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22 fall: path > Test 2: 12 liver 1 > Flashcards

Test 2: 12 liver 1 Flashcards

1
Q

liver gets blood from

A

Portal Circulation

hepatic artery

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2
Q

red?

A

centriloblar lobule- zone 3
midzonal lobule- zone 2
periportal lobule- zone 1

blood flows from portal triad to the central vein

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3
Q

portal triad includes

A

portal venule
hepatic arteriole
bile ductule

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4
Q
A

kupffer cells (macrophages of liver)

stellate cells

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5
Q

leakage enzymes such as — live — in the hepatocytes

A

ALT- Alanine Aminotransferase
AST- Aspartate Aminotransferase
SDH- Sorbitol Dehydrogenase

cytoplasm

if there is damage to hepatocyte, you will find these in the blood

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6
Q

induced enzymes such as — are found where in the hepatocyte

A

Alkaline Phosphatase- ALP
Gammaglutamyl Transpeptide –GGT

membrane bound- seen with increased stress on hepatocyte- increased metabolic activity

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7
Q

Macrophages within sinusoids/space of Disse

A

kupffer cells

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8
Q

kupffer cells eat —

A

RBC and bacteria, immune complex and endotoxins

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9
Q

kupffer cells will accumulate —

A

iron, ceroid /lipofuscin/lipid

from eating RBC, bacteria and old cells

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10
Q

Stellate cells are involved in — metabolism

A

vit A

found in space of Disse

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11
Q

stellate cells are also called

A

Ito cells or hepatic lipocytes

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12
Q

stellate cells may transform to —

A

myofibroblasts and contribute to
fibrosis, along with other fibroblasts

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13
Q

what proteins does the liver make

A

Albumin
Fibrinogen
Clotting factors
Globulin

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14
Q

primary Photosensitization
is caused by

A

Liver incapable of excreting photodynamic compound

Ingestion of St. John’s wort (Hypericum perforatum)

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15
Q

secondary photosensitization (hepatogenous) is caused by

A

damage to liver

eat food with cholestasis, can’t break down Phylloerythrin (catabolite of chlorophyll) or other
photodynamic compounds

these accumulate in the skin and cause severe sun burn

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16
Q

type 2 Photosensitization

A

congenital porphyria

hereditary defect in heme metabolism

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17
Q

hemoglobin break down

A

kupffer cells with eat iron

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18
Q

bilirubin metabolism

A

RBC breaksdown in spleen, gets attached to albumin complex

unconjugated bilirubin: albumin enters liver

hepatocyte conjugates bilirubin making it water soluble

excreted in bile into the intestine

some reuptake

most degraded to urobilinogen by bacteria and excreted in poop

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19
Q

bile in liver flows

A

in canaliculi opposite direction of blood

will flow toward the portal triad

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20
Q

another name for jaundice

A

icterus
hyperbilirubinemia

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21
Q

prehepatic icterus is caused by

A

massive breakdown of RBC

leading to large amounts of unconjugated bilirubin

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22
Q

hepatic icterus is caused by

A

liver issue- unable to uptake and/or excrete bilirubin

leads to Increased conjugated and unconjugated bilirubin

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23
Q

posthepatic icterus is caused by

A

Bile duct obstruction

Increased conjugated bilirubin

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24
Q

Hepatoencephalopathy can be caused by —

A

portosystemic shunt

blood skips liver- cause too much ammonia in the blood leading to neuro issues

25
Q

3 types of reversible injury to liver

A

also called vacuolar hepatopathy

Hepatocellular swelling *Glycogen accumulation *Hepatic lipidosis

26
Q

hepatocellular swelling is caused by —. and looks —

A

cells accumulate water due to inability to maintain
ionic and fluid homeostasis

issue with sodium pump

marked swelling with
very pale staining cytoplasm

27
Q

hepatocellular swelling is reversible or irreversible

A

reversible but can lead to necrosis if not resolved

28
Q

glycogen accumulation is caused by

A

glycogen accumulation without displacement of
the nucleus from the center

usually midzonal, but can be diffuse, zonal, or
involve individual cells

29
Q

glycogen accumulation in dogs is caused by

A

Steroid Hepatopathy

glucocorticoids (endogenous or exogenous)
* may be seen with stress or other drugs

