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Titi Hep & Endo > Equine Endocrinology > Flashcards

Equine Endocrinology Flashcards

1
Q

What are the main products of the pars intermedia?

A

POMC which can then be cleaved into alpha MSH (main peptide), ACTH, beta lipotropin, beta endorphin and corticotropin-like intermediate peptide (CLIP),

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2
Q

List the products of the cortex and medulla of the adrenal glands.

A

Medulla: related to the sympathetic nervous system; chromaffin cells secrete catecholamines (adrenaline, noradrenaline and dopamine)
Cortex: divided into 3 zones - Zona glomerulosa secretes mineralocorticoids (aldosterone); zona fasciculata secretes glucocorticoids (cortisol); zona reticularis secretes sex steroids (mainly androgens)

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3
Q

What are the systemic effects of cortisol?

A
  • Increases gluconeogenesis
  • Mobilisation of amino acids for gluconeogenesis
  • Decreased glucose utilisation
  • Increased glucose concentrations
  • Inhibits insulin actions on glucose uptake and lipogenesis
  • Increases fat and amino acid mobilisation during stress
  • Endogenous glucocorticoids are antiinflammatory and immunosuppressors.
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4
Q

Why do some premature foals have lower basal cortisol and higher ACTH levels?

A

P450-17 is expressed 5 days before birth in normal foals so if premature this enzyme might limit cortisol production. High ACTH is due to a lack of negative feedback.

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5
Q

Define relative adrenal insufficiency (RAI) and critical illness related corticosteroid insufficiency (CIRCI)

A

RAI: inadequate production of cortisol in relation an increased demand during periods of severe illness and stress (high ACTH:cortisol ratio).
CIRCI: promoted instead of RAI as it considers clinical findings; an exaggerate proinflammatory response from cortisol deficiency and tissue refractoriness to corticosteroids.

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6
Q

List serum biochemical abnormalities that might be seen with adrenal insufficiency.

A

May be normal or; hyponatremia, hypochloremia, hyperkalemia, hypoglycemia.

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7
Q

Differentiate primary versus secondary hypoadrenocorticism.

A

Primary: adrenocortical dysfunction leads to high plasma ACTH (rule out PPID) due to lack of negative feedback.
Secondary: increased use of exogenous glucocorticoids leads to low ACTH levels.

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8
Q

ACTH stimulation test involves what?

A

Baseline heparinised or plain blood for cortisol; administer 1iu/kg natural ACTH IM between 8-10am; take post ACTH blood samples 2 and 4 hours after ACTH administration. A functional adrenal gland results in 2-3fold increase in cortisol compared with baseline.

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9
Q

Treatment of hypoadrenocorticism involves:

A

Treatment with corticosteroids, ideally hydrocortisone or prednisolone at low doses.

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10
Q

What are the clinical signs of CIRCI in foals and recommended treatment protocol?

A

vasopressor-unresponsive hypotension, hypoglycaemia or persistent SIRS. (Ideally to ACTH stim test).
Tx: a short tapering therapy of hydrocortisone (1.3mg/kg/day IV divided every 4 hours).

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11
Q

Where do pheochromocytomas arise?

A

Chromaffin cells of the adrenal medulla

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12
Q

Which catecholamines are produced by pheochromocytomas?

A

Adrenaline and noradrenaline.

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13
Q

What are the clinical signs of pheochromocytomas?

A

Intense adrenergic stimulation, may include: abdominal pain from haematomas or haemoperitoneum, GIT distension secondary to ileus, anxiety, tachycardia, tachypnoea, profuse sweating, muscle tremors, hyperthermia, dry and pale MM, increase CRT, ataxia and mydriasis.

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14
Q

What is the incidence of concurrent endocrine abnormalities or multiple endocrine neoplasia (MEN) in horses with pheochromocytoma?

A

73% had concurrent endocrine abnormalities and 21% of those had changes consistent with MEN.

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15
Q

What are the two cell types in the thyroid gland and what does each secrete?

A

Follicular cells secrete thyroxine (T4 - prohormone) and triiodothyronine (T3 - active hormone). These increase metabolic rate.
Neuroendocrine cells give rise to parafollicular cells that secrete calcitonin (important for calcium metabolism).

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16
Q

Which hormones stimulate and which hormones inhibit thyroid stimulating hormone?

