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MBBS II ERS > L19 -Physiology of adrenal cortex and medulla > Flashcards

L19 -Physiology of adrenal cortex and medulla Flashcards

1
Q

Define the 3 layers of adrenal cortex and the hormone produced?

A

Zona glomerulosa - Mineralcorticoids: Aldosterone

Zona Fasciculata: Glucocorticoids: Cortisol

Zona Reticularis: Androgens

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2
Q

Organelle for production of andrenocortical steroids?

A

ER and mitochondria

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3
Q

Describe the first rate-limiting step in steroidogenesis?

A

transfer of cholesterol from the cytoplasm to the inner mitochondrial membrane:

regulated by steroidogenic acute regulatory protein (StAR protein)

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4
Q

Describe the formation for the immediate precursor of all steroid hormones?

A

Cholesterol –[CYP11A1]–> Pregnenolone**

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5
Q

How is the synthesis of different steroids controlled in the adrenal cortex?

A

Depends on type of enzyme expressed in each cortical zone

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6
Q

Explain why hypersecretion of cortisol can lead to hyperaldosteronism?

A

CYP11B1 = form Cortisol in Zona Fasciculata

CYP11B2 = form Aldosterone in Zona glomerulosa

Loci for the 2 enzymes are closely related, hyperactivation could occur concurrently

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7
Q

Describe the cellular effect of Aldosterone?

A

1) Aldosterone bind to mineralcorticoid receptor (MR) in DCT
2) Aldosterone- MR complex translocate into nucleus&raquo_space; bind HRE in regulatory region of target gene promoters

3)
i) Induction of Na+/K+-ATPase expression on the basolateral membrane

ii) Activate epithelial Na+ channel (ENaC) and renal outer medullary K+ channel (ROMK) on apical membrane

> > > > Na+ reabsorption and K+ excretion + water reabsorption

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8
Q

Describe the regulation of Aldosterone secretion (renin-angiotensin system)?

A

Low Na, Low BP or High K:

1) JG cells secrete renin&raquo_space; convert angiotensin to angiotensin- I from liver
2) Angiotensin converting enzyme in pulmonary blood: convert angiotensin-I to II
3) Angiotensin-II bind to Angiotensin-II receptor on adrenal cortex
4) Increase aldosterone secretion

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9
Q

List the physiological effects of aldosterone?

A

Increase sodium and water retention&raquo_space; increase extracellular fluid volume&raquo_space; increase BP

Increase K secretion

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10
Q

List 3 causes of hyperaldosteronism?

A

1) Functional adenoma (Conn syndrome)
2) Inherited CYP11B2 hyperactivity
3) Renovascular diseases» abnormal renin-angiotensin system activation

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11
Q

Symptoms of hyperaldosteronism?

A

Alkalosis

Shallow respiration
Irritability
Constipation

Weakness, Lethargy
Arrhythmia, Weak pulse

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12
Q

Explain how hyperaldosteronism cause alkalosis?

A
  • Increased excretion of K in kidney
  • Low K stimulates H+/K+- ATPase in collecting duct
  • Excrete H+ to retain K
  • Less [H+] = alkalosis
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13
Q

Explain how hyperaldosteronism causes muscle weakness?

A

Decrease extracellular K increases the -ve membrane potential across membrane

> > more difficult to fire AP

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14
Q

List 4 causes of hypoaldosteronism?

A

1) Adrenal insufficiency (primary, secondary, tertiary)
2) Aldosterone synthase deficiency (CYP11B2 loss of function)
3) Renal insufficiency due to diabetic nephropathy
4) Anti-hypertensive drugs e.g. ACEi, ARB, Renin inhibitors

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15
Q

Symptoms of hypoaldosteronism?

A

All due to hyperkalemia:

  • Hypotension, circulatory shock
  • Arrhythmia, cardiac toxicity
  • Muscle cramps, Abdominal cramping
  • Metabolic acidosis
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16
Q

Which brain regions stimulate the hypothalamic corticotropin-releasing hormone (CRH) neurons in the hypothalamic-pituitary-adrenal (HPA) axis ?

A

1) Brainstem: Nucleus tractus solitarius&raquo_space; stimulate under major distress: blood loss, respiratory distress, pain
2) Amygdala&raquo_space; stimulate under negative emotions, fear, emotion
3) Hippocampus&raquo_space; suppress** HPA to regulate stress

17
Q

Describe the different action of cortisol to alter gene transcription?

A

Glucocorticoid/Cortisol activate glucocorticoid receptor (GR):

1) GR bind with glucocorticoid responsive elements (GRE) = enhance gene transcription
2) GR bind with CREB = repression of gene transcription

18
Q

Summarize the effects of cortisol on energy metabolism? (4)

A
  • Increases expression of liver enzymes for gluconeogenesis
  • Increase muscle proteolysis
  • Inhibit insulin secretion and trigger apoptosis of pancreatic β cells
  • Impairs glucose uptake in peripheral tissues (stop GLUT-4 traffick)
19
Q

Summarize the effects of cortisol on bones and connective tissue?

