Pathology Flashcards

1
Q

covering of the liver

A
  • Glisson’s capsule

- thin layer of connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

production of coagulation factor 8

A
  • endothelial lining
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what ducts join to form the common bile duct

A
  • cystic duct and common hepatic duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

major site of production of RBCs in fetuses

A
  • liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

falciform ligament

A
  • separates right and left lobes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

blood supply to the liver

A
  • portal vein (70-80%)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

porta hepatis

A
  • exit port of the common hepatic duct

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

blood and bile flow

A
  • opposite directions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

shape and function of liver lobule

A
  • hexagonal

- blood flow and synthetic function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

shape and function of portal lobule

A
  • triangular

- bile synthesis and excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

shape and function of hepatic acinus

A
  • diamond shaped

- blood flow and disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

definition of portal lobule

A
  • the area from which bile flows to one branch of the bile duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

function of hepatocytes

A
  • absorption
  • secretion
  • production of bile
  • storage of excess carbohydrate as glycogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

function of Kupffer cells

A
  • filtration of the portal blood through phagocytosis of old RBCs and bacteria
  • secrete growth factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

function of Ito or stellate cells

A
  • store vitamin A
  • synthesize hepatic growth factor
  • produce extracellular matrix
  • formation of fibrosis during cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

5 responses of the liver to injurious events

A
  • degeneration and intracellular accumulation
  • necrosis and apoptosis
  • inflammation
  • regeneration
  • fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

centrilobular necrosis

A
  • characteristic of ischemic injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

midzonal and periportal necrosis

A
  • eclampsia and autoimmune hepatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

councilman bodies

A
  • fragmented nuclei of apoptotic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

structure of gallbladder

A
  • lacks a muscularis mucosa and submucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

spiral valves of Heister

A
  • folds coalesce in the neck of the gallbladder and extend into the cystic duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

focal or spotty necrosis

A
  • limited to scattered cells within hepatic lobules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

interface hepatitis

A
  • limited to the interface between the periportal parenchyma and inflamed portal tracts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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