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
Should you do a LDDST or an ACTH stim?
Practicalities
* ACTH availability
* Duration of test
* ACTH not as sensitive
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Non-adrenal illness: false + LDDST
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Diagnose (& differentiate?) etiology with LDDST
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Sometimes need to do both
ACTH stimulation test - how it works, sn, sp, how to dx
◦ Cortisol increases after ACTH given
◦ Dogs with HAC will have an exaggerated response to ACTH versus normal dog
◦ Sensitivity, specificity ~80%
◦ Measure serum cortisol before & 1 or 2 h after ACTH
Differentiating PDH and ADH with LDDST Results
Suppression of cortisol diagnostic of PDH one or more of:
* 4 hour cortisol <40 nmol/L
* 4 hour cortisol <50% of baseline cortisol (0 hour)
* 8 hour cortisol <50% of the baseline
> But still >40 nmol/L
mechanism of pituitary dependent hyperadrenocorticism
- failure of negative feedback
> anterior pituitary produces a ton of ACTH, which stimulates the adrenals to release a lot of cortisol
> normally, ACTH and cortisol would act on the hypothalamus to stop it from releasing CRH (which stimulates the AP the release ACTH), and cortisol would also inhibit the release of ACTH from the AP > but in PDH these negative feedback loops are broken, and ACTH is continuously released from the AP despite high ACTH and cortisol levels
LDDST
0 hours 150 nmol/L
4 hours 90 nmol/L
8 hours 80 nmol/L
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◦ Can we diagnose HAC? why?
◦ Can we differentiate PDH from ADH?
Can we diagnose HAC?
◦ Yes, 8-hour level is elevated
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Can we differentiate PDH from ADH?
◦ No, have not met one of the suppression criteria
Differentiating Tests for PDH vs ADH
- LDDST
- HDDST
- Endogenous ACTH levels
- Ultrasound
HDDST test - how do we do it, what does it tell us?
◦ Giving 0.1 mg/kg dexamethasone
◦ Will suppress cortisol levels in normal dogs at 4 and 8 hours
◦ Some PDH dogs will also have suppression of cortisol levels at 4 and 8 hours when given this higher dose of dexamethasone
> If cortisol suppresses on the HDDST after diagnosing HAC on another test, likely PDH
◦ ADH dogs won’t suppress
Abdominal Imaging to differentiate PDH from ADH
Abdominal Ultrasound
* Symmetrical adrenal glands – PDH
* ADH: usually 1 enlarged gland, 1 atrophied gland
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Abdominal Radiographs > Poor sensitivity
endogenous ACTH levels to differentiate PDH vs ADH
PDH - ACTH levels are high
ADH - ACTH levels are low
