Hyperadrenocorticism Flashcards
what are the causes of hyperadrenocorticism? what is the prevalance of these types?
Pituitary dependent (80-90%)
- Micro and macro adenomas, adenocarcinomas
- [Subgroup pars intermedia]
Adrenal dependent (10-20%)
- Functional adrenal adenomas and carcinomas (50:50)
Iatrogenic
- Exogenous steroids
what is the signalment, history and clinical signs of a dog with hyperadrenocortisism?
- Middle aged to old dogs
- More females than males
- Polydipsia, Polyuria
- Secondary diabetes insipidus
- Polyphagia
- Muscle wasting and weakness (pot-belly, panting)
- Skin thinning, calcinosis cutis, pigmentation, bruising
- Symmetrical hair loss
- Reproductive dysfunction (most of these animals are neutered)
what is seen on radiographs of a dog with cushings?
Usually incidental findings when investigating other causes of the clinical sx, rarely done for diagnosis
Abdominal radiographs
* Good contrast
* Hepatomegaly
* Pot-bellied appearance
* Calcinosis cutis
* Distended bladder
Thoracic radiographs
* Tracheal and bronchial wall mineralisation
* Pulmonary metastasis - with adenocarcinoma
* Osteoporosis
what would you see on haematology of a dog with hyperadrenocorticism?
what about biochem?
what about urinalysis?
Haematology: Stress leukogram
* Neutrophilia (mature)
* Lymphopaenia
* Monocytosis
* Absolute eosinopaenia
If this is not present then unlikely to be HAC
Biochem:
* Increased alkaline phosphatase activity - There is a steroid induced isoform in the dog
* Increased ALT activity - “steroid hepatopathy”
* Hyperglycaemia - Hepatic gluconeogenesis; * Insulin insensitivity
* Elevated phosphorus - Steroid effect on bone turnover
* Increased cholesterol and triglyceride - Steroid effect of lipid metabolism
* Mildly abnormal bile acids
If the is a significant increase in creatinine unlikey to be HAC as not significant muscle mass to increase it, also if ALP is not increase unlikely to be HAC, if markedly abnormal bile asicds more likely to be primary renal disease
Urinalysis:
* Urine specific gravity < 1.030 despite often mild dehydration
* Mild glucosuria in some cases
* Proteinuria in some cases
* Positive urine culture - Reduced immune function; glucosuria
how is HAC diagnosed and how are the different types differentiated?
Diagnosis
* Low-dose dexamethasone
* ACTH response
* Urinary cortisol:creatinine ratio
* Steroid induced alkaline phosphatase
Differentiation
* Low dose Dexamethasone suppression (high dose rarely done)
* Endogenous ACTH
* Ultrasound - for adrenal tumour
How does the low-dose dexamethasome test work to show HAC?
what is done?
what is the positive result?
Resistance of abnormal pituitary-adrenal axis to suppression by dexamethasone - (in a normal animal should suppress)
0.01 to 0.015 mg/kg dexamethasone IV
3 samples @ at 0, 3 to 6 and 8 hours
8 hour cortisol result > 30 - 40 nmol/L is a positive test result
How does the ACTH response test work to show HAC?
what is done?
what is the positive result?
- Measure of adrenocortical reserve (in normal dog small increase in cortisol, in HAC big increase)
- 0.25 mg Synacthen IV/IM
- Or 5ug/kg IV/IM
- Lower doses reported
- Samples at 0 and 1 hour
- 1 hour cortisol > 500-600nmol/L is positive
- Subnormal responses suggest exogenous steroid
- Consider functional adrenal neoplasia in some flat mid-range and subnormal responses
How can urine be used to test for HAC?
Urinary cortisol: creatinine
* One or more morning urine samples at home in non-stressed environment
* Definition of positive depends on laboratory
* Can combine with repeat after several doses of oral dexamethasone for differentiation
* Day 1
* Day 2
* Day 3 following 3x 0.1mg/kg oral dexamethasone
what are the pros and cons of low dose dex suppression?
Advantages
* Highly sensitive
* Extreme confidence in a negative test result
* May differentiate as well as diagnose
Disadvantages
* Long test (8 hours)
* Poor specificity (up to 56% false positives in Non Adrenal Illness)
* Not appropriate if history of exogenous steroids
what are the pros and cons of ACTH stims?
Advantages
* Short test (1 hour)
* More specific than LDDST
* More confidence in a positive test result (very few false positives)
* Test of choice in suspect iatrogenic and in monitoring trilostane (Vetoryl)
Disadvantages
* Less sensitive than LDDST (especially in adrenal)
* Cannot provide differentiation
What are the pros and cons of the Urinary cortisol: creatinine ratio test?
Advantages
* Inexpensive
* Convenient for owner
* Highly sensitive
* Extreme confidence in negative results (SnOut)
Disadvantages
- Very poor specificity (some as low as 24%) - if positive then can’t rule in
When should you test for cushings?
what diseases of minature Schnauzers and scottish terriers can be misdiagnosed as HAC?
Only test if you could believe a positive result
* Presenting signs
* Age
* ALP increased
* Eosinophils absent
Potentially misdiagnosed as hyperadrenocorticism
- Young Min Schnauzers hypertriglyceridaemia
- Scottish terriers progressive vacuolar hepatopathy
What are the differences in trying to diagnose HAC with diabetes mellitus?
- Can’t rely on usual evidence
- ALKP, ALT, Chol, PU/PD
- Need to look for things we would not expect in a regular diabetic
- Hair loss, thin skin, bruising at venipuncture, persistent high insulin requirement
- Treat DM first (the DM will increase the cortisol, so control with lower the cortisol)
- Provides data on insulin requirement - if insulin requerment is higher than expected then could be HAC as well
- Improves confidence in positive endocrine diagnostic tests
What is the reliability of the different tests for differntiating types of ACTH?
-
Low dose dexamethasone
- sufficient suppression for differentiation in 60% of positive LDDST
-
(High dose dexamethasone)
- 0.1 to 1.0 mg/kg IV - sample at 0, 3-6 and 8 hours
- > 50% suppression makes PDH more likely, but up to 25-30% of PDH will fail to suppress
- Endogenous ACTH – needs special shipping
-
Imaging (ultrasound/CAT/MRI) - depends on skill
ultrasound:- PDH: Adrenal glands - symmetrically enlarged and normal conformation
- ADH: One enlarged gland and one atrophied gland
- May see invasion if a malignant tumour
- Complicated by “incidentalomas”
CT or MRI - Size of a ‘normal vs ‘enlarged’ pituitary not clearly defined
What are the treatment options for HAC?
Medical – remember you are treating a chronic glucocorticoid excess
- Trilostane (Licenced)
- Mitotane (opDDD; Lysodren) – not licenced for animals (special import scheme)
- Selegiline (not effective in majority, poss in combination with trilostane)
Surgical
- Adrenalectomy for ADH
- RVC done some adrenalectomy for PDH
- Hypophysectomy for PDH
- Few centres worldwide (Utrecht, RVC, Highcroft Bristol)
- 3D surgical guides by Highcroft/Vet3D may improve accessibility
