geria Flashcards
aging (what’s not to be expected)
sickness, although common, isn’t part of the normal aging process; emphasis on this during pt. education
chronological vs biological age
chronological - your age in years from date of birth; biological age- your body’s age (affected by different factors, e.g., stress, disease/condition)
body changes when we get older (10)
- decrease in muscle performance (dec ms fiber size, fast-twitch fibers; loss of muscle mass; denervation of ms fibers, decline in total number)
- dec bone tensile strength (more osteoclast, less osteoblasts) [bones get more brittle]
- dec jt flexibility [less flexibility]
- ms mass decline at 30 [less ms]
- by 60-90, 30% of ms force production dec [less ms strength]
difference of fast-twitch and slow-twitch fibers
slow twitch (type I) - slow red ox
- aerobic, endurance exercises; oxygenated
fast-twitch - power / dynamic movement
osteopenia vs osteoporosis
osteopenia - less amount of bone density; osteoporosis - PROGRESSIVE LOSS of bone density
if untreated, osteopenia -> osteoporosis; major cause of fractures, MC women > men
osteosarcopenic obesity syndrome (what is it, describe the process and its components; is it reversible)
sarcopenia (loss of ms mass), osteopenia (loss of bone density), obesity (d/t myosteatosis AKA accumulation of fat in ms tissue)
- also: dynapenia (age-related loss of ms strength)
- these are normal processes in aging that can be addressed but if these 3 are left unchecked they will lead to osteosarcopenic obesity syndrome (NOT normal)
reversible unlike cachexia
sarcopenia vs cachexia
cachexia - loss of ms mass with or w/o fat loss; weight loss usually associated w end-stage diseases; body is wasting away and eating at itself, towards the end of this, pt. usually has to rely on caregivers for basic functions (total dependence); exercise has no effect
sarcopenia - reversible, MC men > women; ms mass loss; can be reversed by training
changes in collagen fibers during aging (4)
- less water in collagen matrix => less shock absorption properties, loss of collagen in IV discs (get shorter/smaller)
- inc crosslinks => scar tissue-like, not as pliable
- dec elastic fibers = skin sagging
- dec ROM - fine as long as fxal
CV changes during aging and consequences (6-9)
- dec HRmax & vo2max- dec aerobic workload capacity
- stiffer vascular tissue - inc BP, dec cardiac output and ventricle filling
- dec contractility in vasc tissue - dec HR, vo2max, aerobic workload capacity
- loss of cells in SA node - dec HR & HR max
- thickened basement membrane in capillary - dec arteriovenous o2 uptake
neurologic system changes during aging (5-6)
- loss of myelin - slowed nerve conduction
- axonal loss - slower ms fibers, loss of fine sensation
- ANS dysfunc - systemic issues (e.g., CV and GI systems)
- loss of sensory neurons - dec ability to discern of temperature and pain
- slower response time - inc fall risk
cognitive changes during aging (5)
- slower info processing
- delays in processing & task execution, learning, and long-standing tasks
- higher cognitive reserves in younger years serve as a neuroprotective resource when we get older (more grey and white matter reserves)
process leading to ADRs (3)
- altered distribution and absorption of drugs, impaired metabolizing of liver, difficulty in excretion => altered drug response and side-effects
distribution - less motile, absorption area, stomach emptying and gastric acid
absorption - less water, ms mass and plasma protein; inc fat
polypharmacy vs ADR
ADR - physiological response
polypharmacy - behavioral; excessive/inappropriate use of drugs
vicious cycle of drug administration (5)
more illness/conditions -> medications taken for conditions -> medications have side-effects -> side-effects are seen as sx. -> more medication taken for those side-effects (cycle repeats)
common ADRs (10) describe (common sx, mechanism, common meds, PT indications)
GI-S-FW-C-A-D-E-E-D-OH
GI issues
- vomiting, nausea, diarrhea, constipation
- NSAIDs, opioids: inhibit both cox inhibitors (inhibition of cox 1 leads to GI bleeding bc dec in mucosal lining)
- antibiotics: mess up gut fauna
- cox 2 inhibitors (eg. celecoxib, celebrex - increase MI risk)
sedation
- sleepiness, drowsiness
- analgesics, sedative-hypnotics, antihistamines, benzos, barbs
- dont lift heavy weights
fatigue & weakness
- ms weakness (more relaxed), less water and electrolytes
- diuretics, HTN meds (-zide, -zone)
confusion
- mild confusion to delirium
- antidepressants, drugs w anticholinergic effect (parasympathetic NS activity), narcotics, analgesics
depression
- barbs, antipsychotics, anti-HTN drugs (clonidine, propanolol, reserpine)
- clonidine: decreases catecholamine output -> inhibition of sympathetic NS
- reserpine: sympatholytic -> directly depresses sympathetic NS
excessive bleeding
- anti-HTN meds (i.e., anti-platelet meds)
extrapyramidal effects
- tardive dyskinesia, dystonia, pseudoparkinsonism
- antipsychotics
anticholinergic effects
- antihistamines, antipsychotics, anticholinergic drugs
- CNS effects (drowsy, dizzy) some PNS (sympathetic activated sx
