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Human Development > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

Describe zona glomerulosa

A

lack 17alphahydroxlase. Produces aldosterone

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2
Q

Describe zona fasiculata

A

lacks aldosterone synthase. Produces cortisol

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3
Q

Describe zona reticularis

A

lacks aldosterone synthase. Produces androstenedione and DHEA -> converted to oestrogen and testosterone in the periphery

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4
Q

What is ACTH derived from

A

POMC (also produces beta endorphin and MSH)

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5
Q

What is cortisol stimulated by

A

Stress and has circadian rhythm

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6
Q

Describe cortisol relese pathway

A

CRH from hypothalamus -> ACTH from anterior pituitary -> stimulates adrenal cortex to synthesise and release cortisol -> negative feedback on corticotrophs

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7
Q

How do steroid hormone bind to receptors

A

Steroid hormone enters cells by diffusion and binds to cytoplasmic receptors -> dissociation of hsp90 from receptor
Hormone-receptor complex dimerises and is translocated to nucleus. Complex binds to hormone responsive element on DNA which leads to an increase in mRNA production

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8
Q

What are the effects of glucocorticoids

A 
Decrease glucose uptake, glucose use, protein synthesis, Ca2+ absorption in gut, activity of osteoblasts
Increase gluconeogenesis (hyperglycaemia), protein breakdown, Ca2+ excretion in kidney, activity of osteoclasts
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9
Q

What the anti-inflam effects of cortisol

A

Early - reduce redness, heat, pain, swelling

Late - reduce wound healing, repair and proliferation

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10
Q

What does cortisol decrease

A 
Expression of COX2
Cytokine production
Complement in plasma
NO production
Histamine release
IgG production
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11
Q

What does cortisol increase

A

annexin-1, which inhibits PLA2 (produces arachidonic acid, which is a precursor to leukotrienes)

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12
Q

What does cortisol do on the mineralocorticoid receptor

A

increase Na retention, K excretion, water retention

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13
Q

What is the prevention mechanism for cortisol activation of mineralocorticoid

A

Cortisol has higher affinity for mineralocorticoid receptor than glucocorticoid receptor
Inactivate cortisol by conversion to cortisone (11bHSD enzyme)
11bHSD2 isoform expressed in aldosterone sensitive tissues: converts cortisol to cortisone
11bHSD1 expressed in liver, adipose, muscle: cortisone -> cortisol

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14
Q

What are the adverse effects of glucocorticoids

A 
Suppression of response to infection
Suppression of endogenous glucocorticoid production
Metabolic effects
Osteoporosis
Iatrogenic Cushing's syndrome
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15
Q

What is the treatment for Cushing’s

A

Metyrapone - 11beta hydroxylase inhibitor
Ketoclonazone - inhibits steroid biosynthesis
Pasireotide - SSTR5 agonist
Cabergolien - dopamine D2 agonist
Mifeprestone - glucocorticoid receptor antagonist

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16
Q

What are the effects of aldosterone

A

Effects in distal tubule and collecting duct
Increased number of sodium channels in apical membrane (ENaC)
Increase in Na+/K+ ATPase in basolateral membrane
Increased Na/K exchange

17
Q

What is spironolactone

A

Aldosterone antagonist

Used as K+ sparring diuretic

18
Q

What is Addison’s

A

chronic adrenal insufficiency

19
Q

What are the signs of Addison’s

A

Weakness, fatigue, anorexia, weight loss
Hyperpigmentation (increase of ACTH from POMC, POMC also activates MSH), hypotension, GI disturbances, salt craving, postural symptoms

20
Q

What is Cushing’s

A

Prolonged exposure to elevated levels of cortisol or exogenous glucocorticoids

21
Q

What are the signs of Cushing’s

A

obesity, hypertension, hirsutism (stimulation of androgen), striae, acne, bruising

22
Q

What are the effects of Cushing’s

A

Osteoporosis
Negative nitrogen balance
Increased appetite obesity
Increased susceptibility to infection

23
Q

What are the causes of primary hypoadrenalism

A

Destruction of adrenal cortex
Abrupt discontinuation of steroids
Autoimmune - Addison’s
TB
Surgery
Haemorrhage/infarction - meningococcal septicaemia (Waterhouse Friderichsen Syndrome)
Infiltration - Malignancy, amyloid (classic with lung cancer)

24
Q

How to investigate primary hypoadrenalism

A 
Random cortisol
Short synacthen test
Plasma ACTH (over 1000)
Urea and electrolytes 
Adrenal antibodies
25
Q

What is the treatment for hypoadrenalism

A

glucocorticoid (hydrocortisone, prednisolone), mineralocorticoid (fludrocortisone)

26
Q

What is the NR of cortisol

A

171-526

27
Q

What is the NR of K

A

3.5-5

28
Q

What is the treatment for Cushing’s

A 
Laparoscopic adrenalectomy (other adrenal gland can also atrophy)
Replacement GC (hydrocortisone, periodic withdrawal) 
Psychological disturbance may continue
29
Q

What is pheochromocytoma

A

Tumour of adrenal medulla - excess of adrenaline
Major impact on CV system
Urine or plasma collection

30
Q

What are the genetic factors for pheochromocytoma

A

MEN2, von Hippel Lindau, NF-1, SDH

31
Q

What are the clinical presentations of phaeo

A

Headaches, palpitations, sense of doom, chest pain, sweating, weight loss

32
Q

How is phaeo diagnosed

A

24 urine metanephrine (metabolites of adrenaline)

Or plasma

33
Q

What is the treatment for phaeo

A

Surgical removal after alpha and beta blockade treatment (phenoxybenzamine, doxazosin)

34
Q

What is Conn’s syndrome

A

primary hyperaldosteronism - Low renin but high aldosterone (autonomous hypersecretion)

35
Q

What are clinical presentations of Conn’s

A

Hypertension, hypokalaemia, alkalosis

36
Q

What is the diagnosis of Conn’s

A

Measurement of PRA (suppressed) and aldosterone in salt-replete individuals
Selective venous sampling (IVC and sample from both adrenal glands, see where aldosterone is coming form)

37
Q

What is the treatment of Conn’s

A

Remove the adenoma (laparoscopic)
Drug treatment:
Spironolactone, eplerenone

Human Development (9 decks)

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