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MD4001 WEEK 10 > The adrenal glands > Flashcards

The adrenal glands Flashcards

1
Q

Describe the location of the adrenal glands.

A

Lie retroperitoneally on the upper pole of the kidneys

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2
Q

How does the adrenal cortex arise?

A

arises from intermediate mesoderm

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3
Q

How does the adrenal medulla arise?

A
  • Develops from neural crest cells
  • CHROMAFFIN cells produce catecholamines
  • Controlled directly by preganglionic sympathetic neurones
    (thus chromaffin cells are equivalent to postganglionic sympathetic neurones)
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4
Q

Describe the anatomy of the adrenal gland.

A 
EXTERNAL TO INTERNAL:
Capsular artery
Capsule
Zona glomerulosa
Zona fasciculata
Zona reticularis
Medulla
Medullary vein
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5
Q

What hormones are released from the medulla?

A

Epinephrine

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6
Q

What hormones are synthesized and released from the zona reticularis?

A

Androgens (DHEA and androstenedione)

and cortisol

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7
Q

What hormones are synthesized and released from the zona fasciculata?

A

Glucocorticoids (e.g.. cortisol)

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8
Q

What hormones are synthesized and released from the zona glomerulosa?

A

Mineralocorticoid (aldosterone)

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9
Q

What is secreted and controls secretion from the zona glomerulosa?
What is it involved in?

A
  • Mineralocorticoids – e.g. aldosterone
  • Controlled by renin – angiotensin
  • Involved in: Electrolyte and fluid homeostasis
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10
Q

What is secreted and controls secretion from the zona fasciculata.
What is it involved in?

A
  • Glucocorticoids – e.g. cortisol
  • Secretion controlled by ACTH
  • Involved in: Carbohydrate, lipid and protein Metabolism
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11
Q

What is secreted and controls secretion from the zona reticularis.
What is it involved in?

A

Sex steroids – androgens

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12
Q

Describe the blood supply of the adrenal cortex.

A

Supplied by the superior middle and inferior adrenal arteries; anastomose under the capsule

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13
Q

Describe the effects of the short term stress response.

A
  1. Increased heart rate
  2. Increased blood pressure
  3. Liver converts glycogen to glucose and releases glucose to blood
  4. Dilation of bronchioles
  5. Changes in blood flow patterns leading to decreased digestive system activity and reduced urine output
  6. Increased metabolic rate
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14
Q

Describe the effects of the long term stress response.

A

MINERALOCORTICOIDS:

  1. Retention of sodium and water by kidneys
  2. Increased blood volume and blood pressure

GLUCOCORTICOIDS:

  1. Proteins and fats converted to glucose or broken down for energy
  2. Increased blood glucose
  3. Suppression of the immune system
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15
Q

What is the role of cortisol?

A

Major role in ability to cope with physical (trauma, infection, allergies) or neurological (anxiety, restraint) stresses

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16
Q

Describe the pharmacology of cortisol.

A

anti-inflammatory / anti-allergic / anti-immune actions

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17
Q

What is Cushing’s disease?

A

glucocorticoid excess

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18
Q

What are the causes of Cushing’s disease?

A
  • ACTH-releasing pituitary tumour
  • Ectopic ACTH-releasing tumour (usually in lungs, pancreas or kidney)
  • Tumour of the adrenal cortex - hyper-secretion of cortisol
  • Administration of pharmacological doses of glucocorticoid drugs
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19
Q

What are the clinical features of Cushing’s disease?

A
  • Hyperglycaemia due to gluconeogenesis in liver- adrenal/steroid diabetes
  • Muscle wasting - loss of protein synthesis in muscle and bone (and most tissues)
  • Increase in FFA in plasma (reduced lipogenesis and enhanced lipolysis)
  • Increased insulin release - redistribution of fat stores to face, neck, upper trunk
    “buffalo hump”; β-cell exhaustion
  • Tissue edema, hypokalemia, hypertension - due to increased glomerular filtration
    (glucocorticoid effect) and water and Na+ retention (mineralocorticoid effects)
  • GI Tract ulceration - due to excess H+ secretion and decreased mucous production
    (alkalosis due to increased H+ loss in GI tract and kidney)
  • Decreases in protein synthesis - increased neural excitability, lymph node lysis,
    inhibition of haematopoiesis and lymphocyte production,
  • immunosuppressive and anti-allergic and anti-inflammatory actions)
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20
Q

What are the treatments for Cushing’s disease?

