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MD4001 Physiology > The Adrenal Glands > Flashcards

The Adrenal Glands Flashcards

1
Q

The superior, middle and inferior adrenal arteries arise from what?

A
  • Inferior phrenic
  • Abdominal aorta
  • Renal
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2
Q

What does the adrenal cortex arise from?

A

Intermediate mesoderm

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3
Q

What does the adrenal medulla arise from?

A

Neural crest cells

  • Chromaffin cells
  • Modified sympathetic ganglion cells
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4
Q

Where do the adrenal glands lie in relation to the peritoneum?

A

Retroperitoneally

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5
Q

What surrounds the adrenal glands?

A

Capsule

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6
Q

What are the 3 layers of the adrenal cortex?

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
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7
Q

What hormones are produced by the cells in the zona glomerulosa?

A

Mineralcorticoid - e.g aldosterone

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8
Q

What hormones are produced by the cells in the zona fasciculata?

A

Glucocorticoids (e.g cortisol)

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9
Q

What hormones are produced by the cells in the zona reticularis?

A

Androgens (DHEA and androstenedione)

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10
Q

How are the cells structured in the zona faciculata?

A
  • Large
  • Arranged in columns which twist and turn
  • Blood vessels run along the side
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11
Q

How are the cells structured in the zona reticularis and glomerulosa?

A

Random assortment (smaller in size than fasciculata)

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12
Q

What are the features of the cells in the adrenal cortex?

A
  • Nuclei located centrally
  • Lots of smooth and rough endoplasmic reticulum
  • Many mitochondria
  • Lots of lipid droplets
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13
Q

What are the features of chromaffin cells (on staining)?

A
  • Smaller cells
  • Loosly aranged
  • Densly staining vesicles
  • Lots of rough endoplasmic reticulum
  • Lots of pre-ganglionic sympathetic nerve terminals
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14
Q

What is the function of mineralocorticoids? (produced by zona glomerulosa)

A

Electrolyte and fluid homeostasis (controlled by renin)

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15
Q

What is the function of glucocorticoids? (produced by zona fasciculata)

A

Carbohydrate, lipid and protein metabolism (particularly in starved state)

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16
Q

What is secretion of glucocorticoids produced by the zona fasciculata controlled by?

A

ACTH

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17
Q

Desribe the adrenal cortex blood supply?

A
  • Superior, middle and inferior adrenal arteries
  • Anastomose under the capsule
  • Short cortical arteries run in parallel with the cords of cells to the medulla
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18
Q

What is the blood supply to the medulla?

A
  • Blood which has drained from the cortex
  • Contains adreno-corticosteroids which influence the production of adrenaline by the medullary cells
  • Fresh arterial blood in long cortical arteries
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19
Q

What part of the adrenal gland is involved in the short term stress response?

A

Adrenal medulla

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20
Q

What part of the adrenal gland is involved in the long term stress response?

A

Adrenal cortex

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21
Q

What are the effects of the short-term stress response by the adrenal medulla?

A
  • Increased HR
  • Increased BP
  • Liver converts glycogen to glucose and releases glucose to blood
  • Dilation of bronchioles
  • Changes in blood flow patterns leading to decreased digestive system activity and reduced urine output
  • Increased metabolic rate
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22
Q

What are the effects of the long-term stress response by the adrenal cortex?

A 
Mineralocorticoids 
- Retention of Na+ and water by kidneys 
- Increased blood volume and BP
Glucocorticoids 
- Proteins and fats converted to glucose or broken down to energy 
- Increased blood glucose 
- Suppression of immune system
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23
Q

What hormone produced in the anterior pituitary stimulates the adrenal cortex?

A

ACTH

- Mainly glucocorticoids (e.g cortisol)

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24
Q

What hormone stimulates the release of ACTH?

A

CRH (corticotropin-releasing hormone)

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25
Q

What is the main purpose / actions of cortisol?

A

To increase blood glucose through increasing gluconeogenesis and decreasing protein synthesis and lipogenesis

  • Glycerol, fatty acids and amino acids used for gluconeogenesis
  • Anti-insulin effect
  • Role in ability to cope with physical (trauma, infection, allergies) or neurological (anxiety, restraint) stresses
  • Anti-inflammatory, Anti-allergic and Anti-immune ations
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26
Q

What is hydrocortisone?

A
  • Immuno-suppressive
  • Anti-inflammatory / anti-allergic and anti-immune actions
  • Interferes in cytokine production and protein-synthesis
  • Can be used in transplants
  • Analog of cortisol
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27
Q

What can be the causes of Cushing’s disease?

A
  • ACTH-releasing pituitary tumour (70-75%)
  • Ectopic ACTH-releasing tumour (usually in lungs, pancreas or kidney)
  • Tumour of adrenal cortex - hyper-secretion of cortisol
  • Administration of pharmacological doses of glucocorticoid drugs (e.g hydrocortisone)
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28
Q

What is Cushings disease due to?

A

Excess glucocorticoid release (cortisol)

29
Q

What are the clinical features of cushing’s disease?

A
  • Hyperglycaemia due to increased 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)
  • Increase in insulin release - redistribution of fat stores to face, neck, upper trunk “buffalo hump”, Beta-cell exhaustion
  • Tissue oedema, hypokkaelemia, hypertension - due to increased glomerular filtration (glucocorticoid effect) (leaky podocytes) and water and Na+ retention (mineralcorticoid effect)
  • 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
30
Q

How is Cushing’s disease treated?

A

Surgical removal of tumour / decreases in drug dosage

31
Q

Aldosterone release from the adrenal cortex is under the control of what 3 factors?

