Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Equine Medicine > Liver Diseases > Flashcards

Liver Diseases Flashcards

1
Q

When are horses naturally slightly icteric?

A

when off feed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the major functions of the liver?

A
  • production of plasma proteins, coagulation factors, and acute phase proteins
  • glycogenolysis
  • gluconeogenesis
  • intermediate metabolism of carbohydrates, proteins, and lipids
  • stores fat-soluble vitamins
  • detoxifying organ
  • first pass metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are some acute and chronic signs of liver disease? When do signs start?

A

ACUTE - most common; hepatic encephalopathy, abnormal behavior, icterus, jaundice

CHRONIC - weight loss, intermittent fever or colic, diarrhea, ascites, pruritus, photosensitization

> 60-80% of parenchyma nonfunctional

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the 2 most common causes of hepatic encephalopathy? What is the most common sign?

A
  1. hepatic dysfunction
  2. portosystemic shunt

behavioral changes - depression, incoordination, aimless wandering, blindness, yawning, stridor, head pressing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 3 main aspects of the pathophysiology of hepatic encephalopathy?

A
  1. buildup of neurotoxic ammonia
  2. release of false neurotransmitters (serotonin)
  3. imbalanced neurotransmission caused by GABA and glutamate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What 2 induction liver enzymes are used for diagnosing liver disease in horses? What specificity do they have?

A

(biliary!)

  1. GGT - liver (screening), kidney, pancreas
  2. ALP - liver, bone, intestine, macrophages, placenta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What problems are most commonly associated with increased GGT and ALP?

A

(biliary!)

GGT - biliary hyperplasia and cholestasis, naturally high in young animals (found in colostrum) and racehorses, right colonic displacement, proximal enteritis

ALP - biliary hyperplasia, cholestasis, increased synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What 3 leakage enzymes are used to diagnose liver disease in horses? What specificity do they have?

A

(liver cytosol!)

  1. IDH (SDH) - liver
  2. AST - liver, muscle, heart
  3. LDH - isoenzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What problems are associated with increased IDH (SDH), AST, and LDH?

A

(liver cytosol!)

IDH (SDH) = acute insult (short life, not stable)

AST = inflammation, infection, metabolic disease, toxins, neoplasia

LDH = acute insult (short life, not specific)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Other than liver enzymes, what biochemistry diagnostics are used to diagnosing liver disease?

A
  • direct (conjugated), indirect (unconjugated) bilirubin
  • bile acids
  • triglycerids
  • clotting factors
  • ammonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the purpose of using ultrasound when diagnosing liver disease? Where is the probed placed to locate the equine liver?

A
  • determine size, location, vessel diameter, and texture
  • abscess, cholelithiasis, neoplasia, and fibrosis location

right last rib to 10th ICS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What must be checked before performing liver biopsies? How are they used? How are they performed?

A

clotting times

diagnosis and etiology —> culture, prognosis

ultrasound guided - at 14th ICS, measure from tuber coxae to point of shoulder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hepatic failure in horses:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are 4 causes of viral liver disease in horses? How are they most commonly diagnosed?

A
  1. Equine parvovirus hepatitis - acute, 33% of horses have antibodies, STRONG association with Theiler’s disease
  2. nonprimate equine Hepacivirus - like huma hepatitis C, acute and chronic, 80% of horses have antibodies, NOT associated with Theiler’s
  3. Equine pegivirus 1 and 2
  4. Equine hepatitis B

PCR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Theiler’s disease? What is thought to be the etiology?

A

common cause of acute liver failure in adult horses - aka serum hepatitis, post-vaccinal hepatitis

VIRAL - Equine Parvovirus Hepatitis (EqPV-H)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are some expected transmission pathways of Theiler’s disease?

A
  • product recipients
  • in contact with product receipients
  • no known contact possible!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are 4 risks to developing Theiler’s disease?

A
  1. biologic product administration (TAT)
  2. broodmares
  3. recent castration
  4. seasonal - Summer to Fall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What clinical signs are most commonly seen with Theiler’s disease? What are 4 atypical signs?

A
  • acute hepatic failure within 2-3 months after biologic product contact
  • anorexia
  • hepatoencephalopathy - pica, yawning
  • icterus
  • fever
  • dermatitis

weight loss, edema, icterus, ARDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What 6 lab results support Theiler’s disease diagnosis? What other tests can be done?

A
  1. increased AST, LDH, SDH, and GGT
  2. increased total and unconjugated bilirubin
  3. increased bile acids
  4. decreased BUN, hyperammonemia
  5. increased PT, PTT
  6. decreased albumin

PCR, biopsy (hepatocyte necrosis - dish rag liver)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the focus of treating Theiler’s disease? In what 7 ways is this done?

