Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Semester 1 > Menopause, ageing, osteoporosis > Flashcards

Menopause, ageing, osteoporosis Flashcards

(90 cards)

Start Studying
1
Q

menopause is

iatragenic menopause definition

A

menopause= the permanent ceasing of menstruation, a part of ageing process for women
usually early 50s. process usually gradual, wax and wane over years

iatragenic menopause= by surgery, radiotherapy, chemo etc. Ovaries removed or stopped from working

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

perimenopause
menopause/ postmenopausal
premature menopause

A

perimenopause= from beginning of menopausal symptoms to postmenopause

menopause= no menstrual periods 12 months

premature menopause= menopause before 40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

describe the hormonal changes and follicular changes in perimenopause

A

number and responsiveness ovarian follicles declines over 40

leads to decrease in oestrogen and inhibin secretion, so negative feedback on GnRH and FSH, LH

so FSH and LH levels increase

leftover responsive follicles increase oestrogen in response

so oestrogen production may be erratic, levels fluctuating normal high and low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hormone changes in menopause/ postmenopausal

A

when no more responsive follicles, negative feedback loop is disrupted. FSH and LH levels stay high, stimulate ovarian stromal cells to synthesise androgens (high FSH is therefore a sign of menopause)

in postmenopause, oestrogen derived from ovarian stroma and adipose tissue, androgens aromatised to oestrogen, but a less active form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what tissues are oestrogen dependent

A 
ovary
endometrium
breast 
bone
fat
blood vessels
hair 
colon
(testes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

acute clinical sympotoms of menopause

A

cessation of menses
vasomotor symptoms- hot flushes, night sweats
mood swings, depression, forgetfulness
headaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

explain hot flushes in menopause

A

70-90% of women experience

hot flushes= vasodilation in face and neck, lasting 1 to 5 mins with profuse sweating

thought caused by narrowing of hypothalmic thermoregulatory set point

    • increasing chance sensitivity to intense heat in response to int and ext environmental triggers
    • activates heat loss responses ie vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

medium term symptoms of menopause

A

urogenital atrophy-
vulval, vaginal, urethral, bladder all oestrogen dependent, loss of leads to thinning of epithelium, atrophies

vagina and vulva- dryness, itching, discomfort

bladder- changes in pH, raised vaginal pH, increased bacterial growth so recurrent UTIs

increased risk urinary incontinence/ urgency/ leakage

Sexual problems-
vaginal dryness may cause painful intercourse. loss of libido.

thinning of skin, brittle nails, generalised pains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

long term impact menopause on obesity

A

prevalence obesity higher in post m than pre

menopause causes increase in total body fat
redistribution of fat from peripheries to trunk

if combine w loss of muscle mass and inactivty- obesity and higher risk diabetes type 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

long term impact menopause cardiovascular

A

oestrogen is vasoactive so promotes vascular remodelling and elasticity so is able to regulate vasodilation and local inflammation

without oestrogen have more vasoconstriction, inflammation so arterial stiffness. may cause atherosclerosis and hypertension

early menopause incr risk of coronary heart diseas, stroke, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

impact menopause on mood

A

menopause causes decline in synthesis of NTs eg acetylcholine, serotonin, dopamine

results in lo mood, irritability, insomnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how is diagnosis of menopause made in over 45s

A

in women over 45 on clinical symptoms alone,

perimenopause- vasomotor symptoms, irregular periods

menopause- no period 12 months AND not on hormonal contraception

if without uterus, based on vasomotor symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how is diagnosis made in under 45s

A 
other conditions need to be excluded, incl PCOS, hypothalmic. pituitary problems so
FSH test (u40s do 2 bloods spaced)

not used in UK but
AMH and antral follicle count on ultrasound indicates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

types of oestrogen and progesterone drugs delivered in HRT

A

oestrogen:
oestradiol
conjugated equine oestrogen

Progesterone:
norethisterone
progesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what type of HRT is most likely to cause cancer

A

oestrogen only has 45% incr risk endometrial cancer

if take prog and oestrgen then reduced to 15%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

