Lecture 22 - Steroid Abnormalities Flashcards

1
Q

Low glucose?

A

hypoglycaemia, glucocorticoid deficiency (cortisol)

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2
Q

High potassium?

A

hyperkalaemia, mineralcorticoid deficiency (aldosterone)

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3
Q

Mechanisms of glucocorticoid (cortisol) deficiency?

A

hyponatraemia (loss of cortisol driven ADH inhibition), hypoglycaemia (loss of gluconeogensis), hypotension (loss of cortisol effect on vascular tone)

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4
Q

Mechanisms of mineralcorticoid (aldosterone) deficiency?

A

hyponatraemia (urine Na+ loss with intravascular volume contraction), hyperkalaemia (reduced K excretion), metabolic acidosis (reduced renal H+ excretion)

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5
Q

Aldosterone homeostasis?

A

Angiotensin II + ACTH + K stimulate aldosterone production by adrenal cortex to increase sodium, water and therefore intravascular volumeq

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6
Q

Types of adrenal failure?

A

primary (adrenal gland) and secondary (hypothalamus/pituitary)

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7
Q

Identifying primary adrenal failure?

A

increased ACTH due to lack of cortisol for negative feedback

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8
Q

Primary Adrenal Failure/A good tan?

A

lack of cortisol inhibition leads to increased POMC leading to increased ACTH and MSH (ATCH contains alpha-MSH also), increase of these products leads to pigmentation

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9
Q

Simple obesity?

A

signs around 3-4yr, taller as kids but reverted to normal height in puberty due to glucocorticoid excess

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10
Q

Other signs of glucocorticoid excess?

A

moon face, thinning skin, myopathy, androgen excess, hypertension, glucose intolerance

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11
Q

Cortisol and receptor affinity?

A

equalt to glucocorticoid and mineralcorticoid, no mineralcorticoid effects due to rapid metabolism, effects occur in excess cortisol

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12
Q

Partial loss of function of glucocorticoid receptor?

A

Glucocorticoid resistance - high cortisol, hypokalaemia, hypotension, hyperandrogenism, fatigue

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13
Q

Loss of function of mineralcorticoid receptor?

A

Pseudohypoaldosteronism - high aldosterone and renin, high K and low Na, depleted ECF

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14
Q

ACTH receptor loss of function mutation?

A

severe cortisol deficiency from birth - hypotension, low Na, hypoglycaemia

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15
Q

XX karyotype leading to male phenotype?

A

defect in 21 hydroxylase -> lowered cortisol synthesis -> high ACTH -> high adrenal precursors and hyperplasia

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