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Reproduction, Development and Aging COPY > Lecture 22: Steroid abnormalities > Flashcards

Lecture 22: Steroid abnormalities Flashcards

1
Q

Case

31 year old woman, one year history of increasing tiredness, presents collapsed and rowsy following a mild “flu”

High pulse rate, low BP, afebrile, TANNED appearance and conspicous freckles

Low Glucose, low Na, K+

Low Co2 and low HCO3

A

Hyponatreamia (low Na+)

Hyperkalaemia (high K+)

Hypoglycaemia (low glucose)

Metabolic acidosis (increased H+)

Intraveascular volume depletion

Likely combined glucocorticoid and mineralocorticoid deficiency

Aldosterone and cortiosol deficiency cause a _low sodium concentratio_n and hypotension

_Mineralocorticoid deficiency (aldoster_one) causes high potassium

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2
Q

Aldosterone and cortiosol deficiency cause ______ and _______

A

Aldosterone and cortiosol deficiency cause a low sodium concentration and hypotension

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3
Q

Mineralocorticoid deficiency (aldosterone) causes_______

A

Mineralocorticoid deficiency (aldosterone) causes high potassium

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4
Q

________deficiency causes high potassium

A

Mineralocorticoid deficiency (aldosterone) causes high potassium

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5
Q

_______and _______deficiency cause a low sodium concentration and hypotension

A

Aldosterone and cortiosol deficiency cause a low sodium concentration and hypotension

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6
Q

What are the mechanism of consequences due to glucocorticoid deficiency

A

1) Hyponatraemia (Low Na+)

  • Unable to excrete a water load (reduced glomerular filtration rate)
  • Loss of cortisol i_nhibition of antidiuretic hormone (ADH)_

2) Hypoglycaemia

-Reduced hepatic gluconeogensis (decreased glucose)

3) Hypotension

-Loss of cortisol effects on vascular tone

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7
Q

Describe the mechanism of mineralocorticoid action on…

1) Hyponatraemia
2) Hyperkalaemia
3) Metabolic acidosis

A

e. g. aldosterone
- Mainly regulates sodium

Hyponatraemia (decreased Na+)

-Urine Na+ loss with intravascular volume contraction (vasocontriction) and secondary ADH/vasopressin secretion

Hyperkalaemia (increased K+)

-Reduced renal K+ excretion due to lack of aldosterone

Metabolic acidosis

-Reduced renal H+ excretion (increased H+)

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8
Q

Dehydration means _____-

A

Loss of SALT AND WATER

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9
Q

How is aldosterone formed?

A

JGA produces renin which converts Angiotensiogen to Angiotensin I

AT1 is converted to AT2 by ACE

AGT2 acts on the adrenal cortex zona glomerulosa (with K+ and ACTH) and Aldosterone is produced

Aldosterone causes Increase in Na+ and H20 and therefore increase in intravascular volume

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10
Q

Angiotensin II acts on the ____________________ (with K+ and ACTH) and Aldosterone is produced

A

AGT2 acts on the adrenal cortex zona glomerulosa (with K+ and ACTH) and Aldosterone is produced

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11
Q

What are the 2 groups of causes of adrenal failure?

A

1) Primary (adrenal gland)
2) Secondary/tertiary (pituitary/hypothalamus)

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12
Q

What is ACTH?

A

Adrenocorticotropic hormone

ACTH is made in the pituitary gland and travels through the bloodstream to the adrenal glands. It stimulates the adrenals to release cortisol, a key factor in many functions in the body’s metabolism of fats, carbohydrates, sodium, potassium, and protein as well as blood pressure.

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13
Q

Describe the hypothalamic-pituitary-adrenal axis

A

Hypothalamus releases corticotropin-releasing hormone

Anterior Pituitary releases Adrenocorticotropic hormone

Adrenal cortex releases Cortisol

Cortisol has a negative feedback on the pituitary and the hypothalamus

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14
Q

If someone has a tan (but hasn’t been in the sun), what can it be an indicator of?

A

Primary Adrenal Failure

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15
Q

How can a tan be an indicator of primary adrenal failure?

A
  • PAF = Increased ACTH
  • MSH (melanocyte stimulating hormone)- causes pigmentation
  • Some POMC cleavage products form 3MSH
  • ACTH contains a-MSH and is also a peptide product of POMC
  • Therefore Increased POMC and Increased ACTH produces Increased MSH -> Pgimentation
  • Increased POMC and Increased ACTH occurs with a lack of feedback inhibition (i.e. decreased cortisol) in primary adrenal failure
  • Some of POMC cleavage products are 3 MSH (Malanoycyte Stimulating Hormones)
  • ACTH is a peptide product of POMC
  • ACTH contains a-MSH
  • Therefore Increased POMC and Increased ACTH produces Increased MSH -> Pgimentation
  • Increased POMC and Increased ACTH occurs with a lack of feedback inhibition (i.e. decreased cortisol) in primary adrenal failure
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16
Q

Where can increased pigmentation be observed in primary adrenal insufficiency?

A

Pigmentation occurs generally, but is more apparent in …

1) Skin flexures (e.g. hand creases)
2) Buccal mucosa (mouth)
3) Old scars
4) freckles
5) Nails

ACTH is regulated by cortisol (i.e. is independent of mineralocorticoid axis)

17
Q

ACTH is regulated by _________(i.e. is independent of __________________axis)

A

ACTH is regulated by cortisol (i.e. is independent of mineralocorticoid axis- like aldosterone)

18
Q

What should you look for (key observations) in children with increasing obesity to determine if its…

1) Simple obesity

vs

2) Glucocorticoid excess

A

Is this an input/output problem simle/exogenous obestiy?

