hep C

A

pegylated IFN alpha, ribavirin

response depends on genome (2 and 3 best response), host genome IL28B gene for IF lambda

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70
Q

superinfection

A

severe acute hepatitis

worse than coinfection

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71
Q

Hep D

A

requires B for replication

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72
Q

demographics Hep E

A

India-sporadic
pig farms in developed world
high mortality in pregnant women

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73
Q

clinical serology Hep E

A

elevated AST, ALT, IgM anti-HEV

RNA and virions in stool, serum before symptoms appear

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74
Q

histology hep B

A

ground glass appearance

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75
Q

histology hep C

A

inflamed portal tract

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76
Q

serology autoimmune hep

A

elevated AST, ALT
autoantibodies
necorinflammatory activity on biopsy

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77
Q

type 1 autoimmune hepatitis

A

middle aged and older

ANA, ASMA mostly

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78
Q

type 2 autoimmune hepatitis

A

children
anti-LKM-1 and ACL-1
LKM-1 attacks CYP2D6 on plasma membrane of cells

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79
Q

genetic predispositions hepatitis-autoimmune

A

HLA-DR3/4

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80
Q

clinical presentation autoimmune heptatitis

A

flu like symptoms, fatigue, jaundice, anorexia, hepatomegaly

concurrent autoimmune conditions-thyroiditis, arthritis, Sjogren

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81
Q

overlap syndrome

A

clinical and histologic features of both autoimmune hepatitis and primary biliary cirrhosis or primary sclerosing cholangitis
chronic disease

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82
Q

laboratory findings autoimmune hep

A

elevated AST ALT
autoantibodies
polyclonal serum Ig
liver biopsy

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83
Q

histology autoimmune hep

A

rosette formation
plasma cells
lobular inflammation

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84
Q

treatment autoimmune hep

A

need to treat early

good response to immunosuppresion

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85
Q

xenobiotics

A

therapeutic agents, environmental toxins

liver turns them into active toxin

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86
Q

attributing drug to liver damage

A

temporal association

recovery on withdrawal of suspected agent

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87
Q

direct cytotoxicity liver

A

chlorpromazine

halothane

88
Q

xenobiotics causing steatohepatitis

A

methotrexate and alcoholic beverages

89
Q

leading cause of liver disease in Western world

A

alcoholic liver disease

90
Q

hepatic steatosis

A

liver may be enlarged
micro and macrovesicular
reversible with abstinence

91
Q

pathogenesis hepatic steatosis

A

increased synthesis of lipid
abnormal lipoproteins
increased peripheral fat catabolism

92
Q

Mallory body

A

thick, ropy perineuclear eosinophilic inclusions composed of cytokeratin intermediate filaments

93
Q

neutrophilic reaction

A

infiltrate in areas of hepatic necrosis and produce free radicals

94
Q

effects of alcohol

A

steatosis

dysfunction of mitochondrial, cellular membranes, hypoxia, oxidative stress

95
Q

hepatocellular steatosis

A

shunting of normal substrates towards lipid synthesis
more reduced NADH leads to more lipogenesis
increased peripheral catabolism of fat

96
Q

labs alcoholic liver disease

A

elevated bilirubin, ALP, neutrophilia

AST>ALT

97
Q

factors dictating severity of alcoholic liver disease

A

gender-women have less AlcDH
AA more cirrhosis than white
Asian ALDH2 variant and acetaldehyde

98
Q

gross appearance alcoholic cirrhosis

A

liver is shrunken, diffusely nodular, firm

99
Q

non-alcoholic fatty liver disease

A

most common chronic liver disease in US

growing due to obesity, T2DM, and metabolic syndrome

100
Q

steatosis

A

greater than 5% fat cells in liver parenchyma

elevated liver enzymes without inflammation, cell death, or fibrosis

101
Q

steatohepatitis

A

steatosis and necroinflammatory changes of hepatitis

102
Q

clinical manifestation non-alcoholic fatty liver disease

A

fatigue, RUQ pain

103
Q

non-alcoholic fatty liver disease in individuals with insulin resistance

A

decreased adiponectin
increased TNF alpha, IL-6
promote fat cell apoptosis

104
Q

pediatric NAFLD

A

more diffuse
more portal fibrosis
mononuclear inflammatory cells in portal and lobule (neutrophils in adult)

105
Q

neonatal hyperbilirubinemia

A

unconjugated bilirubinemia

conjugation and excretion immature until 2 weeks

106
Q

treatment neonatal hyperbilirubinemia

A

phototherapy to convert water soluble isomers Z-lumirubin, E bilirubin
excreted without conjugation

