Equine Endocrine Disease Flashcards
(42 cards)
1
Q
Pituitary Pars Intermedia Dysfunction (PPID)
A
- Hairy horse, most common endocrinopathy
- dopamine from hypothalamus controls melnotrops
- disruption of dopamine = too much ACTH and cortisol
2
Q
Pituitary gland
A
- Three distinct lobes
- Pars distalis
- Pars intermedia
- Pars nervosa
3
Q
Pars intermedia
A
- melanotrop => proopiomelancortin (POMC)
- POMC =>
- alpha - MSH
- beta - Endorphin
- corticotrophin - like intermediate lobe peptide (CLIP)
- some ACTH
- POMC =>
4
Q
Pars distalis
A
- Corticotrophs => different POMC peptides than PI
- POMC => ACTH
5
Q
Positive control of melanotrophs
A
- controlled by THR
- which releases MSH (this increases in the fall-prep for winter)
6
Q
Dysfunction of Pars Intermedia
A
- Loss of dopaminergic inhibition of PI
- Neurons in hypothalamus degenerate = dec dopamine conc
- => neurodegeneration root cause
- Pars intermedia enlarges => compresses remaining gland structures
- hypertrophy => hyperplasia => adenoma formation
- benign hyperplastic process
- secretes a small amount of ACTH (more than a normal horse)
- POMC derived peptides accentuate actions of ACTH
- => more cortisol made by adrenal gland
- POMC derived peptides accentuate actions of ACTH
7
Q
Etiology PPID
Clinical Signs
A
- Etiology
- Older horses more likely to acquire PPID
- Clinical Signs
- Hirsutism (long curly hair that fails to shed)
- PU/PD
- Laminitis
- Muscle wasting/weight loss
- Bulging eyes/perioorbital swelling
- hyperhidrosis (even clipped)
- Immunospuression (skin eye inf, subsolar abscesses, sinusitus)
- Inc apetite
- lethargy
- blindness
- infertility
8
Q
Early Clinical Signs PPID
A
- Delayed haircoat shedding
- Shift in metabolism
- Regional adiposity
- +/- Fertility problems
9
Q
PPID Diagnostic testing
A
- HIRSUTISM
- Endogenous ACTH
- Dexamethasone Suppression Test
- TRH stimulation test
10
Q
Things that later ACTH concentration
A
- EVERYTHING
- Stress
11
Q
Dexamethasone Suppression test
A
- ACTH secreted by PI doesn’t respond to normal feedback in PPID
- exogenous steroids don’t reduce cortisol production
- Antemortem ‘gold standard’
- requires 2 farm visits (overnight test)
- misses early cases
- not 100% sensitive/specific
- perceived risk of laminitis
- seasonal variations
12
Q
Endogenous ACTH
A
- morning, single blood draw
- seasonal effect
- less sensitive than DST
- EDTA tube, spin down, ship on ice, sample good for 12 hours
13
Q
TRH Stimulation Test
A
- Admin TRH (I mg IV), then take blood sample to measure ACTH
- affected horses: sig inc ACTH and cortisol (45-90 min post adm)
- Can also measure a MSH respones to TRH stim
- Avoids conplications from dexamethasone admin
- TRH available as compounded med
- needs to be validated in larger pops and in fall
14
Q
Other PPID tests
Tests that aren’t accurate
A
- Other tests
- screen for insulin resistence in PPID positives
- Not useful
- single/multiple cortisol conc (too many other things affect this)
- Diurnal ‘cortisol rhythm’ concentrations
- Urinary cortisol:creatinine ratio
- Insuline concentration
15
Q
PPID Treatment
Goal
Drugs
A
- Goals: increase dopaminergic control of pituitarty
- Reduce or minimize clinical signs
- Avoid laminitis / founder
- Dx and manage insulin resistence
- Improve fertility…?
- Drugs
- Dopamine agonists
- Serotonin antagonists
16
Q
PPID treatment with Pergolide
A
- Pergolide: dopamine agonists (1 mg/horse)
- now available as Prascend
- Assess response in 30 days
- Primary side effects
- depression
- anorexia
17
Q
PPID treatment with Cyproheptadien
A
- Cyproheptadine: serotonin antagonist
- goal to block ACTH production from PI
- Inconsistent response
- 0.5 mg/kg 1-2 times daily
- may improve clinical signs
- can be used as adjuct to pergalide
18
Q
Managing PPID
A
- 35-45 $ per month (not everyone will treat)
- Clipping hair
- manage feed (trims, rads, therapeutic shoeing)
19
Q
Equine Metaboilc Syndrome (EMS)
Case definition
A
- Insulin resistance
- Obesity and/or regional adiposity
- Prior or current lamiitis
- ‘easy keeper’
- Laminitis assoc with spring grass
20
Q
EMS predisposition
A
- Metabolically thrifty horses
- ponies, morgans, Pasos, Norweigian Fjords
- Aged 5-20 yo
- Most are obese
21
Q
Prolonged hyperinsulinemia
A
- Will induce laminitis
22
Q
EMS Diagnostic testing
A
- Resting Insuline/Glucose concentration
- do in the morning w/o access to sugars/food
- make sure horse isn’t stressed
- Oral Glucose Tolerance Tests
- give oral light karo syrum, draw blood 60-90 minutes later
- high glucose (>115 mg/dL) and insulin (>60 mic/mL) positive for IR and EMS
- Combined Glucose - Insuline Test (can cause hypoglycemia)
- takes about 3 hours
23
Q
Horses with an insuling level > 100
A
- risk foundering immediately this second!
