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Pathology > Liver > Flashcards

Liver Flashcards

1
Q

Jaundice, cholestasis
Hypoalbuminemia
Hypoglycemia
Hyperammonia (defective urea cycle function)
Palmar erythema (local vasodilation)
Spider angioma (central pulsating dilation of arteriole with small vessel radiation)
Hypogonadism (hyperestrogenemia) and gynecomastia
Gynecomastia
Weight loss
Muscle wasting

A

Severe Hepatic Dysfunction

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2
Q 
Ascites with peritonitis
Splenomegaly
Esophageal varices
Hemorrhoids
Caput medusae
A

Portal hypertension associated with Cirrhosis

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3
Q 
Coagulopathy
Hepatic encepalopathy
Hepatorenal syndrome
Portopulmonary hypertension
Hepatopulmonary syndrome
A

Complications of Hepatic failure

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4
Q 
Hepatocyte integrity
(Elevation: Liver disease)
A

AST
ALT
LDH

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5
Q

Biliary excretory function

A

Serum bilirubin (Total, Direct, Delta:linked to albumin)
Urine bilirubin
Serum bile acid
Plasma membrane (damage to bile canaliculi)
Serum alkaline phosphatase
Serum gamma glutamyl transpeptidase
Serum 5’ nucleotidase

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6
Q

Hepatocyte function

A 
Serum albumin
Prothrombin time (V,VII,X,PT,fibrinogen)
Hepatocyte metabolism: 
Serum ammonia
Aminopyrine breath test (heptic demethylation)
Galactose elimination (IV injection)
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7
Q

Most severe consequence of liver disease, end point of progressive damage
Loss of 80-90% hepatic function
Insidious piecemeal destruction, repetitive waves of parenchymal damage or sudden, massive destruction

A

Hepatic failure

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8
Q

Drugs or viral hepatitis
Clinical hepatic insuff to hepatic enceph within 2-3 weeks
MASSIVE HEPATIC NECROSIS
Liver transplant

A

Acute Liver Failure with Massive Hepatic Necrosis

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9
Q

Most common route to hepatic failure, endpoint of chronic liver damage
Parenchymal, biliary or vascular in origin
Ends in cirrhosis

A

Chronic liver disease

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10
Q

Acute liver failure extending more than 3 months

A

subacute

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11
Q

Viable hepatocyte but unable to perform metabolic function
Mitochondrial injury in Reye syndrome
Acute Fatty Liver of pregnancy
Toxin mediated injury

A

Hepatic dysfunction without overt necrosis

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12
Q

Bile two major functions

A

1 primary pathway for elimination of bilirubin, chole and xenobiotics
2 emulsification of fat in gut by bile salt and phospholipid

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13
Q

Yellow discoloration of skin and sclerae icterus occurs when system retention of bilirubin exceeds

A

2 mg/dl jaundice

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14
Q

Systemic retention of bilirubin + BILE SALTS AND CHOLESTEROL

A

Cholestasis

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15
Q

Oxidize heme to biliverdin

Biliverdin is reduced to bilirubin by

A

Heme oxygenase

Biliverdin reductase

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16
Q

Bilirubin hepatocyte uptake

A

Carrier mediated uptake at sinusoidal membrane
Cystosolic protein bindingn and delivery to ER
Conjugation with one or two molecules of glucoronic acid by bilirubin UDP GT uridine diphosphate glucuronosyl transferase
Excretion of water soluble nontoxic bilirubin glucuronides into bile (conjugated)

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17
Q

Conjugated bilirubin is deconjugated by gut bacterial B glucuronidase and degraded to

A

colorless urobilinogen

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18
Q

Physiologic jaundice or neonatal jaundice happens bec hepatic machinery for bilirubin conjugation and excretion only matures at around

A

2 weeks

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19
Q

Common 7% benign heterogenous inherited mild fluctuating unconjugated hyperbilirubinemia
Dec hepatic levels of glucorosyltransferase from mutation in encoding gene
No morbidity

