7. Liver pathology 2

Consequences of disease

true

(TRUE/FALSE): hepatocellular disease may progress to biliary disease and vice-versa.

hepatobiliary disease

The presence of hepatocellular disease and biliary disease is termed

acute

Liver disease can be _________, resulting in recovery or death (if severe/diffuse).

chronic

Acute liver disease can progress to a subacute/_________ disease

true

(TRUE/FALSE): All liver disease can progress to liver failure.

hepatic failure

loss of >75% of functional hepatic mass

true

(TRUE/FALSE): Hepatic failure can occur with small, normal, or enlarged liver.

false

(TREU/FALSE): loss of functional hepatic mass directly correlates with the size of the liver.

advanced

If an animal has clinical signs of liver disease, it is likely to have ___________ liver disease.

true

(TRUE/FALSE): In liver failure, one or more functions often fail before the rest.

false

(TRUE/FALSE): In liver failure, most functions fail simultaneously

hepatic insufficiency

“Loss of synthetic and secretory/excretory function causing clinical disease” is termed liver failure or

clinical signs

________ ______ of hepatic insufficiency do not develop until the reserve is exhausted. By then, the liver damage is usually far advanced and potentially irreversible.

icterus

Cutaneous consequences of hepatic failure include

• __________

• photosensitization

• hepatocutaneous syndrome

photosensitization

Cutaneous consequences of hepatic failure include

• icterus

• ______________

• hepatocutaneous syndrome

hepatocutaneous syndrome

Cutaneous consequences of hepatic failure include

• icterus

• photosensitization

• _____________ ____________

hemolysis, ineffective erythropoiesis

Prehepatic jaundice can be due to

• __________

• ____________ _____________

______________ jaundice can be due to

• hemolysis

• insufficient erythropoiesis

intrahepatic

_______________ jaundice can be caused by

• nonobstructive biliary disease

  • hepatitis

  • cirrhosis

  • congestive hepatopathy

  • cystic fibrosis

• mechanical biliary obstruction

  • tumors of the liver

  • intrahepatic gallstones

  • congestive hepatopathy

nonobstructive

Intrahepatic jaundice can be caused by

• ______________ biliary disease

  • hepatitis

  • cirrhosis

  • congestive hepatopathy

  • cystic fibrosis

• mechanical biliary obstruction

  • tumors of the liver

  • intrahepatic gallstones

  • congestive hepatopathy

mechanical

Intrahepatic jaundice can be caused by

• nonobstructive biliary disease

  • hepatitis

  • cirrhosis

  • congestive hepatopathy

  • cystic fibrosis

• _______________ biliary obstruction

  • tumors of the liver

  • intrahepatic gallstones

  • congestive hepatopathy

posthepatic

______________ jaundice can be caused by

• choledocholithiasis

• inflammation

• malformation of the biliary tract

• pancreatic carcinomas

• bile duct strictures.

hyperbilirubinemia

The most important causes of ____________________ include increased hemolysis, failure of hepatocytes in bilirubin uptake/processing/excretion, and blockage of bile ducts.

hemolysis

The most important causes of hyperbilirubinemia include increased _________, failure of hepatocytes in bilirubin uptake/processing/excretion, and blockage of bile ducts.

hepatocytes

The most important causes of hyperbilirubinemia include increased hemolysis, failure of ______________ in bilirubin uptake/processing/excretion, and blockage of bile ducts.

bile ducts

The most important causes of hyperbilirubinemia include increased hemolysis, failure of hepatocytes in bilirubin uptake/processing/excretion, and blockage of ________ _______.

posthepatic

The presence of choleliths is a cause of ___________ jaundice.

focal

A _______ lesion, such as local cholestasis, may not cause jaundice because bilirubin is cleared by the unaffected parts of the liver.

diffuse

A ________ lesion will more often result in jaundice.

carotenoid

Jaundice seen on post-mortem exam has to be differentiated from yellow staining caused by __________ pigments, autolysis, and other artefacts.

hyperbilirubinemia

Elevated bilirubin in the blood, serum, or plasma.

50

Hyperbilirubinemia does not occur until >____% of excretory capacity of the liver is lost.

excretory capacity

Hyperbilirubinemia does not occur until >50% of _________ _______ of the liver is lost.

bile pigments

The yellow discoloration seen in icteric tissues is due to deposition of

duration

The intensity of the icterus is related to the _________ of hyperbilirubinemia.