A

Surgical removal of tumour / decreases in drug dosage

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21
Q

What is Addison’s disease?

A

primary adrenal cortical insufficiency

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22
Q

What are the primary causes of Addison’s disease?

A
  • Tuberculosis/ metastatic tumours
  • Autoimmune adrenalitis - adrenal failure
  • HIV - decreased immunity and increased viral and bacterial infections
  • Atrophy due to prolonged steroid therapy
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23
Q

What are the clinical features of Addison’s disease?

A
  • Loss of weight/appetite, muscle weakness, nausea, vomiting.
  • Low plasma glucose esp. after fasting (lack of glucocorticoid actions)
  • Low plasma Na+ (hyponatriemia) and high plasma K+ (hyperkalaemia) (due to lack of
    mineralocorticoids) .
  • Dehydration and hypotension due to 3. - systolic blood pressures 50-80 mmHg.
  • Lethargy and dizziness on standing up due to 4.
  • Severe cases present with skin pigmentation due to excess ACTH acting as MSH
24
Q

What is Addison’s disease?

A

primary adrenal cortical insufficiency

25
Q

What do the two populations of chromatin cells secrete?

A

Either:
Epinephrine (adrenaline) (majority of cells) OR
Norepinephrine (noradrenaline)

Also been shown to secrete:
Dopamine
Enkephalins (pain control)

26
Q

What are the adrenocortical hormones?

A
  • Mineralocorticoids (chiefly aldosterone)
  • Glucocorticoids (chiefly cortisol)
  • Gonadocorticoids (chiefly androgens, converted to testosterone or estrogens after release)
27
Q

What are the adrenal medullary hormones?

A
  • Catecholamines (epinephrine and norepinephrine)
28
Q

Describe the regulation of release of Mineralocorticoids.

A

Stimulated by renin-angiotensin mechanism (activated by decreasing blood volume or blood pressure), elevated K+ or low Na+ blood levels, and ACTH (minor influence)

Inhibited by increased blood volume and pressure, increased Na+ and decrease K+ blood levels

29
Q

Describe the target organs and effects of Mineralocorticoids.

A

Kidneys: increase blood levels of Na+ and decrease blood levels of K+; since water reabsorption accompanies sodium retention, blood volume and blood pressure rise.

30
Q

Describe the effects of hyper-secretion and hypo-secretion of Mineralocorticoids.

A

HYPERSECRETION:
Aldosteronism

HYPOSECRETION:
Addison’s disease

31
Q

Describe the regulation of release of Glucocorticoids.

A

Stimulated by ACTH

Inhibited by feedback inhibition exerted by cortisol

32
Q

What are the adrenal medullary hormones?

A
  • Catecholamines (epinephrine and norepinephrine)
33
Q

Describe the effects of hyper-secretion and hypo-secretion of Glucocorticoids.

A

HYPERSECRETION:
Cushing’s syndrome

HYPOSECRETION:
Addison’s disease

34
Q

Describe the regulation of release of Gonadocorticoids.

A

Stimulated by ACTH

Mechanism of inhibition incompletely understood, but feedback inhibition not seen

35
Q

Describe the target organs and effects of Gonadocorticoids.

A

Insignificant effects in males

Responsible for female libido; development of pubic and axillary hair in females; source of estrogen after menopause

36
Q

Describe the effects of hyper-secretion and hypo-secretion of Gonadocorticoids.

A

HYPERSECRETION:
Virilization of females (adrenogenital syndrome)

HYPOSECRETION:
No effects known

37
Q

Describe the regulation of release of Gonadocorticoids.

