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MEDICINE > CEP wk8 - ADRENAL GLAND > Flashcards

CEP wk8 - ADRENAL GLAND Flashcards

1
Q

ANATOMY OF ADRENAL GLAND

A
  • located on top of kidneys & have outer layer called adrenal cortex & inner layer called adrenal medulla
  • zona glomerulosa (outside layer) (makes salt - mineralocorticoids e.g. aldosterone)
  • zona fasciculata (mid layer) (makes sugar - glucocorticoids e.g. cortisol)
  • zona reticularis (determines sex - makes androgens e.g. DHEA)
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2
Q

CORTICOSTEROIDS

A

Lipid soluble so cross the membrane -> bind to specific intracellular receptors -> alter gene transcription directly or indirectly

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3
Q

GLUCOCORTICOIDS JOBS

A
  • co-ordinate body response to stress (important in homeostasis)
  • increase glucose mobilisation (encourage gluconeogenesis, increase lipolysis (break triglycerides -> 3 fatty acids + 1 glycerol), generating amino acids
  • maintain circulation (salt & water balance, vascular tone)
  • modulate immune system
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4
Q

TRANSPORT OF GLUCOCORTICOIDS

A
  • in circulation, glucocorticoids heavily bound to proteins (90% bound to CBG, 5% to albumin & 5% is ‘free’)
  • we measure total not “free” cortisol levels & CBG levels are lower with inflammation so there is less free cortisol
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5
Q

CORTISOL MOVEMENT IN UNSTRESSED VS STRESSED

A

in unstressed state, 95% of the cortisol is bound to CBG and there is only a tiny amount of free cortisol which enters cytoplasm & crosses membrane. HOWEVER, in stressed state (e.g. sepsis), there are far less CBG & much more cleaved CBG (broken) so there is far more free cortisol to enter the cytoplasm

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6
Q

CORTISOL CIRCADIAN RHYTHMS

A

trend in day of how cortisol levels rise & drop (identical to ACTH)

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7
Q

EFFECT OF STRESS ON CORTISOL LEVEL

A
  • after surgery, the circadian rhythm is completely disrupted (serum cortisol level rises dramatically and then comes down to normal over a few days)
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8
Q

REGULATION OF GLUCOCORTICOID SYNTHESIS

A

stressors or circadian rhythm -> release of neurotransmitters to hypothalamus -> release of CRH to anterior pituitary -> release of ACTH to adrenal cortex -> cortisol release (used as negative feedback to inhibit ACTH or CRH release) -> tissue action

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9
Q

MINERALOCORTICOIDS

A
  • WHERE - made in zona glomerulosa
  • MAIN ONE- aldosterone
  • JOB - salt & water balance in kidney
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10
Q

ALDOSTERONE

A

increases reabsorption of sodium ions & water & release of potassium in collecting ducts & distal convoluted tubule of nephron. (to increase blood volume & therefore, BP)

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11
Q

REGULATION OF ALDOSTERONE BY K IONS

LOOK AT EFFECT OF ACUTE ILLNESS ON CORTISOL LEVELS

A

Excessive K ingestion -> depolarisation of the cells in the kidney -> opens voltage gated Ca channels -> Ca enter -> Aldosterone is produced -> Na reabsorption and K excreted -> ECF of K decreases.

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12
Q

HOW ALDOSTERONE REGULATES BP & WATER BALANCE

A
  1. When blood volume is low, kidneys secrete renin into circulation.
  2. Renin then carries out the conversion of angiotensinogen -> angiotensin I -> angiotensin II (by angiotensin converting enzyme in the lungs)
  3. Angiotensin stimulates secretion of aldosterone from the adrenal cortex.
  4. This causes the tubules to increase reabsorption of Na and water into the blood.
  5. Volume of blood increases, blood pressure increases (Inhibitory effect on the production of renin)
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13
Q

MINERALOCORTICOID RECEPTOR (MR)

A
  • allows both cortisol & aldosterone to bind to it but cortisol binds more frequently
  • To prevent MR being swamped with cortisol, we have pre-receptor regulation of the kidney (MR transactivation) where the enzyme 11 beta HDS2 converts cortisol  cortisone (inactive) so there is less cortisol available to bind to the receptor so only aldosterone binds (too much liquorice = 11Beta HDs2 is inhibited and cortisol will bind to the MR more frequently)
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14
Q

