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2 - MEH > Adrenal Glands > Flashcards

Adrenal Glands Flashcards

1
Q

State the regions of the adrenal gland

A

Capsule on outside, cortex in middle and medulla on inside

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2
Q

State the hormones produced in the adrenal gland and its location

A
  • Cortex has 3 layers - salt, sugar, sex, excitement
    • Zona glomerulosa - mineralocorticoids (aldosterone)
    • Zona fasiculata - glucocorticoids (cortisol)
    • Zona reticularis - glucocorticoids + androgens
  • Medulla - chromaffin cells synthesise and release catecholamines into blood
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3
Q

State the 3 layers of the adrenal cortex

A
  • Zona glomerulosa - outermost
  • Zona fasiculata
  • Zona reticularis - innermost
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4
Q

Explain the mechanism of action of cortisol in target cells

A
  • Bind to receptors of nuclear receptor family to modulate gene transcription - intracellular
    • Diffuses across plasma membrane and binds to glucocorticoid receptors
    • Binding causes dissociation of chaperone protein (heat shock protein 90), allowing receptor-ligand complex to enter nucleus
    • Receptors bind to glucocorticoid response elements (GRE) or other transcription factors
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5
Q

Describe the effects of aldosterone

A
  • Carrier protein - serum albumin and sometimes transcortin
  • Regulates gene transcription - intracellular
  • Regulates plasma Na, K and arterial blood pressure
  • Promotes expression of Na/K pump in nephron to promote reabsorption of Na and excretion of K
    • Influences water retention, blood volume and therefore blood pressure
  • Component of renin-angiotensin-aldosterone system
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6
Q

Explain how cortisol secretion is regulated

A
  • Cortisol regulated by a negative feedback loop
  • Cortisol inhibits CRH release in hypothalamus
  • Also inhibits ACTH release in anterior pituitary
  • CRH increased in response to physical (temperature, pain), chemical (hypoglycaemia) and emotional stressors
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7
Q

Explain how ACTH can lead to hyperpigmentation

A
  • Decreased cortisol leads to negative feedback on anterior pituitary leading to ACTH synthesis
  • More POMC required to synthesize ACTH
    • Produces both ACTH and MSH along with other peptides
    • ACTH itself can also activate melanocortin receptors on melanocytes
  • Melanin stimulating hormone (MSH) overproduction leads to hyperpigmentation due to increased melanin synthesis
  • Hyperpigmentation common in Addison’s disease
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8
Q

How are cortisol and aldosterone carried in the blood

A
  • Aldosterone - serum albumin and sometimes transcortin

- Cortisol - transcortin and sometimes serum albumin

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9
Q

Describe the main physiological actions of cortisol

A
  • Increase gluconeogenesis in liver which increase glucose
    • Stimulates insulin to store glycogen
  • Increase protein breakdown in muscle
    • Inhibits GLUT-4 to prevent glucose uptake in muscles so relies on protein for energy
  • Increased lipolysis in adipose tissue - decreases sensitivity of adipose cells to insulin
    • Redistribution of fat to abdomen
  • Resistance to stress - increase glucose supply, raise blood pressure by making vessels more sensitive to vasoconstrictors
  • Anti-inflammatory effects - mast cell degranulation useful medication against allergies
  • Depression of immune response - organ transplant patients
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10
Q

Explain the actions of chromaffin cell

A
  • Chromaffin cells lack axons but act as postganglionic nerve fibres that release adrenaline and noradrenaline into the blood
    • Convert tyrosine into dopamine and then into noradrenaline
    • 20% chromaffin cells lack N-methyl transferase enzyme needed to convert noradrenaline to adrenaline
      • Adrenaline - 80%, noradrenaline 20%
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11
Q

What are the actions of androgens

A
  • DHEA and androstenedione secreted
  • Partially regulated by ACTH and CRH
  • In male, DHEA converted to testosterone in testes
    • Insignificant after puberty as testes release far more testosterone
  • In female, adrenal androgens promote libido and are converted to oestrogen by other tissues
    • After menopause, only sources of oestrogen
  • Promote axillary and public hair growth in both sexes
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12
Q

Explain the actions of adrenaline on adrenergic receptors

A
  • Activate GPCRs
  • Binds to alpha 1,2 and beta 1,2 receptors
    • Alpha 1 receptors activate Gq which stimulates phospholipase C to produce DAG and IP3
      • PKC and calcium release via IP3 receptor on SR/ER
    • Alpha 2 receptor activate Gi which inhibits adenylyl cyclase
    • Beta 1,2 receptors activate Gs which stimulate adenylyl cyclase to produce cAMP and then protein kinase A
      • Can phosphorylate and open VOCC
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13
Q

Describe how adrenaline can increase heart rate

A
  • Adrenaline binds to ß-1 receptors which activate Gs and stimulate adenylyl cyclase to produce cAMP
    • cAMP activates HCN channels - responsible for funny current
    • Increase slope and shortens duration
  • cAMP activates protein kinase A
    • PKA phosphorylation of HCN channels modulates function
    • PKA phosphorylation of L-type Ca channels - potentiates opening
      • Increase slope of upstroke of SA action potential
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14
Q

Explain how the RAAS system works and state its effects

A
  • Stimulated by hypovolaemia or hypotension
  • Decrease in renal perfusion, drop in blood pressure and increased sympathetic tone from baroreceptor activation leads to more renin release from kidney
  • Angiotensinogen produced in the liver cleaved into angiotensin I
  • Angiotensin converting enzyme (ACE) produced in lung endothelial cells convert angiotensin I to angiotensin II
  • Angiotensin II has many effects
    • Causes arterial vasoconstriction
    • Stimulates aldosterone production in adrenal glands which increases expression of Na/K pump leading to water retention
      • Stimulates ADH production from posterior pituitary which moves and opens aquaporin channels to aid water reabsorption
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15
Q