1) Change in appearance over time

  • Check old photos to look for patterns of change
  • Simple obesity becomes apparent usually by 3-4 years of age, with progressive worsening
  • Childhood glucocorticoid excess leads to generalised obesity whilst Adult glucocorticoid excess leads to truncal obesity

2) Growth pattern

  • Simple obesity drives growth
    • Fat kids are taller than you would expect from their genetic potential (parents heights)
    • However they enter puberty earlier and end up a height similar to their parents
  • Glucocorticoid excess causes profound growth failure and corssing of percentiles downwards

3) Other features suggestive of pathological causes

  • Moon face
  • Thinning skin (Bruising, stretch marks)
  • Androgen excess (e.g. hirsutism, amenorrhoea)
  • Myopathy (e.g. proximal weakness)
  • Glucose intolerance (diabetes)
  • Hypertension
  • Osteoporosis
    *
19
Q

If a child is ________________, they often have an underlying cause for their obesity until proven otherwise

A

Short and fat

20
Q

What are Other features suggestive of pathological causes (not just simple obesity)

A
  • Moon face
  • Thinning skin (Bruising, stretch marks)
  • Androgen excess (e.g. hirsutism, amenorrhoea)
  • Myopathy (e.g. proximal weakness)
  • Glucose intolerance (diabetes)
  • Hypertension
  • Osteoporosis
21
Q

What are the differences in growth pattern between simple obesity and pathologically-based obesity?

A

Growth pattern

  • Simple obesity drives growth
    • Fat kids are taller than you would expect from their genetic potential (parents heights)
    • However they enter puberty earlier and end up a height similar to their parents
  • Glucocorticoid excess causes profound growth failure and corssing of percentiles downwards
22
Q

What are the Change in appearance over time between simple obesity and pathologically-based obesity?

A
  • Check old photos to look for patterns of change
  • Simple obesity becomes apparent usually by 3-4 years of age, with progressive worsening
  • Childhood glucocorticoid excess leads to generalised obesity whilst Adult glucocorticoid excess leads to truncal obesity
23
Q

Patient comes in (child)

Symptoms:

Facial plethora

Facila and trunkal hair

Moon face

Violceaous striae over trunk and abdomen

Tests:

Increased urinary free cortisol

Low K+

Low renin (suggest everything is turned off)

What is the issue here?

A

Diagnose: Glucocorticoid excess and probably adrogen excess:

CUSHINGS SYNDROME

due to one of these….

1) Primaryfrunctional adrenal tumour
2) ACTH secreting tumour
3) Exogenous glucocorticoid

Cortisol can bind to mineralocorticoid receptor and glucocorticoid receptor with equal affinity. When it does happen, cortisol has no mineralocorticoid effects because it is metabolised straight away. But with excess, you get aldosterone effects. = hence low K+

24
Q

What is Facial plethora?

A

Redness of face due to i_ncreased level of blood volume_ or increased blood flow. Basically, the term plethora is used for redness due to increased blood volume, so when it occurs on face, it is known as facial plethora

25
Q

What is another word for….Stretch marks

A

Violaceous striae

26
Q

What is the word for….Redness in face due to increased blood to the face?

A

Facial plethora

27
Q

Describe Receptors and Ligand affinity of cortisol to different receptors and its effects

A

Cortisol binds to the mineralocorticoid receptor and glucocorticoid receptor with equal affinity

Cortisol usually has no mineralocorticoid (MC) effects as it is metabolised rapidly to cortisone before it can bind and activate the MC receptor. (renal 11B hydroxysteroid dehydrogenase type 2)

However with excess cortisol states however mineralocorticoid effects are observed. (e.g. low potassium and hypertension)

28
Q

What do you get if you have partial loss of function (resistence) of glucocorticoid receptor in various organs?

A

(if all is lost- you die)

Cortisol won’t bind as well = Glucocorticoid resistance

If the brain doesn’t think there is enough cortisol, it will produce more ACTH which causes the _adrenal glands to get bigge_r and then produce more cortisol.

If there’s too much cortisol, it can bind to the mineralocorticoid receptor, so the patient may go into hypertension and low potassium. and alkalosis

By product of cortisol is androgen so you might get hirutism as well and fatigue (cortisol insensitivity)

29
Q

What is a by-product of high cortisol?

A

Increased androgen- hirutism, amenorrhoea

and/or fatigue (cortisol insensitivity)

30
Q

What are some symptoms of high mineralocorticoid?

A

hypertension and low potassium and alkalosis

31
Q

What symptoms do you see when there is _loss of function (resistence) of the mineralocorticoid recepto_r?

A

Look like aldosterone deficiency (but if you measure aldosterone, it’ll be high) = Mineralocorticoid resistance (pseudohypoaldosteronism)

1) High aldosterone and renin levels
2) Depleted extracellular fluid space
3) High serum K+ and low Na+ concentrations

32
Q

If someone has ACTH receptor mutation and therefore loses its function, what would you observe?

A

Adrenal crisis- low BP and often die.

Small nonfunctioning zona reticularis and fasciculata

Severe cortisol deficiency from birth

  1. Hypotension
  2. Low Na+
  3. Hypoglycaemia
33
Q

What is the function of Aldosterone?

A

The most important physiological effect of aldosterone is s_timulation of sodium resorption_ and potassium secretion by principal cells of the late distal tubule and collecting duct

34
Q

What is ADH?

A

Vasopressin, also named antidiuretic hormone (ADH)

causes the kidneys to reabsorb solute-free water

35
Q

What is Cushing Syndrome

A

A pituitary gland tumor (pituitary adenoma). A noncancerous (benign) tumor of the pituitary gland, located at the base of the brain, secretes an excess amount of ACTH, which in turn stimulates the adrenal glands to make more cortisol.

Reproduction, Development and Aging COPY (32 decks)

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