Presentations Flashcards
botox
botulinum toxin can cause?
CN palsy, paralysis of skeletal muscle, respiratory paralysis, and/or death
how does botox work?
binds to SNARE complex, cleaving proteins (guides vesicles to nerve ending)
prevents ACh from binding to nerve terminal and entering into synapse
by botox preventing ACh release, it can be used to treat…
muscle spasticity, hyperhidrosis, incontinence, overactive bladder, over secretion of saliva, and cosmetic appearance
headaches, malaise, mild nausea, numbness, spreading to surrounding tissues, temporary weakness/paralysis of muscles, erythema/edema/mild
botox
blockage of ACh can be overcome by:
restoration of SNARE proteins
new nerve terminals sprouting from axon
what are amphetamines?
group of synthetic psychoactive drugs that act as a CNS stimulant and appetite suppressant
exogenous dopamine agonists
can be in the form of tablets, capsules, crystals and powder– swallowing takes longer to have affect (30 min), injection provides greatest high
what is the MOA of amphetamines?
cause monoamine, and particularly dopamine release
modify action of dopamine and noradrenaline in the brain (at high doses)
increases the concentration of dopamine in the synaptic cleft
amphetamines have mixed alpha and beta agonist activity
what is the bioavailability of amphetamines?
easily absorbed highly lipid soluble protein binding (15-40%) metabolism is haptic half life =10 hours
what are the uses of amphetamines?
treat ADD in children
increase mental alertness in adults with narcolepsy
suppress apetite or combat normal sleepiness
alleviate fatigue, improve mental and physical performance, elevate mood
what are types of amphetamines?
prescription: schedule II classification: adder all, ritalin, concerta
OTC: caffeine, ephedrine, peynlpropanolamine
what are general effects in the body with amphetamines?
PNS: vasoconstriction, HTN, tachycardia
CNS: agitation, insomnia, increased alertness
short-term side effects: high body temp, nausea, headache, dry mouth
long term: difficulty breathing, malnutrition, skin disorders
what is the dependence to amphetamine?
variable psychic dependence and no physical dependence
slow development of tolerance to many of the effects of the drug
what does amphetamine abuse cause?
feelings of euphoria, unrealistic sense of power, increased alertness, increase in perceived strength
long term abuse can result in psychotic behavior, violence/aggressioin, seizures, malnutrition
what are implications for PT of amphetamines?
amphetamines with PT for patients post stroke (subacute period)
best restoration of independent function
increases in attention, concentration, and performance on motor memory tasks
time PT sessions with when the drug is active in the blood
variety of tasks during sessions to challenge the brain to make connections and increase motor function
focus on functional activities
what are the common signs and symptoms of fibromyalgia?
Hallmark sign= fatigue hx of chronic pain in all extremities pain does not follow a dermatomal pattern tingling/numbness sleep disturbances depression
what are treatment goals for fibromyalgia?
focus on maintain function/reducing symptoms, patient education
what are non pharmacological treatment options for fibromyalgia?
aerobic exercise cognitive behavioral therapy strength training acupuncture hypnotherapy biofeedback balneotherapy
what are pharmacological treatment options for fibromyalgia?
pain meds
antidepressants
muscle relaxants
sleep med
what are specific drugs for fibromyalgia?
cimbalta
lyrica
what is cymbalta?
class?
MOA?
dose?
ADME?
1/2 life?
class: serotonin/NE reuptake inhibitor
MOA: pain inhibitory and antidepressant actions
dosing: 60 mg PO daily (up to 120 mg)
A: food slows absorption
D: protein binding >90%
M: extensive hepatic metabolism
E: renal -70%; fecal 20%
1/2 life= 8-17 hours
what is lyrica?
class?
MOA?
dose?
ADME?
1/2 life?
class: gamma aminobuytyric acid
MOA: GABA analog binds to alpha 2- delta site, reduce release of Ca- dependent neurotransmitters
dosing: 75-150 mg PO bid (225 mg max)
A: food does not have an effect
D: no protein binding
M: negligible hepatic metabolism
E: renal 90-99%
1/2 life: 5-6.5 hours
what are glucocorticoids?
endogenous: a type of adrenocorticosteroid produced by the adrenal cortex– immune system mediators
exogenous: drugs administered orally, topically, IV and intracapsularly– used for systemic inflammation and localized joint inflammation; immunosuppressants
how do glucocorticoid injections affect inflammation?
alters gene’s response to the inflammatory process
- increase production of anti inflammatory proteins
- inhibits production of pro-inflammatory substances
- pain reduction
what are side effects to GC injections?
decreased synthesis of proteoglycans – important for organized healing and viscoelastic properties of tendon
human tendon stem cell (hTSC), tendon degradation, other cells come in (adipocytes, chondrocytes, osteocytes)
what are systemic effects of GC injections?
increased systolic BP
increased blood glucose levels
decrease in adrenocorticotropic hormone (ACTH)
what are common uses for glucocorticoid injections?