A

TRH stimulates thyrotropes of the pars distalis to secrete TSH.
Dopamine and somatostatin released by the hypothalamus inhibit TSH secretion.

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17
Q

Are thyroid hormone levels higher in newborn foals or adults?

A

Approximately 10 fold higher in foals

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18
Q

What is the effect of lactation on thyroid hormone concentrations?

A

Serum T3 and T4 concentrations are higher in lactating mares cf non lactating.

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19
Q

What are the effects of feeding on thyroid hormone secretion?

A
  • Soluble carbohydrates increase secretion of TH
  • Energy deprivation inhibits deiodination of T4 to T3 to decrease T3 but increases rT3 concentrations (may be to reduce metabolic rate and conserve energy)
  • Starvation decreases leptin concentrations which has a flow on effect to decrease TRH and therefore TSH; hence feed restriction decreases while caloric intake increases leptin concentrations and the same in thyroid hormones.
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20
Q

Define non-thyroidal illness syndrome (NTIS) and the relative levels of T3 and T4.

A

NTIS is a reduction in T3 due to suppression of the HPTA from illnesses, systemic inflammation, stress and starvation. T4 can be normal, decreased or increased during NTIS.

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21
Q

Explain the TSH stimulation test, the TRH stimulation test and the T3 suppression test.

A

TSH stim: Baseline blood; inject 2.5-5iu of TSH IV and compare pre- and 3-4h post TSH concentrations of TH. T4 should peak at 2.4 times baseline and T3 peaks at 5 times baseline. An insufficient response is consistent with hypothyroidism (bute decreases TH concentrations but doesn’t affect this test; dex blunts the TH response to the TSH stim test).
TRH stim: baseline blood; inject 1mg TRH IV and compare pre and 2-4h post TRH concentrations of TH. Both T3 and T4 should increase 2-3fold. An inadequate response occurs with primary (thyroid) or secondary (pituitary) hypothyroidism.
T3 suppression test: Baseline blood; inject 2.5mg T3 diluted in 5mL saline IM at 8am and 6pm on days 1, 2 and 3, and at 8am on day 4. Serum T3 concentrations are measured 5min before each T3 dose. Additional samples collected at 6pm on days 4-10. Failure of T3 to suppress after T3 administration indicates autonomous secretion of THs, consistent with hyperthyroidism. In euthyroid horses T4 concentrations decrease by day 4 and remain low until day 10.

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22
Q

Differentiate primary from secondary hypothyroidism

A

Primary (thyroid): low TH, high TSH concentrations and a low response to TSH stimulation suggests thyroid gland dysfunction.
Secondary (pituitary): low TH with low or normal TSH concentration indicate hypothalamic or pituitary gland dysfunction.

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23
Q

What effect do nitrates have on thyroid function in-utero?

A

Proposed as a possible mechanism for development of congenital hypothyroidism and dysmaturity (CHD) in foals; nitrates cross the palcenta and impair foetal thyroid gland function. TH concentrations in foals with CHD are low or within normal and their response to TSH is poor. Prognosis is poor. Gestation is often prolonged and they are often weak to stand, silky short coat with domed head, tendon laxity, incomplete ossification of cuboidal bones, flexural and angular limb deformities and rupture of the common digital extensor tendons.

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24
Q

What is the treatment for hyperthyroidism?

A
  • Hemithyroidectomy if unilateral tumour
  • Glucocorticoids may alleviate signs
  • Eliminate exposure to iodine containing products.
  • Potassium iodide 1g/day may improve signs.
    Propylthiouracil (PTU) 8mg/kg POq24h may be successful and can be decreased to EOD.
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25
Q

List the common thyroid tumours.

A
  • Adenoma (most common), benign and not associated with thyroid function.
  • Adenocarcinoma, malignant and can cause euthyroid, hypo or hyperthyroidism.
  • Medullary carcinoma (C-cell or parafollicular cell tumour), usually unilateral.
  • Multiple endocrine neoplasia (MEN), consider this when you see tumour of the thyroid gland.
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26
Q

List the mechanisms of calcium reabsorption in the cortical thick ascending loop of henle and the distal convoluted tubules of the kidney.

A

CTAL: PTH mediated
- Increases calcium reabsorption (enhances the Na/K/2Cl cotransporter which creates the voltage gradient that enables paracellular reabsorption of Ca).
- Reduces phosphate reasbsoprtion
- Promotes calcitriol synthesis.
DCT:
- Increased calcium reabsorption in in his region is
transcellular mediated by epithelial calcium channels, calbindin, basolateral proteins and the vitamin D receptor.

