endocrinology - vfu · clinical impact •endocrinopathy is underlying cause of 80% laminitis cases...

Endocrinology

2015 Zuzka Drábková

The most common endocrinedisorders in horses

PPID EMS

Clinical impact

• Endocrinopathy is underlying cause of 80% laminitis cases• PPID 5x increased risk of laminitis• EMS 30x increased risk of laminitis

PPID (Pituitary Pars Intermedia Dysfunction) Cushing‘s syndrome


→ Loss of dopaminergic inhibition of parsintermedia because of neurodegeneration

→ Adenomatous hyperplasia of pars intermedia and functional adenomas

→ Overproduction of POMC (and it‘s products –ACTH, MSH, LPH ad.)

→ ??? Adrenal hyperfunction and cortisoloverproduction???

PATOPHYSIOLOGY


• Aged horses• 21% prevalence 15y and older• Youngest clinically diagnosed horse was 7y

• No gender or breed predisposition

RISK FACTORS


• Hirsutism/hair coat abnormalities (70% has PPID)

• Hyperhidrosis• Laminitis• Lethargy• Weight loss (but obesity in 12%)• Muscle wastage• PU/PD• Bulging supraorbital fat• Chronic infections (sinusitis, dermatitis, hoof

abscess, parasitosis, alveolar periostitis, gingivitis)

CLINICAL SIGNS


• Hirsutism/hair coat abnormalities• Hyperhidrosis• Laminitis (33% has hyperinsulinemia)• Lethargy• Weight loss (but obesity in 12%)• Muscle wastage• PU/PD• Bulging supraorbital fat• Chronic infections (sinusitis, dermatitis, hoof


CLINICAL SIGNS


• Hirsutism/hair coat abnormalities• Hyperhidrosis• Laminitis• Lethargy• Weight loss (but obesity in 12%)• Muscle wastage• PU/PD• Bulging supraorbital fat• Chronic infections (sinusitis, dermatitis, hoof


CLINICAL SIGNS


• ACTH – majority, 90% sensitivity and specificity• TRH stimulation test (for ACTH) – if dubious

result of ACTH, gold standard

• Dexametason suppression test • Unreliable in autumn• Less practical(2 visits – after 19h)• Laminitis risk

• αMSH • Comparable ACTH• Rarely available

DIAGNOSTICS


Blood level of ACTH

• EDTA blood, chill within3h, analyse within 12h

• Ref: 29 pg/ml• Aug – Oct 47 pg/ml

„GREY ZONE“• Results between 19 - 40

pg/ml perform TRH stimulation test

• Good correlation with pathology, monitoring of therapy


• Pergolid– Dopaminergic agonist– Registred for horses– Dose 0,85 – 10 µg/kg PO BID (SID)– Starting dose usually 0,5 – 1mg pro toto– In 1-4 w clinical improvement and decrease in ACTH (Recheck

after one months)– Some need 2 – 3 y on therapy– Side effects: anorexia, diarrhoea, colic, lactation suppresion,

lethargy, mild ataxia

• Other small evidence (cyproheptadine, trilostane, Vitex)• Management (hoof care, dentistry, clipping, deworming, nutrition)

THERAPY

EMS (Equine Metabolic Syndrome)

• Obesity/regional adiposity→ Predisposition

• Insulin resistence/hyperinsulinemia→ Patophysiology

• Laminitis/laminitis predisposition→ Clinical effect


• Mirrors obesity in humans

OBESITY/REGIONAL ADIPOSITY



• Causes: overfeeding in winter• Native breeds: pony, Arabian, Fjord, donkey…



• Subjective assessment:• BCS – body condition score (0-5, 0-9)• Weight tape

• Objective assessment :• Body weight• USG – retroperitoneal, subcutis (needs

standardisation)• Bioimpedance ?


INSULIN RESISTENCE/HYPERINSULINEMIA

• Not all obese horses have insulin resistence and vice versa

• Phenotype of EMS horses „easy keepers“ –gain weight from air

• 33% PPID horses• Excessive response to oral carbohydrates


• Diagnostics:!BEFORE ALL TESTS: fasting (6-12h), x stres, x pain (acutelaminitis), x sedation alfa2 agonist, x inflamatory process!

