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Endocrine Physiology > Adrenal Physiology > Flashcards

Adrenal Physiology Flashcards

1
Q

What are the 4 layers of the adrenal gland?

A

Glomerulosa
Fasciculata
Reticularis
Medulla

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2
Q

What does the zona glomerulosa mainly secrete?

A

Mineralocorticoids primarily aldosterone for the kidneys

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3
Q

What does the zona fasciculata mainly secrete?

A

Glucocorticoids - cortisol and corticosterone to most cells for glucose and glycogen formation

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4
Q

What does the zona reticularis mainly secrete?

A

Androgens to skin, bones and other tissues

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5
Q

What does the adrenal medulla secrete?

A

Epinephrine and Norepinephrine to most cells

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6
Q

What is the adrenarche?

A

Maturation of zona reticularis in late childhood associated with increased adrenal androgen (DHEA/DHEAS) secretion

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7
Q

What is adrenopause?

A

Decline in DHEA production with age

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8
Q

Where does adrenocorticoid synthesis take place?

A

ER and mitochondria

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9
Q

What does enzyme deficiency alter?

A

Production of ALL adrenocorticoids

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10
Q

What does the zone glomerulosa secrete?

A

Aldosterone

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11
Q

What increases aldosterone secretion?

A

Angiotensin II and K+

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12
Q

What are the zona glomerulosa actions mediated by?

A

Mineralocorticoid receptor

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13
Q

What is the role of aldosterone?

A

Maintenance of electrolyte balance and ECF/plasma volume
Regulates naturesis in renal distal tubule and collecting ducts
Role in acid/base balance

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14
Q

What are the causes of Conn’s Syndrome?

A

Aldosterone secreting adrenal tumour
Adrenal hyperplasia

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15
Q

How does Conn’s Syndrome affect the renal electrolyte and H2O absorption?

A

Electrolyte imbalances (hypernatremia and hypokalemia)
metabolic alkalosis
water retention
low plasma free calcium level

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16
Q

What does hypernatremia and hypokalemia cause in Conn’s Syndrome?

A

Hypern - muscle cramps (neuronal hyperexcitability)
Hypok - muscle weakness (muscle hypo excitability)

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17
Q

What is the treatment for Conn’s SYndrome?

A

Surgery
Spironolactone (aldosterone receptor antagonists)

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18
Q

What is Addison’s Disease?

A

Autoimmune destruction of adrenal cortex

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19
Q

What does Addison’s disease cause?

A

Glucocorticoid (mineralcorticoid) deficiency
Hypoaldosteronism
cardiac arrythmias and low ECF volume

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20
Q

What are two characteristics of the Zona Fasiculata?

A

Pale cells - numerous lipid droplets
Well developed ER and plentiful mitochondria

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21
Q

What does the Zona Fasiculata synthesize?

A

Cortisol
ACTH
Lesser amounts of androgen/estrogen synthesis

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22
Q

What are the Zona Fasiculata actions mediated by?

A

Glucocorticoid receptor

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23
Q

What are the 4 metabolic actions of the glucocorticoids (cortisol and ACTH)?

A

Increase muscle protein catabolism
Increase triglyceride breakdown
Increase hepatic gluconeogenesis
Decrease muscle insulin sensitivity

24
Q

What is cortisol’s effect on immunity and inflammation?

A

Suppress immune and inflammatory response
Inhibit T and B cell function
Inhibit cytokine production

25
Q

What is cortisol’s effect on vasculature?

A

Maintains normal BP and CO

26
Q

What is cortisol’s effect on water and electrolyte balance?

A

Antidiuretic actions (promotes H2O reabsorption)
Increases Na+ reabsorption and K+ excretion

27
Q

What is cortisol’s effect to stress?

A

Metabolic and vascular actions considered beneficial

28
Q

What is the circadian rhythm?

A

Suprachiasmatic nucleus in hypothalamus that is entrained by visual and light/dark cues
Cortisol and ACTH levels increase at night

29
Q

What are 4 causes of Cushing’s Syndrome (hypercortisolism)?

A

Cortisol secreting tumours
Ectoptic tumours secreting ACTH
Pituitary ACTH excess (Cushings Disease)
Prolonged glucocorticoid therapy

30
Q

What are 3 symptoms relating to metabolic actions of cortisol?

A

Hyperglycemia/glucosuria
Insulin resistance
Obesity
purple stripes
females (amenorrhea and hirstusim)

31
Q

What is Addison’s Disease (hypocortisolism)?

A

Autoimmune destruction of adrenal cortex

32
Q

What are the symptoms of Addison’s Disease?

A

Glucocorticoid (and mineralcorticoid) deficiency
Hypocortisolism

33
Q

What does hypocortisolism cause?

A

Hypoglycemia
ACTH excess
MSH excess (hyperpigmentation)

34
Q

What is the difference between cortisol and aldosterone binding?

A

Cortsiol has equal affinity for glucocorticoid and mineralcorticoid receptors
Aldosterone only binds to mineralcorticoids

35
Q

What is the role of HSD11b2 in mineralcorticoid receptors?

A

Minimizes illicit activation of mineralocorticoid receptor by cortisol

36
Q

Where is HSD11b1 highly active?

A

Most metabolically active tissues

37
Q

When is the zona reticularis fully differentiated?

A

At early childhood (6-8 years old)

38
Q

What does the zona reticularis secrete?

A

Adrenal androgen/estrogen synthesis
DHEA
Estrone and estradiol

39
Q

What regulates secretion from the Zona Reticularis?

A

ACTH (not pituitary gonadotrophins)

40
Q

What is the role of DHEA?

A

Development of secondary sexual characteristics in females
Development of male genitalia in pre-pubertal boys

41
Q

What is congenital Adrenal Hyperplasia?

A

Defective adrenal steroidogenesis
21-beta-hydroxylase deficiency

42
Q

What 4 endocrine disturbances does congenital Adrenal Hyperplasia cause?

A

Lowers cortisol production
Lowers mineralocorticoid production
increases male sex steroids
increases ACTH

43
Q

What are 3 other symptoms of congenital Adrenal Hyperplasia?

A

Adrenal hyperplasia
Mineralocorticoid deficiency (salt-wasting form)
Aberrant development of primary/secondary sex characteristics

44
Q

What is the adrenal medulla derived from?

A

Neural crest of embryonic ectoderm

45
Q

What is a nerve ganglion?

A

Cluster of neural bodies outside CNS

46
Q

What are chromaffin cells?

A

Neuroendocrine cells that are modified postganglionic sympathetic neurons

47
Q

What do chromaffin cells release?

A

Epinephrine that acts as a hormone
Norepinephrine (20%)
Adrenergic receptors

48
Q

What are chromaffin cells innervated by?

A

Preganglionic sympathetic neurons

49
Q

What triggers chromaffin cells?

A

Increases sympathetic nervous sytem activity

50
Q

How does endocrine epinephrine differ to sympathetic effects?

A

Lasts 5-10x longer
Affects a wider range of cell types

51
Q

What receptors do E and NE act via?

A

Plasma membrane adrenoreceptors - G protein coupled adrenergic receptors

52
Q

What allows for tissue specificity and multiplicity of action for E and NE?

A

Multiple receptor subtypes
differential ligand binding affinities
different tissue distribution

53
Q

What do the alpha receptors prefer?

A

NE (more involved in neural pathways)

54
Q

What do beta receptors prefer?

A

Epinephrine and increases cyclic AMP

55
Q

What are 4 effects of epinephrine?

A

Increases HR and CO
Increases breakdown of Glycogen and fat
Increases O2 consumption
Increases skeletal muscle flow

56
Q

What is the role of epinephrine in the stress response?

A

Blood flow diverted to vital organs
Increase in HR, peripheral resistance and strength
Increase gluconeogenesis and glycogenolysis

57
Q

What does a tumour of the chromaffin cells cause?

A

Severe hypertension
Hyperglycemia
Increased metabolic rate
arrhythmias
anxiety

Endocrine Physiology (12 decks)

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