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MEH > The Adrenal Glands > Flashcards

The Adrenal Glands Flashcards

1
Q

What are the layers of the adrenal glands and their products

A

CORTEX:
Zona glomerulosa
Mineralocorticoids (e.g. aldosterone)

Zona fasiculata
Glucocorticoids (e.g. cortisol)

Zona reticularis glucocorticoids + small amounts of androgens

MEDULLA:
Chromaffin cells
Adrenaline (~80%) Noradrenaline (~20%)

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2
Q

What are the hormones o teh adrenal carted

A

Zone glomerulose
Mineralocrticoids eg aldosterone

Zona fasiculate
Glucocorticoids eg CORTISOL, corticosterone, cortisone

Zona reticularis
Dehydroepiandrosterone
Androstenedione
Which can be converted to
Testosterone 
Oestrogens
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3
Q

What are steroid hormones synthesised from and what is their action

A

• Synthesised from cholesterol in adrenal glands and gonads
• Lipid soluble hormones - can pass through plasma membrane
- not water soluble
- much slower acting than water soluble hormones
• Bind to receptors of the nuclear receptor family to modulate gene transcription

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4
Q

How do corticosteroids exert their actions

A

• Corticosteroids readily diffuse across plasma membrane
• Bind to glucocorticoid receptors.
• Binding causes dissociation of chaperone proteins (e.g. heat shock protein 90),
• Receptor ligand complex translocates to nucleus
• Dimerisation with other receptors can occur
• Receptors bind to glucocorticoid response elements (GREs) - (hormone response elements eg glucocorticoid response element - when receptor binds it modulates gene transcription , or other transcription factors (modulate gene transcription)
Both lead to new protein

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5
Q

What is aldosterone synthesised by and what are its actions

A
  • Most abundant mineralocorticoid
  • Synthesised and released by Zona glomerulosa of adrenal cortex
  • Steroid hormone = lipophilic. Carrier protein = mainly serum albumin and to a lesser extent transcortin
  • Aldosterone receptor is intracellular & exerts its actions by regulating gene transcription
  • Plays central role in regulation of plasma Na+, K+ and arterial blood pressure.
  • Main actions in distal tubules and collecting ducts of nephron where it promotes expression of Na+/K+ pump promoting reabsorption of Na+ and excretion of K+ thereby influencing water retention, blood volume & therefore blood pressure.
  • Central component of renin angiotensin-aldosterone system (RAAS)
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6
Q

Give a recap of the rams system

A

See slide

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7
Q

What is primary hyperalsosteronism

A

Primary
Defect in adrenal cortex
• Bilateral idiopathic adrenal hyperplasia (most common)
• Aldosterone secreting adrenal adenoma (Conn’s syndrome)
• Low renin levels (high aldosterone:renin ratio)

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8
Q

What is secondary hyperaldosteronism

A 
Secondary
Due to over activity of the RAAS
• Renin producing tumour (Rare) e.g.
juxtaglomerular tumour. 
• Renal artery stenosis 
• High renin levels (low aldosterone:renin ratio)
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9
Q

What is the best way to dierentiate between primary/secondary hyperaldosteroism

A

1- low renin levels

2 - high renin levels

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10
Q

What are the signs of hyperaldosteronism

A
  • High blood pressure
  • Left ventricular hypertrophy
  • Stroke
  • Hypernatraemia (increasead sodium)
  • Hypokalaemia (low potassium)
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11
Q

What are the treatments for hyperaldosteronism

A

Treatment
• Depends on type
• Aldosterone-producing adenomas removed by surgery
• Spironolactone (mineralocorticoid receptor antagonist)

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12
Q

What is cortisol

A
  • Most abundant corticosteroid & accounts for ~95% of glucocorticoid activity
  • Synthesised and released by Zona fasiculata in response to ACTH
  • Negative feedback to hypothalamus inhibits CRH & ACTH release
  • Steroid hormone. Carrier protein in plasma = transcortin
  • Cortisol receptor exerts its actions by regulating gene transcription
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13
Q

What are the actions of cortisol

A
  • Increased protein breakdown in muscle
  • Increased lipolysis in fat
  • Increased gluconeogenesis in liver
  • Resistance to stress (increased supply of glucose, raise blood pressure by making vessels more sensitive to vasoconstrictors)
  • Anti-inflammatory effects (inhibits macrophage activity + Mast cell degranulation) - useful medication for allergic reactions
  • Depression of immune response (prescribed to organ transplant patients)
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14
Q

Give an overview of the HPA axis

A

See slide

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15
Q

What are the effects of glucocorticoids on metabolism

A 
Liver:
Increase Glucose (gluconeogenesis) leads to increase insulin so liver glycogen stores increase

