Endo

Question 1

what is diagnostic criteria for osteoporosis

Answer 1

T score <-2.5, reduced bone density vulnerable to fractures
if T score -1 to -2.5 = osteopenia (less severe reduce bone density)

Question 2

how does age contribute to osteoporosis

Answer 2

with age, osteoclast activity increases but osteoblast activity doesn’t match this
so overall bone mass decreases - more breakdown than formation

peak bone mass achieved in 20s

Question 3

how is oestrogen linked to bone growth

Answer 3

after menopause, low E2 causes higher rate of age-related bone loss

Question 4

how does long-term corticosteroids cause osteoporosis

Answer 4

corticosteroids cause reduced bone turnover/breakdown with even less bone formation
so overall loss of bone mass

Question 5

how does osteoporosis present

Answer 5

usually asymptomatic
diagnosed after fragility fracture (low impact) - vertebra, distal wrist, proximal NOF

Question 6

what are bone mineral dependent + independent RF

Answer 6

bone mineral dependent:
female - premature menopause (as less E2 to protect)
VitD deficiency
asian, caucasian ethnicities
PMH: Cushing syndrome, hyperPTH, CKD, liver disease

bone mineral independent:
old age
low BMI <18.5
alcohol, smoking
DH: long term corticosteroids (asthma, COPD) - SSRI, anti-E2, anti-epileptic, PPI

Question 7

how is osteoporosis investigated

Answer 7

calculate FRAX score - predicts risk of fragility fracture in next 10yr (women 65yr+, men 75yr+)

if low risk - conservative management (stop smoking/alcohol, weight-bearing exercise, more VitD/Ca intake)

if intermediate risk, FRAX >10 - do DEXA scan (gold standard to diagnose osteoporosis), measures bone density
T score - comparing to young healthy adult
Z score - comparing to average person their age + sex

if high FRAX score, start treatment
if fragility fracture, start treatment

Question 8

what is the difference between T and Z score

Answer 8

T score - comparing to young healthy adult
Z score - comparing to average person their age + sex

Question 9

how is osteopenia managed

Answer 9

osteopenia when T score = -1 to -2.5
repeat DEXA scan in 2yr

Question 10

how is osteoporosis medically managed

Answer 10

conservative management (stop smoking/alcohol, weight-bearing exercise, more VitD/Ca intake)

1 - oral bisphosphonate (alendronate) - interfere with osteoclast activity, preventing bone resorption

2 - try with another bisphosphonate

3 - denosumab (monoclonal Ab) - blocks osteoclast activity via RANK ligand

strontium ranelate - stimulates osteoblasts, blocks osteoclasts
teriparidate - PTH, stimulates bone growth

Question 11

how is osteoporosis managed in pre + post menopausal women

Answer 11

pre = HRT to increase E2
(SE: risk of VTE/stroke, endometrial cancer)

post = raloxifene, selective E2 receptor modulator that stimulates E2 in bone but blocks in breast/uterus
(SE:hot flush, vaginal dryness, risk of VTE/stroke)

Question 12

what are SE/cautions of osteoporosis medication

Answer 12

bisphosphonate - take on empty stomach, while sitting up, 30min before eating
SE: reflux, oesophageal erosion, atypical fracture, osteonecrosis of jaw

denosumab - SC injection every 6 months

Question 13

what are primary + 2ndary causes of hyperaldosteronism

Answer 13

primary:
bilateral idiopathic hyperplasia (most common)
conn syndrome - unilateral adrenal adenoma

2ndary = due to excess renin
renal artery stenosis, HF, liver cirrhosis, ascites

Question 14

how do kidneys increase BP

Answer 14

juxtaglomerular cells of afferent arteriole detects low BP
releases renin

renin causes angiotensinogen (from liver) -> angiotensin 1
ACE (from kidney/lung) causes angiontensin 1 -> angiotensin 2

angiotensin 2 stimulates aldosterone release from zone glomerulosa, adrenal cortex
at DT: more Na absorbed, more K excreted
at collecting duct: more H2 excreted, causing metabolic acidosis

Question 15

why does high BP cause metabolic acidosis

Answer 15

aldosterone release causes more H2 excretion at collecting duct
so metabolic acidosis

Question 16

how is hyperaldosteronism investigated

Answer 16

initial - measure aldosterone:renin ratio
(low renin = primary cause, both high = secondary)

CT/MRI abdo+pelvis for adrenal gland tumour or hyperplasia
if considering surgery, adrenal vein sampling done (unilateral - surgical resection, bilateral - mineralocorticoid antagonists)

for secondary hyperaldosteronism = renal artery stenosis
doppler US -> CT/MR angio (for percutaneous renal artery angioplasty)

Question 17

if considering surgery for primary hyperaldosteronism, what investigations are done + management

Answer 17

adrenal vein sampling

if unilateral = surgical resection
if bilateral = mineralocorticoid receptor antagonist (spironolactone, epleronone)

Question 18

what is phaeochromocytoma

Answer 18

adrenal medulla tumour - rare
presents in 40-50s with FH

neuroendocrine tumour of chromaffin cells in adrenal medulla
causes excess catecholamine secretion (adrenaline), triggering SNS

Question 19

what in FH makes phaeochromocytoma more likely

Answer 19

MEN2A - autosomal dominant - linked to medullary thyroid cancer, primary PTH
NFD1 - autosomal dominant - cafe au lait spots, axillary freckling
von-hippel Lindau syndrome - autosomal dominant - linked to cerebellar/retinal haemangioblastoma

Question 20

how is phaeochromocytoma investigated

Answer 20

plasma free metanephrine OR urine free catecholamine
(serum catecholamines have too short a half-life, so not measured)

CT/MRI abdo+pelvis to look for tumour
genetic testing

Question 21

how is phaeochromocytoma managed

Answer 21

medical optimisation + surgical resection

medication - initially alpha blocker (phenoxybenzamine, doxozosin), then add beta blocker
surgical resection