A
  • Increase bone resorption by inducing Oct maturation (RANKL)
  • Reduces bone formation by inhibiting Ob prolif.
  • Inhibit chondrocyte function in cartilage
  • Inhibit fibroblast proliferation and collagen formation
20
Q

Summarize the effects of cortisol on inflammation and immunity?

A
  • Inhibit mast cell degranulation
  • Decrease T cell in circulation and migration
  • Promote atrophy of thymus + lymphoid tissue
  • Repress pro-inflammatory cytokines production
  • Antipyretic: lower IL-1 release
21
Q

Summarize the effects of cortisol on reproductive function?

A
  • Decrease GnRH release from hypothalamus (like prolactin)

- Inhibit synthesis and release of LH and FSH from pituitary

22
Q

List some synptoms of Cushing’s syndrome?

A 
Hyperglycemia 
Increase risk of infection 
High BP 
Fat redistribution, central obesity 
Osteoporosis
23
Q

Compare the contribution of adrenal androgens in male and female?

A

Male = negligible

Female = 50% circulating active androgens, needed for growth of axillary and pubic hair + libido

24
Q

Explain why Cushing disease can lead to polycystic ovarian syndrome?

A

Cushing disease: Large increase in ACTH:

Stimulate MC2R on Zona fasciulata&raquo_space; Produce cortisol&raquo_space; negative feedback on hypothalamus and pituitary

Stimulat MC2R on Zona reticularis&raquo_space; increase androgen production but NO NEGATIVE FEEDBACK

Excessive androgen = hirsutism and ovarian dysovulation

25
Q

Cause of polycystic ovarian syndrome? Symptoms?

A

Elevated testosterone in female&raquo_space; affect development and release of eggs during ovulation&raquo_space; abnormal eggs in ovary cause thickening

  • Lack of ovulation
  • Lack/ irregular menstruation
  • Facial hair, acne, pelvic pain
  • infertile
26
Q

Site of catecholamine production? Which type predominante?

A

Adrenal medulla: Chromaffin cells

Epinephrine/ Adrenaline = 80%

NE = 20%

27
Q

Describe the regulation of Epinephrine/ NE release?

A

1) Sympathetic preganglionic neuron synapse at chromaffin cells
» increase Tyrosine Hydroxylase activity (rate-limiting)
» Convert Tyrosine to Dopa&raquo_space; to NE/E

2) Cortisol from adrenal cortex induce PNMT expression&raquo_space; increase NE to Epinephrine conversion

28
Q

Describe how Amygdala controls NE and Epinephrine release? Mechanism of NE/E release?

A

Stress&raquo_space; amygdala&raquo_space; Ach from sympathetic preganglionic fiber&raquo_space; chromaffin cell nicotinic receptor

Membrane depol. + Ca entry&raquo_space; activate tyrosine hydroxylase&raquo_space; secrete catecholamines

29
Q

Compare the trigger and functions of α and β adrenergic receptors?

A

α1= bind NE and Epinephrine&raquo_space; GPCR coupled to Gaq&raquo_space; activate PLC&raquo_space; IP3 and DAG&raquo_space; Ca signalling

α2 = bind NE/E&raquo_space; GPCR coupled to Gai&raquo_space; decrease cAMP production

β1 and β2 = bind epinephrine only&raquo_space; GPCR coupled to Gas&raquo_space; cAMP production

30
Q

List some physiological effects caused by both NE and Epinephrine

A

Increase glycogenolysis

Increase gluconeogenesis

Increase cardiac contractility, BP, respiration rate

31
Q

List some physiological effects caused by ephinephrine more than NE?

A

Primarily stimulate β** adrenergic receptor:

Lipolysis ****
Calorigenesis 
Glucagon secretion 
Muscle K uptake 
Increase HR ****
32
Q

List some physiological effects caused by NE more than epinephrine?

A

Primarily stimulate α** adrenergic receptor:

  • Increase arteriole vasoconstriction
  • Increase sphicter contraction
  • Increase platelet aggregation
  • Dilation of pupils
33
Q

List some long term stress response due to chronic NE/E release?

A
  • Increased proteolysis and lipolysis
  • Increased blood glucose
  • Suppressed immune system
  • Adrenal fatigue (weaken, unable to make cortisol)

Alteration of glycogen stores only in short-term response

34
Q

Clinical manifestation of adrenal catecholamine deficiency?

A

None

No clinical consequences

35
Q

Symptoms of adrenal fatigue?

A
  • Chronic fatigue
  • Hunger and weight change
  • Emotional instability
  • Frequent urination
36
Q

Give one cause of adrenal catecholamine hypersecretion?

A

Pheochromocytoma

MBBS II ERS (37 decks)

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