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27
Q

What is the role of calcitonin?

A

It is secreted by the parafollicular cells of the thyroid gland in response to hypercalcaemia and it decreases calcium and phosphate levels by increasing urinary calcium and phosphate excretion and suppressing osteoclastic bone resorption.

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28
Q

What drives humoral hypercalcaemia of malignancy?

A

Secretion of parathyroid hormone related peptide.

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29
Q

What effect does blood pH have on Ca binding to albumin?

A

During acidosis Ca binding is reduced so ionised concentration is higher and during alkalosis Ca binding to albumin is increased so ionised concentration is lower; but in both states total calcium is unchanged.

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30
Q

What do you see with chronic excess and chronic deficiency of phosphorus?

A

Excess: clinical signs of calcium deficiency including osteodystrophia fibrosa or nutritional secondary hyperparathyroidism.
Deficiency: weight loss, weakness, depraved appetite, lameness and DOD.

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31
Q

Explain re-feeding syndrome

A

Occurs when re-feeding starved horses and begins with introduction of carbohydrates, specifically glucose which causes insulin release. Insulin prevents release of free fatty acids and causes an intracellular influx of glucose and selected electrolytes (potassium, magnesium and phosphorus), decreasing serum concentrations of these substances. Depletion of ATP results in RBC dysfunction and inability to release oxygen to tissues. Resultant heart, respiratory and kidney failure contribute to death - neurological signs may or may not occur concurrently.

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32
Q

List the clinical signs of hypocalcaemia

A

Anxiety, depression, synchronous diaphragmatic flutter, hyperexcitability, ataxia, stiff gait, tetany, muscle fasciculations and tremors, tachypnoea with flared nostrils, upper airway stridor, dyspnoea, dysphagia, hypersalivation, hyperhidrosis, ileus, seizures, hypotension, recumbency, collapse and death. tachycardias and cardiac arrhythmias may be present although bradycardia can occur in severe cases due to reduced myocardial contractility.

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33
Q

Explain synchronous diaphragmatic flutter

A

Occurs as a result of ionised hypocalcaemia or hypomagnesaemia. Depolarisation of the right atrium stimulates action potentials in the hyperexcitable phrenic nerve as it crosses over the surface of the heart, causing a rhythmic movement on the flank due to synchronous contraction of the diaphragm with the heartbeat.

34
Q

What electrolytes are affected with hypoparathyroidism?

A

Hypocalcaemia, hyperphosphataemia and decreased serum PTH concentrations. Hypomagnesaemia is often present and may be the cause in secondary hypopaathyroidism.

35
Q

Describe the pathophysiology of exercise-induced hypocalcaemia

A

Sweat losses, calcium shift to the intracellular compartment and increased binding of calcium to albumin due to alkalosis (alkalosis is secondary to hyperventilation (respiratory alkalosis) and chloride loss in sweat). Inadequate response of PTH to hypocalcaemia have also been found in endurance horses which might contribute.

36
Q

What is the cause of nutritional secondary hyperparathyroidism?

A

Increased parathyroid hormone secretion secondary to reduced intestinal calcium absorption. It is usually associated with a diet low in calcium, high in phosphorus or high in oxalate. Other names are bran disease, miller’s disease, big head, osteodystrophia fibrosa, fibrous osteodystrophia etc. Ca : P ratio less than 1:3 predispose.
Hyperphosphataemia stimulates PTH secretion but inhibits renal calcitriol synthesis, as this usually downregulates parathyroid function the inhibition of calcitriol contributes to parathyroid cell hyperplasia and PTH secretion. This in turn increases osteoclastic activity, bone resorption and bone loss. Ionised calcium may remain within normal limits as this is a slow progressive disease and homeostatic mechanisms for calcium are highly effective.

37
Q

What does hypervitaminosis D cause?

A

Mineralisation of soft tissues, including cardiovascular tissues. Also increases bone density and reduces the medullary cavity lumen.

38
Q

What are the endocrine functional units of the pancreas, their four cell types and the hormones secreted by each?

A

Islets of langerhans are the functional units. Each islet has alpha, beta, delta and gamma cells.

