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BOD II > Liver and Biliary > Flashcards

Liver and Biliary Flashcards

1
Q

What part of the hepatocyte is most prone to hypoxia?

A

The cells in the central zone (lobule) as they are farthest from the portal triads where the blood enters.

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2
Q

What constitutes the portal triad?

A

Portal vein
Hepatic artery
Bile duct

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3
Q

What are kupffer cells?

A

Hepatic sinusoidal macrophages

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4
Q

Where is Vitamin A stored

A

Ito (stellate) cells: pericytes found in the perisinusoidal space

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5
Q

What are oval cells?

A

Originate in bone marrow
Involved in liver regeneration
Differentiate into hepatocytes and biliary cells

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6
Q

What is the rich reticulin network?

A

scaffolding for hepatic parenchyma

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7
Q

What is icterus and where might it be found?

A

Accumulation of yellow pigment from bilirubin in blood and tissues
Found in pinna, sclera, blood, urine

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8
Q

What animal has naturally yellow blood?

A

Horses: lots of vitamin A

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9
Q

What causes icterus?

A

A problem with hemoglobin metabolism, ie hemolysis
or bilirubin

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10
Q

What is the difference between indirect and direct bilirubin?

A

Indirect: bilirubin + albumin (incr. w/ hemolysis)
Direct: conjugated (incr. w/ liver or bile flow issue)

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11
Q

What is a problem with uptake in bilirubin metabolism called?

A

Prehepatic (hemolytic) jaundice

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12
Q

What is a problem with conjugation of bilirubin called?

A

Intrahepatic (toxic/infectious) jaundice

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13
Q

What is a problem with bilirubin secretion called?

A

Posthepatic (obstructive) jaundice
(Cholestasis)

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14
Q

Causes of intravascular hemolysis

A

IMHA
Infections (blood parasites > fragile RBCs)
Fragmentation injury (fibrin shearing, DIC)
Toxicities (copper in sheep)

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15
Q

Causes of extravascular hemolysis

A

Hemolysis in macrophages (spleen)
Oxidative injury
Histiocytic disorders
Inherited cell defects (membrane defects)

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16
Q

How does intrahepatic icterus come to be?

A

-Cell swelling compress bile canaliculi (intrahepatic cholestasis)
-Extensive hepatocyte necrosis due to hypoxia or hepatotoxins (lack of physical barrier) > interferes w/ hepatocyte ability to absorb, conjugate, and secrete bilirubin

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17
Q

Causes of posthepatic icterus

A

Obstruction of bile flow (extrahepatic cholestasis)
Choleliths
Parasites
Tumors
Fibrosis

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18
Q

What species are more predisposed to develop icterus?

A

Felids

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19
Q

What gross appearance does chronic venous congestion cause?

A

Nutmeg liver

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20
Q

What causes chronic venous congestion?

A

Usually right heart failure

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21
Q

What is cardiac fibrosis or sclerosis?

A

A condition that develops in which there is fibrosis bridging between zone 3 (centrilobular region) of adjacent acini from continuing chronic hepatic passive congestion

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22
Q

What will happen to bile acids if there is a portosystemic shunt?

A

They will be elevated

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23
Q

Congenital portosystemic shunts

A

Abnormal vascular channel in which the blood bypasses the liver and drain to systemic circulation
Can be intrahepatic (large dogs, persistent ductus venosus) or extrahepatic (small dogs)
The affected dogs are usually stunted
Elevated ammonia conc with ammonium biurate crystals in their urine

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24
Q

Telangiectasis

A

Hepatic sinusoids are dilated and filled with blood and thus appear as dark spots

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25
Q

What does excessive lipid accumulation in the liver cause?

A

Steatosis (fatty liver syndrome)

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26
Q

What does excessive glycogen in the liver cause

A

Glycogenosis (steroid hepatopathy)

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27
Q

What does amyloid deposition in the liver cause

A

Amyloidosis

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28
Q

What type of pigment deposition takes place in the liver?

A

Bile pigments: intrahepatic or extrahepatic cholestasis
Hemosiderin: hemosiderosis

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29
Q

What does copper accumulation in the liver cause?