A

Gilbert Syndrome

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20
Q

Autosomal recessive defect in transport protein for hepatocellular excretion of bilirubin glucuronides across canalicular membrane
Exhibit hyperbilirubinemia
Darkly pigmented liver from polymerized epinephrine metabolites
Hepatomegaly without functional problem

A

Dubin-Johnson Syndrome

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21
Q

Enzyme in bile duct and canaliculi of hepatocyte

Elevated in cholestasis

A

ALP

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22
Q

Hemolytic anemia
Resorption of blood from intestinal hemorrhage
Ineffective EPO syndrome (pernicious, thalassemia)

A

excess bilirubin production

predominantly unconjugated hyperbilirubinemia

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23
Q

drug interference with membrane carrier system

diffuse hepatocellular disease (viral, drug induced)

A

reduced hepatic uptake

predominantly unconjugated hyperbilirubinemia

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24
Q

physiologic jaundice of newborn

A

Impaired bilirubin conjugation

Predominantly unconjugated hyperbilirubinemia

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25
Q

Def of canalicular membrane transporter
Drug induced canalicular membrane dysfunction (ocp cyclosporine)
Hepatocellular damage/toxicity

A

Dec hepatocellular excretion

Predominantly conjugated hyperbilirubinemia

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26
Q

Inflammatory destruction of intrahepatic bile duct (primary sclerosing, graft-vs-host, liver transplant) gallstone, ca of pancreas

A

Impaired intra or extra-hepatic bile flow

Predominantly conjugated hyperbilirubinemia

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27
Q

Most common cause of jaundice involving accumulation of unconjugated bilirubin

A

Hemolytic anemia

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28
Q

Most common cause of jaundice involving accumulation of conjugated bilirubin

A

Hepatitis intra or extrahepatic obstruction

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29
Q 
Rigidity
Hyperreflexia
Nonspecific EEG
Seizure
ASTERIXIS (flapping tremor)
nonrhythmic rapid ext and flex movement of head and extremities esp when arms are held in extension with dorsiflexed wrist
A

Hepatic

Encephalopathy

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30
Q

Factors contributing to hepatic enceph

A

severe loss of hepatocellular function

shunting of blood from portal to systemic circulation around chronically diseased liver

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31
Q

Key pathogenesis in hepatic enceph

A

Elevation in blood ammonia
Impairing neuronal function and promoting generalized brain edema in acute

Deranged neurotrasmitter production monoaminergic, opiodergic, y-aminobutyric acid and endocannabanoid system in chronic

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32
Q

Diffuse process characterized by fibrosis and conversion of normal liver architecture to structurally abnormal nodule

A

Cirrhosis

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33
Q

Cirrhosis main characteristics

A

1 fibrous septa - delicate bands or broad scars around lobules
Long standing fibrosis is irreversible as long as vascular shunts are present, regression if cause reversed
2 parenchymal nodule - small to large, encircled by fibrous bands
Preexistent hepatocyte displaying replecative senescence at time of fibrosis
Newly formed hepatocyte capable of replication gives rise to ductular reactions at periphery of nodules
3 involvement of most of liver

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34
Q

3 processes central to pathogenesis of cirrhosis

A

Death of hepatocyte
Extracellular matrix deposition
Vascular reorganization

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35
Q

In cirrhosis this type of collagen is deposited in space of Disse instead of type IV

A

Type I & III

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36
Q

Major source of excess collagen in cirrhosis normally functioning as storage of Vitamin A
Activate and transform to myofibroblast during fibrosis due to ROS, TNF, IL1 and lymphotoxin

A

Stellate cells of perisinusoid

Ito cells in space of Disse

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37
Q

stellate cells produce that initiate fibrosis formation

A

TGF B

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38
Q

Even in late stage disease this may happen significant restoration or remodelling due to dynamic process of ECM synthesis, deposition and resorption by metalloproteases