HRT regimens

A

oestrogen continuously by itself- only if no uterus as othw 45% incr cancer

continuous combined regimen

sequential combined regimen- prog given sequentially for perimenopausal- 2 weeks on 2 weeks off or 3 months on 2 weeks off, useful to maintainperiods so know when enter menopause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

HRT routes

A

oestrogen:
transdermal (patch/ gel) (local skin irritation)
oral (cost-effecive, acceptable)

vaginal oestrogen- cream, tablets, vaginal rings (for urogenital symptoms)

progesterone:
micronised progesterone
oral derivatives
mirena coil

if HRT not effective for sexual desire, testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

benefits vs risks HRT

A 
benefits:
vasomotor
mood and sleep
urogenital atrophy
osteoporosis

risks:
breast cancer
stroke, venous thromboembolism
ovarian cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

HRT re breast cancer

A

risk greater prog and oestro vs oestro alone
risk increases with duration HRT use

h/e lifestyle factors can increase risk just as much so maybe worhty risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

HRT re venous thromboembolism

A

increases w age and duration HRT
highest with oral oestrogen
no risk with non-oral oestrogens, or micronised progesterone

obesity, smoking also risks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

HRT re cardiovascular disease

A

has beneficial effect at earlier age
in young postmenopausal, oestrogen alone is cardio protective, reduces risk CHD u60

incr risk CHD if start more than 10 y after menopause

h/e combined HRT increases risk CHD, stroke 2.2 times

shouldn’t be used for cardio protection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

contraindications HRT

A 
pregnancy
undiagnosed vaginal bleeding
active or recent VTE/ heart attack
suspected/ active breast or endometrial cancer
acute liver disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

alternative therapies in leieu HRT

A

lifestyle:
exercise, lighter clothing, stress reduction, trigger avoidance (caffeine smoking)

vaginal moisturisers, lube, herbal remedies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

how common is premature ovarian insufficiency and what to do about it

A

in in 100 under 40
1 in 1000 under 30
1 in 10000 under 20

HRT recommended unless contraindicated, until age of natural menopause, to improve physical and psychosocial health