Bilirubin

pigmented waste product of RBC necrosis/hemolysis.

bile acids

Made from cholesterol. Responsible for emulsification and absorption of fat.

phylloerythrin

Breakdown product of chlorophyll in ruminants. Excreted in bile.

photosensitization

Increase in phylloerythrin in serum/tissue can cause

bile

_______ excretion into the intestines is responsible for the characteristic dark color of feces.

acholia

White feces.

unpigmented

Photosensitization typically manifests on areas of ___________ skin

photosensitivity

A severe dermatitis resulting form a heightened reactivity of skin cells and associated dermal tissues upon exposure to sunlight.

photosensitizer

A light absorbing photoreactive molecule that can generate reactive oxygen species. Causes organelle damage and cellular necrosis when deposited in the skin

1

Type ___ photosensitivity is due to ingestion of preformed photodynamic toxins in plants and drugs.

2

Type __ photosensitivity is due to congenital enzyme deficiencies resulting in endogenous pigment accumulation.

bovine

Uroporphyrinogen III cosynthetase deficiency is the cause of ___________ congenital hematopoietic porphyria.

st. john’s wart

The photoreactive molecules found in what plant cause primary PS?

primary

Tetracycline and phenothiazine can cause (PRIMARY/SECONDARY) PS.

cholestasis

Deposition of photoreactive molecules in the skin systemically (not through contact) usually coincides with

hepatogenous

Secondary photosensitization is also called

cholestasis

Photoreactive phylloerythrin is derived from chlorophyl by the GIT microbes, and is normally excreted in bile. Systemic deposition can occur due to diseases resulting in

phylloerythrin

Cholestasis increases _______________ concentration in blood.

phylloerythrin

___________ in blood binds to cells in the dermis. Energy from UV light results in the production of free radicals that cause photosensitive dermatitis of unpigmented skin.

UV

Phylloerythrin in blood binds to cells in the dermis. Energy from ___ light results in the production of free radicals that cause photosensitive dermatitis of unpigmented skin.

free radicals

Phylloerythrin in blood binds to cells in the dermis. Energy from UV light results in the production of ________ _______ that cause photosensitive dermatitis of unpigmented skin.

sporidesmin

Non-haired skin of the nose and eyes sloughs due to injury to dermis following exposure to sun. Secondary to Secondary to __________________ toxicosis of the liver.

australia, new zealand

Facial eczema of sheep (serous exudate and SQ edema) is secondary to sporidesmin toxicosis of the liver. It’s an issue in ___________ and _____ ______________

hepatic encephalopathy

Consequence of hepatic failure manifesting as dullness, mania, and convulsions. Signs can vary between subtle behavioral changes to frenzy.

head pressing

A common behavior seen in animals experiencing hepatic encephalopathy is

ammonia, urea

Hepatic encephalopathy arises from a buildup of __________ in the blood and eventually CNS. This buildup is due to the liver’s failure to synthesize _______.

true

(TRUE/FALSE): Hypoglycemia may contribute to neurologic dysfunction associated with liver disease.

astrocytes

___________ are typically able to handle minor alterations in ammonia presence in the CNS, but massive shifts impact their ability to detoxify the brain altogether.

mitosis

Pyrrolizidine alkaloid inhibits hepatocyte __________

bigger

Hepatocytes affected by pyrrolizidine alkaloid are (BIGGER/SMALLER) than normal hepatocytes.

spongy vacuolation

On postmortem, patients affected by hepatic encephalopathy often have _______ __________ of the white matter of the brain.

foramen magnum

The swelling and vacuolation associated with hepatic encephalopathy can result in herniation of the brain tissue through the

hemorrhagic diathesis

Increased tendency to bleed/bruise easily. May be associated with decreased coagulation factor production.

decrease

Chronic liver failure results in a(n) (INCREASE/DECREASE) in coagulation factor production.

true

(TRUE/FALSE): The decrease in coagulation factor production associated with chronic liver failure can result in increased coagulation times, but rarely hemorrhage unless undergoing trauma or surgery.

false

(TRUE/FALSE): The decrease in coagulation factor production associated with chronic liver failure can often result in spontaneous hemorrhage.

petechial, ecchymotic

Acute liver failure and necrosis often results in widespread __________ and __________ hemorrhages throughout the carcass.

