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Endocrine > Hyperadrenocorticism 2 > Flashcards

Hyperadrenocorticism 2 Flashcards

1
Q

What do you see with ACTH stim in hyperadrenocorticism

A

Excessive over response to stimulation

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2
Q

Is the ACTH stim test a good test?

A
  • poorly diagnostic in a proportion of cases
  • post ACTH cortisol less than upper limit of normal range
  • post ACTH cortisols between 500-750nmol/l
    > extremely accurate with post ACTH >1000nmol/l
    > never discriminatory for PDH v ADH
  • so works in % of cases and is convenient
  • BUT 20% HAC dogs will have negative ACTH stim tests
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3
Q

Outline low dose dex suppression test

A
  • measure plasma cortisol at 0, 4 and 8 hours after administering dexamethosone
  • dose 0.01mg/kg dex IV
  • dexamethosone not assayable
  • BOTH 4 and 8 HR cortisol should be if either are high this is ABNORMAL
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4
Q

Which test is more appropriate for hyperadrenocorticism dx

A

> general rule use SUPPRESSION tests for overactive disorders and STIMULATION tests for underactive disorders
- so dex suppression best for HAC

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5
Q

How can pituitary dependant and adrenal dependant hyperadrenocorticism be distinguished?

A

> PDH
- 70% suppressed at 4 hours post ACTH then increased at 8hrs
- 30% no suppression seen at 4 or 8 hours
ADH
- all show no suppression
- but remember 30% cases PDH also show this profile

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6
Q

Why may some ADH and PDH animals respond the same to low dose dex ?

A
  • with PDH different set points of GC activity seen as normal so if one PDH animal set point x and another set point 2x then results of GC activity induced by dex suppression will differ over time
  • normal dog dex injected, at all time points surplus to requirement so ACTH
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7
Q

What may impair the low dose dex test?

A
  • illness -> false positives because ^ cortisol produced with ANY non-adrenal disease
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8
Q

So which test is most appropriate to confirm hyperA?

A
  • LDDST
  • providing not ill
  • NB: dose very low and must be delivered accurately
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9
Q

Is SHOP test useful?

A

No rubbish don’t use
“ shop stimulation test”
- progesterone

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10
Q

How do we discriminate between ADH and PDH?

A

> when LDDST suppression at 4hrs with rebound at 8hrs (though not seeing this does not rule out)
adrenal ultrasound
- difference l and r
- smaller adrenal smaller than Normal with ADRENAL dependent (d/t negative feedback of ^ cortisol -> v ACTH -> atrophy)
- small min 2 basal plasma ACTH levels (plasma separated and frozen in 30mins, values not subnormal but not elevated either)
- NOT high dose dex suppression test (useless)

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11
Q

Tx PDH

A

> medically
- trilostane (lic)
- mitotane
surgical

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12
Q

Tx ADH

A

> medical
- trilostane
surgical

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13
Q

What is trilostane?

A
  • inhibits 3b hydroxysteroid dehydrogenase
  • inhibits synth of cortisol (and MCs and sex steroids)
  • different efficacy in different species (ineffective humans, variable cats and dogs)
  • potentially safer than mitotane (suppresses rather than destroys)
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14
Q

What protection of dogs do not respond to trilostane?

A

25%

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15
Q

What side effect may trilostane have on the adrenals?

A

> group of PDH Tx with trilostane (NOT very effective for ADH, also less risk of necrosis and haemorrhage in ADH d/t ACTH levels)
- develop adrenal necrosis (seen on ultrasound as hyperlucency in the adrenal cortex fluid accumulation)
-> Hypoadrenocorticism
^ ACTH -> ^ adrenal cortical blood flow -> haemorrhage -> acute v cortisol which can be clinically significant
be ready for addisonian crisis

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16
Q

Which form of cortisol/cortisone is active?

A
  • cortisol active
17
Q

Trilostane dilemma

A
  • inhibits cortisol production for something not making sense (not adrenal haemorrhagic effect, potential peripheral effects)
18
Q

How does 11b HSD2 leukocyte expression change in PDH treatment

A
  • normal levels = non-adrenal illness = PDH untreated
  • PDH treated individuals levels ^ (should be DOWN)
  • this increase not seen in humans (and not effective in humans)
19
Q

How should trilostane be used?

A
  • with food (^ bioavailability)
20
Q

Is low dose BID dosing recommended ?

A

In America yes but here thought not to be such a good idea

  • v compliance
  • don’t overdose BUT low dose ALSO bad(not sure why???)
21
Q

If trilostane not effective what are the options?

A

^ freq dosing
- or use mitotane
> v cortisol by adrenocorticolysis d/t
- direct cytotoxic activity to zona fasiculata and reticularis (GC)
- generalised adrenocorticol destruction (enhanced adrenocorticol blood flow mediated via ^Acth)
> induction and maintainance phases

22
Q

Outline induction and maintainance phases of mitotane

A
  • 25mg/kg/12hr for 5-7d
  • always with food
  • check demeanour and appetite
  • evaluate with ACTH stimulation (24-36hrs after last mitotane,Moore and post cortisols maintainance
  • 25mg/kg/12hr once a week
  • monitor as for induction
  • if control lost RESTART INDUCTION don’t increase maintainance
23
Q

Adverse effects of mitotane

A
  • variably reversible GIT signs
  • lack of sensitivity to mitotane
  • neuropathies (esp cranial nerve palsies)
  • unpredictable onset clinically significant Hypoadrenocorticism
24
Q

Is mitotane still a reasonable Tx?

A
  • YES!! (For pituitary only, ADH needs trilostane)
  • remember adverse effects
  • remember consistency of efficacy (sometimes not very efficacious)
    > only option not requiring daily meds
25
Q

What are the surgical options for hyperadrenocorticism ?

A

> bilateral adrenalectomy and Tx as an addisonian
- RVC only!!
- hydrocortisone sodium succinate infusion implemented at time of surgery
1mg/ml solution, 0.5mg/kg/hr for 24hrs, 0.25mg/kg/HR 24-48hrs
- transfer to oral medication
cortisone acetate 0.5mg/kg/12hr
fludrocortisone acetate 10-15ug/kg/24hrs

26
Q

How can hyperadrenocorticism be diagnosed?

A 
> haem and biochem 
- stress leuckogram 
- liver enzyme ^
- ALP>>ALT
> USG 
- generally unhelpful 
> basal plasma cortisol estimation 
> basal urinary corticosteroid excretion 
> dynamic testing 
- ACTH stim 
- low dose dex suppression testing
27
Q

Outline ACTH stimulation test

A
  • measure plasma cortisol at 0 and 1 hr after administration of synth ACTH
  • tetracosactrin IV/IM
  • expect post ACTH cortisol to be 300-600nmol/l
28
Q

Do all adrenal masses produce cortisol?

A

No may be a medullary mass -> catecholamines

- look for small contralateral adrenal as chronic overproduction cortisol -> v ACTH -> atrophy

29
Q

Summary clinical signs and diagnosis hyperadrenocorticism

A
  • nowadays subtle dz
  • may be just a difficult to manage diabetic mellitis
  • always contextualise test results to clinical picture
30
Q

Summary Tx options hyperadrenocorticism

A
  • medical (trilostane, mitotane)

- surgical (bilateral adrenalectomy and steroid supplements (fludrocortisone, cortisone small dogs

Endocrine (16 decks)

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