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GI 3 > Pathology > Flashcards

Pathology Flashcards

1
Q

covering of the liver

A
  • Glisson’s capsule

- thin layer of connective tissue

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2
Q

production of coagulation factor 8

A
  • endothelial lining
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3
Q

what ducts join to form the common bile duct

A
  • cystic duct and common hepatic duct
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4
Q

major site of production of RBCs in fetuses

A
  • liver
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5
Q

falciform ligament

A
  • separates right and left lobes
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6
Q

blood supply to the liver

A
  • portal vein (70-80%)

- hepatic artery (20-30%), comes from celiac artery

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7
Q

porta hepatis

A
  • exit port of the common hepatic duct

- entry port of the hepatic artery and exit port of portal vein

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8
Q

blood and bile flow

A
  • opposite directions
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9
Q

shape and function of liver lobule

A
  • hexagonal

- blood flow and synthetic function

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10
Q

shape and function of portal lobule

A
  • triangular

- bile synthesis and excretion

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11
Q

shape and function of hepatic acinus

A
  • diamond shaped

- blood flow and disease

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12
Q

zones of hepatic acinus

A
  • zone 1 is best oxygenated but first to see toxins

- zone 3 is least oxygenated and last to see toxins

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13
Q

definition of portal lobule

A
  • the area from which bile flows to one branch of the bile duct
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14
Q

function of hepatocytes

A
  • absorption
  • secretion
  • production of bile
  • storage of excess carbohydrate as glycogen
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15
Q

function of Kupffer cells

A
  • filtration of the portal blood through phagocytosis of old RBCs and bacteria
  • secrete growth factors
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16
Q

function of Ito or stellate cells

A
  • store vitamin A
  • synthesize hepatic growth factor
  • produce extracellular matrix
  • formation of fibrosis during cirrhosis
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17
Q

5 responses of the liver to injurious events

A
  • degeneration and intracellular accumulation
  • necrosis and apoptosis
  • inflammation
  • regeneration
  • fibrosis
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18
Q

centrilobular necrosis

A
  • characteristic of ischemic injury
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19
Q

midzonal and periportal necrosis

A
  • eclampsia and autoimmune hepatitis
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20
Q

councilman bodies

A
  • fragmented nuclei of apoptotic cells
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21
Q

structure of gallbladder

A
  • lacks a muscularis mucosa and submucosa
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22
Q

spiral valves of Heister

A
  • folds coalesce in the neck of the gallbladder and extend into the cystic duct
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23
Q

focal or spotty necrosis

A
  • limited to scattered cells within hepatic lobules
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24
Q

interface hepatitis

A
  • limited to the interface between the periportal parenchyma and inflamed portal tracts
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25
Q

bridging necrosis

A
  • more severe inflammatory injury involving contiguous hepatocytes
  • may span adjacent lobules in portal-to-portal, portal-to-central, or central-to-central fashion
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26
Q

submassive necrosis

A
  • involving entire lobules
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27
Q

massive necrosis

A
  • involving most of the liver parenchyma
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28
Q

regeneration

A
  • when hepatocellular necrosis occurs and connective tissue framework remains intact, almost perfect restitution of liver structure can occur
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29
Q

fibrosis

A
  • generally irreversible hepatic damage
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30
Q

apoptosis

A
  • cells condense and fragment are phagocytized by histiocytes
  • NO inflammatory reaction
  • apoptotic cells are called councilman bodies
31
Q

causes of microvesicular fat in the liver

A
  • Reyes syndrome
  • fatty liver of pregnancy
  • tetracycline or valproic acid toxicity
  • nucleoside analogues in HIV
32
Q

processes of hepatic inflammation

A
  • inflammatory cell infiltration with lymphocytes, monocytes, neutrophils, eosinophils and plasma cells
  • Kupffer cell hyperplasia
  • binucleate cells (regeneration)
  • de-glycogenation
33
Q

PE findings of cirrhosis

A
  • spider angiomata, palmar erythema, nail changes, clubbing, hypertrophic osteoarthropathy
  • Dupurtrens contracture, gynecomastia
  • testicular atrophy, ascites, hepatgomegaly, caput medusa, fetor hepaticus, asterixis
34
Q

lab studies during cirrhosis

A
  • AST higher than ALT
  • globulins increased
  • alkaline phosphatase increased
35
Q

hep A lab values

A
  • serum IgM - acute phase
  • serum IgG - immunity, persists for life
  • high serum bilirubin levels
36
Q

extrahepatic involvement of hep A

A
  • arthritis, oliguria, urticaria, vasculitis

- rare

37
Q

high viral DNA, HBsAg+, HBeAg+

A
  • highest probability to develop cirrhosis and HCC
38
Q

low viral DNA, HBsAg +, HBeAg - and Anti HE +

A
  • does not produce cirrhosis but may generate HCC
39
Q

essential cryoglobulinemia

A
  • seen with HCV

- purpura, arthralgia, and weakness

40
Q

immune complex disease associated with HBV

A
  • polyarteritis nodosa

- glomerulonephritis

41
Q

porphyria cutanea tarda

A
  • associated with HCV

- blisters usually on the hands

42
Q

macrovesicular alcoholic steatosis

A
  • presence of large fat droplets in hepatocytes
  • nuclei are in peripheral location
  • 65% of chronic heavy drinkers develop this type
  • perivenular central zone is initially involved
  • best method to demonstrate fat is osmium tetroxide
43
Q

microvesicular alcoholic steatosis (foamy steatosis)

