Hypoadrenocorticism Flashcards

1
Q

Define CIRCI

A

= critical illness-related corticosteroid insufficiency

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2
Q

What is CIRCI?

A
  • relates to management of ‘pressor resistant septic shock’
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3
Q

Why do you get adrenal haemorrhage with hypoadrenocorticism?

A

Adrenal haemorrhage d/t increased ACTH

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4
Q

2 forms of hypoadrenocorticism

A
  • TYPICAL where’re reduced capacity to produce cortisol and aldosterone
  • ATYPICAL where a proportion of cases have no electrolyte abnormalities
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5
Q

Breeds - hypoadrenocorticism

A
  • standard poodles
  • bearded collies
  • leonburgers
  • NSDT retrievers
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6
Q

Clinical pictures of hypoadrenocorticism

A

2 broad categories:

  1. ) acutely collapsed severely compromised patient
  2. ) variable subtle, unwell animal, has a waxing and waning presence
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7
Q

CS - acute hypoadrenocorticism

A
  • NON-SPECIFIC
  • waxing and waning
  • lethargy, depression, under responsive
  • reduced enthusiasm to exercise
  • weakness
    • inappetance
  • vomiting and or diarrhoea
  • Melena (structural secondary gut disease)
  • heart rate usually unaffected though occasionally bradycardic (
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8
Q

Clinical pathology suggestive of hypoadrenocorticism

A
  • mild to moderate anaemia (non regenerative and or regenerative)
  • hypoproteinaemia (or normoproteinaemic in hypovolaemic patient)
  • eosinophilia and/or lymphocytosis or lack of a stress leukogram
  • hyponatraemia and or hyperkalaemia (some people talk about a ratio between these two. If Na/K is
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9
Q

Clinical pathology - hypoadrenocorticism (typical form)

A

Absence of stress leukogram and either hyponatraemia or hyperkalaemia or both (decreased Na:K ratio)

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10
Q

Desvribe clinical pathology of atypical hypoadrenocorticism

A

Absence of a stress leukogram and normal Na and K levels.

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11
Q

What can over diagnosis of hypoadrenocorticism lead to?

A
  • exacerbation of already compromised organs
  • protracted period of administration of inappropriate medicines with adverse effects
  • once on these meds it is very difficult to investigate things further
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12
Q

Dx - hypoadrenocorticism

A
  • ACTH stimulation test with demonstration of subnormal levels of cortisol before and after ACTH as well as confidence at no prior glucocorticoid therapy could be interfering with test results
  • basal cortisol measurement will give an indication but not definitive answer (if >30mmol then hypoadrenocorticism is unlikely but this is not definitive)
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13
Q

Treating acute presentation of hypoadrenocorticism

A
  • supportive fluids (not too much as particularly fluid sensitive). 0.9% NaCl, absolutely no more than 7-8ml/kg/hour.
  • hormone suuplementation: PN administration, similar degrees of GC and MC activity. Use hydrocortisone sodium succinate.
  • when hydrocortisone is infused IV at 0.5mg/kg/h the amount of cortisol present in circulation provides adequate amounts of GC and MC for seriously stressed dogs
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14
Q

Outline hydrocortisone as tx of hypoadrenocorticism

A
  • PN route
  • 0.5mg/kg/h IV infusion
  • equal GC and MC bioactivity
  • short half-life
  • simple, physiological
  • effective
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15
Q

Tx - chronic hypoadrenocorticism

A
  • ** fludrocortisone (GC and MC) OR:
  • deoxycorricosterone pivalate (USA only)
  • 50% cases need GC supplementation (cortisone acetate or prednisolone)
  • diet (add salt)
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16
Q

Chronic clinical picture - tx principles

A
  • subacute patient with varyingly severe CS featuring # o fdifferent body systems, including:
  • GIT (structural gut dz, IBD biopsies)
  • NMS (weakness, lethargy)
  • indicators of renal dysfunction (azotaemia and inaapropriately dilute urine
  • TX: = appropriately balanced GC and MC activity
17
Q

What is the correct GC dose for chronic hypoadrenocorticism ?

A
  • normal adrenal production in dog (0.2mg/kg/24hr cortisol)

- prednisolone has 5 times GC activity of cortisol

18
Q

With fluorinef (= fludrocortisone), do you need a GC?

A
  • 10-15microg/kg/24 hours
  • 15x GC potency of cortisol so theoretically almost enough GC for general maintenance
  • supplement with least potent GC (cortisone acetate, 0.5mg/kg/12h for 5 days then 0.5mg/kg/24 hr)
19
Q

What if dog has no indications of an electrolyte problem?

A

Perform aldosterone extimates on ACTH test samples BUT cost and assay considerations. Usually tx with GC only.

20
Q

Monitoring hypoadrenocorticism efficacy

A
  • clinical response paramount
  • GC activity evaluated by leukogram
  • MC activity evaluated by Na and K levels
  • don’t do ACTH stim test or basal ACTH test to evaluate
21
Q

Pathophysiology - hypoadrenocorticism

A
  • results in marked adrenolysis
  • often I-M
  • destruction results in diminished adrenocortical reserve: reduced capacity to produce cortisol and aldosterone, may or may not be clinically signficant, proportion of cases have no electrolyte abnormalities
22
Q

T/F: confirm dx of hypoadrenocorticism with an ACTH stim test BEFORE use of cross-reacting GCs

A

True (otherwise test interference)

23
Q

T/F: once stable, minimise GC excess by using cortisone in small dogs

A

True