Diseases Associated with Disorders of Fat Metabolism Flashcards
Compare the similarities and differences between the factors that predispose animals to developing the following disorders of lipid metabolism: Hyperlipidaemia (and/or hyperlipaemia) in the horse, Hepatic lipidosis in the cat, fatty liver syndrome in a dairy cow and pregnancy toxaemia in the ewe?
Hyperlipidaemia in horse: Obesity, native, sudden starvation
Hepatic lipidosis in cat: Obesity, Breed (DSH), sudden starvation, anorexia
Fatty liver syndrome in Dairy Cow: Obesity followed by incorrect nutrition (negative energy balance), parturition
Pregnancy toxaemia in sheep: Multiple lambs, Twin lamb disease, obesity, poor nutrition and negative energy balance.
Why does the liver play a fundamental role in the development of these diseases associated with disorders of fat metabolism? Summarise the pathophysiology of hepatic lipidosis and the change in fat metabolism pathway in animals with hepatic lipidosis.
It occurs due to the accumulation of large amounts of lipid in hepatocytes, altering the morphology of the cells and producing an acute hepatopathy. The mortality rate of this disease is high unless it is treated aggressively.
The lipid that accumulates within hepatocytes is composed of triglyceride which is synthesised from circulating fatty acids in the liver. Circulating fatty acid concentrations are regulated by a number of hormonal factors that act on the enzymes hormone-sensitive lipase (HSL) and lipoprotein lipase (LPL). HSL is responsible for releasing fatty acids from adipose tissue and its action is stimulated by catecholamines, glucagon, corticosteroids and thyroid hormones but inhibited by insulin. LPL degrades circulating lipoprotein complexes allowing fatty acids to be taken back up into adipose stores. The liver and other tissues usually oxidise fatty acids via the Krebs cycle within mitochondria but this pathway is downregulated in animals that receive excessive dietary calories. Additionally, hepatocytes are able to package fatty acids into very low lipoprotein complexes (VLDLs) that are released back into the circulation. If the apolipoproteins that partly constitute the VLDLs are deficient, fatty acids may not be dispatched from the liver. The accumulation of triglycerides in the liver reflects an imbalance between the processes that cause lipid mobilisation, those that lead to fatty acid oxidation and dispatch and those that encourage storage in adipose tissue. One or more mechanisms may be involved and these include increased activation of HSL by catecholamines released in response to stress, failure to produce sufficient insulin (in diabetes mellitus) results in uncontrolled HSL activity and excessive lipid mobilisation induced by anorexia, starvation or illness, partly under the influence of glucagon on HSL. Deficiency of dietary proteins and other nutrients, which reduces the capacity of the liver to produce lipid transport (apolipo-)proteins and to metabolise fat. Recognised micronutrient deficiencies include arginine, carnitine, taurine and methionine. Carnitine has a vital role in carrying fatty acids across the inner mitochondrial membrane and also disturbances in the neural and hormonal mechanisms that control appetite and satiety resulting in inappropriate anorexia, are other factors.
You are called to a 12’2 hand 7 year old grey Welsh section A pony in December that is anorexic. It is body condition score 4/5 and you arrive and is in a field with no hay and there is snow on the ground, but won’t eat its hard feed.
What are the top four differentials as to why this pony is anorexic?
Hyperlipidaemia
Laminitis
Dental disease
Colic
You are called to a 12’2 hand 7 year old grey Welsh section A pony in December that is anorexic. It is body condition score 4/5 and you arrive and is in a field with no hay and there is snow on the ground, but won’t eat its hard feed.
What further questions would you ask and why and what further diagnostic tests would you perform whilst with the pony to try to rule out two of these differentials?
Oral exam for dental disease
Clinical exam to rule out laminitis to assess lameness and digital pulses
Ask when it last had access to forage
When did you last notice it being normal
Clinical GI exam to investigate colic
Take blood sample to investigate hyperlipidaemia
You are called to a 12’2 hand 7 year old grey Welsh section A pony in December that is anorexic. It is body condition score 4/5 and you arrive and is in a field with no hay and there is snow on the ground, but won’t eat its hard feed.
You decide to obtain a blood sample to rule out one of your differentials. What type of blood tube would you require and what is a quick, practical test that you can do by letting the blood settle in the car? What test would you request from the laboratory?
Quick test: EDTA. Let blood settle for 4 hours and assess lipid accumulation on top of sample.
Request from lab: Lipid profile
You are called to a 12’2 hand 7 year old grey Welsh section A pony in December that is anorexic. It is body condition score 4/5 and you arrive and is in a field with no hay and there is snow on the ground, but won’t eat its hard feed.
Your settled blood shows milky serum. What is the likely diagnosis and how high are you expecting the test result you have sent to the laboratory to be (with units)?
Diagnosis: hyperlipidaemia
Plasma or serum triglyceride >500 mg/dL confirm the diagnosis
You are called to a 12’2 hand 7 year old grey Welsh section A pony in December that is anorexic. It is body condition score 4/5 and you arrive and is in a field with no hay and there is snow on the ground, but won’t eat its hard feed.
