Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Y4 EQ - Gastrointestinal tract > Equine liver disease and hyperlipaemia > Flashcards

Equine liver disease and hyperlipaemia Flashcards

(57 cards)

Start Studying
1
Q

List the 5 functions of the equine liver

A

Digestive and secretory (bile salts)
Metabolic (CHO, protein, fat metabolism)
Detoxification/excretory (first pass from GIT)
Synthetic (clotting factors, proteins)
Storage (vitamins, minerals)

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

Describe the approach to investigating liver disease in horses

A
  • History and clinical examination
  • Suspicion -> conformation of liver disease
  • Determine aetiology
  • Assess liver function
  • Assess the severity of pathology and prognosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can you determine the aetiology of liver disease?

A

History
Testing in-contacts
Forage analysis
US
Biopsy
Serology/PCR

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

How can you assess liver function?

A

Blood analysis
Clinical signs

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

How can you assess the severity of pathology and prognosis in liver disease?

A

Liver biopsy
Blood analysis
Clinical signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the generalised clinical signs of liver disease

A
  • Not consistent: may be none, some or all
  • Focal, inflammatory and acute disease are more likely to show signs OR may be signs of liver failure
  • Jaundice
  • Weight loss
  • Depression/CNS signs
  • Skin lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the cause of jaundice?

A

Retention of bilirubin (unconjugated in horses)

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

List the 3 main differentials of jaundice

A

Anorexia (mild increase)
Haemolysis
Liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why does liver disease cause weight loss?

A

Failure of the liver to process nutrients -> negative energy balance

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

What depressive/CNS signs are seen in liver disease?

A

Quiet / dull
Yawning
May progress to:
- Somnolence (drowsiness or strong desire to fall asleep)
- Central blindness
- Head pressing
- Compulsive walking
- Sham chewing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why are CNS signs seen in liver disease?

A

One of the liver functions is to remove toxic substances e.g. ammonia. If these aren’t removed then a horse can develop CNS signs

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

Describe the main skin lesion seen in liver disease

A

Hepatic photosensitisation

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

Describe the pathogenesis of hepatic photosensitisation

A

Toxins in the skin, haven’t been removed by the liver so they are activated by UV light -> photosensitisation

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

List the DDx of hepatic photosensitisation

A
  • Tetracyclines
  • St John’s Wort
  • Immune mediated vasculitis
  • Contact e.g. clover
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List some other non-specific signs of liver disease

A
  • Haemorrhage
  • Colic
  • Oedema
  • Diarrhoea
  • Bilateral laryngeal paralysis
  • Anorexia/inappetence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which liver enzymes are of biliary origin in the liver

A

GGT
ALP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which liver enzymes are of hepatocellular origin in the liver

A

SDH
GLDH
AST
LDH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which 3 liver enzymes are liver specific

A

GGT
SDH
GLDH

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

Which 3 liver enzymes are not liver specific

A

AST
ALP
LDH

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

What are the non-liver sources of AST, ALP and LDH

A

AST - muscle
ALP - bone, intestine, kidney, pancreas, leukocytes
LDH - muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which liver enzyme is a sensitive indicator of liver disease?

A

GGT

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

Which liver enzyme is high in foals, pregnancy and GI disease?

A

ALP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are liver enzymes used to assess?

Study These Flashcards
A

Liver damage, not function

24
Q

Increased GGT and ALP indicate what type of liver disease?

