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MBD > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

What can we do to investigate endocrine disorders?

A

Dynamic tests

  • Measure hormone levels
  • Check if endocrine tissue is functional
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2
Q

What is the function of TSH and TRH?

A

TRH from hypothalamus stimulates pituitary to release TSH

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3
Q

Which of the 2 hormones from the thyroid is more active and which is produced in greater quantities?

A
  • T3 (triiodothyronine) more active
  • T4 (thyroxine) in greater quantities
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4
Q

What are the levels of T3/T4 in primary hypothyroidism?

A

Low

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5
Q

What are the levels of T3/T4 in secondary hypothyroidism?

A

Low

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6
Q

What are the levels of TSH in primary hypothyroidism?

A

High

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7
Q

What are the levels of TSH in secondary hyporthyroidism?

A

Low (could be normal, but should be high - not normal or low)

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8
Q

What are the levels of T3/T4 in primary hyperthyroidism?

A

High

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9
Q

What are the levels of TSH in primary hyperthyroidism?

A

Low

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10
Q

What are the levels of T3/T4 in secondary hyperthyroidism?

A

high

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11
Q

What are the levels of TSH in secondary hyperthyroidism?

A

High

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12
Q

Name the 3 zones of the adrenal cortex

A
  • Zona glomerulosa
  • Zona fasciulata
  • Zona reticularis

Blood flow is from the outer cortex (Z. glomerulosa) to the medulla

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13
Q

What does the Zona glomerulosa synthesise?

A

Mineralocorticoids (aldosterone)

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14
Q

What does the Zona fasciulata secrete?

A

Glucocorticoids (cortisol)

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15
Q

What does the Zona reticularis secrete?

A

Adrenal androgens

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16
Q

What does the adrenal medulla secrete?

A

Catecholamines:

  • adrenaline
  • noradrenaline
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17
Q

What are the types of disorders of adrenocortical function?

A
  • Adrenal steroids
  • Adrenal hyperfunction
  • Adrenal insufficiency
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18
Q

What are the adrenal hyperfunction diseases?

A
  • Cushing’s syndrome
  • Conn’s syndrome
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19
Q

Explain what Cushing’s syndrome is

A

Excess cortisol (may be primary or secondary)

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20
Q

Explain what Conn’s syndrome is

A

Excess aldosterone (primary hyperaldosteronism)

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21
Q

What are the adrenal insufficiency diseases?

A
  • Hypocortisolism
  • Addison’s disease
22
Q

Explain what Addison’s disease is

A

Lack of aldosterone and cortisol (adrenal insufficiency) - primary?

23
Q

What two things can increase aldosterone secretion?

A
  • RAAS
  • Increased plasma K+
24
Q

What is RAAS activated by?

A
  • reduced renal perfusion
  • increased sympathetic activity
25
Q

What is the effect of increased aldosterone?

A

Effect of increased aldosterone is increased reabsorption of Na+ and so increased total amount of Na+ in the blood stream so increased blood volume and increased blood pressure

26
Q

What is aldosterone secretion activated by?

A

RAAS

27
Q

What is caused (symptoms) by hyperaldosteronism?

A

Hypertension

  • hypokalaemia (due to increased k+ secretion)
28
Q

What measurement specifically can we take to diagnose hyperaldosteronism?

A

We can measure plasma aldosterone and plasma renin and measure the ratio of the two to diagnose hyperaldosteronism.

  • In hyperaldosteronism there will be low activation of RAAS and so low renin and there will be high aldosterone so this ratio can be measured
29
Q

Name one possible cause (example) of secondary hyperaldosteronism

A
  • Renal artery stenosis
  • Blockage will cause decreased perfusion of the kidney and so much more activation of RAAS
30
Q

Describe the effect of cortisol on the immune system

A
  • Immunosuppressant
31
Q

Describe effects of excess cortisol on BP

A

Excess cortisol causes high blood pressure

32
Q

Describe the metabolic effects of cortisol

A

Metabolic effects are to preserve plasma glucose - does this by:

  • increasing gluconeogenesis
  • decreases glucose uptake in skeletal muscle
  • increases glycolysis
33
Q

Explain fully why Cushing’s disease causes an increase in body fat

A
  • There is an increase in glucose due to the effects of excess cortisol so there is hyperglycaemia.
  • Hyperglycaemia causes increased insulin but insulin can not cause glucose uptake in the muscle as normal (as cortisol is blocking it) and therefore, glycogenesis occurs in the adipose tissue (excess glucose becomes glycogen in the adipose tissue)
  • This is also why there is wastage of the muscles as well as hypertension
34
Q

Explain fully why Cushing’s disease causes an increase in body fat

A

ADH secretion rises in the absence of cortisol

35
Q

What do exogenous glucocorticoids activate?