A

controlled hepatoencephalopathy

  1. dextrose and balanced electrolytes
  2. diet low in protein and high in carbohydrates - sorghum, milo, beet pulp
  3. antioxidants and antiinflammatories
  4. systemic antimicrobials
  5. Neomycin, lactulose, mineral oil
  6. sedation
  7. corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Tyzzer disease? What is its etiology?

A

common cause of acute hepatitis in foals 7-42 days old (also affects intestines and heart)

Clostridium piliforme - spore-forming intracellular anaerobe, multiple strains found in the environment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How is Tyzer disease transmitted? What are the 2 most common risk factors?

A

colonization in the GIT and liver allows fecal-oral transmission from carriers

  1. time of year - Spring = mare on lush pasture
  2. resident status
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the pathophysiology of Tyzzer disease?

A
  • overgrowth of C. piliforme in the gut of the mare following exposure
  • foal ingests mare feces
  • bacteria is absorbed by portal circulation and reaches the liver

(sporadic or outbreaks seen)

24
Q

What are the 2 most common clinical signs of Tyzzer disease? What else is seen?

A

septic shock and liver failure

  • severe depression, fever
  • icterus,
  • coma, sudden death —> foal commonly found dead without prior signs
25
Q

What are the 4 most common laboratory signs of Tyzzer disease?

A
  1. overwhelming sepsis = leukopenia, hemoconcentration, hyperfibrinemia
  2. hypoglycemia
  3. severe acidosis
  4. increased IDH, AST, LDH, GGT, and ALP
26
Q

How is Tyzzer disease diagnosed?

A
  • post-mortem: acute multifocal hepatitis, lytic necrosis, enteritis and intrahepatocellular filamentous bacteria seen with silver stain
  • culture (difficult!)
  • PCR
27
Q

How is Tyzzer disease treated?

A
  • supportive care
  • high doses of Penicillin, Gentamycin, or Metronidazole
  • septic shock treatment

(highly fatal)

28
Q

What are the 2 major causes of chronic liver disease? What signs are most common with each?

A
  1. cholangiohepatitis - jaundice, fever, occasional colic, anorexia
  2. cholestasis (lithiasis) - recurrent colic and weight loss
29
Q

What are the most common causes if cholangiohepatitis?

A
  1. bacteremia
  2. ascending infection

(causes chronic liver disease)

30
Q

What are the 2 most common presentations of cholestasis? What are the 3 most common risk factors?

A
  1. biliary obstruction and liver disease
  2. incidental findings
  • middle-aged horses
  • cholangiohepatitis
  • stasis of bile
31
Q

What are the 4 most common clinical findings seen with chronic liver disease?

A
  1. recurrent colic
  2. intermittent pyrexia
  3. icterus
  4. weight loss
32
Q

What laboratory findings are indicative of chronic liver disease?

A
  • increased GGT and ALP
  • increased bilirubin
  • increased IDH, LDH, and AST
  • increased bile acids
  • inflammatory profiles
33
Q

How is ultrasound used to diagnose chronic liver disease? Where are choleliths most commonly found?

A
  • hepatomegaly
  • bile duct dilation = increased echogenicity
  • biopsy for histopath and culture

cranioventral part of the right liver - 6-8th ICS

34
Q

What broad-spectrum antimicrobials are most commonly used for chronic liver disease? How long?

A

Penicillin, Gentamycin, 3rd gen Cephalosporins, Trimethoprim/Sulfamethoxazole, Enrofloxacin + Metronidazole

6 weeks past normalization of GGT

35
Q

Other than antimicrobials what treatments are recommended for chronic liver disease?

A
  • DMSO
  • fluids
  • NSAIDs
  • bile salts - anti-inflammatory, choleretic
  • cholelithotomy or cholelithotripsy

prognosis based on fibrosis, clinical signs, and location

36
Q

What causes pyrrolizidine alkaloid toxicity? What does it cause?

A

ingestion of Senecio or Crotalaria plants, most common when horses have sparse access to food, hay, or pellets

chronic, progressive, often delayed liver disease

37
Q

What is the pathophysiology of pyrrolizidine alkaloid toxicity?

A
  • PA is activated into pyrrols in liver
  • pyrrol is absorbed, reach portal circulation, and reaches the liver again
  • pyrrols then cross-link DNA (dose-dependent), having an antimitotic and megalocytic effect
  • hepatocytes then no longer divide and are replaced by connective tissue
  • this causes liver failure, veno-occlusive disease, nad portal hypertension
38
Q

What clinical signs are seen with pyrrolizidine alkaloid toxicity?

