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Y1 DRE Endocrine > L4: the adrenal gland > Flashcards

L4: the adrenal gland Flashcards

1
Q

Location of the adrenal glands

A

Sit above the kidneys

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2
Q

Structure of the adrenal glands

A

1: 40
- 3.5-4.5
- adrenal cortex - split into capsule, zona glomerulosa, zona fasciculata, zona reticularis
- adrenal medulla in the centre
- highly vascularised

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3
Q

What does the adrenal medulla produce?

A

The catecholamines - mainly adrenaline but some noradrenaline and dopamine

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4
Q

About the adrenal medulla

A
  • part of the sympathetic branch of the ANS
  • secretion is increased as part of the diffuse sympathetic discharge in emergencies, i.e. fight or flight
  • rapid/short acting response
  • not vital for survival but does contribute to the stress response
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5
Q

Pathway of hormones for the adrenal medulla

A

5:10
Spinal cord sends signals down preganglionic sympathetic neurones to the adrenal medulla releasing ACh. This stimulates a chromaffin cell (modified postganglionic sympathetic neurone) to release adrenaline which enters the blood and travels to target tissues.

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6
Q

How common is failure of the adrenal medulla?

A

Failure of the adrenal medulla is uncommon and causes hypotension and hypoglycaemia, but the hormones of the adrenal cortex are more important in regulating this.

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7
Q

When are catecholamines released?

A

Catecholamines are synthesised dependent on high local cortisol levels (permissive effect). Released during fight or flight.

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8
Q

What effects to catecholamines have?

A

Major effect on the cardiovascular system:

  • tachycardia and cardiac contractility
  • redistribution of circulating volume
  • gluconeogenesis in liver and muscle
  • lipolysis in adipose tissue
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9
Q

What is a tumour of the adrenal medulla?

A

Pheochromocytoma - causes over release of adrenaline
Symptoms - headache, sweating, palpitations, pallor, nausea, tremor, weakness
Treat by removing the adrenal gland

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10
Q

What does the zona glomerulosa produce?

A

Mineralocorticoids - mainly aldosterone

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11
Q

What does the zona fasciculata produce?

A

Glucocorticoids - mainly cortisol

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12
Q

What does the zona reticularis produce?

A

Androgens which are sex hormones e.g. testosterone

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13
Q

Steroid biosynthesis

A

Pathway at 13:20

Don’t need to know all the enzymes but know the different zones and what the different zones produce.

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14
Q

What are all the adrenal cortex steroid hormones produced from?

A

Cholesterol. StAR secretes cholesterol.

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15
Q

What is the rate limiting step in steroid biosynthesis?

A

CYP11A1 (P450SCC) = an enzyme converting cholesterol into pregnenolone, from which all the other steroid hormones can be made.

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16
Q

Biosynthesis of aldosterone

A

In the zona glomerulosa:

  • pregnenolone is converted to progesterone by 3(beta)-HSD
  • progesterone is converted to DOC by CYP21
  • DOC converted to corticosterone by CYP11(beta)1
  • corticosterone converted to aldosterone by CYP11(beta)2
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17
Q

Biosynthesis of cortisol

A

In the zona fasciculata:

  • CYP17 will pull pregnenolone into the fasciculata and turn it into 17-OH-pregnenolone
  • 3(beta)-HSD will convert 17-OH-pregnenolone into 17-OH-progesterone
  • CYP21 will convert that into 11-deoxycortisol
  • CYP11(beta)1 will convert 11-deoxycortisol into cortisol
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18
Q

Biosynthesis of androgens

A

In the zona reticularis:

  • has a different CYP17 enzyme which pulls 17-OH-pregnenolone in and into DHEA
  • DHEA is converted by 3(beta)-HSD into androstenedione

These precursor androgens are released and are converted further by other tissues.

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19
Q

How is secretion of mineralocorticoids (aldosterone) controlled?

A

Plasma potassium concentration and RAAS system (angiotensin)

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20
Q

How is secretion of glucocorticoids controlled?

A

ACTH

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21
Q

How is secretion of androgens controlled?

A

Somewhat by ACTH - poorly understood

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22
Q

How does ACTH stimulate corticosteroid synthesis?

A

17:50
- adrenal cell will respond to ACTH
- adrenal cells will have an ACTH receptor (G-protein coupled receptor)
- when ACTH binds it causes a cascade of events:
• ATP is converted to cyclic AMP
• cyclic AMP activates protein kinase A
• causes the increase in CEH (cholesterol esters hydrolase), an enzyme
- CEH converts cholesterol esters (from low density lipids LDL in the diet which are stored as lipid droplets) into cholesterol
- cholesterol is then transported in those cells by StAR protein to the mitochondria, where CYP11A1 enzymes are present, converting cholesterol into pregnenolone.