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
osteoporosis is | osteopenia is
osteoporosis is the loss of bone substance, such that fractures of non-traumatic origin are sustained BMD 2.5 SDs or more below a normal, healthy control. osteoporosis is a disease of bone remodelling Osteopenia is 2.5 to 1 SD below normal healthy control
26
how is BMD measured
bone mineral density is measured with DEXA, dual energy x ray absorptiometry, of lower spine and hips x ray sent via 2 energy streams. 1 stream absorbed by soft tissues, other denotes total absorption. Subtract soft from total= bone results. bmd computed over area measured
27
why is bone remodelling important and what is it a balance of
formation and maintenance of skeleton depends on balance between bone formation (osteoblasts) and bone resorption (osteoclasts) bone remodelling is essential as removes defective bone and responds to mechanical pressure
28
define bone modelling vs bone remodelling
bone modelling: responsible for growth and shaping of bones during childhood and adolescence bone remodelling: responsible for maintaining mechanical integrity of skeleton during adult life
29
why is menopause a risk factor for osteoporosis
oestrogen usually enables osteoblasts and inhibits osteoclasts. menopause causes sudden increase in osteoclast activity and accelerates below process in osteoporotic post menopausal, problem is with osteoBlasts osteoblasts no longer able to catch up with activity of osteoclasts, causes deficit in BMD
30
action of oestrogen on osteoblasts
oestrogen has positive effect on osteoblasts - increases collagen type 1 synthesis - stimulates growth factor synthesis - regulates osteoblast proliferation - stimulates expression of osteoblast differentiation and maturation markers
31
action of oestrogen on osteoclasts
oestrogen has negative effect in osteoclasts increases apoptosis of osteoclasts suppresses osteoclast differentiation acts on osteoclasts via osteoblasts
32
how is osteoclast differentiation and maturation usually stimulated
1. RANK is receptor on osteoclast precursor cell, is an effector molecule, acts on DNA to stimulate maturation 2. RANKL (RANK ligand) is located on osteoblast 3. RANKL is stimulated to bind with RANK receptor (by IL1, TNF, Vit D, PTH, PTHrp) 4. this promotes osteoclast maturation and differentiation
33
how does oestrogen interfere with osteoclast maturation and differentiation
1. oestrogen promotes synthesis of OPG (osteoprotegerin) 2. OPG is a decoy of RANK receptor so RANKL binds with OPG instead of RANK 3. prevents osteoclast maturation and so formation of active osteoclasts
34
why don't all women get osteoporosis
1 in 3 women do in both m and w, bone mass deteriorates w age after 45 starts to diminish, women at accelerated rate if have a higher bone mass before the decline will be less impacted peak bone mass is influenced by diet and vitamins and ethnicity- white women and asian women do worse
35
why can't we take a blood test for osteoporosis
bone markers don't appear abnormal as very diluted in blood sample also remodelling process takes 9 months so may be too early to see
36
osteoporosis in men
1 in 12 men higher morbidity and mortality also assoc with falling oestrogen levels may see osteoporosis when oestrogen receptor mutation or aromatase mutation
37
outline vitamin D and calcium regulation
vitamin d: sun on skin, vitamin D3 formation from cholesterol base, goes to liver and is hydroxylated to parent molecule then metabolised to active form of D£ calcium regulation: 1. decrease in calcium causes increase in parathyroid hormone PTH synthesis switches off
38
how do corticosteroids affect calcium regulation
corticosteroids cause calcium resorption to be shut off in the gut PTH levels and vit D levels continue rising, act on bone to release calcium may eventually be shut off but may not only see with high, continuous corticosteroid use
39
how else do corticosteroids affect bone and so total effects are
act on osteoblasts to decrease activity, decreasing collagen 1 synthesis this reduces osteoblast numbers in all, corticosteroids cause calcium to be released from bone and reduce number and activity of osteoblasts so bmd loss
40
osteoporosis treatments
HRT for women with osteoporosis (no longer in favour) Bisphosphonates, iv or oral- decrease osteoclast activity. side effect of osteonecrosis of jaw. oral incr stomach acidity so not well tolerated SERMS- selected oestrogen receptor modulators supplementation calcium and vit D intermitent PTH enhances bone formation (if give continuously increases osteoclast activity) denosumbad- monoclonal antibody for RANK protein. sits on RANKL, inhibits it binding to RANK receptor, much like OPG. therefore inhibits osteoclast activity
41
pharma- changes to absorption with age
not much change some reduction in secretion of gastric acid and enzymes in GI tract reduced total SA, but compensated for by some slowing of gastric emptying and motility
42
pharma- changes to distribution with age
when older- loss muscle mass, loss total body water, increase body fat, total body mass often decreased SO lipid soluble drugs: - bc more fat, greater volume of distribution - can accumulate in fat and brain tissue and have prolonged effects water soluble drugs: - bc less water, smaller volume of distribution - can lead to higher conc serum levels, beware toxicity if drug has narrow therapeutic index