A
  • Increase in plasma K+ (causes depolarisation of zona glomerulosa cells)
  • ACTH - mainly allows the glomerulosa cells to be able to respond to other external stimuli
  • Angiotensin II (mainly) - directly binds to receptors and directly stimulates the synthesis of aldosterone
32
Q

What organ does aldosterone effect?

A

Kidney - receptors

33
Q

What cells does aldosterone affect?

A

Principle cells in collecting ducts and distal collecting tubule where it stimulates reabsorption of Na+ and excretion of K+ and H+

34
Q

What does renin break down?

A

Angiotensinogen into angiotensin I

35
Q

What breaks down agiotens I to angiotensin II

A

ACE in lung

36
Q

What is the main function of aldosterone?

A

Increases Na+ reabsorption in kidney

37
Q

What cells produce renin?

A

juxtaglomerular cells

38
Q

What are the epithelial cells of the distal tubule called?

A

Macula densa cells

39
Q

What does the macula densa sense?

A

The Na/Cl content of the tubular fluid

40
Q

How much more prevelant is cortisol compared with aldosterone levels?

A

50 - 100 x higher

41
Q

Why is aldosterone more important in affecting principle cells than cortisol?

A

Cortisol is broken down by 11 Beta-HSD to cortisone which can not bind to glucocorticoid or mineralocorticoid receptors

42
Q

What breaks down cortisol to cortisone?

A

11 Beta-HSD

43
Q

What inhibitis 11 Beta-HSD?

A

Glycyrrhetinic acid (found in liquorice)

  • Results in mass Na+ recovery
  • Increased BP and volume
44
Q

What is Addison’s disease also known as?

A

Primary adrenal cortical insufficiency

45
Q

What are the primary causes of Addison’s disease?

A
  • Tuberculosis / metastic tumours
  • Autoimmune adrenalitis - adrenal failure (most common ~70% )
  • HIV - decreased immunity and increased viral and bacterial infections
  • Atrophy due to prolonged steroid therapy
46
Q

What are the clinical features of Addison’s disease?

A
  1. Loss of weight / appetite, muscle weakness, nausea, vomitting
  2. Low plasma glucose esp. after fasting (lack of glucocorticoid actions)
  3. Low plasma Na+ (hyponatriemia) and high plasma K+ (hyperkalemia) (due to lack of mineralocorticoids) (metabolic acidosis?)
  4. Dehydration and hypotension due to 3 - systolic BP 50-80 mmHg
  5. Lethargy and dizziness on standing up due to 4
  6. Severe cases present with skin pig,entation due to excess ACTH acting as MSH
47
Q

How is Addison’s disease treated?

A
  • Glucocorticoid replacement therapy - hydrocortisone administration morning (25 mg) / afternoon (12.5 mg)
  • IV saline infusion if severely dehydrated and condition is life-threatening and administration of fludrocortisone (mineralocorticoid agonist)
48
Q

What are the cells called in the adrenal medulla?

A

Chromaffin cells

49
Q

What are chromaffin cells controlled directly by?

A

Preganglionic sympathetic neurons (thus chromaffin cells are equivalent to postganglionic sympathetic neurons)

50
Q

What do the 2 populations of chromaffin cells secrete?

A
  • Adrenaline (epinephrine) (majority)

- Noradrenaline (NA)(norepinephrine)

51
Q

What are chromaffin cells also known to secrete other than NA and adrenaline?

A
  • Dopamine

- Enkephalins (pain control)

52
Q

Catecholamine synthesis:

A 
Tyrosine 
- Tyrosine hydroxylase (TH)
Dihydroxy-phenylalanine (Dopa)
- Amino acid decarboxylase (AADC)
Dopamine 
- Dopamine-Beta-hydroxylase  (DBH)
Norepinephrine / NA
- Phenylethanolamine-N-methyltransferase (PNMT)
Adrenaline / Epinephrine
53
Q

What activates Tyrosine hydroxylase (TH) and Dopamine-Beta-hydroxylase (DBH)?

A

Sympathetic stimulation; ACTH

54
Q

What activates Phenylethanolamine-N-methyltransferase (PNMT)?

A

Cortisol from adrenal cortex via portal circulation

55
Q

What molecule in the catecholamine synthesis pathway is the first to enter the chromaffin granule?

A

Dopamine

56
Q

What does dopamine enter the chromaffin granule via?

A

Vesicular mono-amine transporter (VMAT1)

- Dopamine exchanged for H+

57
Q

How is a high concentration of H+ maintained in the chromaffin granules?

A

H+ ATPase

58
Q

Where is NA converted to Adrenaline?

A

Cytosol by Phenylethanolamine-N-methyltransferase (PNMT)

59
Q

What protein stores NA and adrenaline inside the chromaffin granule?

A

Chromatogranin (along with Ca2+ and ATP) creating storage complex - prevents granule swellin gup / osmotic affects

60
Q

How can adrenaline enter the chromaffin granule?

A

VMAT (in exchange of H+)

61
Q

What causes chromaffin granule exocytosis?

A

Depolarisation by sympathetic stimulation

62
Q

What catecholamine has a higher affinity to alpha-adrenergic receptors?

A

NA

63
Q

What catecholamine has a higher affinity to Beta-adrenergic receptors?

A

Adrenaline

64
Q

What catecholaime causes an increase in cAMP production?

A

Adrenaline (NA decreases)

65
Q

What catecholaime causes an increase in calcium?

A

Adrenaline (NA decreases)

66
Q

What catecholamine increases insulin secretion?

A

Adrenaline (NA decreases)

67
Q

What are the effects of catecholamines of parathyroid?

A
  • Adrenaline increases secretion

- NA decreases secretion

68
Q

How do NA and adrenaline affect renin?

A

Both increase renin secretion

69
Q

Which catecholamine causes SM contraction?

A

NA (adrenaline no effect)

MD4001 Physiology (22 decks)

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