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Y4 SA - urinary & endocrine disease > Hyperadrenocorticism > Flashcards

Hyperadrenocorticism Flashcards

Diagnosis & treatment

1
Q

HAC causes

A
  • 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
  • [Ectopic ACTH]
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2
Q

How does pituitary dependent HAC work?

A
  • making too much ACTH and not listening to negative feedback of cortisol being made in response
  • Much in the anterior lobe but there’s a proportion (particularly in dogs) where do have pars intermedia disease.
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3
Q

PDH vs ADH (re what hormones they increase)

A
  • PDH increases ACTH which increases cortisol
  • ADH just increases cortisol
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3
Q

Why is diagnosis difficult?

A
  • PDH + ADH + psychological stress + chronic illness all cause an increase in cortisol
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4
Q

Canine hyperadrenocorticism - signalment, CS

A
  • 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
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5
Q

Abdominal radiograph findings

A
  • Good contrast
  • Hepatomegaly
  • Pot-bellied appearance
  • Calcinosis cutis
  • Distended bladder
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6
Q

Thoracic radiograph findings

A
  • Tracheal and bronchial wall mineralisation
  • Pulmonary metastasis
  • Osteoporosis
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7
Q

Haematology - what you would expect

A

Stress leukogram
* Neutrophilia (mature)
* Lymphopaenia
* Monocytosis
* Absolute eosinopaenia

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8
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A
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9
Q

Haematology - what would make you question HAC diagnosis, or consider it more complicated

A
  • Neutropaenia
  • Lymphocytosis
  • Band neutrophils
  • Eosinophils present
  • Anaemia
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10
Q

Clinical chemistry - what you would expect

A
  • 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
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11
Q

Clinical chemistry - what would make you question HAC diagnosis, or consider it more complicated?

A
  • Normal alkaline phosphatase
  • Normal ALT
  • Significant elevation in creatinine
  • Hypercalcaemia
  • Markedly abnormal bile acids
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12
Q

Urinalysis - what you would expect

A
  • USG <1.030 despite often mild dehydration
  • Mild glucosuria in some cases
  • Proteinuria in some cases
  • Positive urine culture
    – Reduced immune function
    – glucosuria
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13
Q

Urinalysis - what would make you question HAC diagnosis, or consider it more complicated?

A
  • USG >1.030
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14
Q

Diagnosis of hyperadrenocorticism - what 2 questions to ask

A

1 Is hyperadrenocorticism present?
2 If so, what is the source; pituitary or adrenal?

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15
Q

Endocrine diagnostic tests for diagnosis

A
  • Low-dose dexamethasone
  • ACTH response
  • Urinary cortisol:creatinine ratio
  • Steroid induced alkaline phosphatase
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16
Q

Endocrine diagnostic tests - for differentiation between source

A
  • Dexamethasone suppression (low, high and mega)
  • Endogenous ACTH
17
Q

Low-dose dexamethasone test

A
  • Resistance of abnormal pituitary-adrenal axis to suppression by dexamethasone
  • 0.01 to 0.015 mg/kg dexamethasone (Azium) IV
  • Dexamethasone sodium phosphate acceptable but adjust for active ingredient
    *3samples@ at 0, 3 to 6 and 8 hours
  • 8 hour cortisol result > 30 - 40 nmol/L is a positive test result
18
Q

ACTH response

A
  • Measure of adrenocortical reserve
  • 0.25 mg Synacthen IV/IM
  • Or 5µg/kg IV/IM
    – Lower doses reported
  • Samples at 0 and 1 hour
    *1hourcortisol >500-600nmol/Lispositive
    *Subnormal responses suggest exogenous steroid
  • Consider functional adrenal neoplasia in some flat mid-range and subnormal responses
19
Q

Urinary cortisol: creatinine

A
  • 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
19
Q

Pros & cons of LDDxST

A

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 NAI)
* Not appropriate if history of exogenous steroids

20
Q

Pros & cons of ACTH stim

A

Advantages
* Short test (1 hour)
* More specific than LDDST
* More confidence in a positive test result
* Test of choice in suspect iatrogenic and in monitoring trilostane (Vetoryl)

Disadvantages
* Less sensitive than LDDST (especially in adrenal)
* Cannot provide differentiation

21
Q

Pros & cons of UCCR

A

Advantages
* Inexpensive
* Convenient for owner
* Highly sensitive
* Extreme confidence in negative results (SnOut)

Disadvantages
* Very poor specificity (some as low as 24%)

22
Q

When should I test?

A

Only test if you could believe a positive result
*Presenting signs
*Age
*ALKP
* Eosinophils

23
Q

What conditions could potentially be misdiagnosed as hyperadrenocorticism?