acute

Mechanism of coagulopathy in (ACUTE/CHRONIC) liver failure

• decreased synthesis of coagulation factors by the liver

• increased consumption of coagulation factors due to a hypercoagulative state triggered by sinusoidal damage

• increased fibrinolysis leading to exhaustion of inhibitors

• ±thrombocytopenia

coagulation factors

Mechanism of coagulopathy in acute liver failure

• decreased synthesis of ________ _________ by the liver

• increased consumption of coagulation factors due to a hypercoagulative state triggered by sinusoidal damage

• increased fibrinolysis leading to exhaustion of inhibitors

• ±thrombocytopenia

consumption, hypercoagulable state

Mechanism of coagulopathy in acute liver failure

• decreased synthesis of coagulation factors by the liver

• increased ___________ of coagulation factors due to a ______________ __________ triggered by sinusoidal damage

• increased fibrinolysis leading to exhaustion of inhibitors

• ±thrombocytopenia

fibrinolysis

Mechanism of coagulopathy in acute liver failure

• decreased synthesis of coagulation factors by the liver

• increased consumption of clotting factors due to a hypercoagulative state triggered by sinusoidal damage

• increased _______________ leading to exhaustion of inhibitors

• ±thrombocytopenia

cyanobacterial toxicity

Common cause of massive necrosis

chronic

(ACUTE/CHRONIC) liver failure results in decreased urea production, impairing the kidney’s ability to concentrate urine.

renal

PU/PD arises due to ____________ damage secondary to chronic liver failure.

acute

(ACUTE/CHRONIC) liver failure that results in severe hyperbilirubinemia can produce bilirubin casts and biliary nephrosis.

renal failure

Acute hepatic failure is accompanied by oliguria and biochemical evidence of

acetaminophen

Some toxins, such as _____________, will target the liver and kidneys.

chronic

Generalized edema is a classic finding associated with (ACUTE/CHRONIC) liver failure.

albumen, oncotic

Chronic liver failure results in reduced __________ synthesis, decreasing __________ pressure.

portal hypertension, ascites

Chronic liver failure results in fibrosis and increased resistance to blood flow. The restricted blood flow generates _________ ____________, and the increased hydrostatic pressure results in ___________.

blood flow, hydrostatic

Chronic liver failure results in fibrosis and increased resistance to blood flow. The restricted ________ ______ generates portal hypertension, and the increased ___________ pressure results in ascites.

albumin

Protein responsible for >80% of oncotic pressure. Low levels can result in generalized edema. Horses are most affected in their GIT while dogs are most affected in their lungs.

oncotic

Albumin is responsible for >80% of _________ pressure. Low levels can result in generalized edema. Horses are most affected in their GIT while dogs are most affected in their lungs.

GIT, lungs

Albumin is responsible for >80% of oncotic pressure. Low levels can result in generalized edema. Horses are most affected in their ____ while dogs are most affected in their _______.

horses, dogs

Albumin is responsible for >80% of oncotic pressure. Low levels can result in generalized edema. _________ are most affected in their GIT while _____ are most affected in their lungs.

Portal hypertension

Elevation in BP of the normally low-pressure portal vein due to increased resistance to portal blood flow.

pre-hepatic

Portal hypertension can be broken down into three types based on the anatomic site of resistance. Portal vein thrombosis or compression constitutes

hepatic

Portal hypertension can be broken down into three types based on the anatomic site of resistance. Fibrosis due to any chronic hepatopathy such as cirrhosis and chronic progressive liver disease constitutes

post-hepatic

Portal hypertension can be broken down into three types based on the anatomic site of resistance. Right sided CHF or caudal vena cava compression/thrombosis constitute

acquired portosystemic shunt

Anomalous, tortuous thin-walled veins coursing between the duodenum and other viscera.

extrahepatic

Congenital portosystemic shunts in small breed dogs are usually (INTRAHEPATIC/EXTRAHEPATIC)

intrahepatic

Congenital portosystemic shunts in large breed dogs are sometimes (INTRAHEPATIC/EXTRAHEPATIC)

systemic

Congenital portosystemic shunts result in blood from the portal system bypassing the liver and draining straight into __________ circulation.

hepatocutaneous syndrome

Superficial necrolytic dermatitis arising from chronic liver injury and skin disease.

Hepatocutaneous syndrome manifests mainly on the footpads, mucocutaneous junctions, muzzle, and pressure points.