Week 6- Adrenal Disorders Flashcards
What is the signalment for HyperAdreno?
- Middle-aged to older dogs
- Poodle, Dachsund, Boxer…
What are the clinical signs of Hyperadreno?
- Polyphagia
- Polyuria
- Pot belly
- Calcinosis cutis
What are the clinical signs of cats with hyperadreno?
- Polyphagia
- Pot belly
- Alopecia
- Muscle wasting
- Fragile skin
What is the main treatment for feline hyperadreno?
- Adrenalectomy
What is a UCCR test?
For hyperadreno
Tests urine/ cortisol ratio, highly sensitive
What is an ACTH stimulation test?
hyperadreno
- Tests adrenocortical reserve
- Lower sensitivity than LDDST
- can be affected by other drugs
What is a LDDST test?
Tests the HPA axis’s ability to respond to negati ve glucocorticoid feedback
* May also allow differentiation between PDH and ADH
What are the gold-standard aims of hyperadreno treatment?
- Remove source of autonomous ACTH
- Normalise Cortisol levels
- Eliminate Clinical signs
- Improve the QoL
What is the mode of action for Trilostane?
Inhibits enzyme 3Beta- in the steroid synthesis pathway
What is the dosing for Trilostane?
datasheet 2mg/kg q24hr – however often “escape” signs
within 8-12hr so BID dosing at 0.5-1mg/kg q12hr often used
What is the efficacy for Trilostane?
PDH: effective in ~90% of cases at controlling signs – does not
affect tumour growth
* ADH: variable; does not affect tumour growth
What are the risks/ side effects of Trilostane?
Iatrogenic hypocortisolism – stop treatment; can resume at
lower dose (see datasheets)
* Long term/irreversible HPA axis suppression
How often should you monitor an ACTH’ist?
3-5hr post-pill – peak action of trilostane
* Test of choice if concern for over-suppression: lack of response to ACTH, similar to
hypoadrenocorticism
* Never been validated as a monitoring tool
How often should you monitor pre-pill cortisol?
Better reflection of control (in conjunction with owner history) vs. ACTHst?
* Not appropriate if patient is unwell; not a measure of adrenocortical reserve
What are the consequences of an addisons deficiency?
Hypotension
* Hypoglycaemia
* GI signs
* Decreased fat and protein mobilisation
→ weakness
* Increased susceptibility to stress
* Inability to maintain vascular tone and
endothelial integrity
What is primary hyperadrenocorticism?
bilateral adrenal gland destruction
* >95% of cases
What is secondary hypoadrenocorticism?
reduced ACTH production from
anterior pituitary gland
* Rare!
What is atypical hypoadrenocorticism?
glucocorticoid-deficient hypoadrenocorticism
What are the possible mechanisms of atypical hyperadrenocorticism?
Sparing of zona glomerulosa
* Disparity of rate of destruction of adrenal cells
* Increased dietary sodium intake compensating for increased natriuresis
What is the signalment for addisons?
0.06-0.28% estimated prevalence in dogs
Inherited, autosomal recessive trait in standard poodle,
Portuguese water dog, Nova Scotia duck-tolling retriever
Increased odds: Airedale, Basset hound, bearded collie,
WHWT
Median onset 4yo (4m-14yo)
What is acute addisons?
Collapse
* Marked lethargy/depression,
weakness
* In addition to “less acute” signs
* Uncommon: septic peritonitis (GI
translocation), aspiration pneumonia
(secondary to regurgitation)
What does the haematology look like for addisons?
Non-regenerative anaemia
* Lack of stress leukogram, eosinophilia, lymphocytosis
What does the biochemistry look like for addisons?
Hyponatraemia and hyperkalaemia
* Other DDx for hyperkalaemia?
* Azotaemia – usually pre-renal
* Hypoglycaemia
* Hypercalcaemia
* Low albumin
* Low cholesterol
What is the gold standard for testing
ACTH Stimulation test
What is the acute treatment for hypoadrenocorticism?
Correct dehydration/hypovolaemia:
* Fluid boluses to restore circulating volume – check blood pressure
* 0.9% NaCl: historic solution, no potassium, but lack buffer → worsen acidosis?
* Hartmann’s: low K+ concentration, improves acidosis = fluid of choice!
* CARE rate of Na+ correction
How do you correct hyperkalaemia?
Should decrease with IVFT and correcting acidosis. If severe despite IVFT, or if bradyarrhythmias:
* Calcium gluconate: cardioprotective, does not change serum K+
* IV glucose +/- insulin – CARE!
How do you correct acidosis?
rarely necessary if appropriate management with IVFT
* Sodium bicarbonate in severe situations (pH <7.1)
What are the two hormone replacement options for hypoadrenocorticism?
Dexamethasone: pure glucocorticoid
* Dose: variable – 0.05-0.2mg/kg IV (3-10x
physiological dose)
* Hydrocortisone: equal glucocorticoid and
mineralocorticoid
* Dose: CRI 0.5mg/kg/hr IV
What is the glucocorticoid replacement for animals with addisons?
Prednisolone – physiological dose varies <0.05-0.2mg/kg/day
* Start higher initially (0.3-0.5mg/kg/day) and taper to lowest effective dose –
monitor for iatrogenic hyperadrenocorticism
* Stressful situations: consider doubling-tripling dose
What is the mineralcorticoid replacement for animals with addisons?
Desoxycorticosterone pivalate (DOCP; Zycortal) – pure mineralocorticoid
* Datasheet: 2.2mg/kg by subcutaneous injection every 25 days
* In reality – often need lower dose (exception – young patients), and 25d interval
is clunky… compliance better with 28 days?
* After first injection (+ any dose changes): electrolytes after 10-14d and date of
next planned injection (25-28d) – check datasheet for adjustments
* Check the electrolytes themselves, not just Na/K ratio!
* Once stable dose, check electrolytes every 3-6 months
What is CIRCI?
= inadequate cortisol response to critical illness
* Decreased cortisol synthesis?
* Effect of drugs on HPA axis
* Reduced binding of glucocorticoids to target tissues due to pro-inflammatory cytokines
