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Equine Med Final (Old Material) > Hepatic disease (key points only) > Flashcards

Hepatic disease (key points only) Flashcards

1
Q

6 things to look for with chronic infectious disease

A
  1. Neutrophilia (more often than not without a left shift)
  2. Monocytosis (less common in horses)
  3. Normocytic, normochromic, nonregenerative anemia
  4. Hyperfibrinogenemia
  5. Hyperglobulinemia
  6. Thrombocytosis
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2
Q

Hepatocellular injury enzymes in horses

A
  • SDH (best, most specific)

- AST

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3
Q

Biliary tract disease in horses

A
  • GGT is best

- Very specific

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4
Q

Hepatic function assessment

A
  • Bile acids
  • Bilirubin (conjugated vs unconjugated)
  • BUN, ammonia (BUN down, ammonia up)
  • glucose (hypoglycemia; less common in horses)
  • Triglycerides
  • PT/PTT (go down end stage)
  • Albumin, TP
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5
Q

Polyclonal gammopathy in liver dysfunction pathogphysiology

A
  • Inflammatory
  • Can be acute phase globulins
  • Goes up because there is inflammation; liver filters toxins with Kupffer cells
  • If the liver isn’t functioning, then those toxins go systemic
  • Poor prognostic indicator
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6
Q

Things that can increase bile acids

A
  • prolonged fasting
  • Increased in liver disease (more than with fasting alone)
  • concentrations highest with biliary obstruction
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7
Q

Normal ratio of unconjugated to conjugated bilirubin in a healthy horse

A
  • Unconjugated = indirect

- Conjugated = direct bilirubin

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8
Q

Things that increase unconjugated bilirubin

A
  • Hemolysis
  • Anorexia (causes ligandin molecule to go away so that bilirubin can’t get into the liver)
  • Drugs
  • Acute hepatocellular disease (conjugated by the liver)
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9
Q

What should you suspect if conjugated bilirubin is >25% of total bilirubin but <30%?

A

-Suspect hepatocellular disease

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10
Q

What should you suspect if conjugated bilirubin is >30%?

A
  • Biliary disease
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11
Q

Urobilinogen int he urine

A
  • Indicates patent bile duct
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12
Q

Elevated ammonia correlation with severity

A
  • No correlation between blood ammonia and severity
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13
Q

What is the best side of the horse to view the liver on?

A
  • Most of it is on the right side
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14
Q

Scoring system for biopsy

A
  • Fibrosis
  • Megalocytosis or necrosis
  • Leukocytic infiltrate
  • Hemosiderin deposition
  • Biliary hyperplasia
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15
Q

Most severe liver disease changes?

A
  • Biliary hyperplasia
  • Fibrosis
  • These are the most irreversible
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16
Q

Biopsy score and survival

A
  • if 0, 97% survival
  • if 2-6, 67%
  • if 7+, 14%
17
Q

Poor prognostic indicators

A
  • Hepatoencephalopathy
  • Intravascular hemolysis (end stage)
  • Coagulopathy
  • Marked weight loss
  • Severe hepatic fibrosis
  • Increased AP, GGT, bile acids
  • Decreased albumin, increased globulins
  • Decreased BUN
  • Ultrasound abnormalities
18
Q

Supportive care for hepatic encephalopathy

A
  • Decrease absorption of ammonia and other toxic metabolites
  • Mineral oil
  • Activated charcoal
  • NOT lactulose or neomycin
19
Q

Diet for liver disease

A
  • Low protein, high carb diet

- Beet pulp, sorghum, milo

20
Q

Fluid therapy for liver disease

A
  • IV fluids (LRS +/- dextrose) with B vitamins
  • Avoid drugs that require hepatic metabolism and/or excretion
  • Vitamin K1
  • Avoid sunlight (Photosensiization)
21
Q

Cholangiohepatitis/cholelithiasis overall pathogenesis

A
  • Unconjugated bilirubin combines with calcium to form calcium bilirubinate
  • Ascending infection
  • Beta-glucuronidase producing bacteria unconjugate bilirubin in the bile duct
  • Almost always multiple stones and spread
22
Q

Treatment for cholelithiasis

A
  • Long-term antibiotics
  • Usually enteric organisms isolated
  • Penicillin/gentamicin, chloramphenicol, enrofloxacin, TMS, ceftiofur
  • DMSO
  • Ursodiol to increase bile production and make more liquid
  • Surgery is VERY DIFFICULT
23
Q

Prognosis of cholelithiasis

A
  • Depends on extent of hepatic fibrosis, severity of signs
  • Extensive fibrosis CAN resolve
  • 77-85% survival with medical or medical/surgical treatment
24
Q

What can cause icterus in horses?

