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MD4001 Week 10 > 3. The adrenal glands > Flashcards

3. The adrenal glands Flashcards

1
Q

Location of adrenal gland?

A

Lie retroperitoneally on the upper pole of the kidneys

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2
Q

Embryological origin of adrenal cortex and medulla?

A

Adrenal Cortex: arises from intermediate mesoderm

Adrenal Medulla:
Neural crest cells
Chromaffin cells
Modified sympathetic ganglion cells

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3
Q

Layers of the adrenal gland?

A 
Capsule
Zona glomerulosa
Zona Fasciculata
Zona reticularis
Medulla
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4
Q

What hormones are produced by the Zona glomerulosa?

Control and use?

A

Mineralocorticoids – e.g. aldosterone

Controlled by renin – angiotensin

Use:
Electrolyte and fluid homeostasis

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5
Q

What hormones are produced by the Zona Fasciculata?

Control and use?

A

Glucocorticoids – e.g. cortisol

Secretion controlled by ACTH

Use:
Carbohydrate, lipid and protein Metabolism

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6
Q

What hormones are produced by the Zona reticularis?

A

Sex steroids – androgens

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7
Q

What hormones are produced by the medulla?

A

Catecolamines e.g. epinephrine

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8
Q

Adrenal Cortex Produces ______ hormones

A

Adrenal Cortex Produces STEROID hormones

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9
Q

Adrenal Cortex Blood supply?

A

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

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10
Q

Cortex and medulla difference in supply?

A

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

• 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

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11
Q

Adrenal gland involved in …

A

stress response both LONG TERM and SHORT TERM

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12
Q

What makes up the short term stress response by the adrenal gland due to CATECHOLAMINE RELEASE?

A

Increased HR
Increased bp
Liver converts glycogen ot glucose and releases glucose to blood
Brochodilatation
Changes blood distribution causing decreased GI and increased urinary
Increase BMR

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13
Q

What makes up the long term stress response by the adrenal gland due to MINERALOCORTICOID RELEASE?

e.g. aldosterone

A
  1. Retention of Na and water of kidneys

2. Increased BP

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14
Q

What makes up the long term stress response by the adrenal gland due to GLUCOCORTICOID RELEASE?

e.g. cortisol

A
  1. Proteins and fats converted to glucose or broken down for energy
  2. Increased blood glucose
  3. Immune system suppression
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15
Q

Need for ACTH and adrenals

A

Maintains zona glomerulosa hence also mineralocorticoid levels

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16
Q

3 cells where actions of cortisol are located?

A

Muscle
Liver ** mainly for enzyme synthesis involved in gluconeogenesis.
Fat

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17
Q

Action of cortisol at muscle cell

A

Reduces uptake of AA and glucose, which is normally stimulated by insulin

Slows protein synthesis and upregulates proteolysis.

Leads to AA release which contributes to gluconeogenesis at liver cell

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18
Q

Action of cortisol at liver cell

A

Upregulates gluconeogenesis indirectly via enzyme to cause increase in [glucose]

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19
Q

Action of cortisol at fat cell

A

Mainly suppresses glucose uptake to cell.
Limits lipogenesis
So fat stores are being degraded.
Release of glycerol into blood which is then used for gluconeogenesis at liver cells.

ALSO

Lipogenesis is slowed

20
Q

What are the pharmacological effects of cortisol?

A

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

21
Q

Cushing’s disease due to

A

glucocorticoid (e.g. cortisol) excess

22
Q

Causes of cushings?

A
  1. ACTH-releasing pituitary tumour
  2. Ectopic ACTH-releasing tumour (usually in lungs, pancreas or kidney)
  3. Tumour of the adrenal cortex - hyper-secretion of cortisol
  4. Administration of pharmacological doses of glucocorticoid drugs
23
Q

Clinical features of Cushing’s?

A
  1. Hyperglycaemia
  2. Muscle wasting
  3. Increase in FFA in plasma
  4. Increased insulin release
  5. Tissue edema, hypokalemia, hypertension
  6. GIT ulceration
  7. Decreased protein synthesis
24
Q

Cause of hyperglycaemia associated with Cushing’s?

A

Hyperglycaemia due to gluconeogenesis in liver- adrenal/steroid diabetes

25
Q

Cause of muscle wasting associated with Cushing’s?

A

Muscle wasting - loss of protein synthesis in muscle and bone (and most tissues)

26
Q

Cause of increased FFA in plasma associated with Cushing’s?

A

Increase in FFA in plasma (reduced lipogenesis and enhanced lipolysis)

27
Q

Cause of increase insulin release associated with Cushing’s?

A

Increased insulin release - redistribution of fat stores to face, neck, upper trunk
“buffalo hump”; β-cell exhaustion

28
Q

Cause of Tissue edema, hypokalemia, hypertension

A

Tissue edema, hypokalemia, hypertension - due to increased glomerular filtration (glucocorticoid effect) and water and Na+ retention (mineralocorticoid effects)

29
Q

Cause of GIT ulceration associated with Cushing’s?

A

GI Tract ulceration - due to excess H+ secretion and decreased mucous production
(alkalosis due to increased H+ loss in GI tract and kidney)

30
Q

Cause of Decreases in protein synthesis associated with Cushing’s?

A

Decreases in protein synthesis - increased neural excitability, lymph node lysis,
inhibition of haematopoiesis and lymphocyte production,
- immunosuppressive and anti-allergic and anti-inflammatory actions)

31
Q

Treatment of Cushing’s?

