Hypoadrenocorticism Flashcards
Actions of glucocorticoids
Part of the fight or flight response
A ‘stress’ hormone
Counteracts the effects of stress
Essential for life!
Aldosterone regulation
Renin-angiotensin system
- decreased blood pressure (baroreceptors in wall of afferent arteriole, and cardiac and arterial) -> renin release -> angiotensin release -> aldosterone release
Potassium concentration
- Very small increases -> aldosterone release
Function of aldosterone
Regulation of BP
Acts on cells of diatal tubule and collecting duct to increase reabsorption of Na, Cl and water
Stimulates secretion K+ into tubular lumen
Stimulates secretion of H+ in exchange for K+ in the collecting tubules, so regulating acid/base
Aetiology of hypoadrenocorticism
- Primary hypoadrenocorticism - Addison’s
- secondary hypoadrenocorticism - deficiency of ACTH
- Iatrogenic hypoadrenocorticism
Primary hypoadrenocorticism (Addisons)
Deficiency of glucocorticoids (cortisol) and mineralocorticoids (aldosterone).
Occurs with loss of 85-90%
Signalment: young/middle aged, female dogs. Very rare in cats.
Causes of Primary hypoadrenocorticism (Addisons)
Idiopathic atrophy - probably immune mediated destruction
Iatrogenic - drugs (mitotane, trilostane), surgery (bilateral adrenalectomy
Pathophysiology of Primary hypoadrenocorticism (Addisons)
Aldosterone deficiency
- loss of Na+, Cl, H2O
- retention of K+, H+
- Pre-renal failure
Glucocorticoid
- decreased stress tolerance
- GI signs
- Weakness
- appetite loss
- anaemia
- imparied gluconeogenesis
Seconday hypoadrenocorticism
Deficiency of ACTH
Only cortisol deficient as RAS system still stimulating aldosterone
Rare
Iatrogenic hypoadrenocorticism
Exogenous steroids -> adrenal atrophy
Cortisol deficiency only
Patient may have signs of Cushing’s syndrome: PU/PD, alopecia, pot belly, hepatomegaly
May develop signs of Addisons if steroids abruptly discontinued
Clinical signs of a chronic presentation of hypoadrenocorticism
Worsened by stress
Waxing and waning signs
Anorexia
Vomiting
Lethargy
Depression
Weakness
Shivering
Weight loss
PU/PD
Abdominal pain
GI haemorrhage
Acute presentation of Addisonian crisis
Medical emergency, can be fatal
Hypovolaemic shock, with paradoxical relative bradycardia
Collapsed or extremely weak
Hypothermic
History of V+/D+
Abdominal pain
Cardiac abnormalities
Depression
Thin
Weak
Dehydration
Bradycardia
Melena
Blood parameter changes in hypoadrenocorticism
Reflect lack of aldosterone and cortisol, and hypovolaemia
What does lack of aldosterone cause?
Renal loss of water, sodium, and chloride.
Retention of potassium and hydrogen ions.
Pre-renal failure
What does glucocorticoid deficiency cause?
Decreased stress tolerance, appetite loss, impaired gluconeogenesis, normocytic normochromic anaemia.
Biochemistry findings in hypoadrenocorticism
Hyperkalaemia
Hyponatraemia
Hypochloridaemia
Decreased Na:K ratio
10% do not have classic electrolyte findings
Azotaemia (increased renal parameters)
Hypercalcaemia
Hypoglycaemia
Haematology findings in hypoadrenocorticism
Lack of stress leukogram
Lymphocytosis
Eosinophilia
Neutropaenia
Anaemia
Urinalysis findings in hypoadrenocorticism
May be high USG due to dehydration and azotaemia
BUT chronic sodium wasting can reduce urine concentrating - medullary washout
ECG changes in hypoadrenocorticism
Result of the level of hyperkalaemia
> 5.5mmol/l: T wave peaking and Q-T shortening
> 6.5mmol/l: increased QRS duration
> 7.0 mmol/l: P wave decreased, P-R interval prolonged
> 8.5mmol/l: P waves absent and severe bradycardia
Radiographic changes of hypoadrenocorticism
Usually relate to hypovolaemia e.g. microcardia, decreased pulmonary vessel size, reduced caudal vena cava, microhepatica.
Occasionally oesophageal dilation can be seen due to muscle weakness
Features likely to make you suspicious of hypoadrenocorticism
Electrolyte abnormalities (Na+:K+ ratio <23) - but not always abnormal
Lack of stress leukogram in a sick dog
Young dog with a history of chronic illness
Diagnostic tests for hypoadrenocorticism
Basal cortisol
ACTH stimulation
Aldosterone pre and post ACTH
Endogenous ACTH
Basal cortisol in the diagnosis of hypoadrenocorticism
A value >55nmol effectively rules out hypoadrenocorticism.
If lower ACTH stimulation test is needed.
ACTH stimulation test in the diagnosis of hypoadrenocorticism
The most useful test
Can also be used to diagnose atypical hypoadrenocorticism
A dog with hypoadrenocorticism will show no or minimal response to ACTH stimulation
Aldosterone pre and post ACTH in the diagnosis of hypoadrenocorticism
Used to distinguish primary and secondary causes.
If secondary, dog will have raised post ACTH aldosterone, if primary it will have no response.
Endogenous ACTH in the diagnosis of hypoadrenocorticism
Will be high in primary disease and low if secondary or iatrogenic disease
Treatment of an acute Addisonian crisis
- Restore intravascular volume
- Reversal of hyperkalaemia
- Reversal of hyponatraemia
- Provision of glucocorticoids and mineralocorticoids
- (Correction of any life-threatening arrhythmias)
Restoring intravascular volume in an Addisonian crisis
Using aggressive fluid therapy
0.9% NaCl or lactated Ringer’s (Hartmann’s) suitable
20-90 ml/kg/hr
Assess effectiveness frequently
Once volume restored reduce to maintenance rate
Continue fluids until hydratio status, urine output, serum electrolytes, and azotaemia are corrected.
Reversal of hyperkalaemia in an Addisonian crisis
Can be life-threatening due to negative effects on myocardial cells
IV fluid therapy +++
10% Calcium gluconate
Sodium bicarbonate
IV dextrose/glucose
IV soluble insulin
Reversal of hyponatraemia in an Addisonian crisis
Usually IV fluids are all thats needed
Provision of glucocorticoids and mineralocorticoids in an Addisonian crisis
Acute period: IV administration of a rapid acting glucocorticoid
- Dexamethasone (can be used alongside ACTH stimulation test)
- Hydrocortisone
- Methylprednisolone sodium
- Prednisolone
Long term:
- Desoxycortone pivalate (mineralocorticoid replacement, no glucocorticoid activity so needs that too)
- Fludrocortisone (mineralocorticoid and glucocorticoid replacement, oral medication, now very expensive)
Monitoring hypoadrenocorticism therapy
Do not repeat the ACTH stim test!
Clinical signs and electrolytes
Prognosis of Addisonian crisis therapy
Good, providing the dog survives the acute event
Median survival time of 2.5 to 5.5 years following doagnosis