– Insulin • Fasting insulin, ref. 20 mU/L

– Oral glucose test• Fasting, morning 1g/kg glucose in low starch feed (beet pulp),

insulin 2 h later ref. 85 (60) mU/L• Laminitis risk minimal

– CGIT (combined glucose-insulin test)• Fasting, IV glucose (150mg/kg) combined with IV insulin (0,1

IU/kg), glucose back to basal value in 45 min, insulin 45min up to 100 mU/L

• Risk of hypoglycemia

INSULIN RESISTENCE/HYPERINSULINEMIA


LAMINITIS/LAMINITIS PREDISPOSITION

Etiology

Toxemia

colitis

grain overload

colon volvulus

retained placenta

Hyperinsulinemia 80%

EMS

PPID

pasture

Mechanical overload


• Prevention and therapy:

– Diet

– Exercise

– Drug therapy

LAMINITIS/LAMINITIS PREDISPOSITION


• Only hay– 1,5 - 1% actual body weight– soaked several hours

• No grain or treats• Vitamin and mineral supplements• Limited pasture

– Grazing with muzzle– Short period– Pony eats in 3h 40% dd

• Weight loss 1% bwt/w

DIET


EXERCISE

• Increases insulin sensitivity• Residual effect

• In laminitis only when horseis sound


• Až po zvládnutí změn managementu

• Metformin– Decreases glucose production by liver– Increases insulin sensitivity– Poor bioavailability (only 7%)– Dose 30 mg/kg PO TID

• Levothyroxin– Increases mtb decreases bwt– Increases insulin sensitivity– Dose 0,1 mg/kg PO SID

DRUG THERAPY

Thyroid gland

TRH→TSH→T3 (active), T4 (90%)Kalcitonin (parafolicular cells – C-cells)

Thyroid gland

• Adenoma – no endocrine activity, 70% horses over20 y

• Adenocarcinoma – rare

• C-cell tumor – often together withpheochromocytoma

• Cysts – possible swallowing and breathing problems

TUMORS

Thyroid gland

• Rare

• Previously false diagnosed (confused with EMS)

• Effect of exercise, feeding, concurent illness and therapy (phenylbutazon) on the T4 a T3 – unreliable

• Cl.s. adult: exercise intolerance, hair coatabnormalities, bradycardia, ventral edema

• Cl.s. foals: incoordination, weak suckling reflex, hypothermia, ossification abnormalities

HYPOTHYREOSIS

Thyroid gland

• Goiter in foals

– Excessive iodine intake by mother duringpregnancy or dietetary deficiency

– Western syndrome (Canada, USA)

• Dg.: TRH či TSH stimulation test

HYPOTHYREOSIS

Thyroid gland

• 2 cases

• Cl.s.: weight loss, tachypnoe, tachycardia, hyperactivity, ravenous apetite

• Increase in T4

HYPERTYREÓZA

Adrenal medulla

• Any age (6 m – 31 y)

• Usually does not metastasize

• Functional: production of catecholamines

• Cl.s.: profuse sweating, excitation, tachycardia, colic, tremor, mydriasis

• Poor prognosis

PHEOCHROMOCYTOMA

Pankreas

• Definition: persistent hyperglycemia a glucosuria fromhypoinsulinemia or insulin resistence

• Primary DM: rare, after pancreatitis

• Cl.s.: depression, weight loss, Pu/Pd, polyfagia, hair coatabnormalities

• (Secondary DM: EMS rarely hyperglycemia)

• Dg. Hyperglycemia, hypoinsulinemia

DIABETES MELLITUS

Calcium metabolism

• Parathormon/kalcitonin/vitamin D

• Gut, kidneys, bones

Calcium metabolism

• Cl.s.: diaphragmatic flutter, tetany (musclefasciculations, tremor, stiffness, tachypnoe, depression, seizures), ileus, retained placenta

• Causes: sepsis, strenuous exercise, ARF, exertionalrhabdomyolysis, lactation tetany

HYPOCALCEMIA

Calcium metabolism

• (Primary hyperparathyroidism (carcinom), hypervitaminosis D, nutritional secondaryhyperparathyroidism)

• CRF (renal secondary hyperparathyroidism)

• Paraneoplastic hypercalcemia

– Lymfoma

– SCC

– Mesenchymoma

– Ameloblastoma

HYPERCALCEMIA

Calcium metabolism

• Symmetrical proliferation of subperiosteal bone, which occurs on the distal long bones (mtc, mtt)

• Sometimes mandible or maxila, nasal bones

• No articular involvement

• Found in association with intrathoracic lesions (71%)

• Marie‘s disease

HYPERTROPHIC OSTEOPATHY

Calcium metabolism

HYPERTROPHIC OSTEOPATHY

endocrinology - vfu · clinical impact •endocrinopathy is underlying cause of 80% laminitis cases...

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