Hepatic disease (key points only) Flashcards
1
Q
6 things to look for with chronic infectious disease
A
- Neutrophilia (more often than not without a left shift)
- Monocytosis (less common in horses)
- Normocytic, normochromic, nonregenerative anemia
- Hyperfibrinogenemia
- Hyperglobulinemia
- Thrombocytosis
2
Q
Hepatocellular injury enzymes in horses
A
- SDH (best, most specific)
- AST
3
Q
Biliary tract disease in horses
A
- GGT is best
- Very specific
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
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
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
7
Q
Normal ratio of unconjugated to conjugated bilirubin in a healthy horse
A
- Unconjugated = indirect
- Conjugated = direct bilirubin
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)
9
Q
What should you suspect if conjugated bilirubin is >25% of total bilirubin but <30%?
A
-Suspect hepatocellular disease
10
Q
What should you suspect if conjugated bilirubin is >30%?
A
- Biliary disease
11
Q
Urobilinogen int he urine
A
- Indicates patent bile duct
12
Q
Elevated ammonia correlation with severity
A
- No correlation between blood ammonia and severity
13
Q
What is the best side of the horse to view the liver on?
A
- Most of it is on the right side
14
Q
Scoring system for biopsy
A
- Fibrosis
- Megalocytosis or necrosis
- Leukocytic infiltrate
- Hemosiderin deposition
- Biliary hyperplasia
15
Q
Most severe liver disease changes?
A
- Biliary hyperplasia
- Fibrosis
- These are the most irreversible
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
Toxic causes of hepatocellular disease
- Pyrrolizidine alkaloid toxicity
- Aflatoxin
- Alsike clover
- Many others
26
Other dfdx for liver injury
- Toxic hepatopathy (mentioned above)
- Theiler's disease
- Other viral infections?
- Chronic active hepatitis
- Idiopathic hepatic fibrosis
27
Diagnostic plan for non-specific liver injury
- Ultrasound
- Biopsy
- Evaluate feed
- Look at other horses in the same environment
28
PA containing plants
- Senecio
- Croatalaria
- Amsinckia
- Heliotropium
29
Pathogenesis of pyrrolizidine alkaloids
- 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
Theiler's disease
- 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
Lipid metabolism
- 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
Who gets hyperlipemia?
- Ponies and minis
- Relatively insulin insensitive
- Rare for adult horses to be affected
33
PFs for hyperlipemia
- Pregnancy, disease, parasitism, transport, pituitary disease
34
Clinical signs for hyperlipemia
- Icterus
- Anorexia, weakness
- Depression
- Diarrhea, mild colic
- Dependent edema due to microvascular thrombosis and vasculitis
35
Complications of hyperlipemia
- vascular thrombosis, fat embolism
- May lead to renal insufficiency, edema, pancreatitis
- Azotemia prevents lipid removal from blood by inhibiting lipoprotein lipase
36
Diagnosis of hyperlipemia
- 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
Treatment for hyperlipemia
- 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
Prognosis of hyperlipemia
- 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
What is the most common cause of liver enzyme elevations?
- USUALLY a nonspecific cause from an issue somewhere else in the body
