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MEH > 10.1 Adrenal glands > Flashcards

10.1 Adrenal glands Flashcards

1
Q

Where are the adrenal glands situated?

A

Above the kidneys. Enclosed in the renal fascia lata but not part of the kidneys and have a different embryological origin.

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2
Q

Describe the structure of the adrenal glands

A

From outer to inner:
Fibrous capsule
Capsule (Zona Glomerulosa, Zona Fasiculata, Zona reticularis)
Medulla (chromatin cells)

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3
Q

What is the function of the layers of the cortex of the adrenal gland?

A

Salt sugar sex

  1. Zona glomerulosa. Outermost layer secretes mineralcorticoids such as aldosterone. Aldosterone regulates the reabsorption of sodium in the kidney nephrons. SALT
  2. Zona fasiculata. Middle layer secretes glucocorticoids such as cortisol. Cortisol can regulate blood sugar by gluconeogenesis from proteins in the liver. SUGAR
  3. Zona reticularis. Innermost layer secretes glucocorticoids and a small amount of androgens. Androgens such as testosterone is a sex hormone. SEX
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4
Q

What is the function of chromaffin cells?

A

Chromaffin cells act as part of the sympathetic branch of the autonomic nervous system. Releases the amines adrenaline (80%) and noradrenaline (20%) into the bloodstream - endocrine function.

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5
Q

Name the corticosteroids released in the adrenal cortex

A

Zona glomerulosa = mineralcorticoids (aldosterone)
Zona Fasiculata = Glucocorticoids (cortisol, corticosterone, cortisone)
Zona Reticularis = Androgens ( Dehydroepiandrosterone, Androstenedione which is converted to oestrogen and testosterone in peripheral systems.

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6
Q

What are all steroid hormones derived from?

A

Synthesised from cholesterol in adrenal glands and gonads.

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7
Q

What is the mode of action of steroid hormones?

A

As steroid hormones are all derived from cholesterol, they are all lipid soluble. This allows them to diffuse across the plasma membrane with ease.
Steroid hormones bind to receptors of the nuclear receptor family within cells. Binding causes dissociation of chaperone proteins such as heat shock protein 90. Receptor ligand complex translocates to the nucleus. Dimerisation with other receptors can occur. Receptors bind to glucocorticoid response element (GREs) or other transcription factors to modulate gene transcription.

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8
Q

Why is the mode of action of steroid hormones typically much slower than other water soluble hormones?

A

Steroid hormones bind to nuclear receptor to modify gene transcription. Other hormones bind to receptor to modify an existing enzyme/protein. Therefore steroid hormone effects are much slower as the proteins have not yet been formed.

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9
Q

What is the most abundant mineralcorticoid?

A

Aldosterone

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10
Q

Where is aldosterone synthesised?

A

Zona Glomerulosa

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11
Q

How does aldosterone travel in the bloodstream?

A

Lipophillic so cannot travel freely. Travels bound to carrier proteins such as serum albumin and to a lesser extent transcortin.

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12
Q

Describe the aldosterone receptor

A

Aldosterone receptor is intracellular & exerts its actions by regulating gene transcription

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13
Q

What is the function of aldosterone?

A

Plays central role in regulation of plasma Na+, K+ and arterial blood pressure by regulating blood volume

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14
Q

Where does aldosterone exert most of its actions?

A

Main actions in distal tubules and collecting ducts of nephron where it promotes expression of Na+/K+ pump (3 sodium out of the cell / 2 potassium into the cell) promoting reabsorption of Na+ and excretion of K+ thereby influencing water retention, blood volume & therefore blood pressure.

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15
Q

What system does aldosterone form an essential component of?

A

The renin-angiotensin-aldosterone system.

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16
Q

What is the function of the RAAS?

A

To increase blood pressure and increase blood volume through vasoconstriction and increase water reabsorption.

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17
Q

Briefly describe the RAAS pathway

A
  1. Angiotensinogen released in the liver
  2. Angiotensinogen cleaved by renin into angiotensin 1
  3. Angiotensin 1 cleaved by ACE in lung endothelial cells into angiotensin 2
  4. Angiotensin 2 stimulate vasoconstriction, secretion of aldosterone by the adrenal cortex (zona glomerulosa) and secretion of ADH by the posterior pituitary
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18
Q

How is production of renin regulated ?

