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Equine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

Cycle leading to clinical disease w/ insulin dysregulation

A

Feed abundance –> Increased adipose stores –> temporary adverse effects of adipose stores –> continued feed abundance –> temporary effects become permanent –> clinical disease

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2
Q

Pathophys of EMS revolves around (2)

A
  1. increased adipose stores

2. Insulin dysregulation (ID)

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3
Q

what is insulin dysregulation?

A
  • excessive insulin response to NSC
  • fasting hyperinsulinaemia
  • insulin resistance - which is a normal response by cells to a normal level of insulin – to achieve a normal response by cells insulin levels increase
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4
Q

how does obesity affect ID?

A
  • inflammatory cytokines produced by fat
  • adipokines produced by fat
  • excessive metabolism of fat in cells = lipotoxicity

—> interferes w/ insulin signalling, causing insulin resistance/dysregulation

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5
Q

how are obesity, insulin and laminitis linked?

A
  • adipose - increases circulating inflammatory products

- increased insulin shown to cause laminitis + increased glucose may affect laminar vessels

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6
Q

predisposing factors to laminitis?

A
  • excessive pasture exposure
  • carbohydrate overload
  • endotoxaemia, systemic sepsis or toxaemia
  • supporting limb laminitis-laminar failure
  • equine metabolic syndrome/PPID
  • previous episodes of laminitis
  • corticosteroids w/ concurrent metabolic disease
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7
Q

clinical signs of laminitis

A
  • acute onset of lameness (bilateral)
  • forelimbs > HLs
  • reluctant to bear weight, land heel first - ‘heel-toe’ gait
  • look uncomfortable behind
  • increased digital pulses
  • more sore on hard ground, worse on the turn
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8
Q

laminitis hoof tester pain location

A

front of frog

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9
Q

foot exam - laminitis findings

A
  • palpable depression at the coronary band if there is sinking
  • penetration of sole: discolouration, softening, draining pt w/ severe rotation
  • hoof tester pain in front of frog
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10
Q

laminitis blocks to

A

abaxial nerve block

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11
Q

acute laminitis management

A
  • tx primary disease and remove predisposing factors
  • confinement
  • sole support-palmar half of foot to point of frog: sand box, sole pack, dense foam, support shoes
  • analgesia + NSAIDs: flunixin/bute
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12
Q

post acute laminitis management

A
  • farrier: rocker toe (bring break-over back), bar shoe w/ sole-pack/palmar support
  • reg hoof care + analgesia
  • rpt rads to monitor progression
  • avoid predisposing factors
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13
Q

EMS CS

A
  • breeds (ponys), 6-20yo
  • obese, regional adiposity
  • laminitis
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14
Q

EMS ddx

A

PPID, hypoT?

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15
Q

EMS dx

A
  • in feed glucose test/oral sugar test

- mod. insulin tolerance test

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16
Q

fasting insulin levels consistent w/ ID

A

> 20-30uU/ml

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17
Q

describe oral sugar test to dx EMS

A
  • fast as baseline insulin
  • 15ml/100kg corn syrup
  • blood at 60 + 90 mins, normal insulin <45 and 60uU/ml
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18
Q

describe in-feed glucose test to dx EMS

A
  • overnight fast
  • give 0.5-1g/kg BWT glucose powder in non-glycaemic feed
  • measure serum insulin and plasma glucose after 2hrs
  • normal:
    0.5g/kg 2hrs <60uU/ml
    1g/kg dose 2hr insulin <90uU/ml
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19
Q

goal of EMS management

A

decrease ID and restore insulin sensitivity

–> weight reduction: exercise, decrease intake, decrease NSC

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20
Q

EMS diet management

A
  • consume 1.5-1% body weight
  • limit grazing 1hr TID vs. muzzle (only late night/early morning graze)
  • less than 10% NSC - remove grain/concentrates/treats
  • no pasture access during growing season
  • soak hay
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21
Q

diets to maintain energy intake BUT w/ a low glucose and insulin response to manage non-obese EMS

A
  • soaked beet pulp
  • soaked soy hulls
  • rice brain
  • no fat supp
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22
Q

drugs to use for EMS

A
  • thyroxine

- metformin

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23
Q

MOA metformin in EMS

A
  • decreases glucose uptake, utilisation and systemic absorption
  • cause a signif. decrease in plasma glucose and insulin
24
Q

PPID signalment

A

> 15 yo, fluffy (hypertrichiosis), cushings

25
Q

pathophys of PPID

A
  • primarily hypothal disease
  • loss of dopaminergic inhibition of the pars intermedia
  • leading to hyperplasia or adenoma formation of the pars intermedia
  • oxidative stress and increased genetic risk
26
Q

what causes clinical disease in PPID

A

CS dt increased circulation of POMCs and loss of neuroendocrine function of adjacent tissues

27
Q

CS of PPID

A
  • hypertrichiosis - late CS
  • LAMINITIS (POMC –> ID)
  • hyperhydrosis
  • supraorbital fat pads/bags under eyes
  • weight loss/wasted topline + pot belly
  • PU/PD
  • lethargy
  • recurrent infections (dt suppression of IL-1, T-cells, APCs)
28
Q

less common CS of PPID

A
  • Neuro: blindness, collapse, seizures

- infertility?? age related

29
Q

Clinicopath abnormalities of PPID

A
  • mild anaemia
  • leukocytosis
  • hyperglycaemia and glucosuria
  • hyperinsulinaemia
  • cortisol not indicative
    +/- hepatic enzymes
30
Q

dx of PPID

A
  1. ACTH stims –> measure increased POMCs
  2. TRH stim test –> testing hypothal pit axis
  3. Dexamethasone suppression test –> tests hypothalmic pituitary adrenal axis
31
Q