A

Stimulated by ACTH

Mechanism of inhibition incompletely understood, but feedback inhibition not seen

38
Q

Describe the target organs and effects of Gonadocorticoids.

A

Insignificant effects in males

Responsible for female libido; development of pubic and axillary hair in females; source of estrogen after menopause

39
Q

Describe the effects of hyper-secretion and hypo-secretion of Gonadocorticoids.

A

HYPERSECRETION:
Virilization of females (adrenogenital syndrome)

HYPOSECRETION:
No effects known

40
Q

Describe the regulation of release of Catecholamines;

A

Stimulated by preganglionic fibres of the sympathetic nervous system

41
Q

Describe the target organs and effects of Catecholamines.

A

Sympathetic nervous system target organs: Effects mimic sympathetic nervous system activation; increases heart rate and metabolic rate; increase blood pressure by promoting vasoconstriction

42
Q

Describe the effects of hyper-secretion and hypo-secretion of Catecholamines.

A

HYPERSECRETION:
Prolonged fight or flight response; hypertension

HYPOSECRETION:
Unimportant

43
Q

What arteries does the cortex receive?

A

Cortex receives short cortical arteries run in parallel with the cords of cells to the medulla

44
Q

What blood does the medulla receive?

A
  • Medulla receives:
    • blood draining from the cortex (containing
    adreno-corticosteroids which influence the production of adrenaline by the medullary cells)
    • fresh arterial blood in long cortical arteries
45
Q

Describe the process of the short term stress response.

A
  • Impulses passing through the spinal cord
  • Go to preganglionic sympathetic fibres
  • Release acetylcholine to nerve endings in medulla
  • Stimulates chromatin cells to release catecholamines
46
Q

Describe the process of the long term stress response.

A
  • Stress occurs for long time
  • Stimulates release of CRH from hypothalamus
  • Travels down capillary networks down into anterior pituitary
  • Binds to corticotrophs cells of anterior pituitary
  • This stimulates release of ACTH
  • ACTH goes to the adrenal cortex to bind to cells in the zona reticular and fasciculate to stimulate synthesize and release of glucocorticoid (cortisol)
47
Q

What three inputs do the zona glomerulosa cells respond to?

A
  • ACTH
  • Increased plasma potassium (depolarizes plasma membrane)
  • Angiotensin II
48
Q

Describe the process of the short-term stress response.

A

Impulses passing down through the spinal cord into preganglionic sympathetic fibres release acetylcholine, which goes to nerve endings in the medulla to stimulate chromaffin cells to release catecholamines

49
Q

Describe the process of the long-term stress response.

A

If stress occurs for a longer time, it stimulates the release of CRH from the hypothalamus. This travels down capillary networks and down the anterior pituitary. Binds to corticotrophs, stimulating the release of ACTH. ACTH goes to the adrenal cortex to stimulate the release of mineralocorticoids and glucocorticoids.

50
Q

What are the actions of cortisol?

A

Stimulate gluconeogenesis in the liver cells (produced enzymes important for it)
Inhibit protein synthesis in the muscle cells
Inhibit lipogenesis in the fat cells

51
Q

What is the treatment for Addison’s disease?

A

Glucocorticoid replacement therapy - hydrocortisone administration (25mg in morning, 12.5mg in afternoon)
Intravenous saline infusion if severely dehydrated and condition is life threatening, and administrating of fludrocortisone (mineralocorticoid agonist)

52
Q

What is the precursor for catecholamines?

A

L-Tyrosine

53
Q

What is the action of tyrosine hydroxyls?

A

Converts L-Tyrosine to L-Dopa

Rate limiting step

54
Q

What is the action of amino acid decarboxylase?

A

Converts L-Dopa to dopamine

55
Q

What is the action of Dopamine B- hydroxylase?

A

Converts dopamine to noradrenaline

56
Q

What converts norepinephrine to epinephrine?

A

Phenylthanolamine-N-methyltransferase

MD4001 WEEK 10 (12 decks)

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