A

cirrhotic regression

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39
Q

Vascular lesions that contribute to liver function defect

A

Loss of sinusoidal endothelial fenestration and inc basement membrane formation -> thin walled sinusoid becoming fast flowing vascular channel -> impaired protein movement
Portal vein-hepatic vein shunt
Hepatic artery-portal vein shunt

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40
Q

Dominant intrahepatic cause of portal hypertension

A

cirrhosis

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41
Q

Inc resistance to portal flow and compression of central vein by perivenular fibrosis and parenchymal nodule
Inc blood flow to portal vein from vasodilation of splanchnic circulation (hyperdynamic circulation) from inc NO from bacterial DNA
Imposed arterial pressure on normally low pressure portal veins

A

Portal hypertension

42
Q

Collection of excess fluid in peritoneal cavity at least 500 ml to be clinically detectable
Serous, 3g/dL of albumin
Serum ascites:albumin gradient >/= 1.1 g/dL
scant mesothelial cell and mono

A

Ascites

Neutrophilic -infection
RBC -cancer

Hydrothorax on right from peritoneal fluid seepage through diaphragm lymphatics

43
Q

Ascites pathogenesis

A

Inc movement of intravascular fluid into spase of Disse by sinusoidal HTN and hypoalbuminemia
Leakage of fluid from hepatic interstitium to peritoneum. Hepatic lymph flow >20l (normal 800-1000ml) which is rich in proteins and low in TAG
Renal retention of Na and water 2 to hyperaldosteronism despite total body sodium mass more than normal

44
Q

Principal sites of portosystemic shunt

A

Rectal veins
CEJ veins
Retroperitoneum and falciform ligament of liver (periumbilical and abdominal)

45
Q

Renal failure without primary abnormality of kidney in severe liver failure bec splanchnic vasodilation and systemic vasoconstriction leading to dec renal blood flow of cortex
Dec UO and inc BUN, Crea
Hyperosmolar urine devoid of protein and abn sediment (low in sodium) vs RTN
Tx: transplant, HD

A

Hepatorenal syndrome

Exclude circulatory collapse

46
Q

Pulmonary arterial HTN assoc with liver disease or portal HTN
Excessive pulmo vasocon and vaso remodelling leading to R HF

Most common clinical manifestation are

A

Portopulmonary HTN
Hepatopulmonary HTN

Dyspnea with severe arterial hypoxemia and cyanosis

47
Q

Pathognomonic of hepatopulmonary HTN

A

Platypnea (easier breathing while lying down vs sitting and standing)
Orthodeoxia (fall of arterial blood oxygen with upright posture)

48
Q

Most common cause of drug induced acute liver failure

A

Acetaminophen

49
Q

Agent that causes cholestasis in those who metabolize it slowly

A

chlorpromazine

50
Q

Fatal immune-mediates hepatitis in persons exposed to this anesthetic

A

Halothane

51
Q

Bland hepatocellular cholestasis without inflamm

OCP, anabolic steroid, ERT use

A

Cholestatic injury

52
Q

Cholestasis with lobular inflamm and necrosis bile duct destruction
Antibiotics
Phenothiazine

A

Cholestatic hepatitis

53
Q 
Spotty hepatocyte necrosis (methyldopa, phenytoin)
Submassive necrosis of zone 3 (acetaminophen, halothane)
Massive necrosis (isoniazid, phenytoin)
A

Hepatocellular necrosis

54
Q

Macrovesicular

Ethanol, methotrexate, corticosteroids, TPN

A

Steatosis

55
Q

Microvesicular
Mallory body
Amiodarone
Ethanol

A

Steatohepatitis

56
Q

Periportal
Pericellular fibrosis
Methotrexate, isoniazid, enalapril

A

Fibrosis

Cirrhosis

57
Q

Noncaseating epitheloid granuloma

Sulfonamide

A

Granulomas

58
Q

Sinusoidal obstruction
Obliteration of central vein (high dose chemo, bush tea)
Budd-Chiari (OCP)
Sinusoidal dilation (OCP, others)
Peliosis hepatis: blood filled cavities not lined by epithelial cell (Anabolic steroids, tamoxifen)

