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Neuro Pharm Flashcards

1
Q

Why is skeletal muscle pharmacology important for PT

A

our treatments rely on control of muscle spasms and spasticity

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2
Q

what does spasticity involve

A
  • exaggerated muscle stretch reflex that is velocity dependent
  • involves diminished supra-spinal inhibition or control secondary to lesion of SC or brain
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3
Q

What is spasm

A
  • increased and involuntary muscle tension seen after musculoskeletal injury
  • Involves afferent, nociceptive input from peripheral pain receptors, causing excitation of outflow to muscles
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4
Q

Seth wants you to know GABA pathway

A

its on slide 5

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5
Q

mechanism of muscle spasm

A

a pain reflex results in increased muscle activity (tone)

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6
Q

targets of frugs for muscle spasm

A
  • alpha motor neuron or supra-spinal neurons that activate alpha motor neurons
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7
Q

Two sub-classes of anti-spasm medications

A
  • benzodiazepines
  • polysynaptic inhibitors
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8
Q

Benzodiazapines

A

 Diazapam (Valium) and a few others
 All stimulate GABA-ergic synapses on SC alpha-motor neurons
Indications: musculoskeletal injuries such as LB

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9
Q

Polysynaptic Inhibitors

A

 Cyclobenzaprine (Flexeril) & methocarbamol (Robaxin) or in preparation with analgesic: Norgesic (orphenadrine combined aspirin)
 Function as general CNS relaxants, but have no specific effects on alpha-motor neurons
 Often used as adjunctive Rx with rest and PT

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10
Q

Side effects of anti-spasm agents

A
  • primary side effects: drowsiness, sedation, and dizziness
  • Tolerance (long term)
  • Addiction: not recommended for long term use
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11
Q

Very important side effect of valium and muscle relaxants

A
  • anterograde memory loss
  • esp valium
  • don’t count on pt remembering instructions
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12
Q

what is epilepsy

A

neurological condition in which the brain experiences seizures or episodes of intense
involuntary and synchronized neuronal activity

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13
Q

What are seizures?

A

Spontaneous burst of neuronal activity caused
by a group of neurons (or focus) that are
“hyperexcitable” or “irritable”

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14
Q

Status Epilepticus

A
  • a state of “continual seizure activity” brought on by withdrawal of antiepileptic drugs, ETOH or drug withdrawal, CVA or severe intracranial infection
  • Seizures activity > 5 minutes or seizures occurring so close together the patient does have time to recover from the previous one
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15
Q

Are seizures usually “self-limiting?”

A

Yes - except in Status Epilepticus
 the high level of neuronal activity can’t be sustained and neurons become refractory
 most seizures do not last longer than 2 minutes. The longer a seizure lasts, the less likely it will stop on its own without medication. Very long seizures (i.e., status epilepticus) are dangerous and increase the chance of permanent brain damage or deat

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16
Q

Harmful Seizures:

A

 uncontrolled seizures may damage healthy and already injured neurons
 potential for fall or accident
 cardiac arrhythmia or cardiac arrest
* sidelying is the safest position

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17
Q

What do drugs for seizure disorder focus on?

A
  • suppressing the excitability of cortical neurons that trigger the seizure by promoting inhibitory effects of GABA or decreasing Na+ ion permeability – both result in decreased depolarization
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18
Q

GABA

A

 gamma-aminobutyric acid (GABA): inhibitory NT found throughout the brain
 most drugs that suppress seizures work by enhancing the action of GABA

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19
Q

Side Effects of Antiepileptics (& sedative-hypnotics/anxiolytics)

A

 Drowsiness/sedation is the primary side effect
 Ataxia & dizziness
 Antero-grade memory loss (especially w/ valium)
 Memory loss period related to half life of drug
 Cognitive effects with Topiramate

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20
Q

Barbituates:

A
  • Pentobarbital (Solfoton). This class of drugs are given for nearly all seizures, but work best for “grand mal” type
     All increase inhibitory effect of GABA, may block excitatory effect of glutamate
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21
Q

Side Effects of Barbituates

A
  • sedation, ataxia, nystagmus, folate &
    Vit-K deficiency
     May paradoxically increase seizures and hyperactivity in children
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22
Q

Benzodiazepines

A
  • Diazepam (Valium) works best for “status epilepticus”, Clonazepam (Klonopin) works best for absence or petit mal
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23
Q