  • Alpha cells secrete glucagon
  • Beta cells secrete insulin (as well as urocortin-3 and C-peptide)
  • Delta cells secrete somatostatin
  • Gamma cells secrete pancreatic polypeptide.
39
Q

Which hormones influence insulin release?

A

Stimulates: glucose is the most profound; also glucagon, some amino acids and incretin hormones
Inhibits: somatostatin.

40
Q

What influence does the sympathetic and parasympathetic nervous system have on pancreatic endocrine function?

A

Sympathetic system inhibits insulin and stimulates glucagon secretion
Parasympathetic system stimulates insulin secretion during food intake

41
Q

List the effects of insulin in its three major tissue sites

A

Liver: insulin decreases glycogenolysis, gluconeogenesis and ketogenesis and stimulates glycogenesis, glycolysis and fatty acid synthesis.
Adipose tissue: insulin decreases lipolysis and stimulates fatty acid uptake, synthesis and esterification.
Skeletal muscle: insulin decreases proteolysis and amino acid output and increase glucose and amino acid uptake, protein synthesis and glycogen synthesis.

42
Q

Which feed groups stimulate incretins?

A

Carbohydrates, fatty acids and amino acids

43
Q

What differentiates insulin resistance from Type II diabetes?

A

In almost all instances horses remain euglycaemic which is in contrast to Type II diabetes in which the patient is hyperinsulinaemic and hyperglycaemic with glucosuria - this can occur in rare equine cases.

44
Q

Is hyperinsulinaemia due to increased secretion, decreased clearance or both?

A

Both, but more evidence to support increased secretion and beta cell hyperplasia.

45
Q

What are the common clinical findings with acute pancreatitis?

A
  • Colic
  • Reflux
  • Gastric dilation
  • Peritonitis
  • Abdominal fat necrosis
    May be helpful to measure serum and peritoneal fluid lipase and amylase activities.
46
Q

How has somatostatin been implicated in equine IR?

A

Somatostatin inhibits insulin and glucagon secretion and when a somatostatin analogue (octreotide) was administered suppression of insulin was less profound in horses with IR, supporting a lack of beta-cell inhibition as a mechanism for hyperinsulinaemia.

47
Q

What is the mechanism for increased triglyceride levels in horses with insulin resistance?

A

Decreased insulin-mediated inhibition of hormone-sensitive lipase in adipose tissue, and decreased inhibition of hepatic synthesis and secretion of very low density lipoproteins.

48
Q

List complications of obesity.

A
  • EMS/IR
  • Impaired lymphatic drainage leading to oedema
  • Development of pedunculated lipomas at an earlier age
  • Abnormal reproductive cycling in mares
49
Q

Is measurement of basal insulin and oral sugar test of equivalent sensitivity in all breeds?

A

No, it has lower sensitivity in light breed horses - a positive result is still very likely to indicate IR but a negative result doesn’t rule out IR.

50
Q

Explain the IV glucose tolerance test, combined glucose and insulin test and oral sugar test protocols.

A

Starve for 6-8hrs before testing (some evidence suggests allowing access to soaked hay)
IVGTT: Collect baseline sample; administer 150-300mg/kg dextrose as a 50% solution IV; collect blood at 30 minute intervals for 180 minutes, and measure glucose. Should return to normal by 150 min. If glucose is elevated at 180 min, IR is likely.
CGIT: Collect baseline for glucose and insulin; administer 150mg/kg dextrose as a 50% solution IV followed immediately by 0.1iu/kg regular insulin. Blood collection at 0, 1, 5, 15, 25, 35, 45, 60, 75, 90, 105, 120, 135 and 150 min for glucose and also measure insulin at the 45 min sample. IR is diagnosed if blood glucose is above baseline at 45min or if insulin is >100uIU/mL at 45 min. Watch for hypoglycaemia; have rescue glucose available. *Note: the glucose curve is shifted to the right in donkeys; their nadir is 120 min cf 75 for horses and can take 240 min to return to normal.
OST: Take baseline sample; administer karo syrup at 45mL/100kg and collect samples at 60 and 90 min. Insulin >60uIU/mL at 60 or 90 min after administration have IR. Current recommendation is 2 samples 15 min apart taken between 60 & 90 min; ie 60 & 75, 75&90 etc. Blood glucose >125mg/dl at 60-90 min is associated with IR.

51
Q

Which glucose transporter is most involved in uptake of glucose into skeletal muscle?

A

GLUT 4 receptor.

