Endo Flashcards
Describe the signs and symptoms of menopause
change in menstrual cycle
vasomotor sxs (hot flashes, night sweats)
vulvovaginal sxs (dryness) => painful sex
sleep disturbances
weight gain - 5 lbs
menopause
stop period
after 12 months without period
perimenopause
1st signs of endocrine change
irregular period
ends 1 year after last period
natural/spontaneous menopause
12 months after last period confirmed
induced menopause
stopped periods manually
peri-menopause - menopause transition
starts when you see sxs
ends 12 months after last period
post-menopause
years after last period
bioidentical hormone therapy (BHT)
v similar to hormones of the body
estrogen therapy (ET)
unopposed estrogen for:
- systemic use for women without uterus
- local for women with dryness
estrogen-progestogen (EPT)
progestogen added to ET
protect women with uterus from endometrial cancer (estrogen can cause cancer)
FDA approved indications for HT
Vasomotor sxs
prevention of bone loss
premature estrogen loss
genitourinary sxs
How can contraceptives help with perimenopause symptoms?
less hot flashes more predictable period less cramps improve BMD decrease risk cancer
What is the physiological effect of PTH
Bone: increase expression and secretion of RANK ligand from osteoblasts
RANKL causes osteoclast formation => bone resorption
Kidney: decrease phosphate transporter => decrease phosphate uptake
What is the physiological effect of calcitonin
increases cAMP to inhibit osteoclasts
What is the physiological effect of vitamin D
Bone: osteoblasts have Vit D receptors. Cause blasts to make cytokines that activate clasts to resorb Ca which make blasts deposit Ca. BONE MOBILIZING ACTION
Kidney: increase Ca reabsorption
Intestine: Increase Ca absorption
List the causes of primary osteoporosis
aging, menopause, andropause
list the causes of secondary osteoporosis
endocrine, liver/kidney disease, malignancies, malnutrition, GI disease (no Ca abs), genetic disease
name the drugs used in treatment of osteoporosis
bisphosphonates denosumab (Prolia) estrogen/progestins & SERMs calcitonin teriparatide abaloparatide
MOA of bisphosphonates
- get deposited onto bone
- gets eaten by clast
- cause clast apoptosis
MOA of Denosumab
decrease binding of RANKL to RANK so prevent clast formation and activation
MOA of SERMs
Ex: raloxifene (Evista)
estrogen receptor agonist: decrease bone resorption
MOA of calcitonin
activate G protein receptor on clasts
increase cAMP
inhibit clast
MOA of estrogen/progestin
make less cytokines which activate clasts
estrogen bind to blast => decrease making RANKL => decrease clast activity
MOA of teriparatide
low dose causes increase in blasts and bone formation
MOA of abaloparatide
low dose causes increase in blasts and bone formation
who should be tested for osteoporosis
women over 65 post menopause/perimenopause men over 70 men 50-69 with risk factors fracture after 50 years condition/medication: glucocorticoids, RA
Risk factors of osteoporosis
vit D deficient hyperprolact hyperPTH Cushings Diabetes
Meds associated with osteoporosis
depo-medroxyprogesterone
thiazolidenediones
glucocorticoids
thyroid hormone
T-scores
- 1 and up: normal
- 1 to -2.5: osteopenia
- 2.5 and less: osteoporosis
- 2.5 and less and hx of fracture: severe