OH
- anti-HTN, anti-anginal meds
- inc risk for falls
dizziness & falls
- sedation and OH-inducing drugs
frailty hallmarks (5)
- at least 3/5: (less than 3 pre-frail)
1. weight loss (10 lbs > in a year)
2. exhaustion
3. weak grip strength
4. low PA
5. slow walking speed
MC cause of injury and leading cause of injury death in persons 65+
falls
5 types of fallers
- accidental versus nonaccidental,
- syncopal versus nonsyncopal (fainted vs not),
- intrinsically versus extrinsically driven,
- falls with injury versus falls without injury
- single fall incident versus recurrent falling
criteria for recurrent faller
at least 2 falls in the last 6-12mos
FOF (causes, what to do, mechanisms that affect it)
causes: previous falls, injury
what to do: dethreaten movement
mechanisms that can affect: “freezing episodes”
MCI (difference to dementia, and hallmarks (4), types (2))
mci lies bet normal ageing and dementia
- abnormal cognitive measures compared to population-related norms
- doesn’t affect ADLs
- normal gen cognitive fxn
- memory complaints
amnestic vs non amnestic
delirium vs dementia
dementia - condition, progressively worsening degenerative of cognitive processes, irreversible; start with sx of mci and delirium
delirium - sudden onset, state (transient); can be agitated or hypoactive ; can happen in isolation
essential feature of dementia (2-4)
- devt of multiple cognitive deficits and at least 1 of the ff: agnosia, aphasia, apraxia, disturbance in executive fxning
types of apraxia (2) and aphasia (2)
ideational apraxia (lost idea of task) and ideomotor aphasia (can physically do task but cannot process cue)
broca’s aphasia (motor issue when speaking) and wernicke’s aphasia (cognitive issue - speech doesnt make sense)
types of dementia (4) (origin, clinical sx)
- lewy body
- d/t build-up of a-synuclein protein
- visual hallucination, parkinsonian sx., sensitive to antipsychotics - frontotemporal
- buildup of proteins in frontotemporal regions
- personality, thinking, judgment - alzheimers
- MC, d/t build-up of beta-amyloid proteins and neurofibrillary tangles (build-up of tau protein), loss of white matter
- memory, sx more severe w stress/tiredness (sundowning), aphasia, confusion/getting lost, lack of insight - vascular
- depending on area of infarct (small vessel, larger areas [multiple infarcts]); the only one that is SPONTANEOUS
- depending on the area, slowed thinking/cognitive processes
stages of AD devt in order (9)
- Early stages: [memory impairments!!], lapses in judgment, subtle changes in personality
- depression d/t awareness of cognitive decline
- IADLs difficulty (memory and language )
- getting lost, visuospatial probs
- disoriented, delusional, hostile
- motor control fxn loss
- behavioral probs
- dysphagia + incontinence
- not remembering family members and difficulty speaking
- death bc brain shrinks and organ shuts down
EDIGDMBDN
lewy body dementia (how common, sx, cause)
a-synuclein protein build-up
one of the most common progressive dementias
- progressive cognitive decline and 3 addtnal features:
1. fluctuations in alertness and attention
2. visual hallucination
3. parkinson-like sx. (EXTRA-pyramid)
karvonen
220-age= MHR
((MHR-RHR)(target intensity)) +RHR = THR
RPE table (mRPE, RPE, % effort, perceived workload, talk test)
6, 7, 8- 20, 30, 40
1- 9- 50- very very light - rest
2 - 10 - 55
3- 11 - 60 - fairly light - strolling
12- 65 -
4 - 13 - 70 - somewhat hard - brisk walking
- 14 - 75 -
5 - 15 - 80 - hard - 4-5 words
16 - 85
7 - 17 - 90 - very hard - cant talk
8 - 18 - 95 -
9 - 19 - 100
10 - 20 - exhaustion
norms for 6MWT (community ambu, walking speed)
300-400m = community ambu
0.8-1.5 m/s = fast enough to cross street
fun, function, frail, failure values for gait speed, 6mwt, 30STS, SCT, floor transfer
gait speed: fxn: 0.8-1.5m/s; frail 0.3-0.8m/s
6MWT: fxn: 300-400m; frail: 200-350m
30STS: fxn: 8-15; frail: <8
CST: fxn: 10-30s; frail: 30-50s
floor transfer - fxn: 10-30s; frail: >30s
balance and gait tests cut-off scores (8)
B46, T19, TUG13, 4S5S15, DGI20, FGA22, ABC67
recommended intensity
not lower than 60% intensity or 15RM
reactive balance control strategies (3)
hip, ankle, stepping strategy
primary goals for dementia management (2)
improve quality, maximize functional performance
main goals of PT in dementia mgmt (3)
- assist pt., caregiver, family to maximize functional performance and slow down physical decline
- simplifying or modifying envt to help with activity performance
- help caregivers create safe, functional, meaningful and pleasant activities
approach for dementia pt.s w behavioral issues
antecedent-behavior-consequence (ABCs)
contraindications for exercise (3 absolute CIs and 6 general precautions)
absolute CIs: RHR above 100, systolic above 200mmHg/diastolic above 120mmHg, stretching-jt. instability
- use safety equipment if needed
- proper form, avoid valsalva/holding breath
- safe envt (not too hot, cluttered, etc.)
- never exercise unsupervised in high intensity (min. 75-90% 1RM)
- know their meds, possible side effects
- provide encouragement
