Module 17 > Hyperadrenocorticism > Flashcards

Hyperadrenocorticism Flashcards

(38 cards)

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1
Q

what are the causes of hyperadrenocorticism

A

Spontaneous:Pituitary dependent: 85%

Pituitary tumour: >90%

Adrenal dependent

Adrenal tumour: >90%

Iatrogenic

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2
Q

what is the pathophysiology of pituitary dependent HAC

A

Functional adrenocorticotropic hormone (ACTH) secreting pituitary tumour in approx. 85% of dogs

  1. Excessive secretion of ACTH causes bilateral adrenocortical hyperplasia and excess cortisol secretion from the adrenal cortex
  2. Because normal feedback inhibitor of ACTH secretion by cortisol is missing excessive ACTH secretion persists despite increased adrenocortical secretion of cortisol
  3. Episodic secretion of ACTH and cortisol is common and results in fluctuating plasma concentrations that at times may be in the reference range
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3
Q

how is HAC diagnosed

A
  1. clinical signs
  2. screening tests
  3. specific tests: confirming, identifying the cause
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4
Q

what is the signalment of HAC (5)

A
  1. Typically in dogs 6 years and older (median 10 years) but can be in younger dogs
  2. No sex predisposition (but ADH may be more common in female dogs)
  3. Poodle, Dachsunds, Terriers, GSD, Boxers, Boston terriers
  4. PDH more common in small dogs
  5. ADH more common in larger dogs
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5
Q

what are the most common clinical signs of HAC (7)

A
  1. Polyuria, polydipsia, polyphagia
  2. Respiratory signs: panting
  3. Abdominal enlargement
  4. Endocrine alopecia
  5. Mild muscle weakness
  6. Lethargy
  7. obesity
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6
Q

what are the dermatological changes seen in HAC (3)

A
  1. Non-pruritic truncal alopecia
  2. Thin skin
  3. Failure to regrow shaved hair
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7
Q

what are uncommon clinical signs seen in HAC (7)

A
  1. Suppression of pituitary function –> persistent anestrus, testicular atrophy, secondary hypothyroidism
  2. Laxity of ligaments may lead to lameness
  3. Hypercoagulability may result in formation of spontaneous thrombi, typically involving pulmonary vessels and resulting in acute resp distress
  4. Cortisol insulin resistance
  5. Persistent hypertension
  6. Neurological signs: obtunded, dopey, fall asleep, apparently blind
  7. Myotonia: relaxation of muscle is impaired
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8
Q

what is iatrogenic HAC

A

too long of steroid course

make sure you search in history if there has been steroid use

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9
Q

what can be seen on serum bioch with HAC (6)

A
  1. increased ALP: steroid induced production
  2. increased cholesterol
  3. increased glucose (only slightly)
  4. increased ALT, GGT, AST (won’t increase to the extent of ALP)
  5. increased bile salts (steroid hepatopathy)
  6. decreased urea and creatinine (PUPD)
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10
Q

what can be seen on hematology in HAC

A

stress leukogram

  • neutrophilia
  • lymphopenia
  • eosinophilia
  • monocyotosis
  • erthrocytosis
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11
Q

what can be seen in urinalysis HAC (4)

A
  1. low SG (< 1.020)
  2. proteinuria
  3. urinary tract infection
  4. glucosuria
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12
Q

what radiographic changes can be seen in HAC (2)

A
  1. many changes largely non-specific
  2. prognostic important: adrenal masses, thoracic metastases, intercurrent disease
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13
Q

what is the principle of the ACTH stimulation tests

A

ACTH stimulates adrenal cortex to maxillary secrete cortisol

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14
Q

how is an ACTH stimulation test done (3)

A
  1. take blood sample for basal cortisol
  2. administer 0.2 mg ACTH IV or IM
  3. take second blood sample 0.5-2 hours
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15
Q

what is the sensitivity with ACTH stimulation

A

only 50% of dogs with AD-HAC will be indentified

only 85% of dogs with PD-HAC will be identified

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16
Q

how do you interpret the results of ACTH stimulation test

Study These Flashcards
A

Dogs with hyperadrenocorticism have an increased post-ACTH admin cortisol increase