A

Acute and chronic poisoning

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30
Q

Causes of fatty liver syndrome

A

Diet
Toxins
Hypoxia
Ketosis, pregnancy toxemia
Feline hepatic lipidosis
Endocrine (diabetes mellitus, build up of sugars)

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31
Q

Pathogenesis of hepatic lipidosis

A

Increased supply of FFAs
> increased conversion of FFA to triglyceride (w/ decreased oxidation of FFAs)
> triglyceride accumulation

Decreased apoprotein synthesis > decreased lipoprotein export
> triglyceride accumulation

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32
Q

Hepatic glycogenosis pathogenesis

A

Glucocorticoids (steroids) > glycogen synthetase > increased storage > hepatocyte swelling (midzonal)

Grossly: big, rounded, swollen, pale

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33
Q

Pathogenesis of amyloidosis

A

Abnormal proteins (beta-pleated sheets)
Fragile liver, can rupture
Can affect kidneys as well

34
Q

Copper accumulation in the liver

A

Ceruloplasmin, metallothionein
Diet
low molybdenum (Mo)
pyrrolizidize alkaloids
genetics, impaired secretion (Bedlington terriers, WHW terriers, Dobies)

35
Q

What causes white liver disease?

A

Cobalt/cobalamin deficiency

Synthesis of Vit B12 and other enzymes requires cobalt > anemia > centrilobular degeneration/necrosis with pallor

36
Q

What causes hepatosis dietitica

A

Selenium/vitamin E deficiency (young, rapidly growing pigs)

37
Q

What is cholangitis

A

Bile duct inflammation

38
Q

What is cholcystitis?

A

Gall bladder inflammation

39
Q

What is Cholangiohepatitis?

A

Inflammation of the bile ducts w/ in the liver

40
Q

Feline cholangitis

A

Often associated with IBD and chronic pancreatitis
CS: ascites, jaundice, polyphagia and weight loss
Ascending inflammation via the bile duct

41
Q

Gallbladder inflammation causes

A

Cholecystitis&raquo_space; salmonella enteritidis Dublin

Cholelithiasis&raquo_space; local irritation

Cystic mucinous hyperplasia and gall bladder mucocoele&raquo_space; backflow and retrograde infection

Gall bladder adenoma/adenocarcinoma w/ necrosis and secondary infection

42
Q

Acute hepatitis

A

Degeneration/necrosis of hepatocytes
Leuks in periportal CT and/or within sinusoids
-Bacterial: neutrophils
-Viral: lymphocytes

43
Q

Chronic hepatitis

A

Periportal infiltration by lymphocytes and plasma cells
Progressive periportal fibrosis > bridging fibrosis
(band will contract causing a pucker in liver surface)

44
Q

Chronic-Active Hepatitis

A

Dogs (dobies)
Activity is determined by quantity of inflammation and extent of hepatocellular death
Causes: lepto, infectious canine hepatitis, aflatoxicosis, copper tox
End stage = cirrhosis (nodular regeneration and fibrosis)

45
Q

Causes of viral hepatitis

A

Occurs in the course of systemic infection - viraemia
Infectious canine hepatitis (ICH) -adenovirus
Equine herpes virus (EHV)
Bovine herpesvirus 1 (IBR)
Suid herpes virus (SHV)
Rabbit hemorrhagic disease (RHD) -calicivirus
Feline calicivirus (FCV)
FIP -coronavirus

46
Q

Infectious canine hepatitiso)

A

Canine adenovirus type 1

Path: oral/nasal infection > lymph > blood: viraemia

Intranuclear viral inclusions in hepatocytes and kuppfer cells
(also eye, kidney, vessels path)

Outcome: high titer -acute necrotizing hepatitis
low titer -chronic hepatitis, fibrosis, persistent infection

47
Q

EHV 1

A

Equine herpes virus type 1 (rarely type 4)
Path: transplacental infection > placental detachment > late abortion (7mo)
In fetus: multifocal necrosis in liver and other organs

48
Q

Canine herpes virus 1

A

Path: fetal infection > abortion and stillbirth
neonatal infection > fading puppy syndrome > diffuse necrotizing vasculitis and multifocal hemorrhagic necrosis in organs (liver, kidney, brain) -turkey egg kidney, piecemeal necrosis

49
Q

Rabbit hemorrhagic disease

A

Calici virus
Path: fecal oral

Massive necrosis of hepatocytes, DIC (consumptive coagulopathy)

50
Q

FIP

A

Mutated feline coronavirus (enteric)

Oral infection > enterocytes >viremia > granulomatous vaso-centric serositis/hepatitis

51
Q

3 Patterns of Injury to the liver

A

Random
Zonal
-Centrilobular
-Midzonal
-Periportal
Massive

52
Q

Centrilobular Necrosis

A

Common since this is the least oxygenated zone of hepatocytes
also has greatest enzymatic activity
(Zone 3, periacinar)

53
Q

What does pyknosis mean?

