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Endocrine > Equine Endocrinopathies > Flashcards

Equine Endocrinopathies Flashcards

1
Q

What is PPID Also known as?

A
  • equine Cushings disease ( don’t use this term, nothing wrong with adrenal)
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2
Q

What is the pituitary? Outline the anatomy and what is produced here

A

> gland base of brain, produces hormones in response to signals from hypothalamus
anatomy: 2 lobes
- anterior adenohypophysis
~ divided into pars intermedia, pars distalis, pars tuberalis
- posterior neurohypophysis
~ pars nervosa produces ADH and oxytocin

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3
Q

What section of the pituitary is affected in “equine Cushings” and in other animals?

A
  • horses pars intermedia

- other animals pars distalis

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4
Q

What cells is the pars intermedia comprised of?

A

Melanotropes

- process POMC -> b endorphin, aMSH, CLIP &

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5
Q

How is production of ACTH regulated?

A
  • unaffected by GC

- regulated by dopamine (-ve) and 5-HT (+ve) from hypothalamus

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6
Q

Outline Pathophysiology of PPID

A
  • cause unknown
  • loss of dolaminergic inhibition of pars intermedia d/t oxidative damage (slowly progressive)
  • marked overproduction of pars intermedia derived hormones (b-endorphin, aMSH, CLIP
  • modest increase in ACTH
    > GC effects are d/t modest increase in ACTH AND INCREASED ACTIVITY of ACTH plus NO NEGATIVE FEEDBACK
  • not simply excess ACTH like in dogs or humans
  • less important compression of surrounding pituitary and brain -> reduction in hormones (ADH, OT) and seizures and blindness
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7
Q

Epidemiology PPID

A
  • old horses average 19yo, rarely horses
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8
Q

Clinical signs of PPID

A

> hypertrichosis
-common, pathognomonic
- delayed shedding/thick curly coat
- affects 55-80% cases
- poss d/t excess melatonin or corticoid/androgen effect or pressure on hypothalamic thermoreg centre
laminitis
- recurrent or chronic
- probs d/t excess cortisol and/or insulin
- often cause of eventual euthanasia
weight loss
- 90%cases
- metabolic effects of cortisol
- ^ susceptibility to infection (parasitism)
- poor management of old horses (dental care, feeding, v excercise d/t retirement or OA)
hyperhydrosis
- long hair causing overheating
- b adrenergic sweat glands affected by ^ catecholamines
PUPD
- can concentrate if water deprived
- d/t cortisol antagonising action ADH, causing hyperglyceamia with concurrent osmotic diuresis, destruction of other areas pituitary v ADH production or combo of these
bulging supra orbital fat
susceptibility to infections (sinusitis, parasitism, skin)
- v neutrophil function d/t excess hormones
lethargy
- endorphin/cortisol effect?
- may not notice until Tx

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9
Q

Diagnosis PPID

A

> Hx, signalment, clinical signs
hormone assays
- basal ACTH conc (results vary in PPID and normal horses - peak in Autumn, affected by feeding, may not detect early cases, variation in relevance in individual animals so if conc 19-40pg/ml consider further testing)
dynamic testing
- new test so seasonally adjusted range not yet decided
-TRH stim test (not logical but TRH physiologic release factor for pituitary - measure ACTH not cortisol - at 0 & 10m or 30mins
- ACTH >100pg/ml @10mins or >36pg/ml @ 30mins =PPID
- seasonal effect greatest July-Nov cf Februrary
insulin dysregulation
- feature in some but not all case
- may be d/t cortisol antagonising insulin -> ^ release, CLIP stimulating insulin or low grade inflam and oxidative stress from EMS -> PPID
- tests as for EMS. ASSOCIATED WITH LAMINITIS AND WORSE PROG
histology
- hard to dx, even histopath cannot agree

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10
Q

Will all owners opt to Tx PPID?

A

No depends on clinical signs and severity

  • normally laminitis most limiting
  • manage clinical signs only
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11
Q

Tx PPID

A

> DA agonists
- replace lost inhibition of pituitary gland
- PERGOLIDE (prascend) lic so must be 1* line choice of Tx
- 65-80% effective
- 1mg/500kg/day
5-HT antagonists
- replace lost inhibition of pituitary gland
- CYPRIHEPTIDINE (indirect ^ DA)
- less effective cf. DA ags
cortisol antagonists (OUT OF FASHION, USED IN SMALLIES)
- TRILOSTANE - inhibits at level of adrenal: 3b-HSD inhibitor so only prevents effects d/t cortisol

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12
Q

Side effects of prascend?

A
  • D+
  • depression
  • anorexia
  • colic
    > stop and restart at lower dose
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13
Q

What happens to all pituitary hormones in the horse throughout the year?