Diagnosis - hyperlipidaemia
You call the owner. What advice are you going to give her on the telephone and on your return to the pony what options are you going to offer?
Need to get pony feeding asap
Supportive therapy: CRI glucose, Fluids
Option to bring into practice for hospital treatment
Treatment must be prompt and aggressive. Nutritional support is the most important part of treatment. Constant slow infusion of glucose IV (dextrose 5%) should be given initially. Followed by protamine zinc insulin and glucose or high energy gruel based on barley or oats given by stomach tube and supportive amino acids. Heparin may be given in an attempt to reduce plasma triglycerides but will not correct the underlying cause and may alter haemostasis
You are called to a 12’2 hand 7 year old grey Welsh section A pony in December that is anorexic. It is body condition score 4/5 and you arrive and is in a field with no hay and there is snow on the ground, but won’t eat its hard feed.
Diagnosis - hyperlipidaemia
The owner explains that the pony is not insured, but is willing to spend up to £1000 on treating the animal either at home or at the practice. What is the best veterinary treatment you can provide for this animal (with rough costings) for this amount of money?
Nasogastric tube in place, placed at home by vet. Vet wrapped to head collar for owner to tube feed. Initial treatments at home give initial infusion of glucose followed by insulin. Recheck naso-gastric tube in few days. Warn owner of grave prognosis.
You are called to a 12’2 hand 7 year old grey Welsh section A pony in December that is anorexic. It is body condition score 4/5 and you arrive and is in a field with no hay and there is snow on the ground, but won’t eat its hard feed.
Diagnosis - hyperlipidaemia
How might your treatment change if this animal was 10 months in foal?
Get foal out?
Treatment won’t change drastically – just have to consider the foal i.e. might be recommended to hospitalise and increase the intensity of the monitoring/treatment
You are called to five Suffolk ewes due in a group that are due to lamb within the two weeks that have clinical signs of anorexia, weakness, depression, appear blind and are star-gazing. This is the third visit to this farm in the previous ten days to animals with similar clinical signs.
What are your 5 differential diagnoses in these animals in addition to preganancy toxaemia ?
- Pregnancy toxaemia
- Listeria
- Hypocalcaemia
- Copper poisoning
- Polioencephalomalacia (thiamine deficiency and high sulphur intake)
You are called to five Suffolk ewes due in a group that are due to lamb within the two weeks that have clinical signs of anorexia, weakness, depression, appear blind and are star-gazing. This is the third visit to this farm in the previous ten days to animals with similar clinical signs.
What additional blood tests would you request for a ruminant that has suspected disorders of lipid metabolism?
What tests would you request to some of the less likely differential diagnoses? (list was pregnancy toxaemia, listeria, hypocalcaemia, copper poisoning, polioencophalomalacia)
Heparin blood samples looking for BHB and calcium
What tests would you request to some of the less likely differential diagnoses listed in part a:
Listeria: PM, CSF tap
Hypocalcaemia: Done on same blood test for BHB
Copper poisoning: Ask food company, check food yourself
Polioencephalomalacia (thiamine deficiency and high sulphur intake): Check the feed and call feed company,
You are called to five Suffolk ewes due in a group that are due to lamb within the two weeks that have clinical signs of anorexia, weakness, depression, appear blind and are star-gazing. This is the third visit to this farm in the previous ten days to animals with similar clinical signs
What is the most appropriate treatment for these animals? What is the prognosis in these animals with and without treatment?
- Give glucose but consider glucocorticoid carefully as this may cause abortion but it may be that far gone that we need to abort to save the ewes.
- Grave.
You are called to five Suffolk ewes due in a group that are due to lamb within the two weeks that have clinical signs of anorexia, weakness, depression, appear blind and are star-gazing. This is the third visit to this farm in the previous ten days to animals with similar clinical signs
How can this be prevented in animals next year?
- Scan the ewes and separate singles/ triplets/ twins to feed appropriately for metabolic requirements and to confirm they are actually pregnant
- Better condition prior to lambing e.g. 3/3.5
- BCS ewes
- Take blood samples to test for ketones and calcium early in a random sample (or urine)
- Better nutrition advice- use nutritionist
You are called to five Suffolk ewes due in a group that are due to lamb within the two weeks that have clinical signs of anorexia, weakness, depression, appear blind and are star-gazing. This is the third visit to this farm in the previous ten days to animals with similar clinical signs
Why is this condition a rarer finding in Welsh Mountain and Scottish Blackface ewes?
?
Hill breeds so are very hardy. Whereas lowland breeds are more likely to get stressed by the weather and lack of food and get low glucose. Hill breeds are better at finding food and dealing with lack of food. Also they are more likely to have singles and sometimes twins and the lambs come out very small and hardly ever have big lambs so the foetuses are stealing less energy than the big mule twins and triplets. There could be a weird genetic thing but I think overall they can just deal with lack of glucose as they are not use to lots of concentrates, lush grass they’ve just got the hill Scrubs and rough grass.