A
  • hepatocytes have small fat droplets throughout the cytoplasm
  • nuclei are centrally located
  • no Mallory bodies are seen
  • jaundice and elevation of alkaline phosphatase are seen but no fever or leukocytosis like in alcoholic hepatitis
44
Q

alcoholic hepatitis

A
  • most useful test is GGT
  • necrosis and inflammation is in centrolobular area
  • Mallory bodies present
  • “chicken wire” fibrosis
45
Q

alcoholic siderosis

A
  • increased stainable iron

- synergy with hemochromatosis

46
Q

Aflatoxin B

A
  • mold foods

- causes jaundice, fatty liver, Reyes, HCC, and phlebitis

47
Q

Amanita phalloides

A
  • mushrooms

- centrolobular and massive necrosis

48
Q

lead poisoning

A
  • nuclear inclusions

- steatosis and hepatitis

49
Q

drug induced hepatitis

A
  • indistinguishable from viral hepatitis
  • most often causes from oral contraceptives and anabolic steroids
  • presence of non-caseating granulomas
50
Q

autoimmune hepatitis

A
  • female predominance
  • absence of viral serologic markers
  • elevated serum IgG levels
  • high serum levels of autoantibodies (ANA, SMA, LKM)
  • rosetting or piecemeal necrosis of hepatocytes
  • should have good response to steroids with or without azathioprine
51
Q

gene associated with hemochromatosis

A
  • HFE gene (C282Y, H63D)
52
Q

hemochromatosis

A
  • increased intestinal iron absorption causing excessive deposition in tissues
  • “bronze diabetes”
53
Q

screening for hemochromatosis

A
  • ferritin levels >200 in men and >150 in women
  • iron saturation >45-60
  • hepatic iron index (HII) of 1.9 consistent with disease
54
Q

treatment of hemochromatosis

A
  • phlebotomy
55
Q

presentation of alpha 1-antitrypsin deficiency

A
  • accumulated AAT appears as inclusions within hepatocytes that stain positively with PAS reagent but resist digestion by diastase
  • PAS (+), diastase (-)
56
Q

function of AAT

A
  • proteolytic enzyme of elastase
57
Q

Wilsons disease

A
  • defect of cellular copper export
  • Kayser-Fleischer ring
  • accumulation of copper in liver, brain and other tissues
58
Q

lab findings in Wilsons

A
  • decreased serum ceruloplasmin
  • elevated 24 hour urinary copper excretion
  • elevated quantitative hepatic copper
59
Q

treatment of Wilsons

A
  • copper chelators

- D-penicillamine

60
Q
  • Budd-Chiara syndrome
A
  • hypercoaguable state
  • occlusion of main hepatic veins
  • usually a sudden thrombotic accident or slow fibrous occlusion
  • dilated sinusoids will have lysed RBCs are difference with passive congestion due to heart failure
  • if occlusion is sudden and massive: sudden massive ascites, ab pain, liver failure in a few days
61
Q

Veno-occlusive disesae of small intrahepatic veins

A
  • concentric occlusion of the affected veins by loose connective tissue
62
Q

Gilberts

A
  • unconjugated hyperbilirubinemia
  • mild deficiency of glucuronyl transferase
  • does not cause problems
63
Q

Crigler Najjar, type 1

A
  • severe deficiency of glucuronyl transferase
  • death within 1-2 years with kernicterus
  • unconjugated bilirubinemina
64
Q

Crigler Najjar, type 2

A
  • moderate deficiency of glucuronyl transferase
  • normal development but may suffer bilirubin encephalopathy, kernicterus
  • unconjugated bilirubinemina
65
Q

Dubin-Johnson

A
  • no pruritis or elevation of serum alkaline phosphatase, liver is black but normal
  • chronic benign jaundice
  • conjugated hyperbilirubinemia
66
Q

Familial Recurrent Intrahepatic Cholestasis of Pregnancy

A
  • occurs during 3rd trimester
  • safe for the mother but not the fetus
  • premature births and stillbirths due to placental infarcts
  • Sometimes the disorder manifests itself only with presence of pruritus without jaundice (Pruritus gravidarum)
67
Q

pathogenesis of primary biliary cirrhosis

A
  • ongoing immunologic attack on the intralobular bile ducts that eventually leads to cirrhosis and liver failure
  • T lymphocyte mediated
  • primarily affects women
  • Antimitochondrial antibodies (AMA) are normally found
68
Q

symptoms of PBC

A
  • epithelial damage, granuloma formation

- bile duct atrophy, periductal hepatitis

69
Q

treatment for PBC

A
  • ursodeoxycholic acid
70
Q

primary sclerosing cholangitis

A
  • chronic cholestatic disease
  • can lead to end stage liver disease
  • progressive inflammation, fibrosis and stricturing of the intrahepatic and extrahepatic bile ducts
  • beaded appearance
  • ANA, SMA, P-ANCA in 75% of patients
71
Q

associations with PSC

A
  • 90% of patients also have UC

- 70% of patients are men

72
Q

treatment of PSC

A
  • ursodeoxychoic acid and liver transplant
73
Q

Klatskin tumor

A
  • Tumor arising from common bile duct between cystic duct and right and left hepatic ducts

GI 3 (12 decks)

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