29. Diseases of the hypophysis in dogs and cats. Flashcards

1
Q

Hypophysiotropic hormones?

A

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

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2
Q

Pituitary hormones?

A

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

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3
Q

Congenital Hyposomatotropism?

A

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

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4
Q

Alopecia X?

A

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

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5
Q

Acromegaly?

A

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

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6
Q

Diabetes Insipidus>

A

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

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