Presentations Flashcards

1
Q

botox

botulinum toxin can cause?

A

CN palsy, paralysis of skeletal muscle, respiratory paralysis, and/or death

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2
Q

how does botox work?

A

binds to SNARE complex, cleaving proteins (guides vesicles to nerve ending)

prevents ACh from binding to nerve terminal and entering into synapse

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3
Q

by botox preventing ACh release, it can be used to treat…

A

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

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4
Q

botox

blockage of ACh can be overcome by:

A

restoration of SNARE proteins

new nerve terminals sprouting from axon

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5
Q

what are amphetamines?

A

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

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6
Q

what is the MOA of amphetamines?

A

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

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7
Q

what is the bioavailability of amphetamines?

A
easily absorbed
highly lipid soluble
protein binding (15-40%)
metabolism is haptic
half life =10 hours
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8
Q

what are the uses of amphetamines?

A

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

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9
Q

what are types of amphetamines?

A

prescription: schedule II classification: adder all, ritalin, concerta

OTC: caffeine, ephedrine, peynlpropanolamine

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10
Q

what are general effects in the body with amphetamines?

A

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

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11
Q

what is the dependence to amphetamine?

A

variable psychic dependence and no physical dependence

slow development of tolerance to many of the effects of the drug

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12
Q

what does amphetamine abuse cause?

A

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

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13
Q

what are implications for PT of amphetamines?

A

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

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14
Q

what are the common signs and symptoms of fibromyalgia?

A
Hallmark sign= fatigue
hx of chronic pain in all extremities
pain does not follow a dermatomal pattern
tingling/numbness
sleep disturbances
depression
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15
Q

what are treatment goals for fibromyalgia?

A

focus on maintain function/reducing symptoms, patient education

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16
Q

what are non pharmacological treatment options for fibromyalgia?

A
aerobic exercise
cognitive behavioral therapy
strength training
acupuncture
hypnotherapy
biofeedback
balneotherapy
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17
Q

what are pharmacological treatment options for fibromyalgia?

A

pain meds
antidepressants
muscle relaxants
sleep med

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18
Q

what are specific drugs for fibromyalgia?

A

cimbalta

lyrica

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19
Q

what is cymbalta?

class?
MOA?
dose?

ADME?

1/2 life?

A

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

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20
Q

what is lyrica?

class?
MOA?
dose?

ADME?

1/2 life?

A

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

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21
Q

what are glucocorticoids?

A

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

22
Q

how do glucocorticoid injections affect inflammation?

A

alters gene’s response to the inflammatory process

  • increase production of anti inflammatory proteins
  • inhibits production of pro-inflammatory substances
  • pain reduction
23
Q

what are side effects to GC injections?

A

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)

24
Q

what are systemic effects of GC injections?

A

increased systolic BP
increased blood glucose levels
decrease in adrenocorticotropic hormone (ACTH)

25
what are common uses for glucocorticoid injections?
``` dequervain's trigger finger OA/RA bursitis tendonitis synovitis fascitis CTS epicondylagia adhesive capsulitis facet syndrome ```
26
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
27
-itis vs. -algia ?
itis= inflammation algia= microdamage must address initial insult to instigate inflammation process leads to continued injury with use and possible rupture
28
when are GC injections appropriate?
``` bursitis adhesive capsulitis trigger fibers dequervins contraction RA ```
29
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
30
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
31
what are types of MS?
relapse remitting primary-progressive secondary progressive progressive relapsing
32
what is the etiology of MS?
genetics | viral infection
33
what is the pathogenesis of MS?
inflammation demyelination axon loss
34
what are the clinical manifestations of MS?
sensory changes optic neuritis SC lesion
35
what is the old treatment for MS?
treat symptoms baclofen: - administered orally or intrathecally - treatment of muscle spasticity
36
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
37
what are PT implications for MS?
side effects scheduling psychosocial considerations patient education complementary and alternative meds (CAM)
38
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
39
what are clinical manifestations of parkinsons?
rigidity, trembling, forward trunk tilt, shuffling gait, reduced arm swing
40
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
41
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
42
what are PT implications for parkinsons?
time meds with exercise fall prevention modify ADLs big program speech and occupational therapy
43
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 ```
44
what are examples of statins?
``` atorvastatin (lipitor) lovstatin (mevacor) rosuvastatin (crestor) fluvastatin (lescol) simvastatin (zocor) pravastatin (pravachol) ```
45
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
46
what are statins primarily used for?
hypercholesterolemia cardiovascular disease when risk factors for cardiovascular disease are present-- diabetes
47
what are secondary benefits of statins?
cancer dementia osteoporosis
48
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
49
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
50
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