ACTH stim test as dx of PPID

A
  • reference ranges vary depending on time of year and geographic location
  • horses that exceed the reference interval do not necessarily have the disease - needs to be taken in light of CS
  • ‘grey zone’ –> rest test during best time OR TRH stim
  • best time to test: FEB- APRIL (peak of dynamic phase)
32
Q

management of PPID horse

A
  • reg. teeth care + worming
  • aggressive tx of infections
  • address laminitis/risk + hoof care
  • pharmacological: pergolide
33
Q

pergolide MOA in PPID horse

A

Dopamine agonist –> increases dopaminergic control of the pituitary gland using dopamine agonists

34
Q

response to pergolide tx in PPID horses monitoring

A

7 days: ACTH levels improve
30 days: improved demeanour/attitude, ACTH/other hormones
6 months: hair coat improvement
Long-term: other CS improvements

35
Q

recommended protocol for PPID/ID horses

A
  1. Document findings:
    - baseline feet
    - plasma ACTH
    - insulin concentration/in-feed glucose test
  2. Encourage O to monitor appetite, hair coat, water intake, urination, BCS and general demeanour monthly
  3. Pergolide low dose –> reassess in 1-2months
  4. One or more CS should have improved + ACTH improved
    * ** test at same time of day and under the same conditions

4b) if no improvement –> increased pergolide by 0.001mg/kg —> until max dose 0.01mg/kg reached
5. Vet monitor 2x/yr ongoing

36
Q

describe the progression of CS with hyperlipidaemia

A
  1. Initial: assoc. w/ primary disease
    - depression, failure to drink, lethargy, reduce GIT motility and faecal output
  2. Mid: mild colic (stretching liver capsule), D+, icterus, SC oedema, CNS signs, HE
  3. Late: recumbency, convulsions, death

Clinical course: days to 3 weeks

37
Q

dx of hyperlipidaemia

A

TGL >85mg/dl up to 500mg/dl

38
Q

dx of hyperlipaemia

A

TGL >500mg/dl and opalescent plasma

39
Q

other clinicopath parameters of hyperlipaemia

A
  • liver enzymes elevated
  • azotaemia
  • glucose
  • metabolic acidosis
40
Q

treatment goals of hyperlipaemia

A
  1. Tx primary disease
  2. Improve energy intake and balance: IV glucose
  3. Decrease circulating TGL and improve uptake by peripheral tissue
  4. Tx liver disease
41
Q

hyperlipaemia prognosis and mortality

A
  1. Primary: mortality 80%

2. Secondary mortality 25-50% (depends on underlying dz)

42
Q

re. calcium homeostasis horses have —

A
  • high total and ionized calcium concentrations
  • poorly regulated intestinal calcium absorption
  • high urinary fractional excretion of calcium
  • low serum concentration of Vit.D metabolites
43
Q

acute CS of hypocalcaemia

A
  • when calcium is low sodium channels become activated by smaller changes in the RMP causing CS of increased neuromuscular excitability
  • decreased extracellular calcium leads to decreased smooth muscle contractility
  • –> tremors
  • –> SDF: synchronous diaphragmatic flutter (frenic nerve stim. of diaphragm)
44
Q

CS of lactation tetany

A
  • can occur from 2wks prior to foaling up to weaning dt large loss of calcium in milk
  • varied CS: profuse sweating, termors, anxious expression, tachy +/- arrhythmia, ileus, may present w/ colic
45
Q

tx of SDF

A
  • self correct once alkalosis resolved + lytes replaced orally via feed/water
  • or IV calcium
46
Q

how do you give calcium borogluconate?

A

500mls Ca borogluconate in 5L until CS improve then slow to 50mls/hr

47
Q

what conc. of calcigol is safe at 3x maintenance?

A

20ml/L

48
Q

divisions of hypercalcaemia by cause

A
  1. Dt parathyroid dysfunction–> primary vs. secondary

2. Independent of parathyroid dysfunction

49
Q

what causes nutritional secondary hyperparathyroidism?

A
  • diet rich in phosphorous and low in calcium
  • high oxalate pastures
  • -> increased PTH
50
Q

CS of nutritional secondary hyperparathyroidism

A
  • enlargement of the facial bones
  • shifting lameness
  • loose teeth
  • pathologic fxs
51
Q

dx of nutritional secondary hyperparathroidism

A
  1. Bloods: serum calcium normal/low, P normal/high, serum PTH increased
  2. Urinary fractional excretion of calcium is low + phosphorus high >4%
  3. Faeces: Ca:P ratio elevated dt oxalates
52
Q

tx of nutritional secondary hyperparathyroidism

A
  1. Diet: Ca:P ration >4:1 (increase lucerne hay, reduce grain and supp. calcium)
    Prevention diet: Ca:P ratio >1:1
53
Q

influences of baseline thyroid levels

A
  • age, daily rhythm, environment, exercise
  • non-thyroidal illness syndrome
  • decreased T3 and T4 dt corticosteroids, higher dietary iodine, PBZ
54
Q

tx of hypothyroidism

A
  • synthetic thyroxine
  • iodinated casein
  • bovine thyroid extract
55
Q

what is anhidrosis?

A
  • decreased ability to sweat in response to hyperthermia
56
Q

dx of anhidrosis

A

intradermal sweat test w/ terbutaline dilutions

- normal horse sweats at 1:1,000,000

57
Q

tx of anhidrosis

A
  • move to cooler/drier climate + aircon boxes
  • supplement thyroxine
  • feeding combination of KCl and NaCl for chloride replacement

Equine (7 decks)

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