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SA Endocrinology > Hyperadrenocorticism > Flashcards

Hyperadrenocorticism Flashcards

1
Q

What does the adrenal cortex synthesise and secrete?

A

Steroid hormones

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1
Q

What does the adrenal medulla synthesise and secrete?

A

Amines

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2
Q

Feedback system for glucocorticoids

A

Hypothalamus -> CRH
Pituitary -> ACTH
Adrenal cortex -> glucocorticoids
GLucocorticoids negatively feedback on CRH and ACTH production

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3
Q

WHat are steroid hormones made of?

A

Cholesterol

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4
Q

Actions of ACTH

A

Stimulation of cholesterol delivery to mitochondria, where P450scc enzyme is located.

Long term actions include stimulation of genes coding for steroidogenic enzymes.

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5
Q

Canine hyperadrenocorticism

A

‘Cushing’s’

Can either be spontaneous or iatrogenic (exogenous prednisolone treatment).

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6
Q

Two forms of spontaneous hyperadrenocorticism

A

Pituitary-dependent (PDH)
Adrenal-dependent (ADH)

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7
Q

Pituitary dependent hyperadrenocorticism

A

80-90%

Caused by excess ACTH secretion (can be episodic) and bilateral hyperplasia

Normal negative feedback systems fail

Most tumours are microadenomas (<10mm)

Macroadenomas as slow growing and don’t always produce neurological signs

Seen in middle aged, small dogs

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8
Q

Adrenal dependent hyperadrenocorticism

A

10-20%

50% caused by adrtenal adenomas, 50% caused by carcinomas. DIfficult to distinguish.

Independent of pituitary control and plasma ACTH conc is usually low- often leads to atrophy of contralateral gland.

Generally older, larger dogs

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9
Q

Clinical signs of hyperadrenocorticism

A

Abdominal enlargement
Polyphagia
PU/PD

Hepatomegaly
Muscle wasting
Lethargy/exercise intolerance
Skin changes
Reproductive changes

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10
Q

Definition of polydipsia

A

> 100ml/kg/day

Usually manifests as incontinence or nocturia

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11
Q

Skin changes found in hyperadrenocorticism

A

Thinning and reduced elasticity
Prominent abdominal veins
Excessive scale and comedomes
Change in coat colour
Calcinosis cutis

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12
Q

Biochemical abnormalities often found in hyperadrenocorticism

A

Elevated: ALP (in 90%) , ALT, cholesterol, bile acids, lipids, fasting glucose

Reduced: Urea (BUN)

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13
Q

Haematological changes in hyperadrenocorticism

A

Stress leucogram

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14
Q

What is a stress leucogram?

A

Lymphopenia
Eosinopenia
Neutrophilia
Monocytosis
Erythrocytosis

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15
Q

Changes on urinalysis in hyperadrenocorticism

A

Isosthenuria or hyposthenuria
USG is often less than 1.010
UTIs are common

16
Q

Radiographic findings in hyperadrenocorticism

A

Hepatomegaly, pot bellied, calcinosis cutis, distended bladder, +/- calculi, adrenal enlargement/calcification, +/- osteoporosis.

Thoracic can show mets if a carcinoma, tracheal and bronchial wall mineralisation, osteoporosis

17
Q

Ultrasonographic findings in hyperadrenocorticism

A

Hyperplastic adrenals are larger but normal echogenicity
Compare size of both glands
Thickness >7.5mm for left gland considered sensitive

18
Q

Diagnostic tests for hyperadrenocorticism

A

ACTH stimulation test

Low dose dexamethasone suppression test

High dose dexamethasone suppression test

Endogenous ACTH assay

17-alpha-OH progesterone assay

Urinary cortisol:creatinine ratio

19
Q

Urine cortisol:creatinine ratio

A

Very sensitive screening test for HAC
Not very specific
Negative result will rule out HAC
Collect urine samples in stress free environment

20
Q

ACTH stimulation test

A

Easy and quick
Quite specific, poor sensitivity
Detects approx 85% of PDH and >50% of ADH cases
Cannot differentiate between PDH and ADH

21
Q

Protocol for ACTH stimulation test

A

Starve overnight
Collect heparin sample time 0
Inject Synacthen IV
Collect second sample 30-60mins later (heparin tube)

Normal result: pre stim <200nmol/l, post stim <600nmol/l

Positive result: post stim >600nmol/l

22
Q

Low dose dexamethasone suppression test

A

Induces negative feedback to the pituitary, causing cortisol levels to fall if normal.

More sensitive - detects nearly 95% of PDH and most ADH

Cannot detect iatrogenic disease, and cannot be used to monitor treatment as specificity is reduced

23
Q

Protocol for LDDS test

A

Starve overnight
Collect baseline heparin sample
Inject 0.01mg/kg dexamethasone IV
Collect heparin samples at 3 and 8 hours

Normal animals will suppress to <50% basal cortisol by 3hrs and remain suppressed
Postive result: Resting cortisol >40nmol/l at 8hrs (not supressed)

24
Q

17 alpha-OH progesterone test

A

Elevated above control levels post ACTH.
Suggests an abnormality in cortisol production pathway rather than simply overproduction.
Not that specific.

25
Q

Suggested sequence of screening tests for HAC

A

Low suspicion: try to rule out using urine cortisol:creatinine ratio

If suspicious: ACTH stimulation test - if clearly positive and fits with other findings then treat.

If negative but still suspicious do LDDS test - if positive treat.

If negative consider other DDX.

If equivocal results re test later

26
Q

Tests to differentiate the cause of hyperadrenocorticism

A

Plasma endogenous ACTH concentration

Diagnostic imaging

High dose dexamethasone suppression test (no longer recommended)

27
Q

Plasma endogenous ACTH concentration test

A

Endogenous ACTH concentrations in normal dogs: 13-46pg/ml

Dogs with adrenal tumours: <5pg/ml

PDH: >28pg/ml

28
Q

Diagnostic imaging for differentiating ADH and PDH

A

US: if adrenals are similar size and normal shape it suggests PDH. A mass in adrenal area suggests ADH

Can use radiogrpahy to look for adrenal masses or mets of adrenal carcinoma

CT or MRI can be used to look for pituitary tumour

29
Q

Treatment of PDH

A

Trilostane should be first choice drug.
Synthetic steroid, competitive inhibitor of enzyme system that synthesizes glucocorticoids, mineralocorticoids, and sex hormones.
Starting dose in 2mg/kg, then use lowest dose necessary. Monitor with ACTH stimulation test or single cortisol value pre-pill.

30
Q

Treatment of ADH

A

Best prognosis if tumour can be completely removed surgically.
Pre-operative staging.
Complicated surgery- high morbidity and mortality rate.

Mitotane therapy also recommended.

Trilostane has had some success in controlling clinical signs - but only symptomatic treatment not treating underlying neoplasia.

SA Endocrinology (11 decks)

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