52
Q

How does insulin resistance develop?

A

Insulin sensitive tissues (liver, skeletal muscle and adipose tissue) fail to respond normally to insulin levels Insulin receptors, downstream signalling pathways and glucose transporters (eg GLUT4) are potential sites for dysregulation. As the tissues fail to respond to the insulin, more insulin is released from beta cells to compensate for reduced tissue insulin sensitivity, hence you get hyperinsulinaemia.

53
Q

What is uncompensated insulin resistance?

A

When the pancreas fails to sustain the higher rate of insulin secretion necessary to compensate for reduced tissue insulin sensitivity, and hyperglycaemia develops as a consequence. If there is also glucosuria then this is technically Type II diabetes mellitus.

54
Q

What are the broad mechanisms by which IR may predispose to laminitis?

A
  1. Altered blood flow or endothelial cell dysfunction within blood vessels of the food.
  2. Impaired nutrient deliver to hoof tissues.
  3. A proinflammatory or prooxidative state induced by chronic obesity and IR.
55
Q

What is the ideal NSC level in feed for horses with IR?

A

Less than 10% as fed.

56
Q

What is the benefit of molasses-free beet pulp?

A

When rinsed and then soaked it induces a low glycaemic response but provides calories through hindgut fermentation and VFA production.

57
Q

What is your target feed amount for weight loss and how can this be modified in patients that don’t lose weight initially?

A

Start with hay at 1.5-2% body weight if hay (ideally soaked). If weight loss is not achieved, lower this over several weeks to 1.5% of target BW rather than actual BW. Do not restrict to less than 1% body weight/day.

58
Q

What is the highest risk time for grazing?

A

Night time, potentially any time of the day during rapid growth in spring or senescence in fall. Typically early mornings are safer, unless there has been a hard frost (grass will accumulate sugar in this case).

59
Q

Why is it important to control diet in conjunction with levothyroxine treatment?

A

Appetite/feed intake may increase in horses treated with levo so dietary modification/restriction is an equally important component of weight loss during treatment.

60
Q

What is the MOA of metformin?

A

It is a functional AMPK agonist that promotes glucose uptake in horses with clinical evidence of IR. AMPK kinase results in broad changes in carbohydrate, lipid and protein metabolism that in general decreases energy consuption and increases energy production. In skeletal muscle it has been shown to be partly responsible for the insulin sensitising and non-insulin dependent effects on glucose transport following exercise.

61
Q

Why do the clinical signs of PPID vary among individuals?

A

Only a subset of the POMC-derived peptides may be secreted in any one individual and the degree of compression of adjacent neuroendocrine tissues may occur. Hypertrichosis is the most consistent sign, present in up to 80% of case. Weight loss and repartitioning is another common finding in up to 88% of cases.

62
Q

What is a proposed mechanism for increased docility and lethargy in horses with PPID?

A

Horses with PPID have increased plasma and CSF concentrations of beta endorphin which may lead to these signs. This may also explain the reduced responsiveness to painful stimuli and corneal stimulation that is observed in affected animals, and associated with the increased occurrence of ulcerative keratitis.

63
Q

What are the proposed mechanism for development of narcolepsy with PPID?

A

? Removal of dopaminergic control may alter the sleep-wake cycle (occurs in humans).
? Narcolepsy can result from decreased orexin activity in the hypothalamus (orexin is a hypocretin/peptide neurotransmitter expressed in the hypothalamus that is important for the sleep-wake cycle). Horses with PPID have decreased CSF concentrations of orexin.

64
Q

What are the proposed mechanisms for immune impairment in horses with PPID?

A

? Increased concentration of immunosuppressive hormones (alpha-MSH, cortisol, insulin, beta-endorphin).
? Neutrophils from PPID affected horses display reduced oxidative burst capacity and functional adhesion which may increase the animals risk for opportunistic infections.

65
Q

What is the typical signalment of horses with PPID?

A

Ponies and morgans may be predisposed but can occur in any breed.
No sex predilection
Typically a disease of aged horses (19-21 at diagnosis) but has been diagnosed in horses as young as 7yrs.

66
Q

What is the pathogenesis of PPID?

A

Loss of inhibitory control of the pars intermedia cell function is associated with triggering unregulated cell proliferation and the development of adenomas. This occurs due to loss of dopaminergic input to the pars intermedia as a consequence of neurodegeneration of the periventricular neurons (loss of dopaminergic cell bodies in the periventricular nucleus of the hypothalamus and the nerve terminals in the pars intermedia).

