29. Diseases of the hypophysis in dogs and cats. Flashcards
Hypophysiotropic hormones?
HYPOPHYSIOTROPIC HORMONES
Hormones produced by the endocrine cells in the hypothalamus
Hypophysis = Pituitary gland; Hypophysis ≠ Hypothalamus
§ GHRH - Growth hormone releasing hormone
§ LHRH - Luteinising hormone RH
§ TRH - Thyrotropin RH
§ CR - Corticotropin RH
Pituitary hormones?
PITUITARY HORMONES
Hormones secreted directly into the blood stream from the pituitary gland
§ ACTH – Adrenocorticotropic H
§ GH - Growth hormone
§ PRL – Prolactin
§ TSH – Thyroid Stimulating H
§ LH – Luteinising H
§ FSH – Follicle SH
§ aMSH –ɑ-melanocyte SH
§ AVP/ADH – Arginine vasopressin/Anti-diuretic H
§ Oxytocin
Congenital Hyposomatotropism?
Congenital Hyposomatotropism
“Pituitary dwarfism”
Autosomal recessive inheritance
PATHOGENESIS
Cyst formation of the anterior pituitary lobe → ↓ GH → ↓ TSH →
↓ T4 (Results in secondary hypothyroidism)
Predisposed: German Shepherd; Karelian bear dogs
CLINICAL SIGNS
§ Poor growth in puppies (but normal body proportions)
§ Retention of lanugo (missing guard hairs; thin hairs)
Later:
§ Alopecia § Hyperpigmentation
§ Thin skin § Brachygnathia inferior
From 2-3 years (severe):
§ ↓ Activity
§ ↓ Appetite
§ Renal failure
Animals at this level of severity should be euthanised
DIAGNOSIS
Skin biopsy: Show a ↓ in elastic fibres
Insulin-like growth factor
Xylazine-Stimulation test
Clonidine-Stimulation test } GH Measurement
GHRH-Stimulation test
TSH/TRH-stimulation tests
TREATMENT
§ Bovine-GH; Porcine-GH; Human-GH: Antibody
development occurs (note that this is not a permanent
solution)
§ T4 therapy
Prognosis: Animal will likely live until max. 5 years – Euthanasia
usually due to anorexia/renal failure
Alopecia X?
Alopecia X
Endocrine-induced hair-loss; Arrest of the hair cycle
Umbrella term for the following previously named syndromes:
§ GH-responsive dermatosis
§ Castration-responsive dermatosis
§ Oestrogen-responsive dermatosis
§ Biopsy-responsive dermatosis
§ Adrenal hyperplasia-like syndrome
PATHOGENESIS
Not completely understood
Predisposed: Nordic breeds; Poodle; “Fluffy” breeds: Pomeranian;
Chow -how; Samoyed
66% of cases have low GH level
Possible causes:
§ ↑ Androgen production (by adrenal glands)
§ Mild Cushing’s syndrome
CLINICAL SIGNS
Only significant cosmetically, no other impact
§ Symmetrical non-inflammatory alopecia (see Fig. 29.1)
§ Hyperpigmentation on the neck, trunk & caudal surfaces of the thighs
A Pomeranian showing clinical signs associated with alopecia-X
TREATMENT
Some cases may recover without treatment
§ Castration; Testosterone therapy
§ Trilostane (blocks adrenal synthesis of glucocorticoids)
§ Melatonin
Acromegaly?
Acromegaly
Mature animals with excess GH
PATHOGENESIS
Predisposed
Middle-aged bitches:
§ Exogenous progestogens (iatrogenic)
§ Mammary tumour
§ Metoestrous or Ovarian cyst → ↑ Progesterone
Middle/old-aged & male cats:
§ Pituitary tumour
CLINICAL SIGNS
§ Large head § Loose skin
§ Large paws § Snoring
§ ↑ Interdental space § Dyspnoea
§ Distended abdomen § PU/PD
§ Prognathia inferior § Protruding tongue
§ Cats: Insulin-resistant DM
Lab. D: Glucosuria
TREATMENT
Insulin therapy (temporary treatment)
Dog (good prognosis)
GH excess from mammary gland
§ Progestogen + Agleprisone (progesterone rec. blocker)
§ Excision of mammary tumour
Ovarian cysts: Ovariectomy
Cat (poor prognosis)
§ Hypophysectomy
§ Cobalt irradiation
§ Somatostatin
Diabetes Insipidus>
Diabetes Insipidus (DI)
↓ ADH action due to either:
§ ↓ Production
§ ↓ Sensitivity of the kidneys
Role of ADH: Renal water resorption control; Urine production & concentration
PATHOGENESIS
Predisposed: Middle/old-aged bitches; Rare in cats
Central DI (most severe)
§ Partial → ↓ ADH
§ Complete → Ø ADH
§ Causes
§ Pituitary tumour § Inflammation
§ Hypothalamic tumour § Trauma
§ Hypophysectomy
Nephrogenic DI (most common)
§ Impaired action of ADH on the kidneys; ↓ Sensitivity
§ Potentially reversible after eliminating the cause
§ Causes:
§ Kidney Failure § Addison’s
§ Liver Failure § Cushing’s
§ Hypercalcaemia § Pyometra
CLINICAL SIGNS
§ PU/PD
§ If water intake is impossible → Dehydration; Death
DIAGNOSIS
Think of differential diagnosis for PU/PD whilst using:
§ Urine sample: USG >1.020 → DI can be ruled-out
§ Blood sample
§ Abdominal US
§ Cortisol measurement
Distinguishing nephrogenic DI & central DI
Modified water deprivation test
§ Consider that dehydration is risky in DI patients (shock)
§ Used to assess the effects of dehydration on the USG
§ Normal: Dehydration → USG >1.030
§ If this isn’t the case, the animal is administered exogenous
ADH to differentiate between NDI & CDI
§ CDI = USG >1.030
§ NDI = Ø Change
Desmopressin test
§ Alternative to the modified water deprivation test; All other
causes of PU/PD should be ruled out first (see earlier)
§ Desmopressin application for 7 days
§ CDI: ↓ PU/PD by day 7; ↑ USG
§ NDI: Minimal improvement
ADH measurement during hypertonic saline infusion
TREATMENT
Central DI: Desmopressin (ADH receptor stimulator; Similar
structure to physiological vasopressin)
Nephrogenic DI
§ ↓ Na diet
§ Provide continuous source of water
§ Thiazide diuretics