A

Vascular lesion

59
Q 
Hepatic adenoma (OCP, anabolic)
Hepatocellular CA
(Thorotrast)
Cholangiocarcinoma (Thorotrast)
Angiosarcoma (Thorotrast, vinyl chloride)
A

Neoplasm

60
Q

Nodular masses of liver separated by granulation tissue and scar
Nodularity and scarring entire or patchy involvement
Mononuclear infiltrates predominate all phases bec of T cell immunity
Ballooning degeneration, empty cell with pale cytoplasm rupturing and undergoing necrosis cytolysis (dropped out appearance) and apoptosis eosinophilic shrunk hepatocyte
If awat from portal tract and in parenchyma (lobar hepatitis)
Central-portal bridging necrosis followed by parenchymal collapse

A

Hepatitis

61
Q

Minimal or absent portal inflamm

A

Acute hepatitis

62
Q

Dense MONONUCLEAR portal infiltrate of variable prominence
Interface hepatitis
Scarring
Fibrous septa -> cirrhosis

Dx

A

Chronic hepatitis

Liver biopsy

63
Q

Distinction between acute and chronic hep is based on

A

Pattern of cell injury
Severity of inflammation

Acute hep- less inflammation and more hepatocyte death than chronic

64
Q

Hexagon centered on a central vein with portal tract at three of its apices

Regions: periportal, midzonal, centrilobular

A

Hepatic lobule

65
Q

Blood supply as reference with portal vessels at their base

on the basis of distance from blood supply, 3 zones

1 closest to blood source
2 and 3 farther

A

Hepatic acinus

66
Q

Appears before onset of symptom
Peaks in overt disease
Declines undetectable at 3-6 m

A

HBsAg

67
Q

Does not rise until acute disease is over and not detectable for few weeks to months after disappearance of
HBsAg
May persist for life conferring immunity
Basis for vaccination

A

Anti-HBs

68
Q

Appear in serum soon after HBsAg
Signify active viral replication

Persistence indicates continued viral replication infectivity and progression to chronic hepatitis

A

HBeAg
HBV-DNA
DNA polymerase

69
Q

Implies that acute infection has peaked and on the wane

A

anti-Hbe

70
Q

Detectable in serum shortly before the onset of symptoms, concurrent elevation of serum AST ALT
Replaced by IgG

A

IgM Anti-HBc

71
Q

Accumulation of HBsAg in cytoplasm

Large pale finely granular pink cytoplasm inclusions on ER

A

Ground glass hepatocyte in chronic hep B

72
Q

Fatty change from altered lipid metab
Lymphoid infiltrates in portal tract with fully formed lymphoid follicle
Bile duct injury by direct infection of cholangiocyte

A

Hepatitis C

73
Q

Pathognomonic of yellow fever

Apoptosis of hepatocyte, eosinophilic

A

Councilman bodies

74
Q

Only causes acute hepatitis

A

Hepa A

Hepa E

75
Q

Cause chronic hepatitis

A

Hepa B, C, D

76
Q

Inflammatory cells in both acute and chronic Hep

Difference in pattern of injury

A

T cell

77
Q

Most important for grading and staging of disease used to decide whether px will undergo antiviral tx

A

Liver biopsy in chronic hep

78
Q 
sSRNA
Hepatovirus, Picornavirus
Fecal oral 
Incubation: 2-6 w
Freq of chronic liver disease: Never
Lab dx: Detection of serum IgM
A

Hepatitis A

79
Q 
Partially dsDNA
Hepadnavirus
Parenteral, sexual contact, perinatal
Incubation: 4-26w
Freq of chronic liver: 10%
Dx: Detection of HBsAg or HBcAg ab
A