ADRENAL ANDROGENS

A
  • WHERE - made in zona reticularis
  • E.G. - most abundant adrenal steroid is DHEA
  • JOB - increases in adrenal androgens -> more sex thoughts, higher sexual interest, higher satisfaction with the mental & physical aspects of sex life
  • REGULATION - production regulated by ACTH
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15
Q

ADRENAL MEDULLA

A
  • WHAT - specialised ganglia supplied by sympathetic pre-ganglionic neurones from CNS (AcH as transmitter)
  • JOB - Synthesises catecholamines (e.g. adrenaline (80%) & noradrenaline (20%))
  • WHEN - released during defence mechanism (increased fat breakdown)
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16
Q

JOB OF CATECHOLAMINES

A
  • released to prepare body for physical activity (fight or flight)
  • Redistributing circulating volume -> decreased digestive, excretory & reproductive system activity
17
Q

CONSEQUENCES OF LOW CORTISOL (ADRENAL INSUFFICIENCY)

A
  • anorexia, weakness, fatigue, weight loss
18
Q

ADDISONS CAUSES

A

vitiligo, autoimmune hyper/hypothyroidism, autoimmune adrenalitis

19
Q

DIAGNOSING ADDISONS

A
  • ACTH stimulation test (expect cortisol level to shoot up after ACTH but if <450, it is adrenal insufficiency)
  • hyperpigmentation in areas of friction, fatigue, decreased appetite
20
Q

PRIMARY ADRENAL INSUFFICIENCY (ADDISONS)

A
  • low cortisol but high ACTH (as no -ve feedback from cortisol telling hypothalamus to not make CRH)
  • DIAGNOSIS - 1. look for adrenal autoimmune antibodies 2. check long chain fatty acids 3. CT of adrenal (if steps 1 & 2 were negative)
  • CAUSES - surgery to remove adrenal glands or autoimmune adrenalitis (Addisons)
21
Q

SECONDARY ADRENAL INSUFFICIENCY

A
  • low cortisol and low ACTH (as faulty pituitary too)

- CAUSES - steroid tablets (as lead to decreased ACTH release from hypothalamus) & pituitary tumour

22
Q

TREATING ADRENAL INSUFFICIENCY

A
  • give hydrocortisone (active cortisone) or prednisolone
  • LONG-TERM
    - replace glucocorticoids with hydrocortisone
    - replace mineralocorticoids with fludrocortisone
    - give adrenal androgens
23
Q

TREATING ADRENAL CRISIS

A
  • give saline to treat the shock

- give hydrocortisone

24
Q

PREVENTING ADRENL CRISIS

A
  • patients have high NA (due to aldosterone deficiency) & low blood sugar (low glucocorticoids) so give glucocorticoids to replace low cortisol
  • steroid card, sick day rule 1 (if fever, double daily glucocorticoid dose), sick day rule 2 (100mg hydrocortisone then continuous infusion of 200mg over 24hr)
25
Q

CUSHING

A

high cortisol leading to purplish stretch marks, thin skin, easy bruising, osteoporosis, facial fullness

26
Q

CUSHING CAUSES

A
  • IATROGENIC - synthetic corticosteroids
  • ACTH-DEPENDENT - pituitary or ectopic tumour leads to hyper-secretion of ACTH
  • ACTH-INDEPENDENT - adrenal tumour hyper-secreting cortisol
27
Q

DIAGNOSING CUSHING

A
  • dexamethasone suppression test (mimics effect of cortisol & binds to glucocorticoid receptor to lower ACTH by -ve feedback BUT cushing patients dont have -ve feedback so ACTH & cortisol stays high)
  • midnight cortisol (should be v low), urinary cortisol over 24hr
28
Q

CAUSE OF CUSHING ONCE CONFIRMED

A
  • measure ACTH (if low = adrenal tumour (do CT)) (if normal/high = pituitary or ectopic (do MRI)
  • CRH test (should increase ACTH in Cushing but not ectopic tumour)
29
Q

TREATING CUSHING

A

surgery or drugs (block glucocorticoid receptor or cortisol producing adrenal enzymes)

MEDICINE (27 decks)

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