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The Adrenal Gland Flashcards

1
Q

Adrenal medulla synthesises________________.

A

Catecholamines

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2
Q

Name the three zones of the adrenal cortex and what each zone synthesises

A

Zona golmerulosa - synthesises mineralcorticoids
Zona fasciculata - synthesises glucocorticoids
Zona reticularis - adrenal androgens

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3
Q

ACTH

A

Adrenocorticotrophic hormone
Stimulates production of cortisol (a glucocorticoid)
Cortisol exhibits negative feedback on ACTH release

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4
Q

CRH

A

Corticotrophin releasing hormone

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5
Q

Cortisol effects (4)

A

Increase hepatic gluconeogenesis and muscle glycogen storage
Increasing breakdown of plasma and muscle protein to amino acids
Increasing release of glycerol & free fatty acids from adipose tissue
Anti-inflammatory effects

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6
Q

___________is the precursor for adrenal steroid hormone synthesis.

A

Cholesterol

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7
Q

Cortisol measurement

A

95% bound to transcortin
Level of free cortisol is very small
Measured by immunoassay

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8
Q

Diurnal rhythm

A

Levels are high in the morning and low at night

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9
Q

Main function of ______________ is to promote sodium reabsorption and potassium excretion in the kidney.

A

Aldosterone

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10
Q

Aldosterone synthesis also sensitive to changes in circulating ___________ levels.

A

Potassium

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11
Q

Steps in steroid metabolism in aldosterone

A

Cholesterol
Pregnenolone
Progesterone
11-deoxycorticosterone
Corticosterone
18-hydroxycorticosterone
Aldosterone

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12
Q

Steroid metabolism of cortisol

A

Pregnenolone -> 17a-hydroxypregnenolone or progesterone ->17a-hydroxyprogesterone
11-Deoxycortisol
Cortisol

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13
Q

Steroid metabolism of androgens (dehydroepiandrosterone (DHEA) and androstenedione)

A

17a-hydroxypregnenolone or 17a-hydroxyprogesterone

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14
Q

The role of the adrenal gland in the renin-angiotensin system

A

Angiotensin II stimulates aldosterone (mineralcorticoid) release from adrenal cortex

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15
Q

Where is angiotensinogen produced?

A

Liver

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16
Q

Where is renin released?

A

Kidneys

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17
Q

Where is ACE produced?

A

Lungs

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18
Q

Posture affects ______________.

A

Plasma aldosterone

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19
Q

Addison’s disease

A

Hypofunction of the adrenal cortex
Acute adrenal insufficiency => life-threatening emergency

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20
Q

Clinical features of Addison’s disease

A

Lethargy
Weakness
Anorexia
Weight loss

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21
Q

Features of acute adrenal crisis

A

Severe hypovolaemia
Shock
Hypoglycaemia

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22
Q

Treatments of addisons disease

A

Life-long glucocorticoid & mineralcorticoid replacement therapy

23
Q

Causes of addisons disease (primary adrenal hypofunction)

A

Autoimmune destruction of the adrenal gland
Tb
Adrenal haemorrhage

24
Q

Causes of secondary adrenal hypofunction

A

Sudden withdrawal of glucocorticoid drugs
Secondary to hypopituitarism as a result of ACTH stimulation