67
Q

What is the normal process of dopaminergic inhibition on the pars intermedia in horses without PPID?

A

The periventricular neurons that link the hypothalamus with the pars intermedia via the infundibular stalk release dopamine which interaacts with dopaminergic D2 receptors which act to inhibit POMC mRNA expression and POMC derived intermediate lobe hormone release.

68
Q

Why is the TRH stimulation test effective?

A

TRH is a direct releasing factor for equine melanotrophes, hence it increased the secretion of alpha-MSH and ACTH in both normal horses and those with PPID. However the ACTH concentration will be higher and more prolonged in horses with PPID than normal horses.

69
Q

What are the possible side effects of TRH that the owner should be warned about?

A 
Star-gazing
Yawning
Lip movements
Trembling
Salivation
Coughing
70
Q

What are the treatment options for PPID?

A
  • Pergolide 0.2-5mg/horse/day (dopamine D2 receptor agonist)
  • Bromocriptine 0.03-0.09mg/kg BID (dopamine D2 receptor agonist)
  • Cabergoline 2-3mg PO SID-BID for a 500kg (dopamine D2 receptor agonist)
  • Cyprohepatadine 0.25mg/kg PO SID (serotonin antagonist). Can be in conjunction with pergolide; can also be increased to twice daily in refractory cases.
71
Q

How quickly do you expect ACTH to return to previous values after discontinuing pergolide?

A

Approximately 10 days

72
Q

What are the predisposing risk factors for development of anhidrosis?

A
  • Familial history of anhidrosis
  • TB and WB breeds
  • Horses born in non-tropical/colder climates that then move to the tropics.
73
Q

What are the important features of equine sweat glands?

A

They are an apogrine gland associated with the hair follicle and consist of a secretory portion and a serpentine duct that opens into the follicular canal. They have a rich capillary network that is different from other species.

74
Q

Describe the regulatory mechanisms for sweating in horses.

A

Neural regulation: mainly sympathetic beta-adrenergic innervation.
Endocrine: beta-adrenergic receptor stimulation by circulating catecholamines.
Vascular: via an indirect neural influence controlling blood flow.

75
Q

What are the proposed mechanisms of anhidrosis?

A
  • Deficiency of beta2 adrenoreceptor agnoists (deficient beta2 adrenergic stimulation)
  • Poor sweat gland response to beta2 adrenergic stimulation (receptor refractoriness or downregulation).
  • Inflammation (minimal evidence)
    Likely results from a combination of insufficient neural and endocrine stimulation. Horses with skin denervation can sweat although their response to thermal stimulation is impaired.
76
Q

What are the clinical signs of anhidrosis?

A
  • Depression
  • Anorexia
  • Poor performance
  • Tachypnoea
  • Hyperthermia
  • Absent or reduced sweating
  • Dry coat/flaky skin
  • Alopecia
77
Q

What are the diagnostic options for anhidrosis?

A

Clinical signs are important.

  • Adrenaline intradermal test (delayed or absent sweat response) but as this is not specific for B2 receptors the alpha adrenergic effects may mask the response.
  • B2 receptor agonists (terbutaline and salbutamol) are better. Inject several dilutions of saline and salbutamol or terbutaline (terbutaline is a 1mg/mL in tenfold dilutions with 0.9%NaCl (1000, 100, 10, 1, 0.1, -.01, 0.001 and 0mg/L) with a volume of 0.1mL injected at each site 5cm apart. Horses with anhidrosis have minimal or no response to any dilution, normal horses sweat from most dilutions.
78
Q

What is another differential for persistent hyperthermia and tachypnoea in certain foal breeds?

A

Draft breeds have idiopathic hyperthermia - resolves within 3-7 days with supportive management.

79
Q

What are the treatment options for anhidrosis?

A

Symptomatic.

  • Some success with levothyroxine (thyroid hormones may enhance B2 adrenoreceptor sensitivity) but be aware of complications associated with this drug (weight loss etc)
  • B2 recepor agonists are controversial as B2 receptor dowregulation is likely due to excessive adrenergic stimulation, however some clinicians report benefit from use of clenbuterol.
80
Q

What is the prognosis for horses with anhidrosis?

A

Guarded and dictated by severity of the condition

Titi Hep & Endo (7 decks)

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