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Gabe's Endocrinology > Diagnosis of adrenal disorders > Flashcards

Diagnosis of adrenal disorders Flashcards

1
Q

What is the function of the adrenal cortex?

A
  • Steroid hormone synthesis and function
  • Glucocorticoids (cortisol)
  • Mineralocorticoids (aldosterone)
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2
Q

Which two disease states are associated with the adrenal cortex?

A

Cushing’s disease and Addison’s disease.

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3
Q

What is the funciton of the adrenal medulla?

A
  • Catecholamine synthesis and functions
  • Adrenaline and noradrenaline
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4
Q

What is a disease state associated with the adrenal medulla?

A

Pheochromocytomas

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5
Q

What is the chemical structure of aldosterone and cortisol common to?

A

4 ring structure common to all steroids

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6
Q

What is released from the glomerulosa of the adrenal cortex?

A

Mineralocorticoids (aldosterone)

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7
Q

What is released from the fasciculata of the adrenal cortex?

A

Glucocorticoids (cortisol) and some androgens

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8
Q

What is released from the reticularis of the adrenal cortex?

A

Sex steroids, androgens and some cortisol

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9
Q

What is hydrocortisone?

A

Cortisol

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10
Q

What is cortisone?

A
  • Biologically almost inactive metabolite of cortisol, doesn’t actually have much activity.
  • In liver, is metabolised back to cortisol, hence its use as a therapeutic.
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11
Q

What is the major glucocorticoid?

A

Cortisol

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12
Q

What is cortisone acetate?

A
  • Very weak glucocorticoid
  • Metabolite of cortisol
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13
Q

What do aldosterone, cortisol and tesosterone/oestrogen originate from?

A

Cholesterol

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14
Q

What are the 4 actions of glucocorticoids?

A
  • Stimulation of gluconeogenesis (liver)
  • Mobilisation of amino acids (muscle)
  • Stimulation of lipolysis (adipose tissues)
  • Immunosuppression
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15
Q

What does too much cortisol lead to?

A
  • Weight gain
  • Wasting of muscle, skin and bone
  • Hyperglycaemia
    • (muscle amino acid → glucose)
  • Hypertension (salt retention)
  • Inhibition of linear growth (if before puberty)
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16
Q

What are the 2 different types of hypercortisolism?

A

ACTH-dependent and ACTH-independent

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17
Q

What is ACTH-dependent hypercortisolism usually caused by?

A
  • Pituitary adenoma (“Cushing’s disease”)
  • Ectopic ACTH syndrome
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18
Q

What is ACTH-independent hypercortisolism usually caused by?

A
  • Adrenal adenoma or carcinoma
  • ACTH-independent nodular hyperplasia
  • Administration of glucocorticoids (common side effect of treatment) – most common cause
19
Q

What is the most common cause of ACTH-independent hypercortisolism?

A

Administration of glucocorticoids.

20
Q

What are the signs and symptoms of Cushing’s disease hyperadrenocortisolism?

A
  • Hypertension
  • Apparent obesity
  • Muscle wasting, think skin, metabolic derangements (e.g. diabetes)
  • All direct actions of glucocorticoids
21
Q

How is endocrine testing performed?

A
  1. Biochemical Testing first then radiology
  2. Repeat the test
  3. Do not measure random hormones, measure:
  • Hormone and trophic hormone
  • Stimulation if underactive
  • Suppresion if overactive
  • Regulated reagent and hormone (ca/PTH), glc/insulin
  • 24hr urine assay
22
Q

Instead of measuring random hormones, what is measured?

A
  • Hormone and trophic hormone
  • Stimulation if underactive
  • Suppresion if overactive
  • Regulated reagent and hormone (ca/PTH), glc/insulin
  • 24hr urine assay
23
Q

What are the different ways of diagnosis by hormone measurement?

A
  • Assay of hormone and regulated metabolite Ca & PTH, glucose & insulin
  • Assay of hormone and trophic factor
    • T4 and TSH
    • Cortisol and ACTH
    • Oestrogen and FSH/LH
    • Testosterone and LH
  • Stimulation or suppression test
  • 24 hour urine test
24
Q

How is suspected Cushing’s syndrome investigated?