107
Q

breastmilk jaundice

A

beta-glucuronidase deconjugates conjugated bilirubin

108
Q

kernicterus

A

excessive levels of UCB crosses blood brain barrier-toxic to brain

109
Q

Crigler-Najjar type 1

A

AR UDGPT deficiency
kernicterus-hypotonia, deafness, oculomotor palsy, lethargy
fatal-unless transplant

110
Q

Crigler-Najjar type 2

A

AD UGT1A1 activity (monoglucuronide only)

mild jaundice, non-fatal

111
Q

Dubin Johnson syndrome

A

AR mutated gene for MRP2 (transports glucuronate conjugated bilirubin from liver cell to canaliculi)
benign relapsing conjugated hyperbilirubinemia

112
Q

lab findings Dubin Johnson

A

normal liver transaminases and conjugated hyperbilirubinemia
non-pruritic jaundice in teens, asymptomatic
pigmented liver

113
Q

Rotor syndrome

A

AR liver not pigmented

increased urinary coproporphyrin excretion

114
Q

Gilbert syndrome

A

AR
intermittent unconjugated hyperbilirubinemia
precipitated by stress, calorie reduction, fasting, drug intake

115
Q

lab findings Gilbert syndrome

A

increase ratio urinary coproporphyrin I to III

116
Q

causes of large bile duct obstruction

A

gallstones
malignancies (biliary tree or head of pancreas)
strictures from surgery

117
Q

surgery for large bile duct obstruction

A

only works if extrahepatic

intrahepatic may develop biliary cirrhosis

118
Q

ascending cholangitis

A

subtotal/intermittent obstruction

secondary bacterial infection from gut

119
Q

suppurative cholangitis

A

bile pus fills bile ducts

sepsis dominates

120
Q

canalicular cholestasis

A

centrilobular canalicular bile plugs
Kupffer cell activation, mild portal inflammation
scant/absent hepatocyte necrosis

121
Q

forms of sepsis associated cholestasis

A

canalicular cholestasis and ductular cholestasis

122
Q

ductular cholestasis

A

worse pathology

dilated canals of Hering and bile ducts

123
Q

neonatal cholestasis

A

prolonged conjugated hyperbilirubinemia in newborn

124
Q

causes neonatal cholestasis

A

neonatal hepatitis

cholangiopathies-biliary atresia

125
Q

neonatal hepatitis

A

giant cell transformation

necrosis

126
Q

biliary atresia

A

complete/partial obstruction extrahepatic biliary tree in first 3 months

127
Q

clinical manifestations biliary atresia

A

asymptomatic

jaundice, dark urine, pale stools

128
Q

associations perinatal biliary atresia

A

viruses-rotavirus, reovirus, echovirus, CMV

129
Q

hereditary hemochromatosis

A

iron overload in tissues, organs such as liver due to AR genetic mutations

130
Q

secondary hemochromatosis

A

iron accumulates from excess iron-multiple transfusions, ineffective erythropoiesis, increased iron intake

131
Q

HFE hemochromatosis

A

decreased hepcidin leads to increased absorption

defect in regulation of intestinal absorption of dietary iron

132
Q

C282Y mutation

A

AA 282 cystine to tyrosine

133
Q

organs iron deposition

A 
liver
pancreas-interstitial fibrosis
heart-interstitial fibrosis
pituitary gland, adrenal gland, thyroid, parathyroid, joints (pseudogout)
skin
134
Q

hepatic iron index

A

iron concentration in liver biopsy measured tissue iron >1.9

135
Q

clinical manifestations hereditary hemochromatosis

A

hepatomegaly, abdominal pain
pancreas-diabetes
skin pigmentation-bronze, slate grey
cardiac dysfunction-arrhythmias, cardiomyopathy

136
Q

treatment hereditary hemochromatosis

A

regular phlebotomy

monitor serum ferritin level

137
Q

secondary iron overload disorders

A 
multiple transfusions
thalassemia
ineffective erythropoiesis (thalassemia, myelodysplasic syndrome)
chronic liver disease
cirrhosis
increased iron intake-Bantu siderosis
138
Q

Wilson disease

A

AR mutation in ATP7B gene
impaired copper excretion into bile
copper not incorporated into ceruloplasmin

139
Q

ATPase and ATP7B gene

A

copper transporting ATPase in trans-Golgi network in canalicular area of hepatocyte

140
Q

absorbed copper

A

complexed with albumin and histidine

should be excreted in bile or incorporated into ceruloplasmin

141
Q

histology Wilson disease

A

resemble viral hepatitis and fatty changes
glycogenated nuclei
copper granules
rhodamine, rubeanic stains