A

Shrunken cell/nucleus

54
Q

Direction of blood flow in the liver

A

Portal vein to central vein

55
Q

Direction of bile flow

A

Central vein to bile duct

56
Q

Midzonal degeneration and necrosis

A

Not common in domestic animals
Aflatoxicosis: pigs and horses

57
Q

Periportal hepatocellular degeneration and necrosis

A

Uncommon
Occurs when toxins do not need to be metabolized to cause inury: injure first hepatocytes encountered

58
Q

Massive necrosis Pathogenesis

A

necrosis of entire lobule or contiguous lobules
> little to no regeneration
results in collapse of lobule and replacement by fibrous scar

59
Q

Causes of massive necrosis

A

Aflatoxin
Amanita mushrooms
Nutritional deficiencies (swine)
Idiosyncratic drug reactions
Acetaminophen in cats
Equine serum hepatitis

60
Q

Bioactivation: phase 1 of biotransformation

A

Adds reactive polar group to lipid soluble compounds
-mainly via oxidation: cytochrome P450
can yield transient reactive intermediates including free radicals (membrane damage > cell death)

61
Q

What is phase 2 of biotransformation

A

Conjugation

62
Q

What is meant by indirect toxic liver injury?

A

The substance is toxic after biotransformation or after metabolism by gastrointestinal microbes

63
Q

Where is the damage likely to occur with compounds metabolized by the cytochrome P450 system? (CCl4, paracetamol)

A

Zone 3 (centrilobular)

64
Q

Where is the damage likely to occur with direct acting toxicants (metal salts)?

A

Zone 1 (periportal)

65
Q

What are obligate toxic substances?

A

Lead to predictable toxic effects in numerous species
-Dose dependent, direct or indirect effects on hepatocytes
CCl4, pyrrolizidine alkaloids, acetaminophen

66
Q

What are idiosyncratic toxic effects?

A

Only in some species or individuals. Unpredictable, usually immunologic
Paracetamol (acetaminophen), halothane

67
Q

Why is acetaminophen toxic to cats?

A

Acetaminophen is conjugated in two ways: glucouronidation and sulfation and cats are deficient in these two pathways.

68
Q

What are local effects of hepatotoxins on hepatocytes?

A

Diffuse or zonal derangement > hydropic degeneration (swelling), lipidosis, or necrosis

69
Q

Outcomes of acute hepatotoxic injury

A

One time, sub-massive necrosis: regeneration is possible
One time, massive necrosis with destruction of reticulin framework/limiting place > fibrosis

70
Q

Outcomes of chronic (or recurrent) hepatotoxic injury

A

Chronic active hepatitis > cirrhosis (fibrosis + hepatocyte nodular regeneration)
Some toxins > hepatic neoplasms

71
Q

Causes of acute hepatotoxicity

A

Acetaminophen (cats)
Carprofen
Microcystin LR (blue-green algae)
alpha-amanitin (Amanitas)
Acute aflatoxicosis

72
Q

How does centrilobular congestion manifest grossly?

A

Nutmeg liver

73
Q

What pathology can heartworm infections cause in the liver?

A

Centrilobuolar congestion
Nutmeg liver

74
Q

What pathology can Fasciola hepatica cause in the liver?

A

Intrahepatic cholangitis
from migration in the bile ducts

75
Q

What are primary types of hepatic neoplasia?

A

Hepatocellular adenoma
Hepatocellular carcinoma
Cholangiocarcinoma
Hemangiosarcoma

76
Q

Structural manifestations of Cirrhosis

A

-Loss of hepatic parenchyma
-Condensation of reticulin framework
-Formation of tracts of fibrous CT that appear as depressions on the surface
-Regeneration of hepatic parenchyma between fibrous bands > leading to nodules that bulge on surface

77
Q

What is the nervous manifestation of hepatic failure?

A

Hepatic encephalopathy (accumulation of urea)

78
Q

What are the cutaneous manifestations of hepatic failure?

A

Hepatocutaneous syndrome: necrolytic migratory erythema etc.
Photosensitization

79
Q

What are the immunologic manifestations of hepatic failure?

A

Reduction of blood filtration by Kupffer cells

80
Q

What are the metabolic disturbances of hepatic failure?

A

Bleeding tendencies: liver makes clotting factors
Hypoalbuminemia (ascites): loss of oncotic molecules

81
Q

What are the vascular and hemodynamic alterations of hepatic failure?

A

Portal hypertension > acquired portosystemic shunts > modified transudate

BOD II (5 decks)

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