Camelid - Endocrine/Metabolic Dz

Question 1

List unusual features of insulin and glucose metabolism in camelids.

Answer 1

• Generally low insulin production; low in neonates compared to other species, drops further in adults.
• High insulin resistance.
• Potentially unrepressed hepatic gluconeogenesis.

Question 2

List processes of energy metabolism stimulated by insulin.

Answer 2

• Uptake of circulating glucose by insulin-sensitive muscle or adipose tissue.
• Uptake of amino acids.
• Uptake of NEFAs from circulating triglycerides.
• Lipogenesis.

Question 3

List processes of energy metabolism suppressed by insulin.

Answer 3

• Mobilisation of glycogen.
• Mobilisation of adipose triglyceride.
• Gluconeogenesis.

Question 4

How are energy needs met in healthy camelids?

Answer 4

• Short-chain fatty acid products of fermentation.
• Glucose is provided by gluconeogenesis to support obligate requirements.
• Amount of insulin req is small as roughage diet and fermentative digestive system do not result in glucose fluctuations, however given insulin resistance blood glucose conc is higher than in other species.

Question 5

How are energy needs met in camelids that have been fasted?

Answer 5

NEFAs are liberated from adipose stores.

Question 6

List insulin antagonists.

Answer 6

• Glucagon.
• Catecholamines (inc fat fractions as well as blood gluc).
• Corticosteroids.
• Thyroid hormone.
• Growth hormone.

Question 7

List bloodwork abnormalities and morphologic changes which may occur following suppression/anatagonism of insulin in camelids.

Answer 7

• Hyperglycaemia.
• Hyperketonaemia.
• High circulating NEFAs.
• Hypertricglyceridaemia.
• +/- hypoalbuminaemia (insulin stim liver alb prod).
• Fatty infiltration of the liver, kidneys and other tissues.

Question 8

List causes of hyperglycaemia in camelids.

Answer 8

• Rapid GI absorption of glucose: unlikely in adults, may occur in crias.
• Exuberant, unmitigated gluconeogenesis or mobilisation of glycogen stores: corticosteroids or catchemolamines i.e. ‘stress’ of any dz.
• Impaired hepatic or peripheral use of glucose.
• Iatrogenic IV glucose administration.

Question 9

Why is hyperglycaemia more common and persistent in camelids than in other species?

Answer 9

• Insulin resistance, lack of insulin response –> slow removal/uptake by peripheral tissues.
• Slow urinary excretion: high urine threshold of 200mg/dL.

Question 10

What represents the greatest risk for a health complication in hyperglycaemic camelids? Why?

Answer 10

• Dehydration due to lack of water intake or another reason related to primary dz.
• Hyperglycaemia –> inc osmotic draw of fluid from ICF to ECF –> water lost through osmotic diuresis –> hypernatraemia –> further fluid loss from ICF –> further cellular dysfunction.
• Concurrent metabolic acidosis and azotemia are additional signs of circulatory compromise.

Question 11

Outline treatment of acute hyperglycaemia in camelids.

Answer 11

• Provision of water (oral or parenteral if not drinking).
• If Na >5mmol/L above the top of the range may need to restrict access to free water and correct Na over 24h.
• Cessation of stressful stimuli.
• Insulin rarely required.

Question 12

Describe hyperosmolar syndrome.

Answer 12

• Occurs in hyperglycaemic camelids when degree of dehydration due to glucorrhesis progresses to a point where CNS function is impaired (Na = 170mEq/L).
• CNS glucose and Na concentrations become elevated.
• CSx: fine head tremors, wide-based stance, +/- recumbency, obtundation, seizures, coma.

Question 13

In what age group of camelids does hyperosmolar syndrome mainly occur? What are risk factors for hyperosmolar syndrome in these animals?

Answer 13

• Neonatal crias.

- Sepsis, prematurity, corticosteroid treatment, bottle-feeding, glucose administration.

Question 14

Outline treatment of hyperosmolar disorder in camelids.

