endocrine Flashcards
define pcos
characterised by oligo/amenorrhoea and hyperadrogenism
risk factors for pcos
environmental factors
genetic variants
hyperinsulinaemia (leads to increased ovarian androgen synthesis and reduced hepatic sex hormone binding globulin synthesis = increase in free androgens)
epidemiology of pcos
most common cause of infertility
presenting symptoms of pcos
menstrual irregularities hirsutism male pattern hair loss acne dysfunctional uterine bleeding
signs of pcos
hirsutism
male pattern hair loss
acne
acanthosis nigricans (severe insulin resistance) - velvety thickening and hyper pigmentation of axilla or neck
investigations for pcos
bloods:
- high LH
- high LH: FSH ratio
- high testosterone, androstenedione and DHEA-s
- low SHBG
test for:
hyperprolactinaemia, hypo/hyperthyroidism, CAH (17OH prog levels), cushings
impaired glucose tolerance tests:
fasting blood glucose
hb1ac
fasting lipids
Define primary hyperaldosteronism
Characterised by autonomous aldosterone overproduction from the adrenal gland with subsequent suppression of plasma renin activity
risk factors of primary hyperaldosteronism
•Adrenal adenoma (Conn’s syndrome) - responsible for 70% of cases
•Adrenal cortex hyperplasia (30% of cases)
RARE:
Glucocorticoid-suppressible hyperaldosteronism
Aldosterone producing adrenal carcinoma
pathophysiology of primary hyperalosteronism
Excess aldosterone leads to increased Na+ and water retention
This leads to hypertension
It also causes increased renal K+ loss leading to hypokalaemia
Renin is suppressed due to NaCl retention
epidemiology of primary hyperaldosteronism
•Conn’s syndrome is more common in WOMEN and YOUNG patients
•Bilateral adrenal hyperplasia is more common in MEN and presents at an older age
presenting symptoms of primary hyperaldosteronism
- Usually ASYMPTOMATIC
- Tends to be an incidental finding on routine blood tests
Symptoms of Hypokalaemia: o Muscle weakness o Polyuria and polydipsia (due to nephrogenic DI) o Paraesthesia o Tetany
signs of primary hyperaldosteronism
Hypertension
Complications of hypertension (e.g. hypertensive retinopathy)
screening investigations for primary hyperaldosteronism
- Low Serum K+
NOTE: Serum Na+ is usually normal because the Na+ reabsorption is matched by water reabsorption
o High Urine K+
o High Plasma Aldosterone Concentration
o High aldosterone: renin activity ratio
confirmatory tests for primary hyperaldosteronism
oSalt Loading (Failure of aldosterone suppression following salt load confirms primary hyperaldosteronism)
Postural Test (Measure plasma aldosterone, renin activity and cortisol when the patient is lying down at 8 am - Measure again after 4 hrs of the patient being upright - Aldosterone-producing adenoma - aldosterone secretion decreases between 8 am and noon •Bilateral adrenal hyperplasia - adrenals respond to standing posture and increase renin production leading to increased aldosterone secretion
oCT/MRI
oBilateral adrenal vein catheterisation
• Measures adrenal vein aldosterone levels and allows you to distinguish between Conn’s syndrome and bilateral adrenal hyperplasia
oRadio-labelled cholesterol scanning
•Unilateral uptake in adrenal adenomas
•Bilateral uptake in bilateral adrenal hyperplasia
management plan for primary hyperaldosteronism
Bilateral Adrenal Hyperplasia
o Spironolactone
o Eplerenone can be used if the spironolactone side-effects are intolerable
o Amiloride (potassium-sparing diuretic)
o Monitor serum K+, creatinine and BP
o ACE inhibitors and CCBs may also be added
Aldosterone Producing Adenomas
o Adrenalectomy
Adrenal Carcinoma
o Surgery
o Post-operative mitotane (antineoplastic)