Adipose:
Chronic high levels of cortisol can result in re-distribution of fat especially in abdomen, supraclavicular fat pads, Dorso-cervical fat pad, (“buffalo hump”), & on face (“moon face”).
Increase glucose utilisation, decreased sensitivity to insulin, increased lypolysis

Muscle:
Cortisol inhibits insulin-induced GLUT4 translocation in muscle (prevents glucose uptake so has glucose sparing effect)
Increased protein degradation, decreased protein synthesis, decreased glucose utilisation, decreased sensitivity to insulin

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16
Q

What are he causes of Cushing’s syndrome

A

External causes: prescribed glucocorticoids (most common)

Endoenous causes: rare

  • Benign pituitary adenoma secreting ACTH (Cushing’s disease)
  • Excess cortisol produced by adrenal tumour (Adrenal Cushing’s)
  • Non pituitary-adrenal tumours producing ACTH (&/or CRH) e.g. small cell lung cancer - very rare
17
Q

What are the signs/symptoms of Cushing’s syndrome

A 
Signs & Symptoms • Plethoric moon-
shaped face
• “Buffalo hump”
• Abdominal obesity • Purple striae
• Acute weight gain • Hyperglycaemia
• Hypertension
18
Q

What are anti-inflammatory and immunomodulatory effects of steroid drugs

A

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

IMPORTANT POINT !! Steroid dosage should be reduced gradually and not stopped suddenly! - bc everything has been downregulated - must wean of gradually

19
Q

What is Addison’s disease

A

• First identified by Thomas Addison in
1855 while working at Guy’s.
• Main cause at time was a complication of Tuberculosis.
• Most common cause now is destructive atrophy from autoimmune response
• Affects more women than men.
• Exact reason for autoimmunity unknown.
• Other, much rarer causes include fungal infection, adrenal cancer & adrenal haemorrhage (e.g. following trauma).

20
Q

What are the signs and symptoms of Addison’s disease

A
  • Postural hypotension
  • Lethargy
  • Weight loss
  • Anorexia
  • Increased skin pigmentation
  • Hypoglycaemia
21
Q

What leads to hypermigmantation in Addison’s

A

Increased MSH as consequence of increased POMC in Addison’s leads to hyperpigmentation. ACTH itself can also activate melanocortin receptors on melanocytes so will also contribute to hyperpigmentation

22
Q

What is adisonian crisis

A 
Life threatening emergency due to adrenal insufficiency
Precipitated by:
• Severe stress
• Salt depravation
• Infection
• Trauma
• Cold exposure
• Over exertion
• Abrupt steroid drug withdrawal
23
Q

What are teh symptoms and treatment of addisoian crisis

A

Symptoms • Nausea • Vomiting • Pyrexia, • Hypotension • Vascular collapse
Treatment • Fluid replacement • Cortisol

24
Q

What are androgens

A
  • Innermost layer of adrenal cortex (zona reticularis) secretes weak androgens
  • Dehydroepiandrosterone (DHEA) and androstenedione
  • Partially regulated by ACTH and CRH • 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.
  • Promote axillary and pubic hair growth in both sexes.
25
Q

What is the adrenal medulla and what are chromaffin cells

A

Adrenal medulla is a modified sympathetic ganglion of autonomic nervous system
Chromaffin cells in adrenal medulla lack axons but act as postganglionic nerve fibres that release hormones into blood: Adrenaline (~80%) Noradrenaline (~20%)
~20% chromaffin cells lack N-methyl transferase enzyme and secrete noradrenaline

26
Q

What is the adrenalmedulla innervated by

A

T5-t9 - greater splanchnic nerve
T10-t11 - lesser splanchnic nerve
Merge in the celiac ganglion

27
Q

Give an overview of the adrenergic receptors

A

See slide

28
Q

Name some tissues and organs which have adrenergic receptors

A

See slide

29
Q

How does adrenaline increase heart rate

A

Direct activation by cAMP of hyperpolarisation-activated, cyclic nucleotide-gated (HCN) channels (responsible for Ifunny (If) or pacemaker current)
PKA phosphorylation of (HCN) channels modulates function
PKA phosphorylation of L-type Ca2+ channels – potentiates opening, increasing the slope of the upstroke of the action potential

30
Q

What is phaeochromocytoma

A

• Phaeo (dark) chromo (color) cyte (cell) oma
(Tumour stains dark with chromium salts)
• Rare, catecholamine-secreting tumour (mainly noradrenaline)
• May precipitate life-threatening hypertension

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

MEH (21 decks)

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