Side Effects of Benzos

A

sedation, ataxia, behavioral changes

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24
Q

Carboxylic Acids

A
  • Valporic acid (Depakene) used to Rx partial seizures in adults & children
  • Increase GABA effects
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25
Q

Side Effects of Carboxylic Acids

A

hair loss, wt gain /loss, bleeding & GI problems

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26
Q

Hydantoins

A
  • Phenytoin (Dilantin): often first drug
    used for focal onset & tonic-clonic seizures.
  • Phenacemide (Phenurone) Rx seizures that
    don’t respond to other medications. Both
    decrease excitability by impairing Na+ entry
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27
Q

Side Effects of Hydantoins

A

cerebellar signs (nystagmus, ataxia, dysarthria, mild sedation, peripheral neuropathy and diminished reflexes

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28
Q

Tricyclic

A

Carbamazepine (Tegretol): Impairs Na+ entry – good for focal seizures

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29
Q

Tricyclic Side Effects

A

GI distress, dizziness, ataxia, visual disturbance – not as much sedation

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30
Q

New 2nd Generation Anti-Epileptics Characteristics

A

 Slight advantage due to fewer side effects
 Not as effective with mono use - Used as adjunct to other anti-epileptics to decrease dose

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31
Q

2nd Generation Anti-Epileptic Drugs

A

 Topiramate (Topomax): blocks Glutamate
neurotransmission and decrease Na+ movement  Gabapentin (Neurontin): increases inhibitory
effect of GABA
 Same side effects as other common anti-
epileptics, but slightly milde

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32
Q

Rehabilitation and Epilepsy Pharmacology

A

 Aware of potential risk of a seizure
 Seizure control versus sedation relationship in
the patient
 Ataxia as side effect versus result of illness
 Exacerbation of seizures by physical stimuli

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33
Q

Ataxia as a side effect versus result of illness:

A

 patients with TBI or CVA may require balance or coordination exercises, but performance may be limited by the medication or they may need even more Rx secondary to the medication

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34
Q

What is Parkinson’s disease characterized by:

A

 resting tremor (4-5/sec)
 bradykinesia (slow movement)
 akinesia (impaired ability to initiate movement)
 rigidity
 postural instability (maintain low posture)
 microphonia (decreased voice volume)
 mask like, expressionless face

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35
Q

When does Parkinson’s disease begin

A

 Begins in 5th or 6th decade (1% of pop > 60)
 progressive over 20-30 years, leading to complete incapacitation

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36
Q

3 Types of Drugs used to treat PD

A
  • Dopamine Precursor
  • Anticholinergic
  • Dopamine Agonist or Stimulators
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37
Q

Dopamine Precursors

A

 Levadopa (L-dopa): primary drug to treat PD –> dopamine precursor that crosses BBB
 Sinemet (1:4 or 1:10 levadopa : carbadopa)
 Carbadopa (DC-inhibitor)

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38
Q

Anticholinergic Drugs to treat PD

A

Benzotropine

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39
Q

Dopamine Agonist or Stimulators to treat PD

A

 Bromocriptine
 Selegiline MAO inhibitors

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40
Q

Levodopa Characteristics

A
  • 1-3% crosses BBB & converted to dopmaine (by dopa carboxylase), so large quantities must be
    given
  • dramatic improvement in symptoms in most cases, but not all patients respond or can tolerate it
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41
Q

What should Levodopa be given with?

A
  • peripheral decarboxylase inhibitor
    (carbadopa) (Sinemet)
  • Allows more to get to brain.
42
Q

Side Effects of Levodopa

A
  • GI Problems: N & V (milder when given with carbadopa)
  • Cardiac Arrhythmia (caution with exercising)
  • Orthostatic Hypotension (quite severe at beginning)
  • Dyskinesia: 80% –> begins 3-7 months after beginning
  • Behavioral Changes: depression, anxiety, confusion, hallucinations, esp in older adults (worse with carbidopa)
  • Diminished Response: 2-3 years after beginning
43
Q

Fluctuations in response to levodopa

A

 End-of -dose akenesia: wears off prior to next
dose
 On-off phenomena: abrupt change in
responsiveness

44
Q

Drug holiday for Levodopa

A

 restores effectiveness, but depends on pt and
may not last
 Risk of death w/ sudden withdrawal of
levadopa - thus not used commonly

45
Q

Anticholinergics for PD

A
  • Treats rigidity and tremor
  • Benzotropine
46
Q

Benzotropine Side Effects

A

N &V, blurred vision, confusion, dry mouth,
hallucinations, sedation, cardiac irregularities

47
Q

Dopamine Agonists or Dopamimetics to treat PD

A
  • Bromocriptine: used with Levodopa or when Levodopa becomes ineffective
  • Selegiline: Inhibits MAOb and dopamine breakdown
48
Q

How do Dopamine agonists affect side effects?

