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Systemic Pathology II > Hepatobiliary System, Pt. 2 > Flashcards

Hepatobiliary System, Pt. 2 Flashcards

1
Q

What are the major functions of the liver?

A
  • bile synthesis and secretion
  • bilirubin metabolism
  • carbohydrate metabolism
  • lipid metabolism
  • protein synthesis
  • ammonia metabolism
  • xenobiotic metabolism
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2
Q

How is bilirubin normally metabolized and eliminated?

A
  • RBC enters spleen and is phagocytized
  • hemoglobulin is broken down into heme and globulin
  • globulin is further broken down into amino acids
  • heme is broken down into iron and porphyrin, which becomes unconjugated bilirubin
  • unconjugated bilirubin binds to albumin and is transported to hepatocytes, which conjugate it and allows to be excreted in the biliary system
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3
Q

What is a common sequel to bilirubin metabolism dysfunction? How does it look grossly?

A

hyperbilirubinemia = icterus (jaundice)

yellow staining of skin, mucous membranes, and fat

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4
Q

What are 3 types of causes for icterus?

A
  1. prehepatic
  2. hepatic
  3. posthepatic
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5
Q

What are 2 causes of prehepatic icterus?

A
  1. increased unconjugated bilirubin
  2. hemolysis (immune-mediated, infectious, metabolic, trauma, toxin)
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6
Q

What are 2 causes of hepatic icterus?

A
  1. defective uptake or conjugation of conjugated or unconjugated bilirubin
  2. liver disease or congenital anomalies
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7
Q

What are 2 causes of posthepatic icterus?

A
  1. increased conjugated bilirubin
  2. bile duct obstruction (thrombus, stone, neoplasia)
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8
Q

What causes canalicular plugging? How does it look histologically?

A

dysfunction of bilirubin metabolism causes it to accumulate in hepatic canaliculi

brown, amorphous globular pigments (bilirubin) in canaliculi

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9
Q

How does the liver control carbohydrate metabolism?

A

regulates plasma glucose concentration by mediating glycogenolysis and glycogenesis

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10
Q

What are 2 causes of glycogen accumulation in the liver?

A
  1. excess glucocorticoids (steroid hepatopathy) in dogs - endogenous (Cushings = increased cortisol) and exogenous
  2. glycogen storage diseases
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11
Q

How does glycogen accumulation in the liver affect its color?

A

diffuse yellow-tan color changes

  • glucocorticoid-induced hepatopathy, dog
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12
Q

How does glycogen accumulation in the liver appear histologically?

A

amorphous pink strands within swollen hepatocytes with central nuclei

  • glucocorticoid-induced hepatopathy, dog
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13
Q

How does lipid metabolism occur in the healthy liver? How does insulin affect this process?

A
  • dietary sugary causes de novo lipogenesis, forming fatty acids within the liver
  • triglycerides from adipose tissue becomes FFA that are delivered to the liver and metabolized into fatty acids
  • lipids within the liver decrease β-oxidation in mitochondria and are transported to tissue by VLDL particles

insulin will block the transformation of triglycerides into FFA to decrease fatty acid metabolism in the liver and blood glucose levels

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14
Q

What happens to lipid metabolism within the diseased liver?

A

increased dietary sugar, obesity, and insulin resistance will increase the rapid formation of FFA and triglyceride accumulation in the liver

  • the liver will be unable to keep up with transportation to tissues, which leads to triglyceride accumulation and lipidosis
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15
Q

What are 6 causes of hepatic lipidosis (fatty change/steatosis)

A
  1. high-fat or cholesterol diet
  2. negative energy balance (secondary to anorexia, pregnancy) causes the liver to work harder to move lipids
  3. toxin
  4. ketosis (DM)
  5. endocrine disordered (DM, hypothyroidism)
  6. idiopathic
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16
Q

In what species is idiopathic hepatic lipidosis commonly seen?

A

miniature horses and donkeys

17
Q

Hepatic lipidosis, cat:

A
  • secondary to DM
  • increased lipids causes a diffuse pallor/yellowish color change
18
Q

Hepatic lipidosis, sheep:

A
  • secondary to pregnancy toxemia
  • negative energy balance
  • rounded edges
19
Q

Hepatic lipidosis, donkey:

A
  • idiopathic equine hyperlipidemia
  • yellow
  • hepatomegaly
20
Q

How does hepatic lipidosis appear histologically?

A

lipid accumulation within hepatocytes causes them to swell, forming vacuoles (without any staining) and push nuclei to the periphery

21
Q

What proteins does the liver produce? How does hepatic failure affect this?

A

albumin, transport proteins, lipoproteins, clotting factors, fibrinolysis proteins, acute phase proteins

hypoproteinemia, metabolic disease, and bleeding tendencies

22
Q

What are 3 examples of how hepatic failure affects protein synthesis?

