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Pathology > Liver > Flashcards

Liver Flashcards

1
Q

size of normal adult liver

A

1400 - 1600 grams

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2
Q

what runs through the liver (4)

A
  1. hectic vein
  2. hepatic artery (30-40%) oxygen
  3. port vein (60-70%)
  4. common bile duct
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3
Q

what does the port vein bring in

A

Heptic blood flow with nutrients and toxins form GI

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4
Q

lobules are organized around ____ of _____ vein

A

terminal tributaries, hectic vein

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5
Q

what are zones

A

gradients of oxygenation and metabolic activity. 1 closest 3 farthest

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6
Q

sinusoids

A

spaces between plates that led blood flow through

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7
Q

endothelial cells

A

line sinusoids and are fenestrated (perforated)

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8
Q

hepatocytes

A

main liver cell, acquire location specific function

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9
Q

stellate cells

A

contain fat help with regeneration

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10
Q

monocytes and neutrophils dendrites

A

not very abundant only seen when inflammation present

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11
Q

Kupffer cells

A

Phagocytic cells

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11
Q

lobule always has three holes which are

A

port vein, bile ducts, hectic artery

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12
Q

how quickly will liver restore if two thirds is removed

A

8-15 days

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13
Q

what happens immediately after liver is cut

A

hepatocyte proliferation due to change and hemodynamics and hypoglycaemia

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14
Q

what happens within minutes of liver being cut

A

change in gene expresión for proliferation of hepatocytes then other cells

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15
Q

3 stimulation pathways of hepatectomy

A
  1. LPS increase release cytokines (IL 6 TNFa)
  2. factors from other organs (overcome checkpoint)
  3. stellate cell release HGF
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16
Q

martix metalloproteases

A

the process of ECM remodelling when the liver regenerates

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17
Q

how does the liver know to stop regenerating

A

Stellate cells release TGFB shut down growth factors

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18
Q

purpose of steam cell in the liver

A

does not depend on on steam cells used only to replace damaged cells

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19
Q

where are liver steam cells located

A

by the bole ducts

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20
Q

steatosis

A

accumulation of fat

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21
Q

when doe hepatocyte necrosis occurs

A

lack of oxygen and oxidative stress

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22
Q

when doe hepatocyte apoptosis occurs

A

acute and chronic hepatitis

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23
Q

____ is the main cell involved in scare deposition

A

Hepatic stellate cell

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24
Q

how do activated stellate cells deposit scars

A

covered into myofibroblasts to produce cytokines and growth factors eventually collagen

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25
Q

ways to stimulate stellate in scar formation

A
  1. chronic inflammation
  2. cytokine and chemokine production
  3. disruption of EMC
  4. direct stimulation through toxins
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26
Q

metalloproteinases MMP

A

break down scar formation

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27
Q

nonalcoholic fatty liver disease

A

accumulation of fat in absence of alcohol intake most commonly due to metabolic syndrome

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28
Q

metabolic syndrom

A

linked to visceral obesity
insulin resistance
dyslipidemia (lipid screwed up)
hypertension

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29
Q

two hit model of NAFLD

A
  1. insulin resistance –> steatosis
  2. hepatocellular oxidative injury resulting in necrosis and inflammation
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30
Q

3 major pathways of NAFLD

A
  1. insulin resistance and adipose tissue
  2. diet, gut permeability and gut liver axis
  3. hectic lipotoxicity hepatocyte injustice inflammation
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31
Q

fasting state

A

Glucogensis: produce hepatic glucose to maintain blood sugar

32
Q

fed state

A

glycolysis break down of sugar

33
Q

Insulin

A

inhibitor of hepatic glucose production and activator of glycolysis

34
Q

what happens when fat laden myoctyes become resistant to insulin

A

do not take up glucose causing high blood glucose and high circulating insulin which increases lipogenesis/

35
Q

role of adipose tissue

A

store triglycerides (fat)

36
Q

what does increase free fatty acid do in the liver

A

development of hepatic steatosis and inflammation

37
Q

insulin resistance and obesity cause _____ which causes _____ leading to cell necrosis and _______

A

hepatic steatosis, inflammation, regressive fibrosis

38
Q

how does improper diet lead to NAFLD (gut liver axis)

A

changer microbiota, alters permeability and increases endotoxin levels which leads to TLRs and inflammation in liver