A

Cortisol receptor

36
Q

What will glucocorticoids do at high doses?

A

Shut down HPA

37
Q

What happens to the adrenal cortex with lack of ACTH stimulation?

A

Atrophies

38
Q

Explain how exogenous glucocorticoids cause Cushing’s syndrome (most common cause of it) what does this cause to the adrenal cortex?

A

High levels of the exogenous glucocorticoid will cause shut down of the HPA due to negative feedback on the hypothalamus and anterior pituitary so shut down of CRH and ACTH production

  • adrenal cortex atrophy (so you need to be gradually taken off of glucocorticoid therapy)
39
Q

Apart from iatrogenic, what other causes of Cushing’s are there and what is Cushing’s disease?

A

ACTH-secreting pituitary adenoma → Cushing’s disease

or an ectopic ACTH source (a tumour somewhere else)

40
Q

What is the dexamethasone suppression test?

A

Dexamethasone is a synthetic glucocorticoid that will suppress HPA - so in healthy people you would expect cortisol levels to be low in the morning (normally high) and if the person has Cushing’s disease or syndrome, you will find that this cortisol reading in the morning has not been suppressed!

  • then you repeat it with high dose of dexamethasone over a few days and after a few days it will be suppressed
  • if it is an ectopic source of ACTH, then dexamethasone will not affect it if it is a high or a low dose
  • if it is a primary tumour of the adrenal cortex then ACTH would be low
41
Q

What is Addison’s disease?

A

Primary adrenal insufficiency - Lack of aldosterone and cortisol (also adrenal androgens)

  • Addison’s is usually due to autoimmune disease causing destruction of the adrenal cortex so loss of all of the hormones from it
42
Q

How does Addison’s disease affect BP, Na+, K+, ACTH and renin?

A
  • low BP (mostly due to lack of aldosterone)
  • Na+ is normal/low
  • K+ is normal/high
  • high ACTH
  • high plasma renin
43
Q

Why can Addison’s disease cause hyperpigmentation?

A

As at very high concentrations, ACTH can bind to melanocortin receptor

44
Q

Explain why Na+ can be low in Addison’s

A

This is NOT due to low aldosterone as aldosterone regulates the total amount of Na+ as it regulated blood volume - not concentration of Na+ (although it is an easy mistake to make as aldosterone increases Na+ reabsorption)

  • With no negative feedback there is also increased ADH as well as CRH and ACTH
  • Increased ADH will increase water reabsorption and so dilute electrolytes
45
Q

Explain why K+ can rise in Addison’s

A

In this case it is due to low aldosterone as aldosterone does promote K+ excretion

  • but due to vomiting (symptom of Addison’s) which causes hypokalaemia, K+ often does not increase
46
Q

How do we test for Addison’s and other adrenal insufficiency?

A
  • We do a dynamic test to see if the adrenal glands (cortex) can produce cortisol in response to ACTH
  • If the problem is secondary then the adrenal gland should be able to do this, if it is primary, then not
47
Q

What are secondary adrenal insufficiencies called?

A

Pituitary or hypothalamic disease

48
Q

What does secondary adrenal insufficiency cause?

A

Insufficient cortisol

49
Q

What is the onset of Addison’s disease?

A

Has a slow onset and can be unmasked by a significant stress or illness – shock, hypotension, volume depletion, adrenal crisis.

50
Q

What are the symptoms of addisons?

A
  • Anorexia
  • Weakness/fatigue
  • Hyperpigmentation
  • GI symptoms
  • Salt cravings
  • Postural dizziness
  • Vitiligo
  • Muscle or joint pain
51
Q

What is addisons hallmarked by?

A
  • High ACTH and low cortisol
52
Q

What is the short and long synacthen test?

A
  • It is measuring cortisol baseline and then levels after injection of a synthetic cortisol (synacthen)
  • Is a dynamic test

MBD (23 decks)

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