A
  • Anorexia

- Liver disease

25
Q

Toxic causes of hepatocellular disease

A
  • Pyrrolizidine alkaloid toxicity
  • Aflatoxin
  • Alsike clover
  • Many others
26
Q

Other dfdx for liver injury

A
  • Toxic hepatopathy (mentioned above)
  • Theiler’s disease
  • Other viral infections?
  • Chronic active hepatitis
  • Idiopathic hepatic fibrosis
27
Q

Diagnostic plan for non-specific liver injury

A
  • Ultrasound
  • Biopsy
  • Evaluate feed
  • Look at other horses in the same environment
28
Q

PA containing plants

A
  • Senecio
  • Croatalaria
  • Amsinckia
  • Heliotropium
29
Q

Pathogenesis of pyrrolizidine alkaloids

A
  • Metabolized to toxic pyrrole derivatives
  • Pyrroles alkylate nucleic acid and proteins
  • Cells cannot divide, so hepatocytes enlarge, forming megalocytes
  • When megalocytes die, fibrosis occurs
  • Liver shrinks, becoming firmer
30
Q

Theiler’s disease

A
  • Acute serum hepatitis
  • Onset of signs acute to subacute
  • Equine origin biological given 4-10 weeks prior
  • Most affected horses will die
  • Thought to be an equine parvovirus
  • Clinically normal horses may be viremic and/or seropositive
31
Q

Lipid metabolism

A
  • Stress, energy balance
  • Deplete glycogen
  • Mobilize fat stores
  • Catecholamines, glucocorticoids
  • Triglyceride and VLDL synthesis
  • Minimal ketone production
  • Hyperlipemia and hepatic lipidosis

VERY MINIMAL KETONE PRODUCTION*

32
Q

Who gets hyperlipemia?

A
  • Ponies and minis
  • Relatively insulin insensitive
  • Rare for adult horses to be affected
33
Q

PFs for hyperlipemia

A
  • Pregnancy, disease, parasitism, transport, pituitary disease
34
Q

Clinical signs for hyperlipemia

A
  • Icterus
  • Anorexia, weakness
  • Depression
  • Diarrhea, mild colic
  • Dependent edema due to microvascular thrombosis and vasculitis
35
Q

Complications of hyperlipemia

A
  • vascular thrombosis, fat embolism
  • May lead to renal insufficiency, edema, pancreatitis
  • Azotemia prevents lipid removal from blood by inhibiting lipoprotein lipase
36
Q

Diagnosis of hyperlipemia

A
  • Stressed pony
  • Hyperlipidemia is TG <500mg/dL
  • Hyperlipemia is TG >500 mg/dL, opalescent plasma
  • Increased liver enzyme activity
  • Also want to check serum creatinine, electrolytes
37
Q

Treatment for hyperlipemia

A
  • Treat hepatic disease
  • Improve energy intake and balance (often hooked up to a slow dextrose drip)
  • Critical care case
  • Eliminate stress or concurrent disease
  • Inhibit fat mobilization from adipose tissue
  • Increase TG uptake by tissues (heparin)
38
Q

Prognosis of hyperlipemia

A
  • Mortality in 60-100% (untreated)
  • Death often results from underlying disease
  • If aggressive, most mini horses with TG <1200 can survive
  • Educate owners to prevent disease
39
Q

What is the most common cause of liver enzyme elevations?

A
  • USUALLY a nonspecific cause from an issue somewhere else in the body

Equine Med Final (Old Material) (11 decks)

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