A
  • may provide same benefits in terms of alleviating symptoms, but with fewer side effects compared to L-Dopa or Sinemet
     Many of the D-agonists are longer acting
    than L-Dopa and can be given 2 times/day rather than 3 or 4 times/day.
     Future research on D-R subtypes may allow
    for even better control of symptoms without side effects.
49
Q

Controversy about when to begin levodopa

A

 should it be saved until symptoms are severe since it looses effectiveness?
 should it be started w/ symptoms since decline in
drug effectiveness is actually due to disease
progression?

50
Q

Tissue Transplantation in patients with PD

A
  • surgically implant dopaminergic cells into substantia nigra
     source of cells: human fetus mesenchymal tissue  difficulty in procedure (keep cells alive, implant them w/o further damage to brain, keep them from
    differentiating)
51
Q

PT with PD Pharmacology

A
  • Coordinate with peak (Levodopa and Sinemet peak in 1 hr)
  • Need PT during drug holiday to prevent decline in function
  • Be aware of side effects: monitor BP and behavioral changes
52
Q

What has optimal beneficial effect for patients with PD

A

PT combine with drug therapy

53
Q

Side effects of Alzheimer’s disease Pharmacology

A
  • Indirect Cholinergic Stimulants
     Similar to the old drug neostigmine and other
    cholinesterase inhibitors – only work early in
    disease process
     Caution in patients with bradycardia, hypotension, and asthma
     Side effects: commonly produces N&V and
    diarrhea, liver dysfunction, muscle cramps,
    anorexia, headache & insomnia
54
Q

Things about Neuropharmacology and PT

A
  • Neuropsychiatric symptoms and the drugs used to control them can and often impact therapy outcomes.
  • Use of the biopsychosocial model can aid in developing a complete approach to patient care - Biological / chemical aspect of mental illness, Psychological/ behavioral aspect, Social/ real world aspect
  • Psychotropic drugs are “partially” effective, numerous, and treat specific symptoms rather than syndromes
55
Q

How many patient who suffer a “major” illness experience some level of depression in the months following?

A

up to 90%

56
Q

For which patent population may the degree of depression be even more severe?

A

CVA, amputation, heart attack, SCI

57
Q

Theories of Depression Pathophysiology

A
  1. Lack of amine neurotransmitters – norepinephrine and serotonin – leads to increased sensitivity of amine serotonin, dopamine & norepinephrine) receptors
  2. Impaired formation of new neurons – deficiency in trophic support for neurons (BDNF) stress and pain decrease BDNF
  3. Hormonal abnormalities – increased HPA axis – increased CRH & ACTH levels
58
Q

3 types of anti-depressant drugs

A
  • Tricyclics Antidepressants
  • Monoamine Oxidase Inhibitors
  • 2nd Generation Antidepressants (SSRIs and SNRIs)
59
Q

How do Tricyclics Antidepressants work?

A

block re-uptake of amine NT into presynaptic membrane

60
Q

How do Monoamine Oxidase Inhibitors work?

A

-block enzymatic breakdown of amines
-Not used today secondary to adverse side effects

61
Q

How do 2nd Generation Antidepressants work?

A

-block amine NT (serotonin and/or norepinephrine) re-uptake or increase serotonin levels
-more rapid onset
-fewer side effects

62
Q

How long do antidepressants take for full effect?

A
  • 2 weeks or longer
  • Fluoxetine (Prozac): 5 days - 5 weeks
  • Sertraline (Zoloft): 2-4 Weeks
63
Q

Serotonin Syndrome

A

 Toxic reaction to excessive build up of serotonin
 May occur when two SSRIs are taken together
 Agitation, HTN, diarrhea, tachycardia, LOC, hyperthermia, hallucinations, ataxia, N&V & hyper-reflexia.
 Potentially fatal

64
Q

Side Effects of Antidepressants

A

 Sedation
 Central & peripheral anti-cholinergic activity (dry
mouth, constipation, confusion & delirium)
 Arrhythmia
 Orthostatic hypotension
 Restlessness, sleep disturbance, irritability, agitation
 HTN (hypertensive crisis)

65
Q

Do 2nd Generation Antidepressants have any advantage over the other types of meds?