Hepatitis B

80
Q

ssRNA
Flaviridae
Parenteral, intranasal cocaine use is risk factor
Incubation: 2-26w
Freq of chronic liver disease: 80%
Dx: PCR assay for HCV RNA, 3rd gen ELISA for ab detection

A

Hepatitis C

81
Q

Circular defective ssRNA
Subviral particle in Deltaviridae
Parenteral
Incubation: 4-26w
Freq of chronic liver: 5% coinfec, = 70% for superinfection
Dx: Detection of IgM and IgG ab, HDV RNA serum, HDAg liver

A

Hepatitis D

82
Q 
ssRNA
Hepevirus
Fecal-oral
Incubation: 2-8 weeks
Freq of chronic liver: Never
Laboratory diagnosis: PCR assay for HEV RNA, detection of IgM and IgG
A

Hepatitis E

83
Q

Female, absent viral serology, inc IgG, high autoantibody, autoimmune disease (RA, Sjogren’s)
Early phase of severe cell injury and inflamm followed by rapid scarring (early wave of hepatocyte damage and necrosis)
Very severe hepatocyte injury with confluent necrosis
Marked inflammation with advanced scarring
Burned out cirrhosis with Little ongoing cell injury or inflamm
Mononuclear infiltrate with abundant PLASMA CELL
Responds to immunosuppresive therapy

A

Autoimmune hepatitis

84
Q

Drugs that induce autoimmune hepatitis

A

Minocycline

Nitrofurantoin

85
Q

Fatty liver disease (3)

A

Steatosis
Hepatitis
Fibrosis

86
Q

Fat accumulation begins in centrilobular area

Small to large dropleta filling and expanding cell displacing the nucleus (central vein -> hepatocyte)

A

Hepatocellular steatosis

87
Q

More pronounced with alcohol use than NAFLD

A

Steatohepatitis with ballooning, Mallory-Denk, neutrophil infiltration

88
Q

Single or scattered foci of cells undergoing swelling and necrosis
Most prominent in centrilobular region

A

Hepatocyte ballooning

89
Q

Tangled skeins of intermediate filament (ubiquinated keratin of 8 and 18)
Visible eosinophilic cytoplasmic inclusion in hepatocyte

A

Mallory-Denk body

90
Q

Neutrophilic infiltration permeating the lobule and accumulating degenerating hepatocyte
Lymph and mac un portal tract

A

Neiutrophil infiltration

91
Q

Fatty liver disease on histology may appear

Fibrosis on perisinusoids

A

chicken wire fence pattern

92
Q

Fibrosis(central vein sclerosis) then Space of disse outwards becoming chicken wire fence creating central-portal fibrous septa
Liver becomes nodular, cirrhotic
Micronodular cirrhosis
Cryptogenic cirrhosis - burned out NASH

A

Fatty liver disease

Laennec cirrhosis

93
Q

Hepatic steatosis
Alcoholic hepatits
Fibrosis and cirrhosis

A

Alcoholic fatty liver disease

94
Q

Ingestion of this amount of ethanol produce mild hepatic change (fatty liver)

Chronic intake of this amount is norderline risk factor for severe

A

80g

40-80g/day

95
Q

Metabolite of ethanol that induces lipid peroxidation and acetal-dehyde protein adduct for maturation disrupting cytoskeleton and membrane function

A

Acetaldehyde

96
Q

Generated during oxidation of ethanol by microsomal ethanol oxidizing system reacting with damage membranes and protein

A

ROS

97
Q

Major feature of alcoholic hepatitis and liver disease
TNF is main effector of injury
IL1, 6 and 8

A

Cytokine mediated inflammation

98
Q

Most susceptibe region to toxic injury

A

Centrilobular

99
Q

Major accelerator of liver disease in alcoholic

A

Concurrent Hepa C

100
Q

In patients with metabolic syndrome, the best predictor of severe fibrosis and disease progression in NAFLD are

A

Type 2 DM
Obesity

Others: HTN, Dyslipidemia

Pathology (24 decks)

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