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SYSTEMIC PATHOLOGY 2 > 2 - Liver II > Flashcards

2 - Liver II Flashcards

1
Q

Hepatic failure: clinical term (can’t determine when dead)

A
  • Loss of adequate haptic function as a consequence of either acute or chronic hepatic damage
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2
Q

What are the consequences of hepatic failure

A
  1. Hepatic encephalopathy
  2. Metabolic abnormalities
  3. Vascular and hemodynamic alterations
  4. Cutaneous manifestations
    *can happen in all animals
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3
Q

Hepatic encephalopathy due to hepatic failure

A
  • Accumulation of ammonia due to reduced uptake by liver
  • *ammonia=TOXIC TO BRAIN
    o Abnormal neurotransmission in the CNS and neuromuscular system
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4
Q

Metabolic abnormalities due to hepatic failure

A
  • Bleeding tendences due to: decreased synthesis of coagulation factors
  • Decreased albumin synthesis lead to EDEMA everywhere
    o Means it’s quite far along
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5
Q

Vascular and hemodynamic alterations due to hepatic failure

A
  • Ex. portosystemic shunt (extrahepatic shunt)
  • *abnormal communication between portal vein and systemic circulation
  • *can also get an intrahepatic shunt
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6
Q

**How does ci portosystemic shunt occur?

A
  • *secondary to liver failure
    1. Injury and diffuse liver fibrosis
    1. Portal vein bring blood into a noncompliant firm liver=resistance to blood flow
    1. 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
    1. Ascites: due to increase pressure and decreased albumin synthesis
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7
Q

What are some other consequences of an acquired portosystemic shunt?

A
  • Serum acid bile acids go up (REDUCED UPTAKE)
  • Serum ammonia go up
  • Ammonia biurate crystals (bladder, urine)
  • Hepatic encephalopathy
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8
Q

What are the different cutaneous manifestations from hepatic failure?

A
  • Superficial necrolytic dermatitis
  • Photosensitization secondary to hepatic dysfunction
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9
Q

Superficial necrolytic dermatitis (due to hepatic failure)

A
  • 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
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10
Q

Photosensitization secondary to hepatic dysfunction

A
  • *more COMMON (more in RUMINANTS)
    1. Eat plants with chlorophyl and converted to Phylloerythrin by GI bacteria
    1. Phylloerythrin is absorbed and goes to portal vein to be excreted in bile
    1. WHEN liver damage: phylloerythrin accumulates in SKIN=absorbs UV light=oxidative damage and necrosis
  • **RESTRICTED TO NON-PIGEMENTED AREAS
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11
Q

What is primary photosensitization from?

A
  • Eating toxic materials in plants
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12
Q

What are some developmental anomalies and incidental findings in the liver?

A
  • Congenital biliary cysts
  • Polycystic disease
  • Tension lipidosis
  • Capsular fibrosis
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13
Q

Congenital biliary cysts

A
  • Single or few cysts can be found=INCDIENTAL FINDING
  • *more common in CATS
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14
Q

Polycystic disease

A
  • 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
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15
Q

Tension lipidosis

A
  • Incidental finding
  • Pale areas in livers of HORSES and CATLLE
  • Occur adjacent to insertion of ligament (serosal) attachment
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16
Q

Capsular fibrosis

A
  • Incidental finding in HORSE
  • Thought to be related to STRONGYLE SP. Migration
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17
Q

Post mortem changes to the liver

A
  • Pale
  • Blue green staining from bile
  • Very friable
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18
Q

What are some metabolic disturbances of the liver?

A
  • Hepatocellular lipidosis (steatosis
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19
Q

What is hepatic lipidosis?

A
  • When lipid accumulates within liver
    o Mainly TRIGLYCERIDES that are accumulated
  • Several mechanisms
  • *yellow, float, rounded edges
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20
Q

What is the gross appearance of hepatic lipidosis: mild and severe?

A
  • Mild: enhanced lobular patterns
  • Sever: YELLOW
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21
Q

What are the several mechanisms of hepatic lipidosis?

A
  • 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
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22
Q

When might there be increased mobilization of FFA from adipose tissues?

A
  • 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
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23
Q

What happens when there is decreased O2 and energy (anemia, hypoxia) and hepatic lipidosis?

A
  • Processes that need oxygen do NOT happen
  • TGs are NOT being used, so they ACCUMULATE
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24
Q

What happens with decreased protein intake (starvation) and hepatic lipidosis?

A
  • Using fat stores (lipolysis)
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25
Q

Hormonal abnormalities (insulin) and hepatic lipidosis?

A
  • *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
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26
Q

Toxin induced fatty change and hepatic lipidosis

A
  • *too many toxins!
27
Q

What are some examples of hepatic lipidosis in vet med?

A
  • Pregnancy toxemia
  • Bovine fatty liver disease
  • Feline fatty liver syndrome
  • Hyperlipemia
  • Endocrine disorders (diabetes and hypothyroidism)
28
Q

Pregnancy toxemia: species and when

A
  • Sheep in late pregnancy
29
Q

Bovine fatty liver disease

A
  • 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
30
Q

Feline fatty liver syndrome

A
  • Obese fats become anorectic for unknown reason and start mobilizing fat
31
Q

Hyperlipemia

A
  • Syndrome in ponies, miniature horses and donkeys
  • Associated with increased demand on energy
  • Occurs after an event causing anorexia
32
Q

Endocrine disorders (diabetes and hypothyroidism)

A
  • Insulin is anabolic hormone
    o Lack of insulin or insulin response=increased mobilization of fat
  • Hypothyroidism=hypercholesterolemia and increased serum lipids
    o OLDER DOGS
33
Q

Glycogen accumulation (steroid hepatopathy): species and 2 causes

A
  • DOGS
  • 2 causes
    o Prolonged administration of corticosteroids (external)
    o Secondary to hyperadrenocorticism
34
Q

What is the mechanism of glycogen accumulation steroid hepatopathy)?