The absence of a response is suggestive of adrenocortical neoplasia or iatrogenic hyperadrenocorticism

17
Q

what is the priniciple of low dose dexamethasone suppression test

Study These Flashcards
A

Dexamethasone suppresses ACTH secretion

Rapid recovery, or failure to suppress, in HAC

18
Q

how is a low dose dexamethasone test done (3)

Study These Flashcards
A
  1. take blood sample for basal cortisol
  2. administer 0.015 mg/kg dexamethasone IV
  3. take blood sample 3 and 8 hours later
19
Q

how do you interpret the results of a low dose dexamethasone suppression test

Study These Flashcards
A

in an AD/PD-HAC dog dexamethasone will not suppress cortisol at all

in a PD-HAC dog it will be able to suppress it for some time but then cortisol levels will increase again

normal dogs will suppress cortisol

20
Q

what other tests can diagnose HAC (2)

Study These Flashcards
A
  1. 17 hydroxyprogesterone: cortisol precursor
  2. urine corticoid:creatinine ratio approximation of 24 hour total urine cortisol
21
Q

what is an ACTH assay used for

Study These Flashcards
A

to identify the cause of HAC

22
Q

how is an ACTH assay done

Study These Flashcards
A

ACTH decays very quickly at room temp

send frozen EDTA plasma to a specialist lab

23
Q

how is an ACTH assay interpreted

Study These Flashcards
A

PD-HAC results in increased ACTH concentrations

AD-HAC results in suppression of ACTH secretion

24
Q

is HAC common in cats

25
what is another name for HAC
Cushing's
26
what are the clinical characteristics of HAC in cats
Similar to those seen in dogs Differences: Strong association with diabetes mellitus Progressive relentless weight loss leading to cachexia Dermal and epidermal atrophy leading to extremely fragile, thin and easily torn and ulcerated skin
27
how is PD-HAC treated (5)
1. trilostane (steroid enzyme inhibitor) 2. mitotate (adrenolytic) 3. ketoconazole (steroid enzyme inhibitor) 4. I-Deprenyl (MAO-type B inhibitor) 5. hypophysectomy
28
how is AD-HAC treated (3)
1. trilostane 2. mitotane 3. unilateral adrenalectomy
29
what are the effects of trilostane
Competitive inhibitor of 3-B-hydroxysteroid dehydrogenase which mediates the conversion of cholesterol into cortisol The net effect is inhibition cortisol, aldosterone and progesterone production
30
how long acting is trilostane
Relatively short acting: Most dogs break out of suppression after 12 hours
31
what is the initial dose of trilostane
2mg/kg q 25h by mouth accurate dosing can be difficult with capsules --\> generally go up
32
what are mild complications that can occur with trilostane
Mild:Electrolyte abnormalities Inconsequential Diarrhea, lethargy, anorexia, vomiting
33
what are serious consequences of trilostane
Hypoadrenocorticism Some can die Most respond to appropriate therapy
34
what are the clinical signs that you should advise owners to monitor when their dog is treated with trilostane
Polyuria/polydipsia, polyphagia, lethargy Alopecia, panting, pot-belly
35
how often should you monitor HAC with a ACTH stimulation test
10-14d 1 month every 3-4 months start 2-4 hours after treatment
36
what is pre-vetoryl cortisol and how is it used
Book appointment just before dog’s next trilostane is due If the dog is normally given trilostane at inconvenient time then ask the owner to give at a convenient time at least the day before Take history and quickly examine the dog Make sure owner has not given trilostane and that nothing stressful has happened this morning (vomiting, injury) Sample Take sample immediately after exam 1-2ml of blood in heparin or serum tube Can be separated and stored for up 1 week Send to external lab
37
how do you interpret the results of pre-vetoryl cortisol
38
which is better SID, BID trilostane
twice daily is better for clinical signs
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