2 - Liver II Flashcards
Hepatic failure: clinical term (can’t determine when dead)
- Loss of adequate haptic function as a consequence of either acute or chronic hepatic damage
What are the consequences of hepatic failure
- Hepatic encephalopathy
- Metabolic abnormalities
- Vascular and hemodynamic alterations
- Cutaneous manifestations
*can happen in all animals
Hepatic encephalopathy due to hepatic failure
- Accumulation of ammonia due to reduced uptake by liver
- *ammonia=TOXIC TO BRAIN
o Abnormal neurotransmission in the CNS and neuromuscular system
Metabolic abnormalities due to hepatic failure
- Bleeding tendences due to: decreased synthesis of coagulation factors
- Decreased albumin synthesis lead to EDEMA everywhere
o Means it’s quite far along
Vascular and hemodynamic alterations due to hepatic failure
- Ex. portosystemic shunt (extrahepatic shunt)
- *abnormal communication between portal vein and systemic circulation
- *can also get an intrahepatic shunt
**How does ci portosystemic shunt occur?
- *secondary to liver failure
- Injury and diffuse liver fibrosis
- Portal vein bring blood into a noncompliant firm liver=resistance to blood flow
- Increase portal pressure (**PORTAL HYPERTENSION)
o New vasculature being formed before the liver: extrahepatic shunt (POROTSYSTEMIC SHUNT) between portal vein and vena cava leading to hepatic encephalopathy
- Increase portal pressure (**PORTAL HYPERTENSION)
- Ascites: due to increase pressure and decreased albumin synthesis
What are some other consequences of an acquired portosystemic shunt?
- Serum acid bile acids go up (REDUCED UPTAKE)
- Serum ammonia go up
- Ammonia biurate crystals (bladder, urine)
- Hepatic encephalopathy
What are the different cutaneous manifestations from hepatic failure?
- Superficial necrolytic dermatitis
- Photosensitization secondary to hepatic dysfunction
Superficial necrolytic dermatitis (due to hepatic failure)
- ONLY IN DOGS
- Crusting and ulceration of epidermis
- Muzzle, mucocutaneous areas of face, footpads, and pressure points of skin
- Unknown mechanism
- *also occurs with diabetes
Photosensitization secondary to hepatic dysfunction
- *more COMMON (more in RUMINANTS)
- Eat plants with chlorophyl and converted to Phylloerythrin by GI bacteria
- Phylloerythrin is absorbed and goes to portal vein to be excreted in bile
- WHEN liver damage: phylloerythrin accumulates in SKIN=absorbs UV light=oxidative damage and necrosis
- **RESTRICTED TO NON-PIGEMENTED AREAS
What is primary photosensitization from?
- Eating toxic materials in plants
What are some developmental anomalies and incidental findings in the liver?
- Congenital biliary cysts
- Polycystic disease
- Tension lipidosis
- Capsular fibrosis
Congenital biliary cysts
- Single or few cysts can be found=INCDIENTAL FINDING
- *more common in CATS
Polycystic disease
- Rare occurrence
- *congenital: Reported in Cairn Terriers, West highland white terriers and Persian cats, pigs and goats
- Extensive cysts within the liver, kidney and pancreas
- *often fatal
Tension lipidosis
- Incidental finding
- Pale areas in livers of HORSES and CATLLE
- Occur adjacent to insertion of ligament (serosal) attachment
Capsular fibrosis
- Incidental finding in HORSE
- Thought to be related to STRONGYLE SP. Migration
Post mortem changes to the liver
- Pale
- Blue green staining from bile
- Very friable
What are some metabolic disturbances of the liver?
- Hepatocellular lipidosis (steatosis
What is hepatic lipidosis?
- When lipid accumulates within liver
o Mainly TRIGLYCERIDES that are accumulated - Several mechanisms
- *yellow, float, rounded edges
What is the gross appearance of hepatic lipidosis: mild and severe?
- Mild: enhanced lobular patterns
- Sever: YELLOW
What are the several mechanisms of hepatic lipidosis?
