Case 8 - Ageing Flashcards
what is the menopause and what age does it begin
no periods for 12 consecutive months
can’t get pregnant naturally
45-55, ave 51
what is primary hypogonadism and give 2 examples
problem w ovaries
POI - menopause before age 40
natural menopause
what are the patterns of results for primary hypogonadism
low estradiol
high fsh/lh
what is secondary HGadism and examples
problem with PT and HT
eg hypothalamic disease bc anorexic
pituitary tumours = non functioning hormones
pattern of results for secondary HGadism
low estradiol
low fsh and lh
5 symptoms of menopause?
joint pain mood swings vasomotor symptoms insomnia vaginal and urogenital dysfunction
what happens w bone loss in menopause and why?
lose 20% of BD
estrogen inhibits resorption of bone so low estrogen = resorption of bone
how can you improve bone loss in menopause
limit alcohol and smoking
healthy diet w adequate calcium and d3
weight bearing exercise
4 treatments for menopause
prescription
HRT
natural = phytoestrogens and acupuncture
lifestyle
how long for and when do you take HRT
in perimenopause you can start
5 years max
3 negatives of HRT
increased risk of breast and womb cancer, VTE and stroke
what HRT do u take with a uterus and why
combined
bc oestrogen causes proliferation of endometrium, progesterone has anti-prolif effects
what HRT do you take if you have had a hysterectomy
oestrogen only
best method of estrogen? what are the other ways of delivering it?
best = transdermal bc no cancer or VTE risk
patch, gel, orally
what is micronized progesterone and why is it good
natural, body identical progesterone
no androgenic or gcc effects like synthetic
what does HRT reduce
all symptoms of menopause basically
what are prescription remedies for HRT
anti-depressants
clonidine - anti hypertensive
developing: neurokinin 3 receptor antagonist, reduces hot flushes and insomnia
when do you give androgen therapy to women
if loss of libido and sexual drive
what is osteomalacia
loss of bone mineral
associated w lack of vitamin d3
can still produce collagen
osteomyelitis?
infection of bone bc of bacterial origin
osteoarthritis?
mechanical in origin, disease of joints
osteoporosis?
loss of entire bone substance including extra-cellular matrix and minerals
fractures of non-traumatic origin are sustained
what is the WHO definition of OP and what are T and Z scores?
BMD 2.5 SD away from a normal healthy control
T score - BMD matched to control
Z - age matched BMD
how is BMD measured
DEXA of lower spine and hips
2 streams - absorbed by total body and one by soft tissue, subtract to get bone
OP in men and women figures
men - 1/12
women 1/3
what is the osteoid
unmineralized matrix, laid down by OB
what is bone remodelling
resp for maintaing mechanical integrity of skeleton in adult life
removes defective bone
responds to mechanical signals
what is the bone metabolic unit
osteoblasts on one side OC on other signalling going on between them osteoid laid down collagen type 1 formed in circles, lamella formed around outside
what is bone modelling
resp for growth and shaping of bones through childhood and adolescence
what does an 18 y old bone look like
epiphyseal plates open
trabeculae thick
corticies visible and thick
bone at menopause?
thinner trabeculae and corticies
fused EP plates
bone after 80?
no corticies, large gaps in trabeculae
what effect does oestrogen reduction have on bone
increases OC
too many for OB to keep up
esp bc sudden reduction
BMD deficit
what does oestrogen do normally on OB
increases alkaline phosphate expression
incr collagen and tf GF synthesis eg IGF
causes reg cell division and proliferation of OB
receptor for colecalciferol is a marker for OB differentiation is stim by oestrogen
what does oestrogen do normally on OC
incr apoptosis
suppresses proliferation
acts on OC via OB bc of rank/l protein
impact of peak bone mass on OP
higher PBM = stronger bones later in life
impact of genetics on PBM
afro-caribean higher than asians and whites
why do men have lower OP levels
bc higher PBM and oestrogen levels decreases slower bc no menopause
what are the bone markers used for OB and OC
alkaline phosphatase and collagen breakdown products
why can’t we use biochem to test for OP
bc disease of bone remodelling, takes approx 9 months to see
DEXA and BMD done every year reflect entire section of skeleton
OP in men risk and risk factors
25% lifetime risk of fractures
HGadism, smoking, alcohol, steroid therapy
effect of oestrogen on bone mass in men
required
bc mutation in aromatase or oestrogen receptors on OB and OC = OP
what is CCS therapy used for
asthma, RA, AID and inflammtory diseases like crohn’s disease
calcium regulation in terms of 1,25 D etc
o Calcium hormone decreases, PTH goes up
o PTH acts in kidney to metabolise 25OH (vitamin D) to 1,25 D (cole-calciferol)
o Vitamin D production in skin;
o Transformed in liver to 25 OH D3
o Major target for active form of vitamin d3: calcium resorption in the gut
o In the gut: many receptors for active form of vitamin D; enable calcium resorption to return calcium levels to normal
how do CCS affect calcium levels
prevents reabsorption through gut, increased levels of PTH left
how to classify fractures
by location - epi,di, metaphyseal
by type: open/closed, complete/incomplete
what is a fracture
condition that changes bone contour
stage 1 of wound healing?
haematoma formation
BV rupture = bleeding
clot forms, closes off injured vessels and leaves meshwork in damaged area
stage 2?
FC callus formation
external callus - organises w in medullary cavity, between broken ends of shaft
external - forms bone at level of fracture
centre: chondrocytes form hyaline cartilage
edges: diff into OB and bridge broken ends together
stage 3?
bony callus formation
OB replace cartilage w spongy bone
struts of sb join broken ends and hold in place
stage 4?
remodelling,
