canine hyperadrenocorticism pt 2 Flashcards
medical treatment options for HAC
Medical options include trilostane, mitotane
◦ Most clinics will use trilostane (Vetoryl)
trilostane mechanism of action, dose schedule
Trilostane
◦ Blocks enzyme in cortisol production and interfere with cortisol secretion (competitive inhibitor of 3β- hydroxysteroid dehydrogenase)
◦ Usually a twice daily medication
Trilostane: Adverse Effects
◦ Mild GI signs, mild lethargy first few days of therapy relatively
common
◦ Hypoadrenocorticism could result
> Generally reversible (trilostane inhibits enzyme in cortisol production)
> Rare reports of adrenal necrosis
Trilostane Therapy: Monitoring
- goals
- best techniques
◦ Goals are to lower cortisol levels to limit clinical signs
◦ Monitoring therapy
> ACTH stimulation rechecks traditional monitoring method
> New evidence to show that pre-pill cortisol levels, clinical signs are superior to establishing response
ACTH Stimulation Rechecks for trilostane
- when to perform
- targets
- how to interpret, meaning of results
Perform at:
◦ 10-14 days (ensure not overdosing)
◦ Then monthly until optimal dose achieved
◦ At 3-months, then every 3-6 months once at optimal dose
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◦ Target post-ACTH cortisol level is 50-150 nmol/L
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◦ Perform test 3-5h after trilostane dose
◦ Interpret along with check on clinical signs
◦ Does not correlate very well to clinical control, costly test
trilostane Pre-pill Cortisol Level
- when would we check
- context
- timing
◦ Check cortisol level just before next dose of trilostane is due
◦ Appropriate in dogs with or without persisting signs of HAC
> Not appropriate if other signs of illness (e.g., hypoadrenocorticism)
◦ Pair with thorough history, examination of dog
> “Cushings Quality of Life score” is helpful to assess response
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Example timing:
◦ Day 1: Start therapy
◦ Day 10: history, clinical exam
◦ Day 28: history, clinical exam, pre-pill cortisol
> Desired cortisol range 40-140 nmol/L
◦ Once no clinical signs, cortisol in target range
> Recheck in 3 months, then every 3-6 months
Pre-pill Cortisol Evaluation at Day 28
- what do we do if patient is clinically unwell?
- No clinical signs of HAC, cortisol <40?
- No clinical signs of HAC, cortisol 40-140?
- No clinical signs of HAC, cortisol >140?
- Clinical signs of HAC, cortisol 40-140?
- Clinical signs of HAC, cortisol >140
Clinically unwell
- Stop trilostane, perform ACTH stimulation
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No clinical signs of HAC, cortisol <40
- Re-evaluate, consider lower dose
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No clinical signs of HAC, cortisol 40-140
- Continue current dose, recheck in 3 months
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No clinical signs of HAC, cortisol >140
- Re-evaluate, change to BID therapy (if not already) or consider small dose increase (by 5-10 mg)
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Clinical signs of HAC, cortisol 40-140
- Change to BID therapy (if not already); consider small dose increase (by 5-10 mg)
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Clinical signs of HAC, cortisol >140
- Change to BID therapy (if not already); consider small dose increase (by 5-10 mg)
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* If increasing dose, re-evaluate with history and PE in 10 days, repeat cortisol in 28 days
if we are treating with trilostane and we need to increase the dose based on what we see at our 28 day check-up, when do we re-check / re-evaluate?
◦ Recheck history, PE, clinical score in 10 days
◦ Recheck cortisol again in 28 days
Hyperadrenocorticism: Systemic Effects
◦ Potential complications of disease
◦ Recurrent or severe infections
◦ Pancreatitis
◦ Diabetes mellitus
◦ Hypertension
◦ Proteinuria
◦ Thromboembolism
◦ Increased risk of gall bladder mucocoele
proteinuria connection with HAC? why? can we fix it?
◦ >50% dogs with HAC have proteinuria at diagnosis
> Corticosteroid: damaging effect on glomerulus, increased pressure
◦ Proteinuria might resolve with treatment of HAC
> 20-40% of treated dogs have persistent proteinuria
what do we do if we find a dog with HAC and proteinuria?
◦ Verify proteinuria with urine protein:creatinine ratio
◦ Verify that proteinuria is persistent even after trilostane treatment
◦ Treat if persisting
HAC with hypertension - how common is it? severity? mechanism? will it resolve? should we treat?
◦ 30-86% dogs with HAC have hypertension
> Usually mild to moderate
> Unknown mechanism: possibly upregulation of RAAS, other
> Often resolves with treatment of HAC
◦ Consider treatment if systolic BP >180 mmHg; re-evaluate when HAC controlled
HAC connection to hypercoagulability? do we need to do anything about this?
HAC causes hypercoagulablity
◦ Thromboembolic events possible but not common
◦ Not routine to treat with thromboprophylaxis (unless other risk factors, evidence of thrombus)
HAC connection with gall bladder mucocoele? how common?
HAC associated with gall bladder mucocoele
◦ Up to 25% of GBM dogs have HAC in several studies
Macroadenoma connection with HAC - what is this?
◦ Dull mentation, other neurological abnormalities