142
Q

brain lesions Wilson disease

A

lenticular-basal ganglia

143
Q

clinical manifestations Wilson disease

A

depression, behavioral abnormalities, liver failure, Kayser-Fleischer rings, arthritis, tubular

144
Q

A1AT deficiency

A

AR defect
serine protease inhibitor mutated ch 14
SERPINA1

145
Q

PiMM

A

most common

146
Q

PiZZ

A

10% A1AT levels

defective migration from ER to golgi

147
Q

PiMZ

A

codominant expression

148
Q

clinical manifestation PiZZ

A

neonatal hepatitis, cholestasis, fibrosis
chronic hepatitis
childhood or adult cirhosis

149
Q

PiZ polypeptide

A

glu to lys at AA 342

fold abnormally

150
Q

primary biliary cirrhosis

A

autoimmune non-suppurative inflammation and destruction of medium-sized intrahepatic bile ducts
results in chronic progressive, often fatal cholestatic liver disease

151
Q

portal stage primary biliary cirrhosis

A

portal infalmmation, bile duct damage

152
Q

peripheral stage primary biliary cirrhosis

A

ductular proliferation, periportal inflammation, fibrosis

153
Q

septal stage primary biliary cirrhosis

A

bridging fibrosis, ductopenia

154
Q

labs primary biliary cirrhosis

A

elevated ALP
GGT
AMA

155
Q

treatment primary biliary cirrhosis

A

ursodiol

156
Q

primary sclerosing cholangitis

A

chronic cholestatic disorder characterized by inflammation and fibrosis that obliterates intrahepatic and extrahepatic bile ducts up to ampulla
creates beading, common with UC

157
Q

histology primary sclerosing cholangitis

A

onion skin scar-periductal fibrosis, preserved ducts dilated due to obstruction down stream

158
Q

clinical manifestation primary sclerosing cholangitis

A

elevated alk phos

jaundice, pruritus

159
Q

primary bile acids

A

made in liver with cholesterol and AA

cholic acid and chenodeoxycholic acid

160
Q

secondary bile acids

A

made in colon from primary bile acids (bacterial metabolites)
deoxycholate, lithocholate

161
Q

risk factors cholelithiasis

A 
middle age
females
hypersecretion of cholesterol
metabolic syndrome
obesity
162
Q

estrogen role in cholelithiasis

A

increase LDL receptors
stimulate hepatic HMG CoA reductase
enhances cholesterol uptake, synthesis

163
Q

hereditary cholelithiasis

A

ABC transporters have associations with gallstone formation

164
Q

cholesterol stones

A

ca carbonate, phosphates
radiolucent
more common in NA

165
Q

formation cholesterol stones

A

cholesterol becomes water soluble by aggregation with water-soluble bile salts
supersaturated, nucleates into solid monohydrate crystals

166
Q

pigment stones

A

beta glucuronidases hydrolyze bilirubin glucuronides

167
Q

complications of gallstones

A 
empyema
perforation
gallstone ileus
fistula formation
obstructive cholestasis 
cholangitis 
pancreatitis
168
Q

acute cholecystitis

A

90% caused by stone obstructing neck

most important complication of gallstones

169
Q

appearance acute cholecystitis

A

serosa with fibrinous exudate

170
Q

clinical manifestations acute cholecystitis

A

RUQ epigastric pain
fever, nausea, tachy, sweating, N/V
if jaundice-common bile duct is obstructed

171
Q

lab findings acute cholecystitis

A

leukocytosis

mildly elevated ALP

172
Q

acute calculous cholecystits

A

surgical emergency if sudden

173
Q

histology chronic cholecystitis

A

subserosal fibrosis
gray-white wall
lumen with green-yellow mucoid bile

174
Q

clinical chronic cholecystitis

A

N/V, intolerance for fatty foods

175
Q

complications cholecystitis

A

bacterial superinfection
gallbladder perforation
gallbladder rupture

176
Q

porcelain gallbladder

A

due to dystrophic calcifications

associated with increased risk for cancer

177
Q

Caroli disease

A 
chronic recurrent fever, pain, jaundice
cholangitis
elevated ESR
dilated bile duct 
risk of cholangiocarcinoma
178
Q

Alagille syndrome

A

paucity of interlobualr bile ducts
mutations in JAGI
leads to deficient bile flow, malabsorption, growth retardation, osteoporosis, neuro deficits

179
Q

laboratory findings Alagille syndrome

A

conjugated hyperbilirubinemia
GGT, ALP elevation
hyperlipidemia

180
Q

pathology alagille syndrome

A 
peripheral stenosis pulmonary artery
hypoplastic pulmonary tree
vertebral arch defects
posterior embryotoxon
hypertelic facies
181
Q

right sided decompensation

A

passive congestion of liver, congestion of centrilobar sinusoids
atrophic liver cell plates

