30. Diseases of the adrenal glands in dogs and cats Flashcards
Hypoadrenocorticism (Addisons disease) pathogenesis ?
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
Clinical signs and lab D of addisons disease?
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
Diagnosis and treatment of addisons disease?
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
Hyperadrenocorticism (Cushings disease)?
Pathogenesis and clinical signs of cushings?
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
Lab D and diagnosis , treatment and prognosis?
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
- 0.01 mg/kg IV dexamethasone given in the morning
- 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)
Hyperadrenocorticism (Cushings disease) of cats ?
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
