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Endocrine > Equine endocrinopathies > Flashcards

Equine endocrinopathies Flashcards

1
Q

Pathophysiology - PPID

A
  • loss of DA inhibitbition of pars intermedia of pituitary gland d/t oxidative damage, cause unknown
  • result is marked over-production of some pars intermedia derived hormones (beta-endorphin, alpha MSH, CLIP and a modest increase in others i.e. ACTH)
  • GC effects relate to mild ACTH increases
  • less importantly: compression of other areas of pituitary with reduction in production of hormones they produce (ADH) and compression of adjacent brain resulting in blindness seizures
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2
Q

What cells comprise the pars intermedia?

A

melanotropes

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3
Q

What hormones are produced in pars intermedia?

A 
Process POMC into:
- beta endorphin (mainly)
- alpha MSH
- CLIP
-
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4
Q

How is production of pars intermedia hormones regulated?

A
  • regulated by DA and 5-HT

- unaffected by GCs

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5
Q

Epidemiology - PPID

A
  • av age 19, rarely horses
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6
Q

CS - PPID

A
  • hypertrichosis
  • laminitis
  • weight loss
  • hyperhidrosis
  • PUPD
  • bulging supraorbital fat
  • susceptibility to infections increased
  • other: lethargy (endorphin effect?)
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7
Q

Describe hypertrichosis of PPID

A
  • common
  • specific
  • varies from delayed shedding to thick curly coat
  • 55-80% cases
  • possibly d/t excess melatonin or corticoid/androgen effect or d/t pressure on hypothalamic thermoregulatory centre
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8
Q

Describe laminitis of PPID

A
  • frequently recurrent or chronic

- usually d/t excess cortisol and/or insulin

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9
Q

Describe weight loss of PPID

A
  • 88% cases
  • d/t metabolic effects of cortisol, possibly related to increased susceptibility to infection (parasitism, poorer management of older horses including dental care and feeding and reduction in exercise d/t retirement or OA)
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10
Q

How does hyperhidrosis occur with PPID?

A
  • may be d/t long hair coat

- beta adrenergic controlled sweat glands (elevated catecholamines)

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11
Q

Describe PUPD of PPID

A
  • can concentrate urine if water deprived
  • d/t cortisol antagonising ADH on CDs, cortisol causing hyperglycaemia and osmotic diuresis, destruction of other areas of pituitary gland with reduced ADH production or combination of thse
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12
Q

Describe infection susceptibility with PPID

A
  • sinusitis
  • parasitism and skin infections
  • reduced neutrophil function d/t excess hormones
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13
Q

Dx - PPID

A
  • based on hx, signalment, CS and then hormone assays and dynamic tests:
    1. HORMONE ASSAY
    2. DYNAMIC TESTS
    3. INSULIN DYSREGULATION
    4. HISTOLOGY
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14
Q

Describe hormone assays for PPID

A

= basal ACTH concentration: one off blood sample

  • results vary in normal and PPID animals with season (autumn peak)
  • affected by feeding
  • may not detect early cases
  • variations of clinical relevance occur in individual animals
  • in conc b/w 19-40pg/ml then consider further testing
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15
Q

Describe dynamic tests in PPID dx

A

= TRH stimulation test

  • TRH is physiological release factor for pituitary
  • inject 1mg TRH IV and then measure ACTH (not cortisol) at 0 and 10 or 30 mins.
  • ACTH >100pg/ml at 10 mins or >36pg/ml at 30 mins = PPID
  • seasonal effect (greater July-November) compared to February
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16
Q

Describe insulin dysregulation in PPID dx

A
  • feature of PPID in some cases
  • may be d/t cortisol antagonising insulin
  • may be d/t CLIP stimulating insulin
  • may be d/t low grade inflammation and oxidate stress from EMS –> PPID
  • tests: see EMS
  • associated with laminitis and worse px
17
Q

Describe histology in dx of PPID

A
  • histologists cannot agree
18
Q

Tx/ management - PPID

A
  • not all owners elect to tx (depends on CS and severity - normall laminitis the most limiting)
  • can manage CS only
  • DOPAMINE AGONISTS
  • SEROTONIN ANTAGONISTS
  • CORTISOL ANTAGONISTS
19
Q

Describe dopamine agonists in PPID tx

A
  • 1st line tx
  • replace lost inhibition of pituitary gland
    = pergolide
  • side effects: diarrhoea, depression, anorexia, colic
  • 65-80% effective
  • licensed!!
  • 2microg/kg/day (=1mg/500kg)
20
Q

Describe serotonin antagonists in PPID tx

A
  • replace lost inhibition of the pituitary galnd
    = Cyproheptidine
  • probably acts by indirectly increasing dopamine
  • less effective than the dopamine agonists
  • works in 28-60%
21
Q