43
pharma- changes to metabolism of drug with age
not lots reduced hepativ blood flow and volume- may cause reductionin metabolism of some drugs or increase bioavailability of others. reduced first pass metabolism
44
pharma- changes to excretion of drug with age
renal function reduces with age may lead to reduced clearance of drugs which are excreted by kidney filtration so may lead to drug and metabolite accumulation an toxicity- may need dose reduction for renally cleared drugs
45
pharma- changes to pharmacodynamics with age
increased pharmacodynamic sensitivity to many drugs so increased pharmacological effects increased susceptibility to ADRs/ side effects increased risk toxicity often need lower doses
46
polypharmacy
use of multiple meds by a pt, usually 5+ v common in elderly as have an ageing pop living w more lifelong chronic conditions instead of dying often working with specialists in isolation
47
how may polypharmacy be inapproporiate or appropriate`
appropriate: medicines used are optimised each achieves its benefit no ADRs or interactions problematic: multiple prescribed inappropriately intended benefit not achieved ADRs/ interactions
48
impact of polypharmacy in older
increasing number of prescribed drugs increases risk ADRs and side effects, drug- drug interactions older pts more susceptible to ADRS and interactions due to changes in pharmacokinetics and pharmacodynamics ADR of a med may be misdiagnosed as an illness and prescribed more meds, etc
49
prescribing cascades
new drug prescribed to treat unrecognised ADR/ symptom between existing meds and diagnosed new condition, cycle goes on
50
how to prevent polypharmacy
only prescribe in necessary and pt agrees consider NNT vs NNH as to whether it is worth it consider deprescribing review regularly explain all clearly use a limited formulary start low and go slow
51
NNT
avg number pts who need to be treated to prevent one additional bad outcome
52
NNH
how many pts need to be exposed to risk factor over a specific period to cause harm in 1 pt
53
what is an iatrogenic illness
caused by medical trtmnt
54
prednisolone is?
a corticosteroid
55
bendroflumethiazide is?
a thiazide like diuretic- for hypertension
56
meds that increase fall risk
antihypertensives diuretics (both lower bp, falls post hypertension) hypoglycaemics sedatives, hypnotics opioda antideps antipsychs sedating antihistamines anticholinergics/ antimuscarinics
57
how do corticosteroids work and what are they
synthetic versions of hormones produced by adrenal glands 2 modes of action: inhibit immune system, so useful for autoimmune conditions suppress inflammation so useful for inflamm conditions
58
anti inflammatory effects of corticosteroids
inhibit vasodilation and increase vascular permeability-- fluids can't enter site, decr swelling reuced number circulating lymphocytes, inhibits their emigration to site inhibit cytokine expression eg IL1 and TNF, integral to mediated response inhibit production phospholipidase, prevents formation of inflamm mediators
59
corticosteroid ADRs
occur with prolonged use of high doses cushings disease ``` cushingid appearance oedema sleep disturbance hypertension osteoporosis diabetis mellitus cataracts ```
60
good prescribing of corticosteroids
use minimum dose that achieves desired effect for minimum duration to limit long term risks taper dose before stopping for courses over 3 weeks to prevent withdrawal and allow adrenal glands to start secreting cortisol again to prevent relapse if using high dose/ long term, consider bone protection (biphosphate) and gastric protection (proton pump inhibitor)
61
what is the disability free life expectancy gap difference poor vs rich
amount of years disability free before death is smaller in poorer equal m and f majority poorer will have disability before pension age
62
how may exercise reduce fall rate and frailty | what exercise
reduces by 20% improves balance strengthens muscle and bone so fewer breaks reduces risk of symptoms of conditions helps continue everyday activities and remain independent improves brain function should combine weight-bearing activity with impact and muscle strenghtening
63
what % UK pop is over 65 | what % of those admitted to hospitals are over 65
25% UK are over 65 | 65% hospital admissions over 65
64
what are the biological, programmed theories of ageing
programmed longevity- sequential switching off of genes endocrine theory- biological clocks imunological theory- measurable decline in immune function as age so susceptible to deathly infection
65
what are the biological, damage/ error theories of ageing
hayflick limit- wear and tear free radical theory- longer around, the more damage to cells and organs glycation theory- glycation end products cause cell damage somatic DNA damage theory- DNA mutations accumulate w more division
66
what are the evolutionary theories of aging
antagonistic pleiotrophy- genes have beneficial effects early and detrimental later on disposable soma thoery- trade off between maintenance and repair vs reproduction
67
what are the cardiovascular effects of ageing
atherosclerotic change in arteries- walls thicken and elasticity reduced baroreceptors less sensitive- postural bp control worse heart valves thicken apoptosis atrial pacemaker cells decreased esponsiveness to adenoreceptor stimulation decrease in maximal achievable HR