A
  • Gluconeogenesis and glycogen storage
  • *enlarged and BRONZE in colour
  • Can cause elevation in liver enzymes clinically
35
Q

Disturbances of outflow

A
  • 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)
36
Q

What happens with acute heart failure? What does it look like grossly?

A
  1. Congestion at centrilobular areas
  2. Hepatocytes within centrilobular areas may undergo fatty degeneration
    GROSSLY: lobular pattern may be slightly enhanced
37
Q

What happens with chronic heart failure? What does it look like grossly?

A
  1. Sinusoids at centrilobular area become DILATE (appear red grossly)
  2. Hepatocytes at centrilobular area undergo atrophy then degeneration and necrosis
  3. Hepatocytes at periportal area undergo fatty change (appear yellow grossly)
    GROSSLY: enlarged (rounded edges) and enhanced lobular pattern (NUTMEG LIVER)
38
Q

What are some disturbances of INFLOW that occur?

A
  1. Anemia (decrease flow)
  2. Congenital portosystemic shunt
39
Q

Anemia (decreased flow): acute vs. chronic

A
  • acute: centrilobular or paracentral DEGENERATION of hepatocytes
  • chronic: ATROPHY of centrilobular hepatocytes
  • GROSSLY: enhanced lobular pattern
40
Q

Congenital portosystemic shunt (age group and 2 types)

A
  • *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
41
Q

What does congenital portosystemic shunt look like grossly? (non-liver)

A
  • Diffuse liver atrophy
  • ‘blue’ in mesentery
  • NO ascites (NO hypertension)
42
Q

Congenital intrahepatic shunt: large breed dogs

A
  • 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
43
Q

Congenital extrahepatic shunt: short breed dogs, what are the consequences?

A
  • Diffuse liver atrophy (NO FIBROSIS)
  • Serum bile acids go up
  • Serum ammonia goes up
  • Ammonian biurate crystals (bladder)
  • Hepatic encephalopathy
44
Q

What is an incidental vascular finding of the liver?

A
  • Telangiectasis
    o Dilated sinusoids
    o *common in cattle, horses and cats (typically older)
    o Appear as red areas in liver
45
Q

Liver infarction

A
  • 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
46
Q

What are 4 types of hepatic accumulations?

A
  • Amyloid: 2 types
  • Copper
  • Hemosiderin
  • Parasite hematin
47
Q

Primary amyloidosis

A
  • Produced by plasma cells that become cancerous (amyloid light chain or AL)
48
Q

What can amyloid accumulation in the liver be secondary to?

A
  • Chronic inflammation (amyloid A)
  • *secondary is more common
49
Q

Amyloidosis: grossly

A
  • Enlarged
  • Orange
  • Friable
50
Q

What can amyloidosis cause?

A
  • Hepatic failure
  • Rarely: hepatic rupture (horses)
51
Q

What is primary copper accumulation/toxicity due to?

A
  • Exposure to high amounts of copper
  • *sheep is very susceptible
  • *acute and chronic form
52
Q

What is the secondary copper poisoning due to?

A
  • DECREASED copper excretion
53
Q

**What are the causes of decreased copper excretion?

A
  1. Secondary to hepatic damage (Ex. ruminants eating hepatotoxic plants)
  2. Hereditary mutation (ex. **Bedlington terrier, due to mutation in COMMD1 gene)
54
Q

Primary copper poisoning chronic form steps

A
  1. Oral exposure
  2. Cooper binds to metallothionein (MTH) within enterocytes
  3. Absorption into blood and Cu binds to ceruloplasmin
  4. Taken up by liver and binds to MTH
    a. Stored in liver and excreted in bile
  5. IF Cu overload
    a. Hepatic damage
    b. Release of Cu to blood
    c. Intravascular hemolysis and hemoglobinuric nephrosis
55
Q

What is the mechanism of chronic of cooper poisoning?

A
  • *cooper=oxidizing agent
  • Oxidative damage to RBC=intravascular hemolysis
  • Oxidative damage to liver=centrilobular to massive necrosis
56
Q

**How would you diagnose copper poisoning?

A
  • Take a FRESH liver sample
  • *tends to happen during pregnancy or delivery
57
Q

Cooper toxicity GROSSLY

A
  • *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
58
Q

What is hemosiderin? What are some examples of hemosiderin accumulation?

A

*iron derived pigment
- 1. Hemolytic anemia
- 2. Hemosiderosis

59
Q

What is hemosiderosis?

A
  • Genetic mutation causing multisystemic accumulation of hemosiderin
  • NO lesions
  • *if lesions develop=call it hemochromatosis
60
Q

Parasite hematin

A
  • Liver flukes produce dark excreta which often stain the migratory tract within the liver
61
Q

What are the 3 portals of entry into the liver?

A
  • Hematogenous
  • Ascending from intestine through bile ducts
  • Direct penetration
62
Q

What is it called if bile ducts and liver are involved in inflammation?

A
  • chollangiohepatitis
63
Q

What does acute hepatitis look like grossly?

A
  • White spots indicative of necrosis and inflammation (NOT RAISED)
  • NO chronic features
  • *can be severe but rare
64
Q

What does chronic hepatitis look like grossly?

A
  • ***Fibrosis: due to being unable to regenerate
  • Nodular regeneration
  • Granulomas: chronic
  • Abscesses: chronic
  • VERY SEVERE

SYSTEMIC PATHOLOGY 2 (8 decks)

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