Answer 14

• Restore circulating volume: oral fluids, water or diluted milk replacer (dec Na conc), IVF (admin slowly).
• Insulin: regular insulin 0.2U/kg q1-4h IV.
• Neuro signs related to rehydration: mannitol.
• Seizures: diazepam.

Question 15

Has hyperadrenocorticism been reported in camelids?

Answer 15

• Natural persistent hyperadrenocorticism has not.

- Pituitary tumours have been reported.

Question 16

Does hypoglycaemia occur in camelids?

Answer 16

• Rare compared to other species, even in fasting animals.
• Reported in 2% adults, 13% crias in one hospital.
• Should always be confirmed by blood gluc measurement before tx due to its rarity.
• Persistent hypoglycaemia indicates severe hepatic dysfunction.

Question 17

Describe serum chemistry abnormalities in camelids with negative energy balance that induces fat store mobilisation

Answer 17

• Circulating NEFAs inc to 0.6-1 mEq/L.
• NEFAs –> liver –> inc BHB production –> blood BHB 1-2 mg/dL.
• Little to no change in circulating triglyceride conc.

Question 18

What is the ramification of short-term negative energy balance for camelids?

Answer 18

• Adapted to periods of fasting lasting for several weeks, therefore bloodwork abnormalities will be mild and there is little to no health ramifications.
• Animals w higher energy requirements e.g. lactation, may be negatively impacted by fasting, but not always.

Question 19

What are the effects of increased circulating BHB in camelids?

Answer 19

Suppression of appetite.

Question 20

What are the effects of increased circulating NEFAs in camelids?

Answer 20

• NEFAs are pro-inflammatory.
• NEFAs are potentially cytotoxic.
• Inhibit glycogen storage.
• May inhibit glucose uptake.
• May increase insulin resistance.

Question 21

Identify the signalment of camelids prone to hepatic lipidosis.

Answer 21

All ages and signalments from crias up.

Question 22

List blood work abnormalities in camelids with hepatic lipidosis.

Answer 22

• NEFAs > 1 mEq/L.
• BHB > 5 mg/dL.
• Hyperglycaemia (pre/lactating may have hypoglycaemia).
• +/- hyperlipaemia (inc cholesterol and triglyceride).

Question 23

Outline factors which may contribute to the development of hepatic lipidosis in camelids.

Answer 23

• Preg/lactating: may be carb insufficiency like preg tox in ewes/cows.
• Stressors that inhibit insulin or promote catecholamines: transport, extreme temp, illness etc.
• Protein deficiency –> AA deficiencies –> prevent export of hepatic fat and formation of protein hormones or enzymes e.g. insulin.
• Hepatic injury or dysfunction e.g. Cu or plant tox.

Question 24

Describe the occurrence of hyperlipaemia in camelids and compare it to cattle.

Answer 24

• Can occur with any age or gender.
• Hyperlipaemia occurs close to death w lipidosis.
• The more severe the hyperlipaemia, the higher NEFAs and BHB will be.
• Cattle w ketosis have much higher BHB but hyperlipaemia occurs much less frequently –> camelids are either more capable than cattle of exporting liver triglyceride or have greater problems with its end use.
• Mild hyperlipaemia may be benign, but gets worse if untreated.
• Occurs w neg energy balance, inflammatory disorders (inhibition of lipoprotein lipase by Pg), lipogranulomas of the foot.

Question 25

Outline treatment of disorders of fat metabolism in camelids.

Answer 25

• Try and restore appetite.
• High palatable feeds: blackberry leaves, grass, alfalfa leaves; milk or milk replacer for crias.
• Avoid grain in excess as may exacerbate acidosis.
• IVFT, correction of acidosis and elec abnormalities; conservative IVF after correction of shock as hypoalbuminaemia is common in these patients.
• More aggressive tx if NEFA > 1mEq/L, BHB >5 mg/dL and triglycerides > 500mg/dL –> force feeding, PPN + insulin, appetite stimulants (transfaunation, companion, B vit, diaz).