Study These Flashcards
A

biliary – e.g. cholangiohepatitis

25
Increased AST, GLDH and LDH indicate what type of liver disease?
hepatocellular – e.g. serum hepatitis
26
How are bile acids used to assess the function of the liver?
Absorption of lipids\lipid soluble vitamins etc Excretion of cholesterol 90% of bile acids get reabsorbed in SI, returns via enterohepatic circulation Liver failure – decreased absorption
27
How is unconjugated bilirubin used as a liver function test?
- Liver failure, haemolysis, anorexia, intestinal obstruction, Gilbert’s syndrome - The liver isn’t conjugating bilirubin - Not water soluble so wont be seen in urine
28
How is conjugated bilirubin used as a liver function test?
>25% of total bilirubin: hepatocellular failure >30% of total bilirubin: choleostasis - Water soluble: when increased can spill over into urine - Bile duct is lost: conjugated bilirubin cant go into the intestine so it leaks out into systemic circulation
29
How is ammonia used to assess liver function?
RBCs produce NH3 Measure within 15mins If not, separate plasma within 15 min Keep on ice / freeze Keep tube stoppered
30
How do the levels of urea change in liver disease?
Decrease - lack of ammonia metabolism
31
How do the levels of globulins change in liver disease?
Increase - failure of Kupffer cells to remove intestinal antigens
32
Why do the levels of triglycerides increase in liver disease?
Inadequate carbohydrate metabolism and gluconeogenesis
33
Describe the ultrasound landmarks on the LHS of the horse to find the liver
6th - 9th ICS Adjacent to spleen
34
Describe the ultrasound landmarks on the RHS of the horse to find the liver
Shoulder + elbow - tuber coxae 7th - 15th ICS
35
Describe how how the anatomy appears on right sided US when assessing the liver
- Lung is bright white due to air - Reverberation artefacts seen – bouncing of sound waves between the probe and a bright white surface i.e. lung – characteristic of gas - Curve = right dorsal colon - Can see vascular structures – hepatic arteries, veins and portal veins in the liver
36
Describe how how the anatomy appears on left sided US when assessing the liver
Always scan R and L lobes Better for atrophied livers Good for comparison to spleen Biopsy possible under US guidance Spleen is a lighter grey compared to the liver
37
List the potential complications of a liver biopsy
- Haemorrhage: do not perform if clinical coagulopathy - Inappropriate sample e.g. focal lesions - Negative culture (>50%) - Infections: cover with antibiotics if septic hepatitis - Pneumothorax: rare
38
Ragwort poisoning causes what kind of toxicity?
Pyrrolizidine alkaloid toxicity Senecio jacobaea
39
How does a horse with liver disease due to ragwort poisoning present?
- Frequently may only see signs of liver failure just prior to death - Liver has 70% reserve function - Can be delayed disease over a year after exposure - Early clinical signs are difficult to detect and non-specific
40
List some other clinical signs of ragwort poisoning
- Inspiratory dyspnoea: laryngeal paralysis - Severe CNS signs - hepatic encephalopathy usually 10 depression, but occasionally maniacal - Colic: gastric impaction - Photosensitisation - Haemorrhages e.g. epistaxis post tubing - Icterus
41
How can ragwort poisoning be diagnosed?
History Clinical presentation Clinical pathology Ultrasound Biopsy
42
How can ragwort poisoning be treated?
- Should you? - Probably not if bile acids > 50umol/l - Can try supportive - fluid therapy, electrolytes, glucose (if required) - Reduce hepatic encephalopathy: moderate to low protein diet, high BCAA’s
43
What is the cause of cholangiohepatitis and cholelithiasis
Ascending bile duct infection from GIT
44
How does cholangiohepatitis and cholelithiasis present?
Fever Jaundice Colic
45
How is cholangiohepatitis and cholelithiasis diagnosed?
- Marked elevations in esp. GGT - Biopsy may yield positive culture: neutrophilic inflammation - Ultrasound can help ID changes - Biopsy useful: histo (neutrophils) & culture
46
Therapy for chronic active hepatitis should include?
Corticosteroids
47
List some causes of acute hepatitis
Theiler's disease-associated virus Other viruses – parvovirus, hepacivirus Aflatoxins Liver fluke (Fasciola hepatica)
48
How should cases of hepatic encephalopathy be approached/treated?
- Avoid sedation but if required, alpha -2 agonist, not diazepam - Reduce production of neurotoxins: metronidazole to reduce ammonia producing bacteria or lactulose - Reduce inflammation and fibrosis: steroids - Diet
49
Describe the diet for a patient with hepatic encephalopathy
- Carbohydrate- based feed – maintain/gain weight - Moderate quantities of high quality protein (branch chain amino acids, not aromatic) - Fat soluble vitamin supplementation (A D E K)
50
Define hyperlipaemia
Increased triglyceride conc of the blood
51
How does the serum appear in cases of hyperlipaemia?
Dense, white, cloudy serum
52
List the risk factors of hyperlipaemia
Breed Obesity Females Age vs insulin sensitivity Underlying disease Transport, stress, lactation Starvation
53
Describe the pathogenesis of Hyperlipaemia
- Breakdown of stored fat (HSL) - FA’s to liver - energy - Liver poor ketogenic capability, energy production overwhelmed - Triglycerides accumulate in liver and in plasma - Ideally want to promote re-uptake in periphery by LPL - clear plasma - But LPL can’t keep up with HSL & liver
54
How do horses with hyperlipaemia present?
Non-specific: anorexia, lethargy, weakness Progress to more severe CNS & other signs Signs may be underlying disease, hyperlipemia or secondary liver disease
55
How is hyperlipaemia diagnosed?
Cloudy serum TG’s > 5 mmol/l = hyperlipaemia TG’s < 5 (but > 1.5) = hyperlipidaemia
56
How is hyperlipaemia treated?
- Treat underlying disease +parasites - POSITIVE ENERGY BALANCE - Correction of dehydration, electrolyte imbalances, acidosis - Other symptomatic therapy - Normalisation of lipid metabolism
57
Describe the prognosis of hyperlipaemia
Guarded to poor (mortality in > 50%) Worse if female, other organ involvement, poor initial response, failure to eat Get them out of the box especially if used to being out

Y4 EQ - Gastrointestinal tract (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions