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Physical Therapy > Physchopharmacology > Flashcards

Physchopharmacology Flashcards

1
Q

What are some psychotropic medications

A

Sedative hypotonic (anti-anxiety)
Anti-depressants
Antipsychotics
Treatments of dementia

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2
Q

Primary goals of the sedative Sedative Hypotonic; Anti anxiety drugs

A

Want to relax the patient
Have good quality sleep
Decrease their anxiety

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3
Q

How do we monitor their sleeping patterns

A

Look at electrocardiogram (EKG)

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4
Q

What are the primary agents for Sedative Hypotonic/Anti anxiety drugs

A

Benzodiazepine and many others

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5
Q

What is one thing we must monitor with anti anxiety drug dosage

A

Do not want to much sedation or sleep so they are still able to perform functions

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6
Q

Explain the Sedative hypotonic Benzodiazepine drugs

A

Popular 20-30 years ago

Were essentially sleeping pills

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7
Q

Explain the antidepressant Benzodiazepine drugs

A

These will have a less sedative effect unless it has a high dosage.
More focused for anxiety can be used for sleep

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8
Q

Types of Sedative hypotonic Benzodiazepine drugs

A

Estazolam
Quazepam
Temazepam
Triazolam (housien)

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9
Q

Types of Anti-Depressant Benzodiazepine drugs

A

Diazepam(Valium)
Chlordiazepoxide
Iorazepam
Alprazolam

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10
Q

How do Benzodiazepines work

A

Increase the inhibitory effects of GABA by binding to receptor
Allows Cl to enter and the neuron becomes harder to excite
Inhibit NT’s and decrease excitation of CNS

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11
Q

What are the new sedative hypnotic drugs

A

Z- drugs (zolpidem and Zalepion)
Eszopiclone(lunesta)
Ramelteon (Rozerem)

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12
Q

Explain how the the z drugs differ and are similar to the benzodiazepines

A

They are chemically different but they will both bind to the GABA receptors.
Will bind to other subunits
May have less problems with discontinuing (less rebound)

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13
Q

Explain Eszopiclone (lunesta)

A

Works similar to benzodiazepine. Will bind to GABA receptor cite. chemically different

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14
Q

Explain Ramelteon

A

It is a melatonin receptor agonist

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15
Q

What are some of the benifits of the newer sedative hypnotic drugs

A

Have been used for treating insomnia(long term effects not established yet)
Having these drug options offer patients the ability to find the drug that works best for them

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16
Q

What are the newer anti-anxiety drugs

A

Azapirones: Buspirone (BuSpar)

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17
Q

How do the Azapirones work

A

Stimulate serotonin receptors in CNS

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18
Q

What are the benefits of Azapirones

A

May decrease anxiety with less sedation and less dependence

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19
Q

What are some drawbacks of the Azapirones

A

There is a slow onset and only moderate efficacy

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20
Q

Who would Azapirones work best for

A

Older patients with anxiety

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21
Q

What can be used with patients who have anxiety and depression

A

Use antidepressants as an anxiolytic (inhibit anxiety)

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22
Q

What are some benifits of using an antidepressant as an anxiolytic

A

Has less addictive effects may have less side effects

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23
Q

What does -quetiapine mean

A

Anti psychotic

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24
Q

What does gabapentin do

A

Anti Seizure

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25
Q

What is pregabalin

A

Anti seizure

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26
Q

What is hydroxygine

A

Anti-histamine

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27
Q

What are some side effects of the sedative hypnotic/anti-anxiety drugsdrugs (5)

A

Sleeping (hangover effect, confused, nauseous)
Agitated
Anterograde: loss of memory (short term memory)
Rebound effect (insomnia, increased anxiety)
Tolerance/Dependence

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28
Q

What are some complex behaviors that can occur from sedative hypnotic/anti-anxiety drugs

A

Sleep eating/walking/ even driving

Due to the dosage being too high

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29
Q

What disease may be associated with sedative hypnotic/anti-anxiety drugs

A

Alzheimer may be linked with benzodiazepines

Numbs the brain

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30
Q

What are some concerns with sedative hypnotic/anti-anxiety drugs

A

They treat the symptoms but do not treat the cause of insomnia or anxiety
Do the benefits outweigh the sedation

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31
Q

How can we make the sedative hypnotic/anti-anxiety drugs more effective

A

Pair the drugs with non pharmacy treatment such as physical therapy

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32
Q

What is the ideal situation while using sedative hypnotic/anti-anxiety drugs

A

Getting quality sleep with less anxiety

Becoming more active and participating socially

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33
Q

Define Depression

A

Sadness that is incapacitating (can’t enjoy life, family or job)