A
  1. coagulopathy
  2. hepatocutaneous syndrome (superficial necrolytic dermatitis)
  3. ascites (decreased osmotic pressure from hypoproteinemia)
23
Q

What is the pathogenesis of rodenticide toxicosis? What are 3 common causes of this?

A
  • inhibition of vitamin K epoxide-reductase blocks the activation of vitamin K
  • this decreases the production of vitamin K-dependent coagulation factors (II, VII, IX, X) leading to hemorrhgae
  1. prescription medications (warfarin, coumadin)
  2. anticoagulant rodenticides (warfarin, brodifacoum)
  3. moldy sweet clover (dicumarol)
24
Q

How is rodenticide toxicosis treated?

A
  • vitamin K
  • blood transfusion
25
Q

How does superficial necrolytic dermatitis present? In what dogs is this most common?

A

hyperkeratosis of the paw pad, distal limbs, and perioral/periocular areas with bilaterally symmetrical erythema, scaling, crusting, erosions, and ulcers

small breed, geriatric

26
Q

What 3 conditions is superficial necrolytic dermatitis associated with? How can it be diagnosed on bloodwork and ultrasound?

A
  1. liver disease
  2. glucagonomas
  3. diabetes mellitus

hypoaminoacidemia, hyperglucagonemia

heterogeneity and nodules on liver

27
Q

What is thought to be the pathogenesis of superficial necrolytic dermatitis?

A

liver disease decreases amino acid synthesis, which leaves little nutrients left for the skin

28
Q

How does liver disease lead to edema and acites?

A
  • hepatitis causes a decrease in protein production
  • the resulting hypoproteinemia then decreases plasma colloid osmotic pressure
  • changed protein gradient causes the leakage of fluid into the abdomen and out of blood vessels
29
Q

How does normal ammonia metabolism occur in the liver?

A
  • metabolism of amino acids forms ammonia
  • ammonia is then converted into urea
  • urea is excreted in the urine
30
Q

What is a common result of ammonia metabolism dysfunction? What is the pathogenesis?

A

hepatic encephalopathy

  • liver failure allows a buildup of ammonia in the blood since it is unable to convert it into urea
  • blood with ammonia reaches the brain and causes abnormal neurotransmission in the CNS
  • this results in encephalopathy
31
Q

What allows for xenobiotic metabolism in the liver?

A

cytochrome P450 in the smooth endoplasmic reticulum (microsomes) of hepatocytes metabolize xenobiotics in preparation for excretion in bile or urine

32
Q

What is the most common pattern of toxicant-induced liver disease? What is a common example that causes this?

A

centrilobular necrosis

photosensitization

33
Q

What are the 3 types of photosensitization dermatitis?

A

TYPE 1 = primary; ingestion of exogenous agents, like plants and drugs)

TYPE 2 = endogenous; congenital erythropoietic porphyria (porphyrin accumulates and is photodynamic)

TYPE 3 = hepatogenous photosensitization; ingestion of photodynamic plant toxins (Lantana camara, Senecio spp.) and mycotoxins that are transported to the skin

34
Q

How does hepatogenous photosensitization present? What causes this?

A

sun-exposed skin of the face, ears and lightly pigmented regions become intensively pruritic and erythema forms, progressing into crusts, erosion, ulcers, and sloughing of the skin

impaired capacity of the liver to excrete phytophorphyrins causes their accumulation in the blood and delivery to the skin, causing dermatitis

35
Q

What are the 2 major aspects of the immune response in the liver?

A
  1. synthesis and release of acute phase proteins, like C-reactive protein, amyloid A, α1-antitrypsin, and complement factors
  2. enriched with innate immune cells, like Kupfer cells, dendritic cells, NK cells, and NK T-lymphocytes
36
Q

Where are Kupfer cells found in the liver?

A

found within sinusoids, closely associated with hepatocytes —> disc-shaped

  • stained with antibodies against myeloperoxidase
37
Q

What is the most common cause of amyloidosis in the liver? How does this affect the liver?

A

chronic inflammation causes macrophage activation and production of IL-1 and IL-6, which causes hepatocytes to produce increased amounts of serum amyloid associated protein and deposit amyloid into the space of Disse

deposition of amyloid compresses hepatocytes, causes atrophy, interferes with sinusoidal transfer of blood and nutrients, and predisposes the liver to rupture

38
Q

Hepatic amyloidosis, duck:

A
  • diffusely yellow/orange
  • feels waxy
39
Q

How does hepatic amyloidosis look histologically? How can it be stained?

A

pink amorphous material (amyloid) dilates sinusoids and compresses hepatocytes, causing a disruption in their basement membranes and usual chord/plate appearance (messy reticulin stain)

Congo red —> birefringent apple green

Systemic Pathology II (24 decks)

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