A

^ in Autumn.

- PPID horses do a greater ^ in Autumn

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14
Q

How can PPID horses be monitored?

A
  • monitor clinical response (min 2 months initially, can take up to a year)
  • adjust dose monthly
  • +- repeat testing
  • repeat initial test after 30d (if neg keep on same dose, recheck q6mo)
  • if positive, but clinical response, can keep dose same or increase
  • if positive and NO clinical response, increase dose by 1-2mg/kg/d, recheck after 30d
    > probably better to base on clinical signs but some people think you need to normalise lab numbers
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15
Q

Prognosis for PPID?

A
  • lifelong Tx and management
  • some can continue for several years comfortably
  • doesn’t usually -> death, if it does likely d/t laminitis
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16
Q

What is EMS?

A
  • cluster of clinical/metabolic abnormalities associated with ^ risk of laminitis
  • stems from human form of dz
    > characterised by
  • obesity
  • insulin
  • dysregulation
  • hypertension
  • abnormal plasma lipid profile
  • pro-inflammatory state
  • altered adipokines
  • develops in genetically susceptible individuals with excessive dietary intake and inactivity over time
    > risk factor for CV dz and type 2 diabetes, and laminitis
17
Q

What was previously EMS classified as?

A
  • generalised/regional adiposity + IR + recurrent laminitis

- features that define EMS still Up for debate as obesity/IR/plasma lipid vary between studies and individuals

18
Q

Most common features of EMS thought now?

A
  • insulin dysfunction
  • ^ fasting TG
  • altered adipokines
  • not necessarily obese but may exacerbate components of phenotype and marker of underlying metabolic factors
  • EMS horses get laminitis WHEN GRAZING PASTURE esp with ^ WSC [water soluble carbs]content
  • promotes pronounced insulinaemic response -> induces laminitis (poss via endothelial dysfunction) may also -> hind hut carb overload -> inflammatory injury to lamellae
  • high planes of nutrition or changes in pasture do not induce laminitis in all animals, only individuals pdf genetically
19
Q

How is EMS diagnosed

A
  • Hx, signalment, clinical signs
  • detection insulin dysfunction
  • assessment of contributing factors for obesity
  • signalment
20
Q

What are the 2 main players for ^ EMS risk?

A

Genetics and environment NEED BOTH

21
Q

What are the clinical signs of EMS

A
  • altered adipokines
  • insulin dysregulation
  • hypertriglyceridaemia
  • ^ risk lamnitnies (recurrent with no apparent cause)
    +- obesity
    +- hypertension
    +- pro-inflammatory state
    > studies do not agree on all signs
22
Q

How can insulin dysregulation be identified?

A
  • resting insulin and glucose concentrations - hyperinsulinaemia (rarely hyperglycaemia) after 6hrs overnight fasting
  • combined glucose insulin test (infusion glucose and insulin after 6hr fast, IR if blood glucose is above baseline and insulin >100uIU/ml @ 45mins)
  • oral glucose test (feed 1g/kg glucose after 6 hr fast, ID if blood glucose >85uIU/ml @ 120mins)
  • oral sugar test (0.15ml/kh PO Karo light syrup, ID if blood glucose >60uIU/ml @ 60-75mins)
23
Q

Tx EMS

A
  • wt loss to reduce omental fat if obese only
  • limit sioluble carbs (ideally feed hay only 1.5% body weight - can add beet pulp substitute 11lb beet pulp for 1.5lb hay)
  • can add vit and mineral supplement esp if soaking, avoid fat supplement as worsens IR
  • excerce promotes glucose uptake and use by skeletal muscle by an insulin -independent route and ^ insulin sensitivity. v inflammaotion and feed intake
  • diet and exercise should be sufficient but is hard work!!*
    > pharmacological interventions
  • reserve for short term 3-6mo while management changes take effect
  • METFORMIN (now out of fashion) used human type 2 diabetes. Improves insulin sensitivity and vascular endothelial function. Low bioavailbility in horses. MAY work by v intestinal glucose absorption)
  • THYROXINE (0.1mg/kg SID PO can ^ 0.15 @ 3mo) ^ metabolic rate
  • BUT UK have to use dog tablets -> prohibitively expensive
  • side effects: hyperphagia, wean off when wt lost
    > supplements and neutraceuticals
  • no evidence
24
Q

Egs of supplements and neutracueticals suggested for use with EMS

A
  • chromium
  • magnesium
  • cinnamon
  • chasteberry
    > NO EVIDENCE
  • supposedly insulin sensitising
  • but if it helps owner do mamagement changes may be useul

Endocrine (16 decks)

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