A

Treatment:

1. Surgical removal of tumour / decreases in drug dosage

32
Q

Mechanism’s controlling aldosterone secretion i.e. RAAS

A

Stimulating inputs to adrenal cortex:

  • Renin-angiotensin cascade
  • ACTH from Ant Pit
  • Increase [K+]

Aldosterone is released as a mineralocorticoid from the adrenal cortex
Aldosterone acts on the kidneys to cause:
-Renin release
-Na+ and H20 retention. K+ excretion

Renin-angiotensin cascade:

  • -> Renin release
  • -> Conversion of angiotensinogen to angiotensin I @ liver
  • -> Angiotensinogen II
  • -> Back to kidney to increase Na+ and H2O retention
33
Q

Structure of juxta-glomular apparatus

A

The juxtaglomerular apparatus is a specialized structure formed by the distal convoluted tubule and the glomerular afferent arteriole. It is located near the vascular pole of the glomerulus and its main function is to regulate blood pressure and the filtration rate of the glomerulus.

34
Q

What is addison’s disease?

A

Primary adrenal cortical insufficiency

UNDERSECRETION

35
Q

Cause of Addison’s?

A

Primary Causes:

  1. Tuberculosis/ metastatic tumours
  2. Autoimmune adrenalitis - adrenal failure
  3. HIV - decreased immunity and increased viral and bacterial infections
  4. Atrophy due to prolonged steroid therapy
36
Q

Clinical features of Addison’s?

A
  1. Loss of weight/appetite, muscle weakness, nausea, vomiting.
  2. Low plasma glucose esp. after fasting (lack of glucocorticoid actions)
  3. Low plasma Na+ (hyponatriemia) and high plasma K+ (hyperkalaemia) (due to lack of
    mineralocorticoids) .
  4. Dehydration and hypotension due to 3. - systolic blood pressures 50-80 mmHg.
  5. Lethargy and dizziness on standing up due to 4.
  6. Severe cases present with skin pigmentation due to excess ACTH acting as MSH
37
Q

Treatment of addison’s?

A

Treatment:

  1. Glucocorticoid replacement therapy – hydrocortisone administration morning (25mg) /afternoon (12.5 mg)
  2. Intravenous saline infusion if severely dehydrated and condition is life- threatening and administration of fludrocortisone (mineralocorticoid agonist)
38
Q

Development of adrenal medulla?

A

Develops from neural crest cells

39
Q

Cells of the adrenal medulla?

A

• CHROMAFFIN cells produce catecholamines

Two populations of chromaffin cells secrete:
• either Epinephrine (adrenaline) (majority of cells) • or Norepinephrine (noradrenaline)

40
Q

Control of the adrenal medulla?

A

• Controlled directly by preganglionic sympathetic neurones (thus chromaffin cells are equivalent to postganglionic sympathetic neurones)

41
Q

Secretions from adrenal medulla?

A

Chromaffin cells: Adrenaline and NA

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

42
Q

Synthesis of adrenal catecholamines

A
  1. Tyrosine —TH—>
  2. Dopa —AADC—>
  3. Dopamine —- DBH—>
  4. NE—PNMT–>
  5. Epinephrine

*****Process is stimulated by ACTH and SYMPATHETIC stimulation **

1-3 in the cytosol of adrenal cortex cells
4-5 in the chromaffin granule
Storage complex within the chramaffin granule

43
Q

How is glucocorticoid activity suppressed in renal cortical tubular cells?
Result?

A

Normally the cortisol is taken into the tubular cell and metabolised to an inactive metabolite by 11beta-HSD enzyme.
This prevents it from binding to the MR and GR.
Aldosterone, which isn’t metabolised, then occupies the MR and GR
Glycyrrhetinic acid inhibits this 11beta-HSD, hence cortisol binds to MR and GR instead of aldosterone.
(MR= Mineralocortiocoid receptor
GR= Glucocorticoid receptor)

Result?
Cells that are responsive to aldosterone produce effects of both GR and MR

44
Q

Mineralocorticoids e.g. aldosterone
Regulation of release?
Target organ and effect?
Effect of hypersecretion and hyposecretion?

adrenocortical hormone

A

Regulation of release, stimulated by…

  • RAAS due to low blood volume
  • High K or low Na
  • ACTH

Target organ and effect?
Kidneys
–> Increase blood Na and volume

Effect of hypersecretion and hyposecretion?

  • High is aldosteronism
  • Low is Addison’s disease
45
Q

Glucocorticoids e.g. cortisol
Regulation of release?
Target organ and effect?
Effect of hypersecretion and hyposecretion?

adrenocortical hormone

A

Regulation of release?

  • Stimulation by ACTH
  • Inhibition by neg feedback
Target organ and effect?
At body cells
-->Gluconeogenesis and hyperglycaemia
--> Mobilise fats for energy metabolism
--> Protein catabolism 
--> Inflammation and immune suppression

Effect of hypersecretion and hyposecretion?

  • High is Cushing’s
  • Low is Addison’s
46
Q

Gonadocorticiods e.g. testosterone
Regulation of release?
Target organ and effect?
Effect of hypersecretion and hyposecretion?

adrenocortical hormone

A

Regulation of release?
-stimulation by ACTH

Target organ and effect?
Source of libido
Pubic and axillary hair growth
Oestrogen source post-menopause

Effect of hypersecretion and hyposecretion?

  • High is virilisation of females
  • Low has nil effect
47
Q

Catecholamines e.g. epinephrine
Regulation of release?
Target organ and effect?
Effect of hypersecretion and hyposecretion?

adrenal medullary hormone

A

Regulation of release?
Preganglionic sympathetic NS

Target organ and effect?
Symp target organs
–> Increase HR and BMR
–> Vasoconstriction leads to increase bp

Effect of hypersecretion and hyposecretion?
-High is prolonged f-or-f response and hypertension

MD4001 Week 10 (11 decks)

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