30. Diseases of the adrenal glands in dogs and cats Flashcards

1
Q

Hypoadrenocorticism (Addisons disease) pathogenesis ?

A

Hypoadrenocorticism (Addison’s Disease)

↓ Adrenal gland hormones; Rare but life-threatening

Uncommon in dog; Very rare in cat

PATHOGENESIS

Predisposed: Young/middle-aged animals; Bitches

Great Dane; Rottweiler; Poodle; Schnauzer; Westie; Bearded colie;

English cocker spaniel

Primary Addison’s (if 90% of adrenal cortex tissue is lost)

§ ↓ Cortisol & aldosterone; ↑ ACTH

§ Causes

Autoimmune destruction of the AC (most common)

Bilateral adrenal tumour

Amyloidosis

Infection

Iatrogenic treatment of Cushing’s disease → Cortisol & aldosterone

deficiency

Secondary Addison’s

§ ↓ Cortisol; Normal aldosterone; ↓ ACTH

§ Causes

Long term glucocorticoid therapy with abrupt stop

Hypophyseal tumour

Pituitary tumour

Trauma; Inflammation

Glucocorticoid/Cortisol deficiency
§ ↓ GNG & ↓ GGL → ↓ Energy metabolism

§ ↓ Fat metabolism; ↓ Water excretion; ↓ Mentation & stress

tolerance

Aldosterone (mineralocorticoid) deficiency

§ Loss of: Na; Cl; H2O

§ Retention of: K+

§ → Hypovolaemic shock; ↓ Cardiac conduction; ↓ Cardiac

output; ↓ BP; ↓ Renal perfusion; Muscle weakness; Nausea

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2
Q

Clinical signs and lab D of addisons disease?

A

CLINICAL SIGNS

“Addisonian crisis” CSx:

§ Vomiting § PU/PD

§ Diarrhoea § Anorexia

§ Weakness § Lethargy

Other CSx:

§ ↓ Stress response § Tremor

§ Dehydration § Hypothermia

§ Abdominal pain § Depression

§ Weight loss

Acute/end-stage CSx:

§ Shock § ↑ CRT

§ Bradycardia

§ Weak pulse → Hypovolaemic shock → Death

LAB. D

§ Mild normocytic normochromic anaemia

§ Eosinophilia; Lymphocytosis

§ ↓Na+; ↓Cl-

; ↑ Ca2+; ↑ K+

§ ↓ Cholesterol

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3
Q

Diagnosis and treatment of addisons disease?

A

DIAGNOSIS

ACTH-Stimulation test (frequently used)

§ Administer 5μg/kg IV Tetracosactite (synthetic ACTH)

§ Blood sample taken at T=0 & T=1 hour

§ Positive result: T=0 <28nmol/l; T=1 hour <100nmol/l

ECG:

§ Spiked T-Wave

§ ↑ Q-T distance

§ Wider QRS complex

§ ↓ P-wave

§ ↑ P-R distance

§ Bradycardia

Radiology: Microcardia; V. cava caudalis is smaller

Abdominal US: Thinner adrenal glands

TREATMENT

Addisonian crisis

§ Correct any perfusion & dehydration deficits

§ Correct any electrolyte & acid-base imbalances

§ Steroid supplement: Hydrocortisone then Dexamethasone

§ Mineralocorticoid supplement: Desoxycortone

Maintenance therapy

§ Fludrocortisone/DOCP

§ Prednisolone

§ NaCl mixed with food

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4
Q

Hyperadrenocorticism (Cushings disease)?

A
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5
Q

Pathogenesis and clinical signs of cushings?

A

PATHOGENESIS

Predisposed: Middle/old-aged dogs

Poodle; Dachshund; Yorkie; Vizsla; Boxer

Pituitary dependent Cushing’s (PDH) (85% chance) (small dogs)

§ ↑ Cortisol; ↑ ACTH

§ Excess ACTH secretion (unresponsive to negative

feedback) → Bilateral AC hyperplasia

§ Causes: Hypophysis hyperplasia; Adenoma

Adrenocortical tumours (large dogs)

§ ↑ Cortisol; ↓ ACTH

§ Independent from ACTH; ↑ Cortisol excretion → ACTH

feedback leads to contralateral adrenal hyperplasia

§ Causes: Adenoma; Carcinoma

Iatrogenic form

§ Long-lasting glucocorticoid therapy

§ ↓ Cortisol (due to AC atrophy); ↓ ACTH

CLINICAL SIGNS

§ Polyphagia § PU/PD

§ Centripetal obesity § Hepatomegaly

§ Abdominal enlargement § Thin skin

§ Muscle wasting § Atrophied skin

§ Secondary infections § Alopecia

§ Hyperpigmentation § Panting

§ Calcinosis cutis § Anoestrous

§ Testicular atrophy § Keratin plugs

Risk of pulmonary embolism → Associated CSx

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6
Q

Lab D and diagnosis , treatment and prognosis?

A

LAB. D

§ ↑ Proteolysis; ↑ GNG; ↑ Lipogenesis (due to ↑ GC)

§ Leucocytosis; Neutrophilia

§ ↑ ALP (steroid induced alkaline phosphatase)

§ ↑ Cholesterol; Lipaemia; ↑ Blood glucose

§ ↓ USG

DIAGNOSIS

See “Lab. D” & “Clinical signs”

Low dose dexamethasone suppression test (LDDS)

Procedure

  1. 0.01 mg/kg IV dexamethasone given in the morning
  2. Blood sample at: T= 0; T= 4 hours; T= 8 hours

Results

§ Positive: T= 8 cortisol >40nmol/l

§ PDH: T= 4 cortisol < 0.5 times T= 0 cortisol

ACTH Stimulation test

Indication: If the cause is iatrogenic; If there is concurrent illness;

Monitoring the response of the patient

Procedure: See under “Hypoadrenocorticism” earlier in the topic

Results

§ Normal: 2/3-fold ↑ in cortisol

§ Cushing’s disease: T=1 cortisol >550nmol/l

§ Adrenocortical atrophy: Reduced response

Discrimination test (differentiate between PDG & ADH)

§ Measurement of endogenous ACTH

§ Abdominal US:

Bilateral enlargement – PDH

Unilateral enlargement – ADH

§ High-dose dexamethasone suppression test

See LDDS for method

0.1 mg/kg dose instead

PDH: T= 4 or T= 8 cortisol < 0.5 T= 0

PDH: T= 4 or T= 8 cortisol < 40 nmol/l

§ Urinary cortisol/creatinine ratio (Non-specific)

§ Ultrasound: Adrenal glands; Metastasis

§ Radiology: Hepatomegaly; Osteoporosis; Calcinosis cutis;

Lung metastasis; Calcification of AG (15% of cases)

§ CT: Pituitary tumour

§ Blood pressure

TREATMENT

§ Mitotane (selective destruction of AC)

§ Trilostane

§ Hypophysectomy

§ Adrenalectomy

PROGNOSIS

Good → Poor; Average lifespan is 2 years (due to complications)

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7
Q

Hyperadrenocorticism (Cushings disease) of cats ?

A

Hyperadrenocorticism (Cushing’s Disease) of Cats

↑ Cortisol; Rare disease

Predisposed: Middle/old-aged cats

CLINICAL SIGNS

§ Alopecia § Keratin plugs

§ Hyperpigmentation § Fragile skin

§ DM

TREATMENT

Mitotane is ineffective

§ Trilostane

§ Hypophysectomy

§ Bilateral adrenalectomy

Prognosis: Guarded → Poor

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