39
Q

NALFD morphology

A

steatosis (big white droplets)
chicken wire collagen deposits
inflammation

40
Q

when does NALFD become irreversible

A

between NASH and Cirrhosis

41
Q

Alcoholic liver disease

A

excessive amount of ethanol

42
Q

how does ethanol metabolism effect the liver (3)

A

1.Create ROS,
2. decrease NAD (accumilation of fat) and create
3. acetaldehyde ( alters protein function)

43
Q

how does exc sessile NADH generation cause steatosis

A

inability to maintain redox homeostasis, alters kerb cycle and fattyacid oxidation

44
Q

alcohol causes the reals of endotoxin LPS which

A

stimulates inflammation in the liver

45
Q

all changes in ALD begin in zone ___ and go outward

A

3

46
Q

fatty liver is ____ if abstention from alcohol

A

reversible

47
Q

mallory denk bodige

A

tangled knots of intermediate filaments (keratin)

48
Q

only different betters ALD and NAFLD morphologically .

A

mallory denk bodige

49
Q

Alcoholic steatofiborsis

A

activation in sinusoidal stellate cells chicken wire fencing of scar tissue

50
Q

alcoholic cirrhosis

A

not reversible small nodules entrapped in fibrosis tissue. fatty accumulation

51
Q

hepatic tumors classification

A

benign (hepatocellular adenoma and hemangioma) or malignant (hepatoblastoma and hepatocellular carcinoma)

52
Q

how does hepatocellular adenoma develop

A

from hepatocytes

53
Q

monoclonal tumors

A

occurs from a single cell

54
Q

what cancer is associated with oral contraceptives or androgen containing steroid anabolic drugs

A

Hepatocellular adenoma

55
Q

Hepatocellular adenoma morphology

A

solitary symptomatic mass, hypervascularity

56
Q

why are lover tutors prone to hemorrhage

A

lack a true capsule

57
Q

treatment of Hepatocellular adenoma

A

regress in size after discontinuation of inciting factors

58
Q

Hepatocellular adenoma three subtypes

A
  1. HNF1a inactivated
  2. b Catenin activated
  3. inflammatory
59
Q

HNF1a inactivated Hepatocellular adenoma mechanism

A

inactivation repress glucogensis activation of glycologysisi.

60
Q

Beta Catenin

A

dual function protein that regulates cell adhesion and gene transcription

60
Q

HNF1

A

transcription factor regulated glucose and fatty acid metabolism.

61
Q

b Catenin activated Hepatocellular adenoma mechanism

A

impart phosphorylation and degradation causes over expression of rage genes

62
Q

b Catenin activated Hepatocellular adenoma staining

A

IHC GS (glutamine synthetase)

63
Q

HNF1a inactivated Hepatocellular adenoma staining

A

IHC; LFABP liver fatty acid binding protein

64
Q

inflammatory Hepatocellular adenoma mechanism

A

associated with NAFLD. mutation in gp130 promote tutor infiltration by lymphocytes

65
Q

gp130

A

co receptor for IL6 (cytokines and chemokine)

66
Q

inflammatory Hepatocellular adenoma staining

A

IHC of CRP (C creative protein) due to activation of JAK/STAT

67
Q

main risks of Hepatocellular adenoma

A

hemorrhage and malignant transformation

68
Q

hepatoblatoma time line

A

most common in early childhood. older you are worse prognosis

69
Q

hematoblast

A

what hepatoblastoma is composed of

70
Q

Two anatomical variants of

A
  1. epithelial type
  2. mixed epithelial and mesenchymal
71
Q

activation of Wnt/B-catenin singalong

A

characteristic feature of hepatoblatoma (key in zoning

72
Q

hepatoblastoma main clinical significane

A

untreated will be fatal, treatment of surgery and chemotherapy

73
Q

most common liver cancer

A

Hepatocellular carcinoma (HCC)

74
Q

underlying factors of Hepatocellular carcinoma (HCC) (2)

A
  1. viral infection (HBV HCV),
  2. toxic injury ( alcohol)
75
Q

Hepatocellular carcinoma gross morphology (3)

A
  1. unifocal (large mass)
  2. multifocal (distributed)
  3. diffusely infiltrative cancer
76
Q

most common Hepatocellular carcinoma (3)

A
  1. TERT promotor (telomerase)
  2. TP53 (accumulate mutation)
  3. B catenin (stimulates)
77
Q

main clinical significance

A
  1. starts as big mrs before metastasizes
  2. bigger tumor worse outcome
  3. small tumors have good outcomes
  4. liver transplant in some cases

Pathology (14 decks)

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