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23
Q

Summary of the effects of ACTH

A
  • upregulates CEH
  • upregulate CYPP11A activity
  • uoregulate StAR protein
24
Q

Steroid backbone

A

20:10

25
Q

Different structures of steroids

A

Small structural modifications can substantially alter specificity for steroid receptors.

26
Q

How do steroid hormones act?

A
  • lipid soluble so pass through biological membranes
  • bind to specific intracellular receptors, e.g. mineralocorticoid receptor or glucocorticoid receptor
  • alter gene transcription directly or indirectly
  • exact action depends on structure, ability to bind to specific receptors (and recruit cofactors)
27
Q

What is CYP11B2 also known as?

A

Aldosterone synthase

28
Q

What are the main mineralocorticoids?

A

Aldosterone, 3% DOC

29
Q

What is aldosterone critical to?

A

Without aldosterone we would lose 10-20g sodium per day. Critical to salt and water balance in the kidney (mainly), colon, pancreas, salivary glands, sweat glands.

30
Q

RAAS system

A
  • baroreceptors on the kidney will detect a fall in blood pressure
  • secretes renin
  • acts on angiotensinogen, converting it into angiotensin I
  • angiotensin I is converted by ACE into angiotensin II (active)
  • angiotensin II will cause a vasoconstriction hence increasing BP, and will stimulate the zona glomerulosa cells of the adrenal cortex to synthesis aldosterone
31
Q

Effects of aldosterone on the kidney

A
  • salt retention - so reabsorbs more sodium into the blood in exchange for potassium (which enters the urine)
  • water follows by osmosis hence maintaining body fluid volume and increasing BP and effective circulation
32
Q

How does aldosterone have its effect (molecular level)

A

7:15 - LOOK AT THIS PIC
Cells of the DCT/collecting ducts:
- have a mineralocorticoid receptor
- sodium potassium ATPase on the interstitial side
- normally, sodium passively enters the cells from the lumen side and potassium moves out with H+ into the lumen from the cell
- aldosterone binding to the MR receptor will cause the insertion of more sodium channels into the cell, and increase the sodium potassium ATPase. This drives more sodium into the interstitium and push potassium out.

33
Q

Regulation of aldosterone by potassium concentration

A

If you are hyperkalaemic (high levels of ECF potassium), the adrenal gland will sense high levels of potassium and will synthesis and secrete aldosterone, which will go to the kidney and increase potassium excretion and increase sodium reabsorption.

34
Q

What happens in hyperaldosteronism/primary aldosteronism (excess aldosterone)?

A

Retention of too much sodium leads to hypertension. Increase of aldosterone also suppresses renin, causing hypertension due to sodium retention and potassium secretion in urine - causing hypokalaemia. Can cause cardiovascular damage over time.

35
Q

Causes of primary aldosteronism/hyperaldosteronism

A
  • adrenal adenoma (Conn’s syndrome) - autonomous aldosterone secretion
  • bilateral adrenal hyperplasia - excessive aldosterone secretion for prevailing angiotensin II
36
Q

Treatment for hyperaldosteronism

A
  • surgery for the adenoma - removal

- medical therapy for rest e.g. hyperplasia, e.g. blocking the MR receptor to limit aldosterone’s effects

37
Q

What is the action of glucocorticoids?

A

Actions on most tissues. Their actions are permissive = they do not directly initiate but allow to occur in the presence of other factors. ‘Permissive’ actions only apparent with deficiency.

38
Q

When are glucocorticoids important?

A

They are essential to life.
Important in homeostasis e.g. conditioning the body’s response to stress. Essential for survival and resistance to stress.

39
Q

How do glucocorticoids exist?

A

80% bound to CBG - corticotropin binding globulin. Increasing the amount of binding hormone will increase the total concentration of the plasma hormone.

40
Q

What is stress?

A

The sum of the bodies responses to adverse stimuli. E.g., infection, trauma, haemorrhage, medical illness, psychological, exercise/exhaustion

41
Q

Actions of glucocorticoids

A
  • maintain blood glucose levels by: augmenting gluconeogenesis, amino acid generation, increased lipolysis of fat cells
  • maintenance of circulation (permissive): maintains vascular tone /circulation, salt and water balance (homeostasis)
  • immunomodulation: dampen the immune response (to control infections)
42
Q

How is the action of cortisol controlled?

A
  • controlled by the HPA axis
  • hypothalamus recognises stress, stimulating it to release corticotropin releasing hormone CRH.
  • this will travel in the portal vein to the anterior pituitary gland, stimulating it to release ACTH
  • ACTH will have a negative feedback on the system, switching it off, and will also travel to the adrenal cortex and stimulate it to secrete cortisol
  • cortisol has its negative feedback on the hypothalamus and on the anterior pituitary.
43
Q

How does ACTH vary during the day?