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34
Q

How common is depression

A

Is the most common mental illness based on incidence and prevalence

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35
Q

What is the basis of neurochemical study of depression

A

If we understand the neurochemistry of depression we can better treat the pt

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36
Q

What is the current theory in neurophysiology on depression

A

Caused by a deficit of biogenic amines or neurotransmitters in the CNS

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37
Q

What are some biogenic amines that would cause depression if they were in deficit

A

Norepinephrine
Dopamine
Serotonin

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38
Q

What is the strategy of anti depression drugs

A

Prolong the effects of the biogenic amines

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39
Q

What are the types of antidepressants

A

Tricyclics
Monoamine oxidase (MAO) inhibitors
Second generation drugs
Selective serotonin reuptake Inhibitors (SSRI)
Serotonin-norenepherine Reuptake Inhibitor (SNRI)

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40
Q

What are some SSRI’s

A

Prozac
Zoloft
Lexapro
Celexa

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41
Q

What are some SNRI.

A

Pristiq
Cymbalta
Effexor

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42
Q

What is the goal of SSRI

A

Works on the limbic system
Is a famous anti-depressant
Will have little to no effect on NEP or dopamine

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43
Q

What is the goal of SNRI

A

Works only on the serotonin and NEP.

No effect on dopamine

44
Q

What are Tricyclics

A

Oldest form of antidepressants

Not well known but very effective

45
Q

What are the names of some tricyclic drugs

A

Elavil
Ascending
Norpramin

46
Q

What are the MAO drugs used for

A

Used as a last resort for ant depression

47
Q

What do the drugs nefaodone and Trazodone do

A

Block serotonin receptors and serotonin uptake

48
Q

What does the drug bupripion do

A

It is a Norepinephrine and dopamine reuptake inhibitor

49
Q

What does the drug mirtazapine do

A

May clock the presynaptic but is very complicated

50
Q

How do the antidepressant drugs work

A

They will prolong the effects of the amine neurotransmitter by

1) inhibiting the NT reuptake (SSRI/SNRI)
2) Preventing the NT breakdown (MAO inhibitor)

51
Q

How will MAO inhibitors prevent the breakdown of NT’s

A

1) They will recycle the NT by reuptaking them into the presynaptic neuron
2) Inhibit the enzymes that break down the NT’s

52
Q

How will tricyclics and 2nd generation drugs work on NT

A

They cause the NT to remain in the synapse so they activate the receptors on the postsynaptic neuron over and over

53
Q

Adverse effects of Tricyclics

A

Sedation
Anticholinergic (dry mouth, seizures, could be fatal)
Orthostatic hypertension (sudden increase in blood pressure when someone stands up)

54
Q

Adverse effects of MAO inhibitors

A

CNS excitation

Increase blood pressure (especially those who eat femented foods)

55
Q

Adverse effects of Second generation drugs

A

These are generally better tolerated but can have some GI issues with overdose

56
Q

Which second generation drugs are more tolerable

A

SSRI and SNRI

57
Q

What is Serotonin syndrome

A

Occurs when the serotonin receptors are over stimulated

58
Q

What are some symptoms of serotonin syndrome (5)

A 
High blood pressure and HR 
Shivering 
Dyskinesia 
Muscle pain 
GI problems
59
Q

Is serotonin syndrome reversible

A

Usually if it is caught early

If unchecked it could be fatal

60
Q

What are some concerns with anti depressants

A

May be 1-2 weeks before we see effects
Could become more depressed if they are not getting better fast enough
Could cause harm to themselves (mood swing)

61
Q

How long do we wait before the antidepressant is deemed ineffective

A

6 weeks

62
Q

What drug is used to treat bipolar syndrome

A

Lithium

63
Q

What is the mechanism of action for lithium

A

Unclear, thought to prevent manic episode

May stabilize neurons (neuroprotective)

64
Q

How is lithium eliminated

A

Remains intact and eliminated through kidneys

65
Q

What is lithium toxicity

A

Accumulation of lithium in the kidney

66
Q

Symptoms of mild lithium toxicity (4)

A

Metallic taste
Fine Tremor in hands
Nausea
Generalized weakness

67
Q

Symptoms of moderate lithium toxicity (5)

A 
Vomiting 
Diarrhea 
Increased tremors 
Dizziness/incoordination 
Blurred vision
68
Q

Symptoms of severe lithium toxicity

A 
Confusion 
Hallucinations 
Nystagmus (involuntary eye movement) 
Dysarthia (motor speech)
Fasciculation (muscle twitching)
69
Q

How will lithium toxicity progress

A

It could be slow or rapid
Need to monitor closely
Need to catch early or it will damage the cerebellum

70
Q

What are anti-manic effects

A

Prevent swing from manic to depressed

71
Q

What are some other bipolar treatments

A

Anti-seizure

Antipsychotic

72
Q

What are some drawbacks of using drugs other than lithium to treat bipolar disorders