- Increased mobilization of FFA from adipose tissue
- Increased intake of at or carbs
- Decreased O2 and energy (anemia, hypoxia)
- Decreased protein intake or synthesis (starvation)
- Hormonal abnormalities (insulin)
- Toxin induced fatty change
When might there be increased mobilization of FFA from adipose tissues?
- periods of increased demand (lactation and pregnancy)
- increased TGs
- FFA can be converted to ketone bodies leading to KETOSIS
o Using FFA as an energy source but brain can’t use FFA, but CAN USE KETONE BODIES
What happens when there is decreased O2 and energy (anemia, hypoxia) and hepatic lipidosis?
- Processes that need oxygen do NOT happen
- TGs are NOT being used, so they ACCUMULATE
What happens with decreased protein intake (starvation) and hepatic lipidosis?
- Using fat stores (lipolysis)
Hormonal abnormalities (insulin) and hepatic lipidosis?
- *no insulin=glucose can’t be utilized as energy source
- Low insulin causes fat to be used as an energy source instead of glucose and INCREASES mobilization of FFA
Toxin induced fatty change and hepatic lipidosis
- *too many toxins!
What are some examples of hepatic lipidosis in vet med?
- Pregnancy toxemia
- Bovine fatty liver disease
- Feline fatty liver syndrome
- Hyperlipemia
- Endocrine disorders (diabetes and hypothyroidism)
Pregnancy toxemia: species and when
- Sheep in late pregnancy
Bovine fatty liver disease
- Dairy cattle (lactation)
- Beef cattle (pregnancy)
- *something that causes them to be off feed and start mobilising fat from adipose tissue=increased production of ketone bodies
Feline fatty liver syndrome
- Obese fats become anorectic for unknown reason and start mobilizing fat
Hyperlipemia
- Syndrome in ponies, miniature horses and donkeys
- Associated with increased demand on energy
- Occurs after an event causing anorexia
Endocrine disorders (diabetes and hypothyroidism)
- Insulin is anabolic hormone
o Lack of insulin or insulin response=increased mobilization of fat - Hypothyroidism=hypercholesterolemia and increased serum lipids
o OLDER DOGS
Glycogen accumulation (steroid hepatopathy): species and 2 causes
- DOGS
- 2 causes
o Prolonged administration of corticosteroids (external)
o Secondary to hyperadrenocorticism
What is the mechanism of glycogen accumulation steroid hepatopathy)?
- Gluconeogenesis and glycogen storage
- *enlarged and BRONZE in colour
- Can cause elevation in liver enzymes clinically
Disturbances of outflow
- Central passive congestion within the liver
- *secondary to R-SIDED HEART FAILURE (ex. nutmeg liver)
o Increased pressure within vena cava and central vein (ie. Blood can’t get out)
What happens with acute heart failure? What does it look like grossly?
- Congestion at centrilobular areas
- Hepatocytes within centrilobular areas may undergo fatty degeneration
GROSSLY: lobular pattern may be slightly enhanced
What happens with chronic heart failure? What does it look like grossly?
- Sinusoids at centrilobular area become DILATE (appear red grossly)
- Hepatocytes at centrilobular area undergo atrophy then degeneration and necrosis
- Hepatocytes at periportal area undergo fatty change (appear yellow grossly)
GROSSLY: enlarged (rounded edges) and enhanced lobular pattern (NUTMEG LIVER)
What are some disturbances of INFLOW that occur?
- Anemia (decrease flow)
- Congenital portosystemic shunt
Anemia (decreased flow): acute vs. chronic
- acute: centrilobular or paracentral DEGENERATION of hepatocytes
- chronic: ATROPHY of centrilobular hepatocytes
- GROSSLY: enhanced lobular pattern
Congenital portosystemic shunt (age group and 2 types)
- *young animal
- Intra-hepatic
o Failure of closure of ductus venosus
o Most common in large breed dogs - Extra-hepatic
o *connection between portal vein and caudal vena cava
o BYPASSES THE LIVER - **DOES NOT HAVE PORTAL HYPERTENSION (compared to acquired shunts)
o NO FIBROSIS
What does congenital portosystemic shunt look like grossly? (non-liver)
- Diffuse liver atrophy
- ‘blue’ in mesentery
- NO ascites (NO hypertension)
Congenital intrahepatic shunt: large breed dogs
- Umbilical vein brings O2 blood
o 50% goes through liver
o 50% through ductus venous (shunt) - *ductus venous should CLOSE after birth
o When doesn’t=congenital portosystemic shunt
Congenital extrahepatic shunt: short breed dogs, what are the consequences?