A

Regulated by blood pressure and blood volume (hypovolaemia / hypotension)

Baroreceptors in aortic arch and carotid sinus detect the drop in blood pressure and send a signal to the kidneys.
Decrease in renal perfusion, a drop in blood pressure and increased sympathetic tone from baroreceptor activation leads to more renin release from kidney.

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19
Q

Why are angiotensin converting enzyme inhibitors used as a hypertensive drug?

A

As ACE inhibitors stop ACE cleaving angiotensin 1 into angiotensin 2 and therefore inhibit an increase of blood pressure by the RAAS.

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20
Q

What is the function of aldosterone?

A

Increases expression of Na+/K+ pump leads to increased reabsorption of Na+ and water back into blood

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21
Q

What is the function of anti-diuretic hormone?

A

Translocation of aquaporin channels aids reabsorption of water back into the blood

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22
Q

What is hyperaldosteronism?

A

When too much aldosterone is produced

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23
Q

What causes primary hyperaldosteronism?

A

A defect in the adrenal cortex.

  • Bilateral idiopathic adrenal hyperplasia
  • aldosterone secreting adrenal adenoma (conn’s syndrome)
  • Low renin levels (high aldosterone : renin ratio - so problem is in aldosterone secretion not in renin secretion)
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24
Q

What is the most common cause of primary hyperaldosteronism?

A

Bilateral idiopathic adrenal hyperplasia

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25
Q

What causes secondary hyperaldosteronism?

A

Over activity of RAAS.

  • Renin producing tumour (juxtaglomerular tumour)
  • renal artery stenosis (kidney detects low blood supply and increases renin production even though systemic blood pressure may be fine)
  • high renin levels ( low aldosterone: renin ratio)
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26
Q

What is the best way to distinguish between a primary and secondary hyperaldosteronism?

A 
Primary = high aldosterone: renin ratio
Secondary = low aldosterone : renin ratio
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27
Q

What are the signs of hyperaldosteronism?

A

High blood pressure
Left ventricular hypertrophy
Stroke
Hypernatraemia and hypokalaemia (as aldosterone leads to greater expression of the Na+/K+ pump in the nephrons)

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28
Q

What is the treatment for hyperaldosteronism?

A

Aldosterone producing tumour removed by surgery
Spironolactone (mineralocorticoid
receptor antagonist)

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29
Q

What is the most abundant corticosteroid?

A

Cortisol - accounts for 95% of glucocorticoid activity

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30
Q

Where is cortisol synthesised?

A

In the Zona fasiculata, the middle layer of the adrenal cortex.

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31
Q

What regulates the secretion of cortisol?

A

Synthesis is stimulated in response to adreno corticotropic hormone (ACTH)

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32
Q

Cortisol acts via negative feedback on which hormones?

A

Negative feedback to hypothalamus to inhibit CRH (corticotrophin releasing hormone) and ACTH (adrenal cortico tropic hormone ) release

33
Q

How does cortisol travel in blood?

A

Cortisol is a steroid hormone and is lipophillic and therefore cannot travel freely in blood. Travels bound to carrier protein in plasma = transcortin.

34
Q

How does cortisol receptor exert its actions?

A

By regulating gene transcription

35
Q

What are the actions of cortisol?

A
  • Increased protein breakdown in muscle
    effects
  • Increased lipolysis in fat
  • Increased gluconeogenesis in liver
  • Resistance to stress (increased supply of glucose, raise blood
    medication for pressure by making vessels more sensitive to vasoconstrictors)
  • Anti-inflammatory effects (inhibits macrophage activity + Mast cell degranulation)
  • Depression of immune response (prescribed to organ transplant patients)
36
Q

When is cortisol used as a drug?

A

Useful medication for allergic reactions due to cortisol anti-inflammatory affects ( inhibits macrophage activity and mast cell degranulation).
Used after organ transplant as suppresses immune response.

37
Q

Describe the hypothalamic-pituitary- adrenal axis (cortisol)

A
  1. Hypothalamus detects increase in stress
  2. Hypothalamus releases corticotropin releasing hormone CRH
  3. CRH stimulates anterior pituitary to release adreno cortico tropic hormone (ACTH)
  4. ACTH has a stimulates the adrenal cortex to release cortisol
  5. Cortisol stimulates many effects on target cell type.
38
Q

What are the effects of glucocorticoid on metabolism?