A

Diurnal variation (daily variation) of ACTH, Serum cortisol peaks at 4-7am, drops slightly and slight increase after lunchtime, then drifts down after lunch.

44
Q

Effect of ACTH on adrenal size

A

Normal ACTH will have a normal size adrenal gland.
ACTH excess causes adrenal growth
ACTH deficiency causes adrenal gland shrinkage.

45
Q

How do synthetic steroid affect the negative feedback cycle?

A

E.g. dexamethasone, cortisone, hydrocortisone

  • given for immuno-dampening effects e.g. for rheumoid arthritis
  • on these treatments for a long time, the negative feedback cycle is affected
  • if given, the body will react to it as normal and switch off CRH and ACTH by negative feedback
  • so lowered ACTH over time, shrinking them
  • never remove from steroids immediately, otherwise adrenal glands will not be able to produce enough cortisol for patients to survive. Need to wind off the drugs slowly.
46
Q

Glucocorticoid excess - Cushing’s syndrome

A

Iatrogenic Cushing’s (most common):

  • given synthetic corticosteroids and the dose is too high
  • so causes glucocorticoid excess, so adrenal glands shrink
  • in steroid inhalers, causing oral candidiasis by increasing blood glucose and thus saliva glucose levels

Endogenous Cushing’s

  1. ACTH dependent: pituitary tumour (Cushing’s disease) causing too much ACTH, stimulating the adrenals and the negative feedback fails. Hypothalamus responds but adrenal gland doesn’t. Also caused by small cell lung carcinoma, carcinoids.
  2. ACTH independent: adrenal adenoma/carcinoma causing too much cortisol production. Negative feedback works so low ACTH but high cortisol. Shrinkage of adrenal gland.
47
Q

Typical appearance of someone with Cushing’s

A
  • moon face
  • fat pads
  • red cheeks
  • bruisabikity
  • thin skin
  • striae
  • pendulous abdomen
  • poor muscle development
  • poor wound healing
48
Q

Other complications from Cushing’s

A
  • diabetes mellitus
  • osteoporosis - vertebral collapse
  • mental abnormality
  • reduced ability to fight infection (since WBCs are broken down to produce glucose)
  • hypertension
49
Q

Treatment for Cushing’s

A

If due to pituitary or adrenal disease usually surgery is required, followed by radiotherapy and or cortisol synthesis blocking drugs.
If due to steroids, must wind them off the steroids to allow adrenal glands to recover.

50
Q

What are adrenal androgens?

A

Send hormone production is mainly in the gonads (primary reproductive organs). Stimulated by LH and FSH. Androgens converted into testosterone and oestrogens in other tissues.

51
Q

Congenital adrenal hyperplasia (CAH)

A

Causes 21-hydroxylase deficiency. So progesterone does not produce the aldosterone and cortisol, and produces too much adrenal androgens. Causes ambiguous genitalia.

52
Q

Primary adrenal insufficiency/Addisons disease

A
  • failure of adrenals to secret sufficient glucocorticoid in response to stimulation
  • often gradual autoimmune destruction of adrenal e.g. HIV, TB
  • HPA axis compensates until 90% loss or until stress - adrenal crisis/acute adrenal insufficiency
  • weakness, fatigue, hypotension, hyponatremia, hyperkalaemia, dehydration, nausea, vomiting, anorexia, hyperpigmentation
53
Q

Secondary adrenal insufficiency (more common)

A
  • loss of ACTH secretion due to hypopituitarism

- no hyponatremia or hyperpigmentation

54
Q

Why does primary adrenal insufficiency cause hyperpigmentation?

A
  • adrenally insufficient so not responding or producing cortisol
  • so hypothalamus will response to this by increasing CRH and pituitary will increase ACTH
  • ACTH comes in the preprohormone POMC, along with MSH, which causes hyperpigmentation of the skin, usually shown first in the buccal mucosa
55
Q

What is adrenalectomy?

A

Loss of the adrenal glands

  • fatal within a few days as a result of circulatory collapse due to the lack of aldosterone
  • fasting results in fatal hypoglycaemia
  • stress results in collapse and death
56
Q

Summary of what can go wrong with the adrenal glands.

A
  • Over secretion of corticosteroid hormones: Cushing’s syndrome (cortisol), Conn’s syndrome (aldosterone)
  • Under secretion of corticosteroid hormones: Addison’s disease and hypopituitarism, congenital adrenal hyperplasia
  • adrenal lumps and bumps like adenomas and carcinomas
57
Q

Oral manifestations of Cushing’s

A

Moon face, facial hirsutism, osteoporosis (fractures in mouth), delayed healing, muscle weakness - phonation, deglutition, oral candiasis

Y1 DRE Endocrine (7 decks)

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