What are the causes of Cushing’s Syndrome

A
  • Chronic excessive exposure to cortisol
  • Most commonly caused by prescribed glucocorticoid drugs
    • Used to treat inflammatory disorders - asthma, inflammatory bowel disease, rheumatoid arthritis
    • Steroid dosage should be reduced gradually and not stopped suddenly
  • Cushing’s disease - adenoma in pituitary gland secreting ACTH
  • Adrenal Cushing’s - excess cortisol produced by adrenal tumour
    • Secrete glucocorticoids but may also secrete androgens
    • Treatment - adrenalectomy
  • Small cell lung cancer - non pituitary adrenal tumours producing ACTH
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16
Q

What are the signs and symptoms of Cushing’s syndrome

A
  • Abdominal obesity - increased lipogenesis
  • Skinny and weak arms and legs - increased muscle proteolysis
  • ‘Buffalo hump’
  • Plethoric moon-shaped face
  • Purple striae - proteolysis leading to easy bruising because if thin skin
  • Red stretch marks on abdomen
  • High blood pressure and diabetes - sodium and fluid retention
  • Osteoporosis
17
Q

How to test to distinguish between Cushing’s disease and adrenal Cushing’s

A
  • Suppression test used to differentiate between Cushing’s disease and adrenal Cushing’s
  • Use dexamethoasone - synthetic steroid
    • If positive (cortisol suppressed), Cushing’s disease as ACTH will still be inhibited in a pituitary tumour
      • If negative (cortisol not suppressed), adrenal Cushing’s as cortisol produced from adrenal gland regardless of ACTH concentration
18
Q

State the causes of Addison’s disease

A
  • Chronic adrenal insufficiency
  • Caused by destructive atrophy of adrenal glands from autoimmune response
  • Disorders in pituitary or hypothalamus that lead to decreased secretion of ACTH or CRF
19
Q

State the signs and symptoms of Addison’s disease

A
  • Postural hypotension - fluid depletion
  • Lethargy
  • Weight loss
  • Anorexia
  • Abdominal pain
  • Dizziness
  • Hyperpigmentation
  • Hypoglycaemia - sodium and fluid depletion
20
Q

What is Addisonian crisis and its causes

A
  • Life threatening emergency due to adrenal insufficiency (loss of both cortisol and mineralocorticoids)
    • Precipitated by - severe stress, salt depravation, infection, trauma, cold exposure, abrupt steroid drug withdrawal
21
Q

What are the symptoms and treatment of Addisonian crisis

A
  • Symptoms - nausea, vomiting, pyrexia, hypotension, vascular collapse
  • Treatment - fluid replacement (dextrose in normal saline), IV hydrocortisone
22
Q

How would you test for Addison’s disease

A
  • Stimulation test using synthacthen (synthetic analogue of ACTH)
  • If normal, should increase plasma cortisol
23
Q

Discuss the cause, presentation and treatment of Congenital adrenal hyperplasia

A
  • Autosomal recessive
  • Block in adrenal cortex pathway
  • 21 hydroxylase deficiency - less glucocorticoid and mineralocorticoid production
    • Precursor of 21 hydroxylase diverted to produce more androgen - high sex steroid level
    • Result in genital ambiguity in female infants
  • Leads to large amounts of ACTH synthesis - hyperplasia of adrenal cortex
  • Presentation - hypotension, hyponatraemia, hyperkalaemia, hypoglycaemia
  • Treatment - treat adrenal crisis, determine sex of baby
24
Q

Explain primary and secondary hyperaldosteronism and distinguish between the two

A
  • Excess aldosterone produced from adrenal glands
  • Primary - defect in adrenal cortex
    • Bilateral idiopathic adrenal hyperplasia
    • Conn’s syndrome - aldosterone secreting adrenal adenoma
    • Low renin levels (high aldosterone: renin ratio)
      • Low renin does not cause decrease in aldosterone in Conn’s syndrome
  • Secondary - due to over activity of the RAAS
    • Renin producing tumour
    • Renal artery stenosis
    • High renin levels (low aldosterone: renin ratio)
      • Aldosterone increase water retention -> increase blood volume -> increase arterial pressure -> decrease renin production -> decrease aldosterone
25
Q

What are the signs and treatment of hyperaldosteronism

A
  • Signs - high blood pressure
    • Left ventricular hypertrophy
    • Stroke
    • Hypernatraemia
    • Hypokalaemia
  • Treatment - dependent on type
    • Aldosterone-producing adenomas removed by surgery (adrenalectomy)
    • Spironolactone (mineralocorticoid receptor antagonist)
26
Q

What are the symptoms if high androgen levels

A
  • Female - excessive body hair growth, acne, menstrual problems, virilisation (development of male characteristics such as low voice), increased muscle bulk
  • High oestrogen - breast development, broad hips, accumulation of fat in breast and buttocks, body hair distribution
27
Q

Describe the cause and symptoms of phaeochromocytoma

A
  • Genetic inheritance common
  • Tumour of adrenal medulla
  • Symptoms
    • Hypertension
    • Anxiety
    • Palpitations
    • Pallor
    • Sweating
    • Glucose intolerance
    • Headaches
    • Panic attacks
    • Diaphoresis - excessive sweating
    • Weight loss
      • Collapse

2 - MEH (16 decks)

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