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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
What does excessive lipid accumulation in the liver cause?
Steatosis (fatty liver syndrome)
26
What does excessive glycogen in the liver cause
Glycogenosis (steroid hepatopathy)
27
What does amyloid deposition in the liver cause
Amyloidosis
28
What type of pigment deposition takes place in the liver?
Bile pigments: intrahepatic or extrahepatic cholestasis Hemosiderin: hemosiderosis
29
What does copper accumulation in the liver cause?
Acute and chronic poisoning
30
Causes of fatty liver syndrome
Diet Toxins Hypoxia Ketosis, pregnancy toxemia Feline hepatic lipidosis Endocrine (diabetes mellitus, build up of sugars)
31
Pathogenesis of hepatic lipidosis
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
32
Hepatic glycogenosis pathogenesis
Glucocorticoids (steroids) > glycogen synthetase > increased storage > hepatocyte swelling (midzonal) Grossly: big, rounded, swollen, pale
33
Pathogenesis of amyloidosis
Abnormal proteins (beta-pleated sheets) Fragile liver, can rupture Can affect kidneys as well
34
Copper accumulation in the liver
Ceruloplasmin, metallothionein Diet low molybdenum (Mo) pyrrolizidize alkaloids genetics, impaired secretion (Bedlington terriers, WHW terriers, Dobies)
35
What causes white liver disease?
Cobalt/cobalamin deficiency Synthesis of Vit B12 and other enzymes requires cobalt > anemia > centrilobular degeneration/necrosis with pallor
36
What causes hepatosis dietitica
Selenium/vitamin E deficiency (young, rapidly growing pigs)
37
What is cholangitis
Bile duct inflammation
38
What is cholcystitis?
Gall bladder inflammation
39
What is Cholangiohepatitis?
Inflammation of the bile ducts w/ in the liver
40
Feline cholangitis
Often associated with IBD and chronic pancreatitis CS: ascites, jaundice, polyphagia and weight loss Ascending inflammation via the bile duct
41
Gallbladder inflammation causes
Cholecystitis >> salmonella enteritidis Dublin Cholelithiasis >> local irritation Cystic mucinous hyperplasia and gall bladder mucocoele >> backflow and retrograde infection Gall bladder adenoma/adenocarcinoma w/ necrosis and secondary infection
42
Acute hepatitis
Degeneration/necrosis of hepatocytes Leuks in periportal CT and/or within sinusoids -Bacterial: neutrophils -Viral: lymphocytes
43
Chronic hepatitis
Periportal infiltration by lymphocytes and plasma cells Progressive periportal fibrosis > bridging fibrosis (band will contract causing a pucker in liver surface)
44
Chronic-Active Hepatitis
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
Causes of viral hepatitis
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
Infectious canine hepatitiso)
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
EHV 1
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
Canine herpes virus 1
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
Rabbit hemorrhagic disease
Calici virus Path: fecal oral Massive necrosis of hepatocytes, DIC (consumptive coagulopathy)
50
FIP
Mutated feline coronavirus (enteric) Oral infection > enterocytes >viremia > granulomatous vaso-centric serositis/hepatitis
51
3 Patterns of Injury to the liver
Random Zonal -Centrilobular -Midzonal -Periportal Massive
52
Centrilobular Necrosis
Common since this is the least oxygenated zone of hepatocytes also has greatest enzymatic activity (Zone 3, periacinar)
53
What does pyknosis mean?
Shrunken cell/nucleus
54
Direction of blood flow in the liver
Portal vein to central vein
55
Direction of bile flow
Central vein to bile duct
56
Midzonal degeneration and necrosis
Not common in domestic animals Aflatoxicosis: pigs and horses
57
Periportal hepatocellular degeneration and necrosis
Uncommon Occurs when toxins do not need to be metabolized to cause inury: injure first hepatocytes encountered
58
Massive necrosis Pathogenesis
necrosis of entire lobule or contiguous lobules > little to no regeneration results in collapse of lobule and replacement by fibrous scar
59
Causes of massive necrosis
Aflatoxin Amanita mushrooms Nutritional deficiencies (swine) Idiosyncratic drug reactions Acetaminophen in cats Equine serum hepatitis
60
Bioactivation: phase 1 of biotransformation
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
What is phase 2 of biotransformation
Conjugation
62
What is meant by indirect toxic liver injury?
The substance is toxic after biotransformation or after metabolism by gastrointestinal microbes
63
Where is the damage likely to occur with compounds metabolized by the cytochrome P450 system? (CCl4, paracetamol)
Zone 3 (centrilobular)
64
Where is the damage likely to occur with direct acting toxicants (metal salts)?
Zone 1 (periportal)
65
What are obligate toxic substances?
Lead to predictable toxic effects in numerous species -Dose dependent, direct or indirect effects on hepatocytes CCl4, pyrrolizidine alkaloids, acetaminophen
66
What are idiosyncratic toxic effects?
Only in some species or individuals. Unpredictable, usually immunologic Paracetamol (acetaminophen), halothane
67
Why is acetaminophen toxic to cats?
Acetaminophen is conjugated in two ways: glucouronidation and sulfation and cats are deficient in these two pathways.
68
What are local effects of hepatotoxins on hepatocytes?
Diffuse or zonal derangement > hydropic degeneration (swelling), lipidosis, or necrosis
69
Outcomes of acute hepatotoxic injury
One time, sub-massive necrosis: regeneration is possible One time, massive necrosis with destruction of reticulin framework/limiting place > fibrosis
70
Outcomes of chronic (or recurrent) hepatotoxic injury
Chronic active hepatitis > cirrhosis (fibrosis + hepatocyte nodular regeneration) Some toxins > hepatic neoplasms
71
Causes of acute hepatotoxicity
Acetaminophen (cats) Carprofen Microcystin LR (blue-green algae) alpha-amanitin (Amanitas) Acute aflatoxicosis
72
How does centrilobular congestion manifest grossly?
Nutmeg liver
73
What pathology can heartworm infections cause in the liver?
Centrilobuolar congestion Nutmeg liver
74
What pathology can Fasciola hepatica cause in the liver?
Intrahepatic cholangitis from migration in the bile ducts
75
What are primary types of hepatic neoplasia?
Hepatocellular adenoma Hepatocellular carcinoma Cholangiocarcinoma Hemangiosarcoma
76
Structural manifestations of Cirrhosis
-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
What is the nervous manifestation of hepatic failure?
Hepatic encephalopathy (accumulation of urea)
78
What are the cutaneous manifestations of hepatic failure?
Hepatocutaneous syndrome: necrolytic migratory erythema etc. Photosensitization
79
What are the immunologic manifestations of hepatic failure?
Reduction of blood filtration by Kupffer cells
80
What are the metabolic disturbances of hepatic failure?
Bleeding tendencies: liver makes clotting factors Hypoalbuminemia (ascites): loss of oncotic molecules
81
What are the vascular and hemodynamic alterations of hepatic failure?
Portal hypertension > acquired portosystemic shunts > modified transudate

BOD II (5 decks)

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