A 
Increased glucose production
Increased protein degradation 
Decreased sensitivity to insulin
Decreased protein synthesis 
Redistribution of fat
39
Q

What are the effects of glucocorticoid on the liver?

A

Increase glucose storage as glycogen in liver
Increase gluconeogenesis
Increase activity and amounts of liver enzymes

40
Q

What is the affects of glucocorticoid in adipose tissue?

A

Decrease in glucose utilisation
Decrease in sensitivity to insulin
Increase in lypolysis

Chronic high levels of cortisol can result in re-distribution of fat especially in abdomen, supra clavicular fat pads, dorso-cervicular fat pad ( buffalo hump ) and on face (moon face )

41
Q

What is the affect of cortisol on muscle tissue?

A

Increase in protein degradation
Decrease in protein synthesis
Decrease in glucose utilisation
Decrease in sensitivity to insulin

Cortisol inhibits insulin-induced GLUT4 translocation in muscle ( prevents glucose uptake)

42
Q

What is Cushing’s syndrome?

A

Chronic excessive exposure to cortisol that is NOT due to a benign pituitary adenoma secreting ACTH

43
Q

What external causes would cause Cushing syndrome?

A

Prescribed glucocorticoids

44
Q

What are the endogenous causes of Cushing’s syndrome?

A

Excess cortisol produced by adrenal tumour (adrenals cushing’s)

Non pituitary-adrenal tumours producing ACTH (&/or CRH) such as a small cell lung cancer

45
Q

What is Cushing’s disease?

A

Chronic excessive exposure to cortisol due to a benign pituitary adenoma secreting ACTH

46
Q

What are the signs and symptoms of Cushing’s syndrome/ Cushing’s disease?

A 
Plethoric moon-shaped face
Buffalo hump (dorso-cervical fat pad) 
Abdominal obesity 
Purple striae
Acute weight gain
Hyperglycaemia 
Hypertension
47
Q

What type of drugs are prednisolone and dexamethosone?

A

Steroid drugs

48
Q

What effects do steroid drugs have?

A

Anti-inflammatory & immunomodulatory effects

49
Q

What conditions are steroid drugs used to treat?

A

Used to treat inflammatory disorders e.g.
• Asthma
• Inflammatory bowel disease
• Rheumatoid arthritis
• Other auto-immune conditions
Also used to supress immune reaction to organ transplantation

50
Q

What are the side effects of steroid drugs?

A

Side-effects are the same as the effects of higher levels of cortisol, plus can also have mineralocorticoid effects

51
Q

How should steroid usage be stopped?

A

Gradually over time, not suddenly

52
Q

What is Addison’s disease?

A

Chronic adrenal insufficiency

53
Q

What are the main causes of Addison’s disease?

A

Previously main cause was a complication of Tuberculosis

Now main cause is destructive atrophy from autoimmune response.

Rare causes include fungal infection, adrenal cancer and adrenal haemorrhage e.g. following trauma.

54
Q

Who is most likely to suffer from Addison’s disease?

A

Affects more women than men but exact cause of autoimmunity is unknown

55
Q

What are the signs and symptoms of Addison’s disease?

A 
Postural hypotension
Lethargy
Weight loss 
Anorexia
Increased skin pigmentation 
Hypoglycaemia
56
Q

Why is hyperpigmentation a prominent sign in Addison’s disease?

A

Decreased cortisol means that there is less negative feedback on the anterior pituitary gland so secretion of ACTH increases.
More POMC is required to synthesis ACTH, and therefore more MSH is synthesised as a consequence. Increase in MSH leads to hyperpigmentation.
ACTH itself can also activate melanocortin receptors on melanocytes so will also contribute to hyperpigmentation

57
Q

What is pro-opiomelanocortin?

A

Pro-opiomelanocortin a.k.a. POMC is cleaved to form ACTH in the anterior pituitary. When ACTH is cleaved from POMC, other fragments are formed including MSH, which causes hyperpigmentation in high levels.

58
Q

What is MSH?

A

MSH is melanocytes stimulating hormone. It is a hormone derived from POMC alongside ACTH.

59
Q

What is the function of MSH?

A

Alpha melanocytes stimulating hormone effects melanin synthesis, immune response and decreases food intake.

60
Q

What is Addison’s crisis?

A

Uncontrolled Addison’s disease resulting in a life threatening emergency due to adrenal insufficiency

61
Q

What is Addisons crisis precipitated by?