dequervain's trigger finger OA/RA bursitis tendonitis synovitis fascitis CTS epicondylagia adhesive capsulitis facet syndrome
PT vs. steroid
corticosteroids:
- fast pain relief
- high pt satisfaction
- effective in short term
- reduces synovitis, ROM improvement rate with frozen shoulder
- high recurrence rates
- diminshes tissue integrity
PT:
- intermediate and long term
- low recurrence rates
- treats the root of the problem
- stress applied to encourage tissue growth and organized healing
-itis vs. -algia ?
itis= inflammation
algia= microdamage
must address initial insult to instigate inflammation process
leads to continued injury with use and possible rupture
when are GC injections appropriate?
bursitis adhesive capsulitis trigger fibers dequervins contraction RA
what are the implications for PT for GC injections?
determine is condition is biomechanical in etiology
know that effects of GC shots have long effect- take this into account when treating, particularly for any jt mobs to increase ROM
what is MS?
chronic, debilitating, immune-mediated disease causing the body to attack its own CNS by damaging myelin and nerve axons- sclerotic plaques form through SC and brain
what are types of MS?
relapse remitting
primary-progressive
secondary progressive
progressive relapsing
what is the etiology of MS?
genetics
viral infection
what is the pathogenesis of MS?
inflammation
demyelination
axon loss
what are the clinical manifestations of MS?
sensory changes
optic neuritis
SC lesion
what is the old treatment for MS?
treat symptoms
baclofen:
- administered orally or intrathecally
- treatment of muscle spasticity
what is the new treatment for MS?
SLOW PROGRESSION
1-Aubagio
- prescribed for pts with relapsing MS
- immunomodulatory drug with anti-inflammatory properties
2-Tysarbri
- monotherapy for relapsing MS patients
- recommended for patients unable to respond to alternate therapy
- Integrin-receptor antagonist
3- Lemtrada
-not FDA approved
what are PT implications for MS?
side effects
scheduling
psychosocial considerations
patient education
complementary and alternative meds (CAM)
what is the pathogenesis for parkinsons?
proteins responsible for cell autophagy and apoptosis become abnormal
- homeostasis disrupted
- degeneration of dopaminergic neurons in the substantia nigra
- ->decrease dopamine production
- -> dysfunction of basal nuclei- motor coordination, cognition, sleep patterns
formation intraneuronal protein/Lewy bodies
what are clinical manifestations of parkinsons?
rigidity, trembling, forward trunk tilt, shuffling gait, reduced arm swing
what drugs are used for parkinsons?
dopamine replacement therapy
- replaces dopamine in dopaminergic neurons
- improves mobility and functioning
- best in early stages
ex: Levodopa
dopamin agonist
- act on D1 and D2 dopamine receptors
- can be combined with dopamine replacement therapies
- not as effective as replacement therapy
ex: bromocriptine & ropinirole
monoamine oxidase inhibitors:
- inhibit type B enzyme of the MAO family– limit breakdown of dopamine
- may slow progression
- may cause lethal dietary or drug interactions- last line of defense
catechol O-methyltransferase (COMT)
- inhibit enzyme COMT- prevent levodopa conversion
- used as adjunct to levodopa therapy
ex: Tolcapone
amantadine
- blocks N-methyl-D-aspartate (NMDA) receptor in brain
- may reduce dyskinesia and other motor symptoms associated with levodopa therapy
anticholinergics
-block action of ACh in basal ganglia- alleviate tremors and rigidity
exercise & parkinsons
improves: aerobic capacity, strength, balance, gait, quality of life
L dopa & exercise:
-coordinate with peak dose or time of day when pt feels best (peak= 1 hour after dose)
recommend regular, ongoing, lower intensity for longer duration
what are PT implications for parkinsons?
time meds with exercise
fall prevention
modify ADLs
big program
speech and occupational therapy
what are statins?
class of drugs that lower cholesterol levels in the blood (lowers LDL, raises HDL, lowers triglycerides)
slows plaque formation
primary and secondary prevention of cardiac events
improve endothelial function stabilize plaques anti-inflammatory properties anti-cancer effects new blood vessel growth bone formation stimulation
what are examples of statins?
atorvastatin (lipitor) lovstatin (mevacor) rosuvastatin (crestor) fluvastatin (lescol) simvastatin (zocor) pravastatin (pravachol)
how do statins work?
inhibition of the HMG-CoA reductase enzyme
HMG-CoA is a rate limiting enzyme of cholesterol synthesis
cholesterol synthesis occurs primarily in the liver
reduced cholesterol increases cell membrane LDL receptors concentration
what are statins primarily used for?
hypercholesterolemia
cardiovascular disease
when risk factors for cardiovascular disease are present– diabetes
what are secondary benefits of statins?
cancer
dementia
osteoporosis
what are the risks of statins?
if taking multiples– muscle pain & damage
females- liver damage
petite- increased blood sugar/ type 2 diabetes
diabetes- neurological effects
alcohol consumption- rhabdomyolysis
what will you see in PT with statins?
energy and exertional fatigue worsened- esp women
mild muscle injury suggested as a result of increases in creatine kinase
decreased muscle strength??
muscle pain
what are PT implications for statins?
awareness of adverse S/S- PT education
PT may confirm adverse effects
recommendations with S/S are present
delay of tx/recovery
consideration of S/S during tx planning;
muscle groups
type of contraction/exercise
level of exertion
safety concerns and precautions