182
Q

left sided decompensation

A

centrilobular necrosis

ischemic coagulative necrosis

183
Q

systemic circulatory decompensation

A

centrilobular necrosis
ischemic coagulative necrosis
central vein red, surrounding parenchyma tan/brown

184
Q

peliosis hepatitis

A

blood filled cysts with incomplete endothelial lining

185
Q

etiology peliosis hepatitis

A

tamoxifen, corticosteroids, methotrexate, thorotrast, AIDS, bartonella, hairy cell leukemia

186
Q

Budd-Chiari syndrome

A

thrombosis of two or more major hepatic veins or IVC

results in increased intrahepatic blood pressure

187
Q

causes Budd-Chiari syndrome

A

myeloproliferative disorders
deficiencies antithrombin, S,C, V
antiphospholipid syndrome, malignancies (HCC)
pregnancy, OCP

188
Q

sinusoidal obstruction syndrome

A

fibrotic occlusion of small hepatic veins with secondary hepatic congestion
endothelial cell injury, destruction

189
Q

etiology sinusoidal obstruction syndrome

A

herbal teas, pyrrolizidine alkaloids, chemo agents, bone marrow transplant

190
Q

focal nodular hyperplasia

A

20-40 yo women
OC cause tumor to enlarge
no malignant potential

191
Q

nodular regenerative hyperplasia

A

transformation of entire liver into multiple nodules without fibrous septa between nodules
due to heterogenous microcirculation-obliteration of small portal veins and arterialization

192
Q

clinical manifestations nodular regenerative hyperplasia

A

RA, SLE, sclerosis, PAN, polycythemia vera, chronic granulomatous disease, cystinosis, mastocytosis, amyloidosis

193
Q

lab findings nodular regenerative hyperplasia

A

mildly elevated ALP, GGT

194
Q

hepatocellular adenoma

A

benign tumor of hepatocytes
young women of reproductive age OCP and men on androgen therapy
can rupture during pregnancy or change into carcinomas (especially in glycogen stroage disease)

195
Q

cavernous hemangioma

A

most common

discrete subcapsular red-blue soft nodules less than 2 cm

196
Q

complications cavernous hemangioma

A

Kasabach-Merritt syndrome

197
Q

Kasabach-Merritt syndrome

A

MAHA with consumption coagulopathy

erythrocytosis (EPO secretion)

198
Q

liver met adult

A

colon, breast, lung, pancreas

199
Q

liver met children

A

neuroblastoma, Wilms, rhabdomyosarcoma

200
Q

hepatocellular carcinoma

A

malignant tumor of liver from hepatocytes

201
Q

risk factors hepatocellular

A

NASH, hemochormatosis, aflatoxin

202
Q

laboratory findings hepatocellular carcinoma

A

increase AFP

203
Q

biopsy hepatocellular carcinoma

A

paler than surroudning parenchyma

propensity for vascular invasion-intrahepatic mets

204
Q

fibrolamellar HCC

A

young
better prognosis than HCC
large eosinophilic cells

205
Q

cholangiocarcinoma

A

arises from ducts within and outside liver

206
Q

risk factors cholangiocarcinoma

A

PSC, gallstones, liver fluke, thorotrast, choledochal cysts

207
Q

Klatskin tumor

A

hilar location choloangiocarcinoma causes symptoms of biliary obstruction

208
Q

lab cholangiocarcinoma

A

elevated 19.9 (no specific)

209
Q

histology liver angiosarcoma

A

pleomorphic spindle and epithelioid cell with bizarre multinucleated cells

210
Q

liver hepatoblastoma

A

malignant pediatric tumor
epithelial-best prognosis
associated with Beckwith-Wiedemann syndrome, FAP

211
Q

lab findings preeclampsia and eclampsia

A

elevated aminotransferases, ALP, bilirubin

212
Q

pathology pre-eclampsia and eclampsia

A

hematoma may dissect under Glisson’s capsule and rupture

biopsy-periportal sinusoidal deposits fibrin, coagulative hepatocyte necrosis

213
Q

treatment seizures

A

MgSO4

214
Q

HELLP syndrome

A

hemolysis, elevated liver enzymes, low platelets

215
Q

acute fatty liver of pregnancy

A

defects in mitochondrial fatty acid beta-oxidation

216
Q

intrahepatic cholestasis of pregnancy

A

pruritus, jaundice, darkening urine, lightening stool

bile salts increased-cause of pruritus

217
Q

genetics cholestasis of pregnancy

A

mutations in phospholipid translocator B4

DT4 Exam 3 (5 decks)

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