canine hyperadrenocorticism Flashcards
adrenal gland anatomy - zones and what they produce
- zona glomerulosa: mineralcorticoids (regulate mineral balance) eg. aldosterone
<><> - zona fasciculata: glucocorticoids (regulate glucose metabolism) eg. cortisol, corticosterone, cortisone
<><> - zona reticularis: androgens (stimulate masculinization) eg. dehydroepiandrosterone
<><> - adrenal medulla: stress hormones (stimulate sympathetic ANS) eg. epinephrine, norepinephrine
regulation of cortisol secretion
stressors (hypoglycemia, hypotension, fever, trauma, surgery…) act on the hypothalamus > releases CRH, which acts in the pituitary causing the release of ACTH, which act on the adrenals to produce cortisol
> cortisol sends negative feedback to the pituitary and the hypothalamus
> AVP cytokines can also act on the pituitary causing the release of AVP
effects of cortisol on the cardiovascular system
- increase myocardial contractility
- increase cardiac output
- increase catecholamine pressor effect
effects of cortisol on the metabolism
- increase gluconeogenesis
- increase glycogenolysis
- increase proteolysis
- increase lipolysis
Hyperadrenocorticism: Clinical Features
- most common clinical signs
- less common
- uncommon
MOST COMMON:
* Polyuria
* Polydipsia
* Polyphagia
* Excessive panting
* Thin hair coat
* Abdominal distention
* Hepatomegaly
* Muscle weakness
* Systemic hypertension
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LESS COMMON:
* Hyperpigmentation
* Thin skin
* Comedones
* Poor hair regrowth
* Urine leakage
* Recurrent infections
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UNCOMMON:
* Neurological abnormalities
* Myopathy
* Thromboembolism
* GI ulceration / bleeding
Hyperadrenocorticism: Common Laboratory Findings for CBC
- Neutrophilia
- Lymphopenia
- Thrombocytosis
- Mild erythrocytosis
Hyperadrenocorticism: Common Laboratory Findings fro serum biochem
- Increased ALP
- Increased ALT
> (ALP > ALT) - High cholesterol
- High triglycerides
- Mild hyperglycemia
Hyperadrenocorticism: Common Laboratory Findings for urinalysis
- USG <1.020
- Proteinuria
- Possibly indications of UTI
types of hyperadrenocorticism and how common they are
◦ ~85% pituitary dependent (PDH)
◦ ~15% adrenal dependent
(functional adrenal tumour; ADH)
usual signalment for hyperadrenocorticism
◦ Average age 9-11 years
◦ Predisposed breeds:
> PDH: Poodles, Dachshunds, terriers, etc
> ADH: Poodles, Dachshunds, Labs, GSD, terriers
◦ 75% PDH cases <20 kg
Diagnostic Goals: HAC
- Diagnose HAC
*Screening tests - Differentiate PDH from ADH
*Differentiating tests - Detect concurrent diseases, consequences of HAC
*Basic +/- advanced labwork
*Imaging
Screening Tests for HAC: Options, what negative results mean
- Urine cortisol to creatinine ratio
- ACTH stimulation test
- Low dose dexamethasone suppression test
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Negative test result has good likelihood of being a true negative
Urine Cortisol to Creatinine Ratio test characteritics
- sp, sn, sample, result
- Very sensitivity (~100% sensitive)
- Poor specificity
- Urine collected at home = best sample
- Normal ratio = rule out hyperadrenocorticism
Low dose dexamethasone suppression test - is this a good test for HAC? sn, sp
Gold standard screening tool
- Sn ~95%
- Sp 44-73%
Low dose dexamethasone suppression test
- how to differentiate normal dog, from PDH vs ADH?
- how do we diagnose?
Normal dog:
◦ Dexamethasone causes negative feedback on pituitary
◦ ↓ ACTH production
◦ Therefore ↓ cortisol
◦ For ~48h
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PDH dog:
◦ Usually transient ↓ in ACTH (and cortisol) production
◦ Variable, only a few hours
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ADH:
◦ Cortisol secretion from tumour independent of ACTH, no effect
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To diagnose HAC, look at the 8 hour cortisol level
* Usually <40 nmol/L in normal dogs
* Usually >40 nmol/L in dogs with HAC