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Flashcards in Pathology Deck (73):
1

covering of the liver

- Glisson's capsule
- thin layer of connective tissue

2

production of coagulation factor 8

- endothelial lining

3

what ducts join to form the common bile duct

- cystic duct and common hepatic duct

4

major site of production of RBCs in fetuses

- liver

5

falciform ligament

- separates right and left lobes

6

blood supply to the liver

- portal vein (70-80%)
- hepatic artery (20-30%), comes from celiac artery

7

porta hepatis

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

8

blood and bile flow

- opposite directions

9

shape and function of liver lobule

- hexagonal
- blood flow and synthetic function

10

shape and function of portal lobule

- triangular
- bile synthesis and excretion

11

shape and function of hepatic acinus

- diamond shaped
- blood flow and disease

12

zones of hepatic acinus

- zone 1 is best oxygenated but first to see toxins
- zone 3 is least oxygenated and last to see toxins

13

definition of portal lobule

- the area from which bile flows to one branch of the bile duct

14

function of hepatocytes

- absorption
- secretion
- production of bile
- storage of excess carbohydrate as glycogen

15

function of Kupffer cells

- filtration of the portal blood through phagocytosis of old RBCs and bacteria
- secrete growth factors

16

function of Ito or stellate cells

- store vitamin A
- synthesize hepatic growth factor
- produce extracellular matrix
- formation of fibrosis during cirrhosis

17

5 responses of the liver to injurious events

- degeneration and intracellular accumulation
- necrosis and apoptosis
- inflammation
- regeneration
- fibrosis

18

centrilobular necrosis

- characteristic of ischemic injury

19

midzonal and periportal necrosis

- eclampsia and autoimmune hepatitis

20

councilman bodies

- fragmented nuclei of apoptotic cells

21

structure of gallbladder

- lacks a muscularis mucosa and submucosa

22

spiral valves of Heister

- folds coalesce in the neck of the gallbladder and extend into the cystic duct

23

focal or spotty necrosis

- limited to scattered cells within hepatic lobules

24

interface hepatitis

- limited to the interface between the periportal parenchyma and inflamed portal tracts

25

bridging necrosis

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

26

submassive necrosis

- involving entire lobules

27

massive necrosis

- involving most of the liver parenchyma

28

regeneration

- when hepatocellular necrosis occurs and connective tissue framework remains intact, almost perfect restitution of liver structure can occur

29

fibrosis

- generally irreversible hepatic damage

30

apoptosis

- cells condense and fragment are phagocytized by histiocytes
- NO inflammatory reaction
- apoptotic cells are called councilman bodies

31

causes of microvesicular fat in the liver

- Reyes syndrome
- fatty liver of pregnancy
- tetracycline or valproic acid toxicity
- nucleoside analogues in HIV

32

processes of hepatic inflammation

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

33

PE findings of cirrhosis

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

34

lab studies during cirrhosis

- AST higher than ALT
- globulins increased
- alkaline phosphatase increased

35

hep A lab values

- serum IgM - acute phase
- serum IgG - immunity, persists for life
- high serum bilirubin levels

36

extrahepatic involvement of hep A

- arthritis, oliguria, urticaria, vasculitis

- rare

37

high viral DNA, HBsAg+, HBeAg+

- highest probability to develop cirrhosis and HCC

38

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

- does not produce cirrhosis but may generate HCC

39

essential cryoglobulinemia

- seen with HCV
- purpura, arthralgia, and weakness

40

immune complex disease associated with HBV

- polyarteritis nodosa
- glomerulonephritis

41

porphyria cutanea tarda

- associated with HCV
- blisters usually on the hands

42

macrovesicular alcoholic steatosis

- 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

microvesicular alcoholic steatosis (foamy steatosis)

- 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

alcoholic hepatitis

- most useful test is GGT
- necrosis and inflammation is in centrolobular area
- Mallory bodies present
- "chicken wire" fibrosis

45

alcoholic siderosis

- increased stainable iron
- synergy with hemochromatosis

46

Aflatoxin B

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

47

Amanita phalloides

- mushrooms
- centrolobular and massive necrosis

48

lead poisoning

- nuclear inclusions
- steatosis and hepatitis

49

drug induced hepatitis

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

50

autoimmune hepatitis

- 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

gene associated with hemochromatosis

- HFE gene (C282Y, H63D)

52

hemochromatosis

- increased intestinal iron absorption causing excessive deposition in tissues
- "bronze diabetes"

53

screening for hemochromatosis

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

54

treatment of hemochromatosis

- phlebotomy

55

presentation of alpha 1-antitrypsin deficiency

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

56

function of AAT

- proteolytic enzyme of elastase

57

Wilsons disease

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

58

lab findings in Wilsons

- decreased serum ceruloplasmin
- elevated 24 hour urinary copper excretion
- elevated quantitative hepatic copper

59

treatment of Wilsons

- copper chelators
- D-penicillamine

60

- Budd-Chiara syndrome

- 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

Veno-occlusive disesae of small intrahepatic veins

- concentric occlusion of the affected veins by loose connective tissue

62

Gilberts

- unconjugated hyperbilirubinemia
- mild deficiency of glucuronyl transferase
- does not cause problems

63

Crigler Najjar, type 1

- severe deficiency of glucuronyl transferase
- death within 1-2 years with kernicterus
- unconjugated bilirubinemina

64

Crigler Najjar, type 2

- moderate deficiency of glucuronyl transferase
- normal development but may suffer bilirubin encephalopathy, kernicterus
- unconjugated bilirubinemina

65

Dubin-Johnson

- no pruritis or elevation of serum alkaline phosphatase, liver is black but normal
- chronic benign jaundice
- conjugated hyperbilirubinemia

66

Familial Recurrent Intrahepatic Cholestasis of Pregnancy

- 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

pathogenesis of primary biliary cirrhosis

- 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

symptoms of PBC

- epithelial damage, granuloma formation
- bile duct atrophy, periductal hepatitis

69

treatment for PBC

- ursodeoxycholic acid

70

primary sclerosing cholangitis

- 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

associations with PSC

- 90% of patients also have UC
- 70% of patients are men

72

treatment of PSC

- ursodeoxychoic acid and liver transplant

73

Klatskin tumor

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