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Pharmacology > Presentations > Flashcards

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
Q

what are common uses for glucocorticoid injections?

A 
dequervain's 
trigger finger
OA/RA
bursitis
tendonitis
synovitis
fascitis
CTS
epicondylagia
adhesive capsulitis
facet syndrome
26
Q

PT vs. steroid

A

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
Q

-itis vs. -algia ?

A

itis= inflammation

algia= microdamage

must address initial insult to instigate inflammation process

leads to continued injury with use and possible rupture

28
Q

when are GC injections appropriate?

A 
bursitis
adhesive capsulitis
trigger fibers
dequervins contraction
RA
29
Q

what are the implications for PT for GC injections?

A

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
Q

what is MS?

A

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
Q

what are types of MS?

A

relapse remitting

primary-progressive

secondary progressive

progressive relapsing

32
Q

what is the etiology of MS?

A

genetics

viral infection

33
Q

what is the pathogenesis of MS?

A

inflammation
demyelination
axon loss

34
Q

what are the clinical manifestations of MS?

A

sensory changes
optic neuritis
SC lesion

35
Q

what is the old treatment for MS?

A

treat symptoms

baclofen:

  • administered orally or intrathecally
  • treatment of muscle spasticity
36
Q

what is the new treatment for MS?

A

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
Q

what are PT implications for MS?

A

side effects

scheduling

psychosocial considerations

patient education

complementary and alternative meds (CAM)

38
Q

what is the pathogenesis for parkinsons?

A

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
Q

what are clinical manifestations of parkinsons?

A

rigidity, trembling, forward trunk tilt, shuffling gait, reduced arm swing

40
Q

what drugs are used for parkinsons?

A

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
Q

exercise & parkinsons

A

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
Q

what are PT implications for parkinsons?

A

time meds with exercise
fall prevention
modify ADLs
big program

speech and occupational therapy

43
Q

what are statins?

A

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
Q

what are examples of statins?

A 
atorvastatin (lipitor)
lovstatin (mevacor)
rosuvastatin (crestor)
fluvastatin (lescol)
simvastatin (zocor)
pravastatin (pravachol)
45
Q

how do statins work?

A

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
Q

what are statins primarily used for?

A

hypercholesterolemia
cardiovascular disease
when risk factors for cardiovascular disease are present– diabetes

47
Q

what are secondary benefits of statins?

A

cancer
dementia
osteoporosis

48
Q

what are the risks of statins?

A

if taking multiples– muscle pain & damage

females- liver damage

petite- increased blood sugar/ type 2 diabetes

diabetes- neurological effects

alcohol consumption- rhabdomyolysis

49
Q

what will you see in PT with statins?

A

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
Q

what are PT implications for statins?

A

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

Pharmacology (8 decks)

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