A

May cause some movement disorders or other side effects associated with Anti-seizure or antipsychotic drugs

73
Q

What is psychosis

A

More severe than depression or anxiety
May see or hear things
Have fragmented thoughts

74
Q

What causes psychosis

A

Increase dopamine acting on the CNS as well as other NTs

75
Q

How do antipsychotic drugs work

A

They block the dopamine receptors in the CNS specifically the D2 receptors

76
Q

How much dopamine is blocked with antipsychotic drugs

A

Not all of the dopamine, just enough

Called normalize dopamine

77
Q

Why are the new antipsychotic drugs called atypical agents

A

They do not have the typical side effects as the traditional drugs

78
Q

What NT may antipsychotic drugs improve

A

Serotonin

79
Q

What are some adverse side effects of the traditional antipsychotic drugs

A

Orthostatic hypertension
Sedation
Anticholinergic effects

80
Q

What are some adverse side effects of atypical antipsychotic drugs

A

Weight gain

Disturbed fat and sugar digestion

81
Q

What is the primary concern of antipsychotic drugs

A

Motor side effects (MOST IMPORTANT)

82
Q

What are some extrapyramidal side effects of antipsychotic drugs (4)

A

Tardive Dyskinesia
Psuedoparkinsonism
Akathisia
Other dystonias or dyskensisa of extremities ( Chorea Athletoid)

83
Q

What is Tardive Dyskinesia

A

Oral facial movements; lips, tongue, jaw, grimacing

*Could be permanent even if found early

84
Q

What is Psuedoparkinsonism

A

Decrease in dopamine activity
We want to decrease it but in a different par of the brain
May go away after taken off drug

85
Q

What is akathisia

A

Severe restlessness

86
Q

What causes Tardive Dyskinesia

A

Denervation will occur and then new synapses are formed

87
Q

What is the prevalence of Tardive Dyskinesia

A

1/4 of patients with long term antipsychotic drugs

88
Q

What puts you at risk for Tardive Dyskinesia

A

Genetic issues
Mood disorders
Using antipsychotic drugs over 6 months

89
Q

What is neuroleptic malignant syndrome

A

Cancerous
Can occur with all antipsychotic drugs
Can be fatal

90
Q

What are some symptoms of neuroleptic malignant syndrome (4)

A

Rigidity
Catatonia(unresponsive)
Tremors
Fever

91
Q

What is Alzheimer’s disease

A

Irreversible dementia

Due to shrinking of the brain

92
Q

What will change in the CNS (3)

A 
Neuronal structure 
Neuronal function (Loss of neuronal activity) 
Will not be a minor change, will be profound throughout the entire brain
93
Q

What are the goals when treating dementia

A

Improve their cognitive and intellectual abilities

Improve their behavior

94
Q

How to improve function in patients with dementia

A

Neuronal changes decrease acetylcholine activity in brain
Effects the higher part of the cortex (involved in memory)
Cholinergic stimulants used to increase ACH activity either indirectly or directly

95
Q

How do indirect Cholinergic drugs effect dementia

A

Will not directly effect the ACH receptor

Inhibits enzyme that breaks down ACH

96
Q

What enzyme will break down ACH

A

Cholinesterase

97
Q

What are the Cholinergic stimulants in Alzheimer disease

A

Aricept
Razadyne
Exelon
Cognex

98
Q

What are some indications to use Cholinergic stimulants

A

To improve cognition
Behavior function
Memory

99
Q

What determines the efficacy of Cholinergic stimulants

A

If it helps them retain more cognitive information in the early stages of Alzheimer’s

100
Q

When will Cholinergic stimulants be ineffective in treating AD

A

When there is rapid progression of the disease.

Due to not producing neurotransmitters

101
Q

What is memantine

A

New form of AD drug which blocks NMDA-glutamate receptors in the brain

102
Q

What does glutamate do to the brain

A

Excitatory amino acid that is used in memory and learning

103
Q

What is the mechanism of Memantine

A

During AD glutamate activity is disrupted. Drug will normalize glutamate influence

104
Q

What is a potential problem of memantine

A

Too little or too much dosage could be harmful and actually advance the disease.

105
Q

What are some drugs used to modify or improve behavior

A

Antidepressants
Anti-Anxiety agents
Antipsychotic

106
Q

What role did the government play in antipsychotic drugs

A

Placed regulations on the use of drugs due to OD

-Can’t just use antipsychotic just because the pt’s behavior is “unacceptable

107
Q

What is symptom specific medication, and what disease is it associated with

A

Using the type of medication based on the problems the patient presents with.
Alzheimer’s

Physical Therapy (18 decks)

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