- Diffuse liver atrophy (NO FIBROSIS)
- Serum bile acids go up
- Serum ammonia goes up
- Ammonian biurate crystals (bladder)
- Hepatic encephalopathy
What is an incidental vascular finding of the liver?
- Telangiectasis
o Dilated sinusoids
o *common in cattle, horses and cats (typically older)
o Appear as red areas in liver
Liver infarction
- Uncommon due to dual blood supply
- Can occur secondary to
o Torsion of an individual hepatic lobe
o Thrombosis - *infarction is NECROSIS, secondary to lack of blood flow
What are 4 types of hepatic accumulations?
- Amyloid: 2 types
- Copper
- Hemosiderin
- Parasite hematin
Primary amyloidosis
- Produced by plasma cells that become cancerous (amyloid light chain or AL)
What can amyloid accumulation in the liver be secondary to?
- Chronic inflammation (amyloid A)
- *secondary is more common
Amyloidosis: grossly
- Enlarged
- Orange
- Friable
What can amyloidosis cause?
- Hepatic failure
- Rarely: hepatic rupture (horses)
What is primary copper accumulation/toxicity due to?
- Exposure to high amounts of copper
- *sheep is very susceptible
- *acute and chronic form
What is the secondary copper poisoning due to?
- DECREASED copper excretion
**What are the causes of decreased copper excretion?
- Secondary to hepatic damage (Ex. ruminants eating hepatotoxic plants)
- Hereditary mutation (ex. **Bedlington terrier, due to mutation in COMMD1 gene)
Primary copper poisoning chronic form steps
- Oral exposure
- Cooper binds to metallothionein (MTH) within enterocytes
- Absorption into blood and Cu binds to ceruloplasmin
- Taken up by liver and binds to MTH
a. Stored in liver and excreted in bile - IF Cu overload
a. Hepatic damage
b. Release of Cu to blood
c. Intravascular hemolysis and hemoglobinuric nephrosis
What is the mechanism of chronic of cooper poisoning?
- *cooper=oxidizing agent
- Oxidative damage to RBC=intravascular hemolysis
- Oxidative damage to liver=centrilobular to massive necrosis
**How would you diagnose copper poisoning?
- Take a FRESH liver sample
- *tends to happen during pregnancy or delivery
Cooper toxicity GROSSLY
- *black kidneys (due to hemoglobinuric nephrosis)
- Icterus due to destruction of RBCs and increased bilirubin AND liver is damaged (pre-hepatic and hepatic causes of icterus)
- Enlarged spleen: activation of macrophages
What is hemosiderin? What are some examples of hemosiderin accumulation?
*iron derived pigment
- 1. Hemolytic anemia
- 2. Hemosiderosis
What is hemosiderosis?
- Genetic mutation causing multisystemic accumulation of hemosiderin
- NO lesions
- *if lesions develop=call it hemochromatosis
Parasite hematin
- Liver flukes produce dark excreta which often stain the migratory tract within the liver
What are the 3 portals of entry into the liver?
- Hematogenous
- Ascending from intestine through bile ducts
- Direct penetration
What is it called if bile ducts and liver are involved in inflammation?
- chollangiohepatitis
What does acute hepatitis look like grossly?
- White spots indicative of necrosis and inflammation (NOT RAISED)
- NO chronic features
- *can be severe but rare
What does chronic hepatitis look like grossly?
- ***Fibrosis: due to being unable to regenerate
- Nodular regeneration
- Granulomas: chronic
- Abscesses: chronic
- VERY SEVERE