A
  • nope just fewer side effects
  • may exacerbate depression/suicidal ideation
66
Q

Off Level Uses of Antidepressants

A
  • Pain
  • OCD
  • ADHD
  • Anxiety Disorder
67
Q

How can antidepressants help pain?

A
  • Depression linked to “helplessness” due to intractable pain or physical limitations
     Even when no symptoms of depression are present, patients with chronic pain report improvement with anti-depressant therapy
     improved sleep patterns or alter the
    patient’s perception of pain
68
Q

What do anxiety disorders include?

A

panic and social anxiety disorders, generalized anxiety, OCD and post-traumatic stress disorder

69
Q

50% of hospitalized patients are prescribed what?

A

Anxiolytic Agents (anti-anxiety)

70
Q

What are well recognized complications of TBI

A

Anxiety and OCD

71
Q

OCD is related to many different conditions:

A

over-eating, panic disorders, repetitive hand-
washing compulsions, etc

72
Q

Sedative-Hypnotic Drugs

A
  • Used to Rx anxiety: induce relaxation (sedation),
    sleep (hypnosis) & anesthesia
  • Most sedative-hypnotics have anesthesia effects
    at high doses: act as “CNS-depressants”
73
Q

Why are many patients prescribed sedative-hypnotic drugs in rehab?

A

Due to apprehension caused by either the injury itself or rehabilitation/hospitalization (esp for TBI)

74
Q

Barbituates Facts

A

 narrow therapeutic
 highly addictive
 tolerance (liver enzymes)
 lipid soluble (fat storage, hang-over & retro amnesia)
 acts on GABA- benzodiazapine-Cl-receptor, also inhibit pre-synaptic NT release

75
Q

Benzodiazepines Facts

A
  • Broader Therapeutic Window
  • Addictive
  • Moderate Tolerance
  • Lipid soluble (fat storage, hang-over and retro-amnesia)
  • GABA-Benzodiazapine-Cl-channel
76
Q

What is the prototype of Benzodiazepines

A
  • Valium
  • Sedative properties at low dose, preferentially affect limbic system
77
Q

Limitations of Benzodiazepines

A

 “Relatively safe” compared to barbiturates –> preferentially bind GABA-Cl- channels in limbic
system, rather than in reticular activating system, so less hypnosis
 Due to lipid solubility, hangover and
retrograde amnesia are still a problem
 Caution when giving these drugs to patients who are depressed secondary to potential
for suicide

78
Q

Other anti-anxiety Medications

A
  • Sedative Hypnotics: Azapriones (Busprone or BuSpar)- serotonin agonist –> Useful for anxiety associated with OCD, post-traumatic stress, panic disorders
  • Beta-Adrenergic Blockers (Propranolol etc…) –> Help control physical signs of anxiety and “anticipatory” anxiety
  • Anti-depressants (SSRIs) –> useful for OCD and panic disorder
79
Q

Anti-Anxiety Meds and Rehab

A

 All tend to cause sedation, lethargy and somnolence –> need to be titrated to minimize does to achieve anxiolytic effect.
 Drug interactions are common when more than one anxiolytic agent is used or with any CNS depressants.
 Hangover and retrograde amnesia are problematic
 Addiction and abuse
 Rebound anxiety when discontinued
 Scheduling: 2-4 hour peak action, so schedule
therapy accordingly

80
Q

What is Psychosis:

A

 Group of severe mental illnesses characterized by
marked thought disturbance & impaired
perception of reality
 Schizophrenia: affects 1 % of population
 Paranoid disorders
 Psychotic depression
 Often associated with TBI and less often CVA- 48% of patients with TBI in acute care setting received neuroleptics

81
Q

What is pharmacology associated with?

A
  • Excessive dopamine activity
  • Based on findings that D-R blockers have beneficial effect
  • Most anti-psychotics are dopamine receptor blockers
  • Atypical anti-psychotics block both dopamine and serotonin
82
Q

Dopamine facts

A

~ Fluidity of movement (in BG, cerebellum)
~ Fluidity of thought
~ Satisfaction
~ Repetition drive

83
Q

Traditional Anti-Psychotic Drugs

A

Dopamine receptor antagonists:
Haloperidol (Haldol)- high potency D-R blocker
Chloropromazine (Thorazine)- lower potency
Both are associated with “extra-pyramidal side effects” –> Dystonic reactions, akathisia, tardive dyskinesia