A

CHRONIC liver failure due to insult over many years —> signs seem acute

  • weight loss
  • icterus
  • abnormal behavior
  • ohotosensitization
  • stridor, diarrhea
39
Q

How is pyrrolizidine alkaloid toxicity diagnosed with bloodwork? U/S? Biopsy?

A

increased GGT, ALP, bile acids, and bilirubin

increased echogenicity

chronic hepatitis - fibrosis, bile duct proliferation, megalocytosis

40
Q

What treatment is recommended for pyrrolizidine alkaloid toxicity? What also needs to be considered?

A
  • supportive therapy for liver failure
  • Pentoxifylline
  • SAMe
  • may improve with treatment and relapse once stopped (still ingesting!)

other horse on pasture need to be checked for toxicity on blood work, look out for toxic plants

41
Q

What are some other toxicities that can cause chronic liver failure?

A
  • alsike clover poisoning
  • panicum toxicity
  • iron toxicity
  • drug-induced hepatotoxicity
42
Q

What causes hyperlipemia/hepatic lipidosis? What are 3 risk factors?

A

high caloric need, but low intake results in life-threatening, fatty liver disease with cloudy serum

  1. well-conditioned, middle-aged
  2. ponies and donkeys
  3. early lactation, late pregnancy
43
Q

What is the pathophysiology of hyperlipemia?

A

high caloric need and stress with low intake cause a negative energy balance, resulting in….

  • fat mobilization
  • TG synthesis
  • secretion VLDL
  • fat accumulation and deposition
44
Q

What clinical signs are associated with hyperlipemia?

A
  • anorexia, depression, weakness
  • incoordination
  • diarrhea, colitis
  • colic
45
Q

What are 4 ways hyperlipemia is diagnosed?

A
  1. opaque plasma due to TG > 500 mg/dL
  2. increased bilirubin
  3. azotemia
  4. fatty liver infiltration (biopsy)
46
Q

How is hyperlipemia treated?

A

emergency!

  • treat negative energy balance
  • IV fluids
  • enteral/parental nutritional support - small volume q2-4hr with critical care meals
  • heparin
  • insulin for hyperglycemia
47
Q

When are antimicrobials used to treat liver disease? Which IV and long-term oral ones are most commonly used?

A

cholelithiasis, cholangitis, cholangiohepatitis

IV - Pen/Gen, Enrofloxacin, Metronidazole

PO - TMS, Enrofloxacin + Metronidazole, Chloramphenicol (careful - liver metabolism!)

48
Q

What is the most important aspect to hepatic encephalopathy treatment?

A

avoid self-trauma, minimize stress and neurological damage

  • sedation (careful with respiratory distress)
  • BZD antagonists - Flumazenil, Sarmazenil
  • antioxidants - SAMe, Acetylcysteine, Pentoxifylline
49
Q

What dietary management is recommended for hepatic encephalopathy?

A

low protein with high BCAA/AAA —> grass/oat hay, beet pulp, cracked corn

  • may need forced enteral or partial parenteral
50
Q

How can ammonia absorption and cerebral edema be decreased in cases of hepatic encephalopathy?

A

Neomycin, Lactulose, Acetic acid, mineral oil, Metronidazole

Furosemide, hypertonic saline, Mannitol 20% solution over 20-30 mins

51
Q

What fluid therapy is recommended for chronic liver disease? What is avoided?

A
  • hydration —> NaCl (0.9%) + Ca + dextrose + KCl, bicarbonate, glucose
  • colloids

whole blood or hetastarch

52
Q

What are 5 treatments used for inflammation and fibrosis associated with chronic liver disease?

A
  1. corticosteroids - Dexamethasone, Prednisolone
  2. NSAIDs
  3. vitamin E
  4. Pentoxyfyllin
  5. Colchicine
53
Q

What antioxidants are recommended for chronic liver disease?

A
  • SAMe
  • N-acetylcysteine
  • DMSO
54
Q

Which enzymes are increased with bile duct obstruction?

a. IDH, AST, LDH
b. GGT, ALP

What other parameters will be elevated?

A

B

  • conjugated BILI > 30% of total
  • bile acids
55
Q

Does the horse have a gallbladder?

A

NO

56
Q

What is the most important treatment in a horse with hepatic encephalopathy?

a. prevent self-trauma and stress, fluid therapy with dextrose
b. antimicrobials and antioxidants
c. fluid therapy alone

A

A

57
Q

Which of the following indicates cholestasis?

a. total BILI 5 mg/dL, conjugated BILI 2 mg/dL
b. total BILI 5 mg/dL, conjugated BILI 1 mg/dL
c. total BILI 5 mg/dL, conjugated BILI 0.5 mg/dL

A

A

Equine Medicine (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions