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Endocrine > Hyperadrenocorticism > Flashcards

Hyperadrenocorticism Flashcards

1
Q

Define hyperadrenocorticism

A
  • clinical problem brought about by sub-acute overexposure to GCs
  • natural (ADH or PDH) or iatrogenic (chronic underdosage of steroids)
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2
Q

Differentiate ADH and DH frequency

A
  • ADH 10-15%

- PDH 85-90%

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3
Q

Clinical picture - hyperadrenocorticism

A
  • subtle changes early in dz
  • insidious onset means presentation occurs at variable stages
  • secondary problems frequently result in death
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4
Q

Hx - hyperadrenocorticism

A
  • PD and PU 85-90%
  • excellent appetite 80%
  • exercise intolerance 60%
  • abdominal distension 50%
  • coat changes 50%
  • alopecia and hyperpigmentation 35%
    anoestrous 90% (of intact females)
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5
Q

CS - hyperadrenocorticism

A
  • panting
  • mm weakness and atrophy
  • hepatomegaly and abdominal distension
  • increased abdominal fat deposition
  • testicular atrophy, increased vulval size
  • dermal changes
  • altered mentation (underwhelmed)
  • appear ‘old for age’ (epaxial mm wasting)
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6
Q

Dermal changes - hyperadrenocorticism

A
  • non-primary skin changes
  • symmetrical alopecia (trunk –> extremities)
  • non-pruritic
  • hyperpigmentation
  • hyperkeratosis and ‘flaking skin’
  • comedones
  • clacinosis cutis
  • infections or infestations (recurring)
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7
Q

Cause of PD and PU in hyperadrenocorticism

A

= PRIMARY PD

- also cortisol interferes with ADH action in CD but this effect is relatively minimal compared with the primary PD

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8
Q

Clinical picture - cat with hyperadrenocorticism

A
  • cat with DM that is difficult to manage
  • varying degrees of IR
  • resent for varying periods of time
  • usually no other CS
  • uncommon problem
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9
Q

Clinical pathology

A
  • eosinopaenia, lymphoctyopaenia (STRESS LEUKOGRAM)
  • increased ALP (dog - much increased, disproportionate cf ALT), increased ALT
  • hypercholesterolaemia
  • increased thrombocyte count
  • ‘low’ USG
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10
Q

Why can’t you remove water from a PUPD dog with hyperadrenocorticism?

A

because they are prone to infections (UTI) –> PUPD that is necessary so would be dangerous to remove water bowl in these instances without testing for and tx the infection.

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11
Q

Dx - hyperadrenocorticism

A
  • haematology and biochemistry (stress leukogram, liver enzyme elevations, USG usually unhelpful) helps raise index of suspicion
  • basal plasma cortisol estimations
  • basal urinary corticoid excretion
  • latter two are poor discriminators hence –> dynamic tests (ACTH stimulation test or low dose dexamethasone suppression test)
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12
Q

Describe ACTH stimulation test

A
  • measure plasma cortisol at 0 hr and 1 hr after administration of synthetic ACTH
  • 5 microg/kg of tetracosactrin IV ORRRRR:
  • 250microg/kg/dog IV or IM
  • except post-ACTH cortisol to be b/w 300-600nmol/L
  • evaluate success of tx
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13
Q

Efficacy - ACTH stimulation test

A
  • poorly diagnostic in a % cases (post ACTH cortisols less than upper limit of normal range, post ACTH cortisols b/w 500 to 700nmol)
  • extremely accutate when post ACTH cortisols are > 1000nmol/L
  • virtually NEVER discriminatory for PDH vs ADH
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14
Q

Outline LDDST

A

= low dose dexamethasone suppression test

  • more appropriate for what we are trying to investigate
  • samples taken over 8 hour period (plasma cortisol measured at 0, 4, 8 hours)
  • 0.01mg/kg dexamethasone IV
  • dexamethasone is NOT assayable
  • expect 4 and 8 hr cortisols to be
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15
Q

Why is LDDST more appropriate (than ACTH stim) for d HAC?

A
  • demonstrates impaired capacity to reduce cortisol production
  • lack of suppression for a given level of GC activity
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16
Q

How do you differentiate PDH and ADH?

A

= LDDST results:
- PDH 4hr post will have low cortisol levels with rebound at 8hr post (i.e cortisol), this is true in 70% PDH cases
- ADH: cortisol high at 4 hr and 8hr post dexamethasone (100% ADH and 30% PDH cases)
= adrenal ultrasonography: adrenomegaly with PDH, adrenal mass with ADH (especially if unilateral, difference in size with other adrenal and the other is smaller i.e. 2-5mm)
= at least two basal plasma ACTH levels (plasma separated and frozen within 30 minutes, values aren’t subnormal but not necessarily elevated)
= NOT WITH high dose dexamethasone suppression test

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17
Q

How to confirm HAC

A
  • ACTH STIM TEST: convenient (within 1 hr, concern of false negatives)
  • LDDST (least convenient, concern of false positives - minimise this risk by not performing on sick patients)
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18
Q

What is the ‘SHOP’ stimulation test?

A
  • designed to dx HAC
  • not worth effort (inadequate precision)
  • 17-OH progesterone levels pre and post ACTH
19
Q

Outline tx - PDH

A
  • ** MEDICALLY: trolostane (L) or mitotane (NL)

- SURGICALLY

20
Q

Outline tx - ADH

A
  • ** SURGICALLY

- MEDICALLY: (trilostane)

21
Q

How does trilostane work?

A
  • inhibits 3 beta-hydroxysteroid dehydrogenase
  • inhibits cortisol synthesis
  • different efficacy vs PDH in different spp (effective in dogs, variably in cats)
  • may be safer than mitotane as ‘simply’ suppresses cortisol production
  • but inhibits cortisol production for
22
Q

Why can trilostane be dangerous?