A
  • Severe stress
  • Salt depravation
  • Infection
  • Trauma
  • Cold exposure
  • Over exertion
  • Abrupt steroid drug withdrawal
62
Q

What are the symptoms of Addisons crisis?

A
  • Nausea
  • Vomiting
  • Pyrexia
  • Hypotension
  • Vascular collapse
63
Q

What is the treatment for Addisons crisis?

A

Fluid replacement

Cortisol

64
Q

Where in the adrenal gland secretes androgens?

A

Innermost layer of the adrenal cortex (Zona Reticularis)secretes weak androgens

65
Q

What androgens are secreted in the adrenal cortex?

A

Dehydroepiandrosterone (DHEA) and androstenedione

66
Q

How s secretion of androgens in the adrenal cortex regulated?

A

Partially regulated by ACTH and CRH

67
Q

What is the function of androgens?

A

• In male DHEA converted to testosterone in testes (after puberty this is insignificant since testes release far
more testosterone themselves)

  • In female adrenal androgens promote libido and are converted to oestrogens by other tissues. After menopause this is only source of oestrogens as androgens from the ovaries cease.
  • Promote axillary and pubic hair growth in both sexes.
68
Q

Why is the adrenal medulla thought of as a modified sympathetic ganglion of the autonomic nervous system?

A

As chromaffin cells in the adrenal medulla lack axons but act as postganglionic nerve fibres that release hormones into blood:
Adrenalin 80%
Noradrenalin 20%

69
Q

Why are some chromaffin cells in the adrenal medulla able to produce adrenaline whilst some aren’t?

A

20% or chromaffin cells lack N-methyl transferase enzymes and therefore cannot produce adrenaline from noradrenaline. These 20% of cells secrete noradrenaline.

70
Q

What amino acid is the primary building block for both noradrenalin and adrenaline?

A

Tyrosine

71
Q

Describe the pathway from GCPR to target protein of a receptor with a Gs linked protein.

A

Gs protein is stimulatory and activates adenylyl cyclase.
Adenylyl cyclase stimulates cAMP.
CAMP activates protein kinase A.
Protein kinase A then goes on to phosphorylase target proteins, initiating a reaction.

72
Q

What effect does G protein Gi have?

A

Gi is an inhibitory protein. It inhibits the activation of adenylyl cyclase. This means that cAMP is not activated by adenylyl cyclase and protein kinase A is not activated. Target proteins are not phosphorylated and effects are down regulated.

73
Q

What is the effect of Gq protein?

A

What Gq protein is activated by a ligand binding to Gqs associated GCPR, it stimulates the activation of phospholipase C. Phospholipase C then stimulates the cleaving of PIP2 membrane bound protein into Diacylglycerol (DAG) and IP3. Both these secondary messengers go on to have effects on target proteins. Most notably Phosphokinase C and calcium release via IP3 receptor.

74
Q

What are the hormonal actions of adrenaline?

A

Adrenaline is a ligand of the sympathetic branch of the autonomic nervous system and is involved in the fight or flight response.

75
Q

What effect does the fight or flight response have on the heart, lungs, blood vessels and kidneys?

A

Heart = increase heart rate and contractility via the B1 receptors

Lungs = stimulate bronchodilation via B2 receptors

Blood vessels = vasoconstriction via a1 receptor (skin and gut ) , vasodilation via b2 receptor (muscle )

Kidney = increase renin secretion via B1 and B2 receptors

76
Q

What effect does the fight or flight response have on the liver, pancreas, muscle and adipose tissue?

A

Muscle = increase glycolysis via a1 and B2, increases glycogenolysis via a1 and b2

Liver = increases glycogenolysis (a1, B2) and increases gluconeogenesis (a1, B2)

Pancreas = increases glucagon secretion (a2) and decreases insulin secretion (a2 and b2 )

Adipose = increases lipolysis (B2)

77
Q

What is a phaeochromocytoma?

A

Chromaffin cell tumour (adrenal medulla) that is a catecholamine-secreting tumour (mainly noradrenaline)

Phaeo (dark) chromo (color) cyte (cell) oma (Tumour stains dark with chromium salts)

May precipitate life-threatening hypertension

78
Q

What are the signs and symptoms of phaeochromocytoma?

A
  • Severe hypertension
  • Headaches
  • Palpitations
  • Diaphoresis (excessive sweating)
  • Anxiety
  • Weight loss
  • Elevated blood glucose

MEH (23 decks)

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