Describe cortisol antagonists in PPID tx

A 
- inhibiti production of excess cortisol by adrenal gland
= TRILOSTANE
- it is a 3 beta-HSD inhibitor
- 75% efficacy 
- only alteres CS d/t cortisol
22
Q

Monitoring - PPID

A
  1. monitor response to tx (give at least 2 months initally, adjust dose monthly)
  2. monitor clinical response + repeat testing: repeat initial test after 30 days, if now negative keep on same dose and recheck q 6months. If test still positive and no clinical response, increase dose by 1-2mg/kg/day and recheck after 30 days.
23
Q

Px - PPID

A
  • life long tx and management
  • some can continue in comfort for many years (50% still alive after 4.5 years)
  • laminitis usually reason for euthanasia
24
Q

What is EMS?

A

= Equine Metabolic Syndrome

  • cluster of clinical/metabolic abnormalities associated with increased risk of laminitis
  • stems from HMS (Human Metabolic Syndrome)
25
Q

Features - EMS

A
  • PREVIOUSLY: generalised/ regional obesity + IR + recurrent laminitis
  • NOW: not all components present in all individuals, obesity/IR/plasma [lipid] vary b/w studies
  • CURRENT THOUGHTS: insulin dysfunction, increased fasting triglyceride concentrations, altered adipokines. Obesity not a requisite feature of EMS, may exacerbate components of phenotype (e.g. IR) and it is a marker of an underlying metabolic dysfunction whose expression is influenced by environmental factors
26
Q

Why do EMS horses develop laminitis?

A
  • when grazing pasture
  • especially under conditions which favour increased WSC contnet
  • this promotes pronounced insulinaemic responce –> i fprolonged can induce laminitis in healthy horses and ponies (possibly through inducing endothelial dysfunction). May also trigger inflammatory injury to lamellae
  • BUT high planes of nutirtion/pasture changes don’t cause laminitis in all animals
  • individual variability may be d/t underlying genetic predisposition involving genetic alleles that result in alterations in insulin, glucose and/oor lipid metabolism which can increase or decrease dz risk and work with environmental influences to determine overall dz risk
27
Q

Dx - EMS

A
  • based on hx, signalment, CS and detection of insulin dysfunction
  • hx: assess contributing factors for obesity
  • signalment:
28
Q

CS - EMS

A
  • ? generalised obesity
  • ? regional adiposity - crest, tail head and shoulders, prepuce or mammary region
  • lean EMS phenotype possible
  • recurrent laminitis with no obvious cause
29
Q

How to detect insulin dysfunction for EMS dx?

A
  • Resting glucose and insulin cocnentrations
  • hyperinsulinaemia (rarely hyperglycaemia) after 6 hours overnight fast
  • combined glucose insulin test:
  • oral glucose test
  • oral sugar test
30
Q

Describe combined glucose - insulin test

A

Infusion of glucose and insulin after 6 hour fast. IR if blood glucose is above baseline value and insulin > 100microIU/ml at 45 minutes

31
Q

Describe oral glucose test

A

Feed 1g/kg glucose after 6 hour fast. ID if blood glucose >85 microIU/ml @ 120mins

32
Q

describe oral sugar test

A

0.15ml/kg po Karo light syrup. ID if blood glucose > 60 microIU/ml @ 60-75 minutes

33
Q

Tx - EMS

A
  • WEIGHT LOSS: to reduce omental fat via diet if obese
  • DIET: limit soluble carbohydrate intake, ideally feed only hay, 1.5% bodyweight, can add beet pulp, substitute 1 lb of beet pulp for 1.lb hay, can add vitamin and mineral supplement, avoid fat supplementation as worsens IR
  • EXERCISE: promotes glucose uptake and use by skeletal mm by insulin-dependent route, imrpoves insulin sensitivity, reduces inflammation and decreases feed intake
  • PHARMACOLOGIC INTERVENTION (metformin vs thyroxine)
34
Q

Describe pharmacologic intervention

A
  • METFORMIN (for human DMtype2): improves insulin sensitivity and vascular endothelial function, low bioavailability in horses (7%), only 2 studies (one no effect, one some beneficial effect), may work by decreasing GT glucose absorption
  • THYROXINE: ++++++++++++++++++++
35
Q

What supplements and neutraceuticals can be used for EMS

A
  • insufficient scientific evidence to support use

- chromium, magnesium, cinnamon and chasteberry commonly recommended as supposedly insulin sensitising

36
Q

Define PPID

A

Pituitary Pars Intermedia Dysfunction

37
Q

Describe thyroxine in pharmacological tx of EMS

A
  • ACTION: increases metabolic rate –> weight loss

- SIDE EFFECTS: hyperphagia so must restrict calories

Endocrine (11 decks)

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