A

inhibits cortisol synthesis and increases ACTH production –> much increased ACTH –> much increased adrenocortical BF –> adrenocortical blood supply very fragile (rate, dogs, cats) –> adrenocortical haemorrhage and damage –> acute reduction in cortisol production which can be clinically significant
* this risk is much greater in PDH than ADH

23
Q

Why is risk of adrenocortical haemorrhage much worse in PDH than ADH?

A
  • ‘efficacy’ reduce in ADH compared to PSH as;
  • in trilostane-tx DH, the rises in ACTH directly damage the adrenal galnds
  • hypOadrenocorticism is still a concern
24
Q

What is another concern with trilostane?

A
  • inhibits cortisol production for
25
Q

Describe trilostane tx

A
  • reduces GC activity through various mechanisms
  • 2-4mg/kg/day, with food (increases bioavailability)
  • ACTH test 2-4 hr post-dose
  • fine to worry about overdosing but DON’T underdose
  • hypOadrenocorticism remains possible
26
Q

How does mitotane work?

A
  • reduces cortisol production through adrenocorticolysis induced by:
    a. direct cytotoxicity to ZF and ZR (GC producing parts of adrenal cortex)
    b. generalised adrenocortical destruction (enhanced adrenocortical blood flow mediated via increased ACTH production)
  • ** induction and maintenance phases of mitotane tx***
27
Q

Outline mitotane induction:

  • dose
  • monitoring
A
  • 25mg/kg/12 hours for 5-7 days
  • ALWAYS with food
  • check demeanor and appetite
  • evaluate with ACTH stimulation (24-36 h after last mitotane, pre- and post-cortisols
28
Q

Outline mitotane maintenance

A
  • 25 mg/kg/12 hour on one day/week
  • ALWAYS with food
  • evaluate with ACTH stimulation (24-36 h after last mitotane, pre- and post-cortisols RESTART induction, don’t use an increased maintenance dose
29
Q

Mitotane - adverse effects

A
  • variably reversible GIT signs
  • lack of sensitivity to mitotane
  • neuropathies (especially CN palsies)
  • unpredictable onset of clinically significant hypoadrenocorticism
30
Q

What is a huge advantage of mitotane?

A

only option not requiring a daily medication

31
Q

Tx action if medical tx of PDH (trilostane and then mitotane) has not worked or long term costs of medical tx are prohibitive

A

= BILATERAL ADRENALECTOMY

  • hydrocortisone infusion started at time of sx
  • post-sx hydrocortisone infusion (hydrocortisone sodium succinate. 1mg/ml solution. 0.5mg/kg/hr for 24 hours then 0.25mg/kg/hr for 24-48 hours).
  • then transfer to oral medication ((cortisone acetate 0.5mg/kg/12 h if
32
Q

What are the earliest signs of hyperadrenocorticism?

A
  • relatively subtle
  • no more than difficult to manage DM patient
  • insidious onset means presentation occurs at variable stages
33
Q

Cost - hyperadrenocorticism tx

A
  • all 3 options (2 medical, 1 surgical) likely expensive
  • assuming 2 yr survival period, cheapest of 3 is bilateral adrenalectomy (especially dogs >20kg)
  • bilateral adrenalectomy needs to be considered with maintenance on fludrocortisone and either cortisone (
34
Q

Causes - hyperadrenocorticism

A
  • Naturally occurring (PDH > ADH)

- iatrogenic (usually chronically administered underdogsage)

35
Q

T/F: secondary hyperadrenocorticism problems frequently result in death

A

True

36
Q

List endocrinopathies of ferrets

A
  • adrenal gland dz (think of as hyperadrenocorticism without increased cortrisol secretion)
  • insulin secreting tumors (endocrine pancreas)
  • DM (endocrine pancreas)
37
Q

Characteristics - ferret hyperadrenocorticism

A
  • middle aged to older ferrets
  • normal pituitary gland
  • marked adrenomegaly (85% unilateral, 15% bilateral)
  • variably explained by hyperplasia, adenomas or adenocarcinomas)
38
Q

Pathogenesis - ferret hyperadrenocorticism

A
  • associated with early neutering (possibly) and neutering (certainly) as –> increased GnRH levels –> increased LH and FSH –> secondary (?) over-expression in adrenal cortex of LH-R
39
Q

CS - hyperadrenocorticism in ferrets

A
  • symmetrical alopecia (usually starts in spring)
  • vulval enlargement (jills)
  • return of sexual behaviour (hobs)
  • pruritis
  • more severe cases: urethral obstruction (hobs), gynecomastia and mammary neoplasia (jills)
40
Q

Dx - hyperadrenocorticism in ferrets

A
  • haematology/biochemistry normal
  • radiography generally unremarkable
  • ABDOMINAL ULTRASOUND: can generally demonstrate an enlarged adrenal gland with normal contralateral gland)
  • serum hormone estimations (expect one or more elevations in: androstenedione, dehydroepiandrosterone, 17-hydroxyprogesterone, estrodiol)
41
Q

Tx - hyperadrenocorticism in ferrets

A
  • ** sx removal - generally unilateral***
  • medical (clinical dependent as to which drug): mitotane, ketoconazole, trilostane)
  • n.b. keotconazole = systemic antifungal
42
Q

Prevention - hyperadrenocorticism in ferrets

A
  • GnRH agonist implants instead of castration

- deslorelin slow release implant

43
Q

Describe the deslorelin implant

A
  • acts on pituitary
  • decreases sex hormone production
  • used for preventing HAC in entire of neutered ferrets
  • lasts 18-24 months depending on time of insertion

Endocrine (11 decks)

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