30
Q
A

glycogen accumulation

31
Q

glycogen accumulation is reversible or irreversible

A

reversible; usually NOT associated with necrosis

32
Q

hepatic lipidosis cause — in the cytoplasm of the hepatocytes

A

vacuoles of lipid

33
Q

hepatic lipidosis is reversible or irreversible

A

reversible form of cellular injury; but may lead to necrosis

34
Q

another name for hepatic lipidosis

A

fatty change or steatosis

35
Q

5 ways fat can accumulate in the liver

A. Excessive entry of FAs due to — (most
common)

B. Excessive FA synthesis and TG formation due to excessive intake of —

C. Decreased — of FAs due to hepatocyte dysfunction

D. Decreased — with subsequent decreased export of lipoproteins

E. Impaired secretion of — (often due to hepatocyte dysfunction)

A

excessive dietary intake or increased mobilization

carbohydrates

oxidation

apoprotein synthesis

lipoprotein

36
Q
A

tension lipidosis

ligaments pull on edge of liver causing decreased blood flow and fat accumulation

37
Q
A

Feline Fatty Liver Syndrome

38
Q

storage disorder in the liver are accumulations in hepatocytes and — due to inherited metabolic disorders

A

Kupffer cells

Common findings include clear vacuoles, vacuoles with granular or hyaline material, or cytoplasmic yellow brown material

39
Q

what causes canine copper-associated hepatopathy

A

not really sure

might be chronic active hepatitis

Cu accumulates in centrilobular hepatocytes → progressive → hepatocellular necrosis and inflammation with copper-laden hepatocytes and macrophages → chronic hepatitis and cirrhosis

40
Q

what type of dogs have genetic mutation in copper transport proteins

A

Bedlington terrier

41
Q

what type of dog has familial association for copper-associated hepatopathy

A

West Highland white terrier, Dalmatian

42
Q

what type of dog has breed predisposition for copper-associated hepatopathy

A

Doberman pinschers, Labrador retrievers, and cocker spaniels

43
Q

Multifocal Random necrosis is caused by

A

Infectious agents (virus, protozoa, bacteria)

44
Q

massive necrosis is caused by

A

Toxic and nutritional

45
Q

zonal necrosis is caused by

A

toxic or hypoxia (zone 3)

Centrilobular (periacinar / zone 3)

Midzonal (midacinar / zone 2) - rare

Periportal (centroacinar / zone 1)

46
Q

inflammation of the liver parenchyma

A

Hepatitis

47
Q

inflammation of the bile ducts

A

Cholangitis

48
Q

inflammation of the bile ducts with extension into the liver parenchyma

A

Cholangiohepatitis:

49
Q

inflammation of the gall bladder

A

Cholecystitis

50
Q

inflammation of the bile ducts

A

Choledochitis

51
Q

Bile stasis is also called

A

cholestasis

52
Q

cholestasis is caused by

A

toxins, inflammation, duct
obstruction

53
Q

cholestasis will cause increased — in circulation

A

inducible enzymes

Alkaline Phosphatase- ALP-dogs and cats

Gammaglutamyl Transpeptide –GGT-Liver and Biliary-All Species

54
Q

— is severe diffuse (bridging) hepatic
fibrosis with nodular regeneration and bile duct hyperplasia

A

cirrhosis

55
Q

necrosis and inflammation in the liver can lead to

A

Regeneration
Fibrosis
Bile Duct Hyperplasia
Cirrhosis

56
Q

liver

A

Fibrosis and Nodular Regeneration

57
Q

Cirrhosis

A

severe diffuse (bridging)
hepatic fibrosis with nodular regeneration and bile duct hyperplasia

58
Q

cirrhosis leads to

A

portal hypertension→ multiple acquired
portosystemic shunts, ascites

Loss of hepatic function →insufficiency →
failure
Coagulopathies
Hyperbilirubinemia
Hepatoencephalopathy
Edema, Ascites (hypoproteinemia)
Photosensitization

22 fall: path (46 decks)

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