84
Q

Second Generation or Non-Traditional Anti-psychotic Drugs

A

distinguished by side effect profile, not
mechanism
Clozapine (Clozaril)
Risperidone (Risperdal)
Fewer side effects and help with affect and “resistance

85
Q

Dopamine Excess vs. Dopamine Deficiency

A

Excess: psychosis, schizophrenia
Deficiency: PD and pseudo PD

86
Q

What is the most common neuroleptic prescribed for patients with TBI

A

Haloperidol - member of Butyrophenone family

87
Q

Pharmacokinetics of Anti-psychotics

A

 For an acute psychotic episode, high dose is
given orally 4 x /day, or intramuscularly
 Cut back to a maintenance dose
 Some tolerance develops
 Side effects usually begin after 12 months and
become progressively worse w/ use
 Antipsychotics may be given to help w/ GI side
effects of Parkinsons medication

88
Q

Extrapyramidal Symptoms of Anti-psychotics

A

 motor side effects resulting from alterations in dopamine imbalance in basal ganglia
 tardive dyskinesia: involuntary and fragmented movements (15 - 20%)
 in some patients symptoms stop when drug is
stopped, but in some patients, irreversible
 “disuse” super-sensitivity of dopamine R’s in BG
 mouth, tongue & jaw movements
 choreoathetiod movements of limbs
 dystonia of trunk & neck
 Pseudoparkinsonism
 Akathisia: motor restlessness
 Dyskinesia and dystonia: bizarre movements of limbs or neck
 Neuroleptic malignant syndrome

89
Q

Pseudoparkinsonism from Anti-Psychotics

A

 PD caused by lack of dopamine transmission in substantia nigra motor synapses
 Antipsychotics deplete dopamine or interfere with dopamine neurotransmission
 resting tremor, bradykinesia and rigidity (especially in elderly), but usually reversibly

90
Q

What is Neuroleptic Malignant Syndrome

A

catatonia, stupor, rigidity, tremor occurring with high doses
- Mortality: 25%
- Affects males <40

91
Q

Time of Onset of Extra-Pyramidal Side Effects:

A

Days 1-3: Acute Dystonic Reactions
Day 3: Akathisia
Day 5: Pseudo-Parkinsonism
Day 90: Tardive Dyskinesia

92
Q

Tardive Dyskinesia due to anti-psychotics

A
  1. Protrusion of Tongue
  2. Puffing of Cheeks
  3. Chewing Movements
  4. Involuntary Movements of Extremities
  5. Involuntary Movement of Trunk
93
Q

Non-Motor Side Effects of Anti-Psychotics

A

 Sedation: all have sedative properties
 Anticholinergic affects (dry mouth, constipation, urinary retention, blurred vision)
 Orthostatic hypotension (with initiation of Rx)
 Light sensitivity
 Withdrawal symptoms (GI distress, N&V)

94
Q

Special Concerns for Anti-Psychotics and Rehab Patients

A

 These drugs can help improve the patient’s
performance in therapy as well as outcome
secondary to improve cooperation, attention,
compliance, etc.
 Need to be aware of serious side effects: Orthostatic hypotension, extra pyramidal motor side effects, neuroleptic Malignant Syndrome

95
Q

Two Categories of Neuro-Stimulants

A

 Amphetamines
 Parasympathomimetics (cholinergic stimulants)

96
Q

What are Neuro-Stimulants used for?

A

 Patients with attention deficit disorder
 Slowed cognitive function
 Delirium
 Dementia

97
Q

Amphetamines: Methylphenidate (Ritalin)

A
  • Indirect Acting sympathomimetic (amphetamine)
  • Blocks re-uptake of norepinephrine at alpha and be a adrenergic synapses and increases dopamine activity
  • Affects RAS & cortex in CNS
  • Mild CNS stimulant
  • Potential for abuse
  • Many CNS side effects: most notably nervousness, insomnia, changes in BP and HR
  • More commonly prescribed for children, but increasingly used in adults
98
Q

Effects of Amphetamines

A
  • Increased use-dependent neuroplasticity following a TBI in humans with d-amphetamine
  • Potential benefit for both patients with TBI and CVA
  • Present problem when BP control is an issue
99
Q

How do drugs for MS work?

A

stimulate the immune system to slow the degeneration of the neurons (Interferons/anti-virals)

100
Q

Common adverse effects of drugs for MS

A

flu-like symptoms, nausea, fatigue, weight loss, hematological toxicities, elevated transaminases, and psychiatric problems (e.g., depression, suicidal ideation)

Pharm (12 decks)

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