68
what are the musculoskeletal effects of ageing
skeletal muscles lose cells and weight lose more fast twitch than slow twitch fibres so less explosive hormone loss and denervation atrophy exacerbated by inactivity/ hospital decreased BMD cartilage thins ligaments less elastic
69
what are the vision and hearing effects of ageing
``` lens stiffens- difficulty focussing cloce lens denser- reduced night vision retina less sensitive to light pupils react slower presbyacuisis- less high pitched hearing ```
70
what are the nervous system effects of ageing
cerebral blood flow decreases 10% loss in brain weight more susceptible to damage some slowing of thought and reflexes from 30
71
what are the immune system effects of ageing
immunosenescence so everything is reduced
72
what are the GI system effects of ageing
``` taste buds lose sensitivitiy gums recede and less saliva food empties stomach slower liver loses cells and reduced blood flow so more toxins and side effects gut transit time decreases ```
73
what are the renal effects of ageing
``` nephron number declines 30-40% kidneys shrink less efficient clearing waste men- prostatic hypertrophy women- urinary incontinence ```
74
what are the endocrine effects of ageing
GH levels decrease reduction in insulin sensitivity, inc diabetes type2 reduction adrenal hormones female menopause
75
frailty is | frailty results in
a state of increased vulnerability to poor resolution of homeostasis after a stressor event, which increases the risk of adverse outcomes not all frail. but frailty increases prevalence with age someone who is frail will take longer to recover than a fit person and may never return to previous level of functional abilities
76
what is the clinical frailty scale
goes 1. very fit to 9. very severely frail to 9. terminally ill useful to know as those more frail have worse outcomes so need to consider
77
what is the comprehensive geriatric assessment
``` treatment approach. uses an MDT considers all when choosing options- medical problems mh function social circumstances environmental assessment ``` has reduced mortality and functional decline and reduced care home admission
78
ways to manage an infection
``` symptomatically if viral topically if superficial removing focus of infection surgically immunotherapies antimicrobials ```
79
antibiotics target? | antibiotics may also be c.... or s.....?
different classes have different targets within bacteria eg cell wall synthesis (broad spectrum antibiotics) nucleic acid damage protein synthesis folic acid metabolism antibiotics may be cidal (kill bacteria) or static (immobilises so immune system can deal with them)
80
types of antibiotic therapy
empiric therapy: treat per guidelines prior to firm diagnosis typicall broad spectrum based on international clinical trials and local epidemiology targeted therapy: initiate when culture report available or switch to therapy: using antibiotics to treat the infection pre-emptive therapy: use antibiotics to treat presumed infection prophylaxis: prevent development of infection
81
infection prevention measures
prophylactic use of antibiotics is OK in certain groups but very limited ``` decontamination PPE sharps management waste disposal laundry ``` isolation of pt severe, made by infection specialist antimicrobial stewardship
82
antimicrobial stewardship
aims to ensure appropriate antibiotic use the right drug at right time adt right dose via right route for right duration for right patient
83
what are the signs of inflammation
redness swelling heat pain severe- loss of function can also be signs of infection
84
what are some signs of infection
``` signs of inflammation suppuration (pus) necrosis lymphoadenopathy fever, rigors fatigue, headache, weakness etc ```
85
staphylococci
gram positive cocci in groups facultative anaerobes- fine in aerobic but do better anaerobic classified acc to ability to coagulase serum ---- staph aureus is coagulase positive coagulase negative are less pathogenic common in medical device infections, UTIs
86
staph aureus
gram positive cocci in groups, coagulase positive seen in superficial skin lesions, localised abscesses, eczema infection. Deep seated infections like pneumonia, osteomyelitis, endocarditis etc food poisoning via toxins and toxic shock syndrome assoc with Panton Valentin toxin (PVL) major cause hospital acquireed infections of surgical wounds
87
MRSA
methycillin resistant staph a resistant to many antibiotics (is an XDR), typically resistant to several classes, especially glycopeptides usually treated with vancomycin, but some vancomyic resistance has been reported
88
antibiotic resistance may develop how
1. natural resistance- an inherent trait that renders it resistant 2. acquired resistance- by means of mutation of transfer of plasmids
89
mechanisms of antibiotic resistance
1. chemically modify the antibiotic with enzymes 2. activate the cells efflux pumps and physically remove antibiotic from cell 3. modify target sites so not recognised by antibiotics
90
MDR XDR PDR antibiotic resistance
MDR multi drug resistance, 1 or more drugs in 2 classes XDR, extensively drug resistant, 3 or more classes PDR, pan drug resistant, all drugs and classes

Semester 1 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions