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ESA2 > MEH - The Adrenal Glands > Flashcards

MEH - The Adrenal Glands Flashcards

1
Q

What are the three layers of the adrenal glands?

Within the capsule and cortex what layers are there and what do each produce?

What des the medulla produce? What cells are here?

A

G Salt
F Sugar
R Sex

CAPSULE: Zona glomerulosa - Mineralocorticoids - Aldosterone

CORTEX: Zona fasiculata - Glucocorticoids - Cortisol
Zona reticularis - Androgens + Glucocorticoids

Adrenaline (80%), NA(20%), chromatin cells

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2
Q

What are DHEA and androstenedione precursors of?

A
  • Testosterone male

- Oestrogen women

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3
Q

What are the three glucocorticoids?

A

Cortisol
Cortisone
Corticosterone

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4
Q

What is an important mineralocorticoid?

A

Aldosterone

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5
Q

What are steroid hormones synthesised from and where?

A

Cholesterol in adrenal glands and gonads

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6
Q

How do they exert their action?

A

Lipid soluble - Bind to nuclear receptors and modulate gene transcription

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7
Q

What exerts a faster action and why? Steroids or catecholamines?

A

Steroids as its takes time to modulate gene transcription and new protein synthesis

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8
Q

How do corticosteroid exert their action in the cell?

A

Diffuse across cell membrane
Binding causes chaperone proteins to dissociate from glucocorticoid receptor (e.g. heat shock protein 90)
Receptor ligand translocates to nucleus
Binds to GREs (glucocorticoid response elements) or other transcription factors

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9
Q

What are GREs (glucocorticoid reposes elements)?

A

Areas in a promotor region of a gene that can turn on transcription when glucocorticoid-receptor binds

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10
Q

Where is aldosterone synthesised exactly?

A

In the zona glomerulosa of the adrenal cortex

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11
Q

Which 2 proteins carry aldosterone in serum? Which is the main one?

A

Albumin - most

Transcortin

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12
Q

Where is the aldosterone receptor and why?

A

Intracellular as it exerts its actions by regulating gene transcription

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13
Q

What are the broad roles of aldosterone?

A

Na K homeostasis - reabsorption of Na excretion of K, absorption of H2O (by increasing expression of NaK pump)
BP balance

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14
Q

Where is ACE made and where does ang I get cleaved to ang II?

A

Primarily in lung endothelial cells

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15
Q

What is the primary role of ADH?

A

Translocation of aquaporins in collecting tubule to increase H2O reabsorption

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16
Q

What happens in hyperaldosterone (6 - 3 primary, 3 secondary) vs hypo?

A

Hyper -
Primary - LOW renin (high aldosterone): Most common is bilateral idiopathic adrenal hyperplasia,Conns syndrome (aldosterone secreting adrenal adenoma) -> increased BP, low K+ arrhythmias, hypernatraemia, LVH

Secondary - HIGH renin (low aldosterone), also renin producing tumours e.g. of juxta glomerular, renal artery stenosis

Hypo - Congenital adrenal hyperplasia - lack of enzyme leads to low cortisol and aldosterone and high androgens (male hormones)

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17
Q

What can cause hyperaldosteronism? (primary vs secondary) What are signs and treatments?

A

Primary - LOW RENIN - defect in adrenal cortex
Most common is bilateral idiopathic adrenal hyperplasia
Conns syndrome

Secondary - HIGH RENIN - Over activation of RAAS
Juxtaglomerular tumour
Renal Artery Stenosis

Signs/Symptoms are:
High BP
Hypernatraemia
Hypokalaemia 
LVH
Stroke

Treatment: Aldosterone antagonist - Spironolactone. Surgery if aldosterone secreting tumour

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18
Q

What is Conn’s syndrome?

A

Aldosterone secreting adrenal adenoma

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19
Q

Where exactly is cortisol synthesised? What it’s major carrier protein?

A

Zona fasiculata in response to ACTH

Transcortin

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20
Q

Are cortisol main actions catabolic or anabolic?

A

Catabolic

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21
Q

What are 6 important actions of cortisol?

A 
Gluconeogenesis 
Proteolysis
Lipolysis
Increase BP - via increased glucose (increases sensitivity of blood to vasoconstrictors)
Anti-inflammatory 
Depression of immune reponse
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22
Q

What is cortisols effect on gluconeogenesis and where?

A

Increase glucose production leads to increased insulin which leads to increased glycogen stores in the liver.

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23
Q

What is cortisol effect on muscle?

A

Inhibits GLUT4 receptor so reduces uptake of glucose by muscles having a glucose sparing effect

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24
Q

What is cortisol effect on fat?

A

Decreased glucose utilisation, decreased sensitivity to insulin, increased lipolysis

Also redistribution of fat especially in abdomen, supraclavicular fat pads (buffalo hump), and on face (moon)

25
Q

What are symptoms of Cushings syndrome? Why do you get striae? What are 4 causes of Cushings syndrome?

A 
Moon face
Buffalo hump
Hyperglycaemia 
Hypertension
Acute weight gain
1) Prescribed glucocorticoids
2) Pituitary ACTH secreting adenoma -Cushings DISEASE
3) Adrenal secreting cortisol adenoma
4) Non pituitary-adrenal tumours secreting ACTH e.g. small cell lung cancer (rate)
26
Q

Name two steroid drugs, what kinds of disorders are they used to treat? What are the side effects like? Why should you reduce steroids gradually and not stop suddenly?

A

Prednisolone
Dexamethasone

Inflammatory - e.g. asthma, IBD, RA

Side effects similar to higher levels of cortisol plus can have mineralocorticoid effects

Must reduce slowly as get adrenal insufficiency (adrenals reduce steroid synthesis whilst you’re on steroids) - would get similar to addison’s crisis

27
Q

What is the most common cause of Addisons?

A

Autoimmune destructive atrophy of adrenal cortex.

28
Q

Who is more likely to get Addisons men or women

A

Women (autoimmune tends to be)

29
Q

What are symptoms of Addisons?

A 
Postural hypotension
Lethargy
Weight loss
Anorexia
Increased skin pigmentation - brown
Hypoglycaemia
30
Q

Why is there more POMC in Addisons? What is the side effect of this?

A

Because ACTH is low, so negative feedback to ant pit reduced, so more POMC is required to synthesis ACTH

Side effect is POMC contains gamma-MSH (melanocyte stimulating hormone) which produces melanin in skin –> colouration

31
Q

How else is melanin and skin pigmentation increased in Addison’s other than POMC?

A

ACTH contains alpha-MSH which acts on melanocortin receptors on melanocytes to increase hyper pigmentation

32
Q

What is Addisonian crisis? What is it precipitated by? Symptoms? Treatment?

A

Life threatening emergency due to adrenal insufficiency

Caused by stress, salt depravation
Infection 
Trauma 
Cold Exposure
Over exertion
Abrupt steroid drug withdrawal

Symptoms are nausea, vomitting, pyrexia, hypotension, vascular collapse

Treatment: Fluid replacement, cortisol

33
Q

Explain how the adrenal medulla is a modified sympathetic ganglion of ANS

A

It receives pre-ganglionic sympathetic input via:
Splanchnic nerves –> celiac ganglia –> chromaffin cells

Chromaffin cells lack axons but release hormones into blood: Adrenaline (80%), Nor adrenaline (20%)

34
Q

Why do 80% chromaffin cells release adrenaline and 20% NA?

A

Because 20% of chromaffin cells lack the enzyme N-Methyl transferase

35
Q

What are NA and adrenaline derived from?

A

Tyrosine

36
Q

How does tyrosine become DA, NA, Adrenaline? Which enzyme converts NA to adrenaline?

A

Tyrosine —> Levodopa —> Dopamine —-> NA —> via N-methyl transferase —> Adrenaline

37
Q

How does hormonal adrenaline increase HR?

A

Binds to beta 1 adrenergic receptors (GPCR) G alpha S pathway

1) Activating PKA that phosphorylates L type Ca2+ channels
2) cAMP - phosphorylates HCN channels increasing funny current
3) PKA - also phosphorylates HCN channels increasing funny current

Potentiates opening
Therefore increasing upslope of the action potential

38
Q

What is pheochromocytoma? What happens?

A

Catecholamine secreting tumour (normally NA)
Can lead to life threatening hypertension

Other symptoms:
Palpitations 
Hyperglycaemia 
Headaches
Anxiety
Weight loss
Excessive sweating
39
Q

Are there any ill-effects from lack of adrenal catecholamines? Compared to corticosteroids?

A

No ill effects from catecholamines

Lack of Corticosteroids is life threatening - must receive cortisol aldosterone (e.g. similar to Addisons disease).

40
Q

What tests would you do for Cushings syndrome and what would you see?

A

Blood test: Midnight cortisol, should be low will be high
Suppression test - Give a steroid drug e.g. dexamethasone for a few days then test cortisol levels should be low but in cushings will stay high.
24hr urine - cortisol levels will be high in Cushings

41
Q

What would you expect to see in tests for Aldosterone insufficiency (e.g. Congenital Adrenal Hyperplasia)? Compared to low ACTH?