25
4x Hyp- of adrenal hypofucntion
Hyponatraemia Hyperkalaemia Hyperuremia Hypoglycaemia
26
What is the test for cortisol?
9am plasma cortisol SynACTHen Tests the capacity of the adrenal cortex to respond to ACTH
27
2 conditions associated with hyperfunction of the adrenal cortex
Cushings’s syndrome - overproduction of cortisol, although increased mineralcorticoid and androgen levels may also be seen Conn’s syndrome - excess production of aldosterone
28
Causes of cushing’s disease
Prolonged exposure to excess cortisol Can lead to hypertension and hypokalaemic Increased androgen => hirsutism
29
Iatrogenic cushings features
Increased cortisol but not increased mineralcorticoid activity as cortisol administered was synthetic
30
Causes of Cushings (4)
Pituitary adenoma - ACTH-producing tumour Ectopic ACTH secretion by various tumours Adrenal adenoma or carcinoma producing cortisol Iatrogenic
31
3 tests used in the initial screening for Cushing’s
24hr urinary free cortisol Overnight dexamethasone suppression 48hr low-dose dexamethasone suppression test
32
Explain the urinary free cortisol test
Increased UFC => cushings/pseudo-cushings/obesity
33
Explain overnight and 48hr low-dose dexamethasone suppression tests
Test for cushing’s Dexamethasone is a synthetic glucocorticoid which binds cortisol receptors in pituitary => suppression of ACTH release => suppression of cortisol secretion by the adrenals in normal individuals Fewer false positives are seen with 48hr low-dose
34
3 tests in finding the cause of hypercortisolism
High dose dexamethasone suppression test Plasma ACTH measurement Corticotrophin-releasing hormone (CRH) test
35
Explain the high dose dexamethasone suppression test
Dexamethasone administered Plasma cortisol measured at 9am over three days Failure of suppression suggests an adrenal tumour or ectopic ACTH source
36
ACTH is ___ when adrenal tumour is the cause of Cushings
Low
37
Explain the CRH test
Distinguishes between Cushing’s disease and ectopic ACTH secretion ACTH and cortisol measured at intervals over 2 hours Rise of both cortisol and ACTH suggests pituitary source No response in ectopic ACTH secretion
38
10% patients with Cushings disease do NOT respond to _____ but they usually show suppression to HDDST
CRH
39
10% of ectopic ACTH syndrome may respond to CRH but these patients fail to suppress with ______________.
Dexamethasone.
40
Causes of Conn’s syndrome
Adrenal adenoma Bilateral hyperplasia of Zona glomerulosa Adrenal carcinoma - rare Glucocorticoid-suppressive hyperaldosteronism (autosomal dominant)
41
Clinical features of Conn’s syndrome
Hypertension (sodium retention) Muscle weakness (hypokalaemia) Tetany (hypokalaemia) Many patients are asymptomatic
42
What enzyme is involved in the in the conversion of cortisol to cortisone?
11beta-Hydroxysteroid dehydrogenase
43
What inhibits 11beta-hydroxysteroid dehydrogenase? (2)
Liquorice & carbenoloxone
44
Secondary hyperaldosteronism
(hyper-reninaemic hyperaldosteronism) More commonly seen than primary hyperaldosteronism Common causes include: Heart failure Liver cirrhosis Nephrotic syndrome
45
Laboratory findings in Conn’s syndrome
Hypokalaemia Plasma sodium slightly above ref range
46
Features of congenital adrenal hyperplasia
CAH is a group of inherited autosomal recessive metabolic disorders of adrenal steroid hormone synthesis Depending on which enzyme in the pathway is deficient 95% due to 21-hydroxylase deficiency Lack of cortisol and negative feedback; ACTH levels are high & drive androgens biosynthesis High levels of 17 hydroxyprogesterone are secreted used in diagnosis
47
Classical CAH
Lack of cortisol and aldosterone => adrenal crisis => dehydration => shock => death Excess adrenal androgen production => ambiguous genitalia or precocious puberty
48
Non-classical CAH
Milder, non-life threatening Partial enzyme deficiency Premature development of pubic hair
49
Diagnosis of CAH (4)
Hormone measurement Clinical evaluation History and physical examination Newborn screening USA
50
Treatment of CAH
Glucocorticoid (dexamethasone) Fludrocortisone (classical CAH deficiency)
51
Phaeochromocytoma
Tumour secreting catecholamines (usually non-adrenaline) 10% malignant Hypertension, headache, pallor
52
Diagnosis of phaeochromocytoma
Measurement of metanephrines
53
Symptoms of Cushing’s Syndrome
Muscle weakness Poor wound healing Easy bruising Moon face Acne Hypertension Skin thinning

Biochemistry (19 decks)

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