A

*Young Min Schnauzers hypertriglyceridaemia
*Scottish terriers progressive vacuolar hepatopathy

24
Q

How to make a diagnosis of HAC in diabetics

A

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
* Provides data on insulin requirement
* Improves confidence in positive endocrine diagnostic tests

25
Q

Differentiating origin

A
  • 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 rules out adrenal source
  • Endogenous ACTH
    *Imaging (ultrasound/CAT/MRI)
26
Q

Adrenal imaging - PDH vs ADH

A
  • PDH: Symmetrically enlarged and normal conformation
  • ADH: One enlarged gland and one atrophied gland
  • May see invasion if a malignant tumour
  • Complicated by “incidentalomas”
27
Q

Pituitary imaging

A
  • CT or MRI
  • Size of a ‘normal vs ‘enlarged’ pituitary not clearly defined
  • Useful if neurological signs to detect the presence of a large pituitary tumour
28
Q

Treatment options - medical

A
  • Trilostane (Licenced)
  • Mitotane (opDDD; Lysodren) – not licenced for animals (special import scheme)
  • Selegiline (not effective in majority, poss in combination with trilostane)
29
Q

Treatment options - surgical

A
  • Adrenalectomy for ADH
    – RVC done some adrenalectomy for PDH
  • Hypophysectomy for PDH
    – Few centres worldwide
    – 3D surgical guides by Highcroft/Vet3D may improve accessibility
30
Q

What is hyperadrenocorticism?

A
  • chronic glucocorticoid excess
31
Q

What is trilostane?

A
  • Modified steroid
    –intereferes with the conversion of the 3 beta end of the molecule that gets converted in the pathways
    – can reversibly bind in the enzyme process.
    – i.e. reversible competitive inhibitor
    – not particularly long lasting
32
Q

What can happen to the adrenal glands are trilostane tx? What is the relevance of this?

A
  • the adrenal glands can initially get bigger
    — reduced neg feedback so increased ACTH release
  • so need to find balance of reduced signs from cortisol but enough to have a bit of neg feedback on the pituitary.
33
Q

Rationale for SID therapy

A
  • Not aiming for ablation of glucocorticoid production
  • Aiming to preserve mineralocorticoid function
  • Plan to allow some negative feedback to mitigate increases in pituitary ACTH output and/or mass enlargement in PDH
  • Avoid Aggressive therapy
    → more complete inhibition of cortisol
    → loss of negative feedback on pituitary mass
    → increased ACTH output/pituitary mass enlargement
    → adrenal stimulation/enlargement
    → higher dose requirement
    → spiralling dose requirements
34
Q

Other adrenal diseases - of the cortex

A
  • Functional adrenal neoplasia (non- cortisol)
  • Aberrant adrenal receptor activity
    – Food (GIP) associated
  • “Atypical” hyperadrenocorticism
  • Ectopic ACTH
  • Congenital adrenal hyperplasia
  • “Alopecia X”
    – ?non-adrenal
    – ?Trilostane responsive
35
Q

Other adrenal diseases - of the medulla

A
  • Phaeochromocytoma
36
Q

Functional adrenocortical tumours

A

Classic:
* Cortisol secreting
– Adrenal dependent hyperAC
* Aldosterone secreting
– “aldosteronoma”
– Conn’s syndrome

Non-classic:
* HyperAC associated with excessive sex hormone production by an adrenocortical tumor
* Hyperaldosteronism and hyperprogesteronism in a cat with an
adrenal cortical carcinoma
* Corticosterone- and aldosterone-secreting adrenocortical tumor
in a dog
* Deoxycorticosterone-secreting adrenocortical carcinoma in
a dog

37
Q

Functional adrenocortical tumours (non-cortisol)

A

Glucocorticoid like:
* Presentation
– Similar to HAC incl stress leukogram, ACTH suppression etc
* Diagnosis
– ACTH stim
-> 17OP, androstenedione
-> Mid range or low cortisol with minimal change
* Treatment
-> Surgical (preferred)
-> Medical

Mineralocorticoid like:
* Presentation
– Related to hypokalaemia
– Muscle weakness
– Cats ventroflexion of neck
* Diagnosis
– ACTH stim
-> aldosterone
* Treatment
– Surgical (preferred)
– Medical
-> Spironolactone

38
Q

Phaechromocytoma - CS

A
  • Weakness/Collapse
  • Weight loss
  • Poor appetite
  • Tachypnoea
  • Polyuria/Polydipsia
  • Tachycardia
  • Hypertension
  • Panting
  • Restlessness
  • High blood glucose: insulin resistance
39
Q

Why might pheochromocytoma be confused with hyperAC?

A
  • PU/PD/Panting
  • Adrenal mass on imaging
  • Hyperglycaemia
40
Q

Phaechromocytoma - diagnosis

A
  • May be diagnosed post-surgically
    – Histology – Tx for ADHAC
  • Pre-surgical diagnosis
    – Urinary catecholamine metabolites
41
Q

Phaechromocytoma - tx

A

Treatment – Surgical
* Local vessel invasion

Medical – symptomatic and pre-surgical * Adrenoceptor antagonists (Sympatholytics)
* Phenoxylbenzamine (alpha)
* Propanolol (Beta)

Y4 SA - urinary & endocrine disease (17 decks)

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