A

High K
Low Na

Low ACTH alone will have Low Na with normal K

42
Q

What would you expect to see on tests for aldosterone excess e.g. Conns, renin secreting juxtaglomerular tumours etc?

A

High BP
High Na
Low K

CT/MRI/MIBG/PET scan - tumours etc

43
Q

How would you test for increased catecholamines? Why avoid things like coffee, coke, bananas before? What might high levels indicate?

A

24hr Urine - catecholamines or metanephrines

Plasma metanephrines - more sensitive than 24hr urine

Because they affect results

Pheochromocytoma

44
Q

What are metanephrines?

A

Metabolites of adrenaline and NA

45
Q

Apart from Addisons what two other causes of reduced cortisol is there?

A

Secondary adrenal failure from hypopituitism - reduced ACTH

Steroid induced hypoadrenalism - ACTH suppression

46
Q

Apart from autoimmune what other causes of primary adrenal failure is there?

A 
Infection - TB
Drugs
Malignancy
Vascular - infarct etc 
Infiltration - amyloidosis etc
47
Q

What is the treatment for Addisons? Why would they have to carry a steroid card?

A

Lifelong:

Glucocortioids - hydrocortisone, prednisolone
Mineralocorticoids - fludrocortison

To ensure health professionals know about crisis that can occur if steroids are stopped suddenly –> gives similar to addison crisis. As ACTH suppressed with long-term steroids so on removal can cause hypo adrenal crisis

48
Q

why would Secondary adrenal failure from hypopituitism - reduced ACTH when compared with Addisons not:

  • Cause pigmentation
  • Not cause hyperkalaemia
  • Cause hyponatraemia
A
  • No ACTH so no gamma-MSH stimulating melanin
  • No mineralocorticoid deficiency unlike can get in addisons
  • Dilutional hyponatraemia (due to absence of normal effect of cortisol on free water excretion)
49
Q

3 causes of Cushings syndrome? State their effects on ACTH

A

Pituitary tumour - increased ACTH
Adrenal Tumour - increased cortisol - reduced ACTH due to negative feedback
Ectopic ACTH - e.g. some small cell lung cancers secrete ACTH

50
Q

Sometimes adrenal tumours causing Cushings also affect androgens - what kinds of symptoms might you see? How would you treat an adrenal tumour?

A 
Hirtuism (excessive hair growth in some areas of body)
Acne
Greasy skin
Clitoromegaly
Deep voice
Androgenic alopecia

Adrenalectomy

51
Q

What is the commonest cause of endocrine hypertension?

A

Primary hyperaldosteronism e.g. Conns or bilateral idiopathic adrenal hyperplasia - can see hypertension at a young age

52
Q

High BP low K - what is the clinical suspicion?

A

Hyperaldosteronism

53
Q

Low Na high K - what is the clinical suspicion?

A

Hypoaldosteronism

54
Q

Low Na normal K

A

ACTH deficiency

55
Q

What is Congenital adrenal hyperplasia? What enzyme? What is the treatment?

A 
Rare autosomal recessive disorder - 
Lack of enzyme 21-hydroxylase causes:
Low cortisol
Low aldosterone
High male hormones (androgens)

Causes genitalia abnormalities and adrenal crisis (Hypotension, hyponatraemia, hyperkalaemia, hypotension, hypoglycaemia, virilisation (development of male characteristics) -

Treat adrenal crisis, determine sex of baby
Corrective surgery may be needed and long term glucocorticoids and mineralocorticoids

56
Q

What is the difference between pheochromocytoma and paraganglioma? What three characteristics make it more likely to be genetically inherited. What are the symptoms of both? What are the investigations? (Type of urine/blood tests/imaging and what is the neuroendocrine marker?)

A

Both catecholamine secreting hormones

Pheo - from adrenal medulla (90%)
Para - extra adrenal tumour (10%)

Genetic if:
Extra adrenal
Malignant
Bilateral

Symptoms are same as anxiety attack - sympathetic surge –> sweating, palpitations, high or low BP, collapse

24hr urine metanephrines
Plasma metanephrines
Neuroendocrine marker is - Chromogranin A (a tumour marker)
CT/MRI/PET

57
Q

What is the treatment for pheochromocytoma and paraganglioma? Why must you alpha block first?

A

alpha antagonists - phenoxybenzamine
beta blockers - bisoprolol
surgery

Must alpha block first because otherwise get unopposed alpha antagonism and this can lead to an pheo crisis.

58
Q

What is phenoxybenzamine?

A

Adrenergic Alpha antagonist

59
Q 
What are 
MEN-2
VHL 
NF1 and 
SDHB/SDHD
A

Familial causes of pheochromocytoma and paraganglioma

ESA2 (37 decks)

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