24
Q
Goals of treatment EMS
A
- Improve insulin sensitivity => inc threshold for laminitis
- Reduce body fat (adiposity inc insulin resistence)
- Avoid high starch/sugar feeds
- Exercise, if possible
25
Managing obesity
* cut forage to 1.5 % BW in hay
* slowly reduce to 1.5% ideal body weight
* Choose hay \< 10% Non-structural carbohydrate
* get crappy hay
* or soak hay for 30 min (leaches out carbs)
* Restrict pasture access (1-2 hours a day)
* Grazing muzzle
26
Pharmacologic approaches to managing EMS
1. Levothyroxine (weight loss strategy)
* short term therapy at very high dose, must wean off
2. Metformin
* not super commin, given at meals
3. Corticosteroids
* associated with laminitis...?
* worse in IR horses...?
27
Thyroid dysfunction
* Hypothyroidism does not exist in horses
28
Euthyroid Sick Syndrome
* aka: non-thyroidal illness syndrom
* changes in thyroid function occur with systemic disease
* dec metabolic rate and preserve body mass...?
* recognized in
* humans and dogs
* amount of suppression correlated with severity of dz
29
Calcium homeostasis
* most regulation in Equine GI system
* most Ca and P found in teeth and bones
* 50% plasma calcium is ionized
* 40% plasma calcium bound to protein
* 5-10% plasma calcium bound to citrate, nitrate and sulfate
* alkalemia =\> low ionized Ca
* acidosis =\> inc ionized Ca
30
Hormones in Ca homeostasis
* PTH =\> inc plasma Ca
* bone, kidney
* Calcitriol (vit D3) =\> inc plasma Ca
* intestine
* Calcitonin =\> decreases plasma Ca
* bone
31
Conditions associated with Hypocalcemia
* Synchronous diaphragmatic flutter: thumps
* Lacation tetany
* Seizures
* Colic-endotoxemia
32
Synchronous Diaphragmatic Flutter
SDF
* Depolarization of the phrenic nerve occurs in time with right atrium
* stimulates contraction of diaphragm
* **Clinical Sign of hypocalcemia**
* thoracic/flank musculature contractions 'ticking' in time with HR
* thumping noise
* horse usually very anxious
* Clin path
* Low Ca, metabolic alkalosis, low K, Na
* alkalosis contributes to hypoCa
* Mg may also be decreased
* TX: give Ca and solve whatever caused hypocalcemia to begin with
\*horse specific
33
Lactation Tetany
* anytime from pre-foaling to post-weaning
* Profuse sweating, anxious
* stiff gain, muscle fasiculations
* Tachycardia/arrhythmia
* Colic w/unremarkable rectal, ileus
* Clin path: dec ionized Ca
34
Sepsis/Endotoxemia/Colic
* common cause of hypoCa in hospital
* Insufficient PTH secretion and intracellular Ca sequestration
35
Blister beetles
* causative agent of hypocalcemia
* reported regularly in FL
* found in alfalfa hay
* Canthardin
* vesicant
* highly irritating
* absorbed in GI and excreted in urine
* GI and renal irritation, muscle damage
* dose dep (1 beetle enough)
36
Blister beetle tox Clinical Signs
* Fever
* Tachycardia/pnea
* PD, dehydration
* Hematuria
Due to HypoCa:
* Muscle fasciculations
* Sweating
* Arrhythmias
* SDF
37
Hypercalcemia
1. Primary/Secondary hyperparathyroidism
2. Hypervitaminosis D
38
Secondary Nutritional Hyperaparathyroidism
* Dec Ca intake or excessive ingestion of P, oxalates
* Stimulates PTH
* CA and P mobilize from bone
* Bone replacedment by fibrous connective tissue
* over months
39
Secondary Nutritional Hyperparathyroidism
History/CS/DX
* History
* Diet low in Ca, high in PO4 (Bran disease)
* CS
* 'big head'
* Bones of maxilla widen
* loosening of teeth
* shifting leg lameness
* pathological fractures
* DX
* history
* PE
40
Secondary Nutritional Hyperparathyroidism
treatment
1. inc Ca, dec P in diet
2. Ca:P ratio 4:1 to induce remission
* alfalfa
* Calcium carbonate
* can take 9-12 months for recovery
\*normal diet: Ca:P ratio of 1:1 - 2:1
41
Anhidrosis
* Catecholamines =\> sweat glands =\> sweat
* Etiology of acute dz unknown
* No known predilection
42
Annhidrosis
Chronic signs/DX/TX
Chronic signs
* **Alopecia on forehead**
* Poor performance
* dry flaky skin
* dec water consumption
DX
* Clinical dx, terbutaline sweat test if someone doesn't believe dx
TX
* change environment or keep cool