A
  • 24h urine free cortisol measurement
  • Check diurnal variation: serum cortisol & plasma ACTH at 0800 and midnight
  • Check that negative feedback loop is working: dexamethasone supp’n test – most common test
  • Cranial MRI/ adrenal CT as indicated
25
Q

What is the most common investigation performs for suspected Cushing’s syndrome?

A

Dexamethasone suppression test - check that the negative feedback loop is working.

26
Q

What does not enough cortisol cause?

A
  • GI symptoms (anorexia, nausea, vomiting, diarrhea, weight loss)
  • Low blood pressure (salt wasting)
  • Darkening of the skin (if ACTH secretion is stimulated)
  • Muscle weakness (both skeletal and cardiac muscle)
  • Increased susceptibility to infection
  • Death
27
Q

What are the causes of adrenocortical insufficiency?

A
  • Genetic: Enzyme defect in cortisol biosynthesis
  • Genetic: metabolic defect: adrenoleukodystrophy
  • Autoimmune adrenal destruction – most common
  • Infectious disease: adrenal destruction by tuberculosis (other countries)
28
Q

What happens to sodium and potassium levels in Addison’s disease?

A

Salt-wasting state results in low serum sodium and high serum potassium

29
Q

What is Addison’s disease treated with?

A

Cortisol and fludrocortisone

30
Q

What are the signs and symptoms of excess adrenal androgens?

A
  • Premature pubic hair
  • Hirsutism, acne
  • Enlargement of penis or clitoris (child)
  • Behavioural changes
  • Linear growth spurt
  • Rapid epiphyseal fusion (child)
  • Muscular habitus
  • Deepening of voice.
31
Q

What is congenital adrenal hyperplasia (CAH)?

A
  • Due to 21-hydroxylase def in 90% of cases
  • Autosomal recessive
  • Variable impairment of cortisol and aldosterone biosynthesis
  • Prenatal ACTH stimulation → adrenal hyperplasia
32
Q

What are the 3 different presentations of CAH in females?

A
  • Infant with ambiguous genitalia OR
  • Premature pubic hair & enlarged clitoris OR
  • Adolescent hirsutism and acne
33
Q

What are the 2 different presentations of CAH in males?

A
  • Adrenal crisis in a baby aged 2-3 weeks OR
  • Premature sexual development at age 2-3 years
34
Q

How is CAH treated?

A

By replacing cortisol

35
Q

What are the clinical uses of glucocorticoids?

A
  • Replacement if inadequate production (pituitary disease, Addison’s disease)
  • Anti-inflammatory and immunosuppressive properties.
  • Used to treat inflammatory conditions e.g. arthritis, dermatitis, asthma, autoimmune diseases
36
Q

Which glucocorticoids have no mineralocorticoid activity?

A

Synthetic glucocorticoids, e.g. Dexamethasone

37
Q

What are the two regulators of aldosterone secretion?

A
  • Increase [K+] in extracellular fluid
  • Angiotensin II
38
Q

What are the actions of mineralocorticoids?

A
  • Aldosterone regulates [Na+], [K+] in extracellular fluids
  • Increased resorption of Na+, water
  • Increased excretion of K+ from the kidney distal tubule
39
Q

What does excess aldosterone result in?

A
  • → hypertension (salt retention)
  • → weakness (hypokalaemia)
40
Q

What does aldosterone deficiency result in?

A
  • → Dehydration, salt depletion & postural hypotension.
  • → Cardiac arrhythmias (hyperkalaemia)
41
Q

What will happen if the adrenal glands are removed surgically?

A

Death within just a few days, due principally to a loss of mineralocorticoid activity.

42
Q

What is Conn’s syndrome?

A
  • Adrenocortical tumour secreting aldosterone (mineralocorticoid excess)
  • Present with hypertension or with weakness due to low potassium
  • High sodium, low potassium, low renin
  • Cured by surgery
43
Q

What happens to renin levels in hyperaldosteronism?

A

Decreases and therefore angiotensin II does, too.

Gabe's Endocrinology (17 decks)

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