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UM - Pharmacology > Medications for anesthesia, neurological conditions, and psychiatric conditions > Flashcards

Medications for anesthesia, neurological conditions, and psychiatric conditions Flashcards

Anesthetics, Sedative-Hypnotics and analytics, Affective Disorders and Psychiatric Disorders, Anti-epileptics, Drugs for PD, Drugs for MS

1
Q

Distinguish difference between general and local anesthetics

A

General is fully body with a patient unconscious whereas local is injected into one area and the patient is still awake

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2
Q

What is induction stage I of general anesthesia

A

Analgesia:

- pt loses somatic sensation but is still conscious and aware of what is happening

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3
Q

What is induction stage II of general anesthesia

A

Excitement (delirium):

  • pt unconscious but agitated/restless
  • want to move quickly thru this to stage III
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4
Q

List different types of general anesthesia and adjuvant medications used during anesthesia

A
  • Pre-op Meds for relax and reduce post op N/V

- Neuromuscular blockers (nondepol and depolarizing)

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5
Q

List some IV anesthetics

A
  • Barbiturates
  • Benzodiazepines
  • Opioid Analgesics
  • ketamine
    [- propofol
  • etomidate
  • dexmedetomidine]
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6
Q

How do barbiturates work

A

CNS depressant to decrease anxiety and facilitate induction of anesthesia used in IV anesthetics

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7
Q

How do benzodiazepines work

A

CNS depressant to decrease anxiety and tension and provide sedation and amnesia used in IV anesthetics

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8
Q

How do opioid analgesics work

A

They provide analgesia, antianxiety and sedative effects used in IV anesthetics

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9
Q

How does ketamine work

A

It produces a dissociative anesthesia that does not cause respiratory or cardiac issues but can cause hallucinations and other rxns during recovery used in IV anesthetics

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10
Q

What is dexmedetomidine

A

It is a newer IV anesthetic used mostly for ST ICU to stimulate certain alpha receptors in the brain

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11
Q

What is the pharmacokinetics of general anesthetics

A
  • IV metabolized in liver and eliminated in kidneys

- inhaled: metabolized and eliminated in the lungs

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12
Q

What is a concern w/anesthetic if a person has liver or lung disease

A

It will take longer for it to be eliminated causing longer periods of confusion, disorientation and lethargy

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13
Q

Age concerns w/pharmacokinetics of general anesthesia

A
  • older adults need smaller doses

- difficult w/children since their organs are immature and they have small body masses

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14
Q

What is the mechanism of action of general anesthesia

A
  • Increases inhibition in the CNS by exciting GABA and glycine
  • Decreases excitation by acting on K+, ACh, NMDA and opioids
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15
Q

In general, how do anesthetics exert their effects?

A

By binding to receptors in the CNS

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16
Q

What are the types of pre-operative meds given w/general anesthesia

A
  • sedatives
  • anti N/V
  • decrease bronchial secretions
  • dec gastric acidity (help w/N/V)
  • post-op pain (opioids and steroids)
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17
Q

What are neuromuscular blockers

A

Adjuvants to general anesthesia that increase skeletal mm paralysis to allow for safe surgery

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18
Q

What are the side effects of neuromuscular blockers

A

tachycardia, increased histamine release, hyperkalemia, residual mm pain and weakness, anaphylaxis

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19
Q

Nondepolarizing blockers vs depolarizing blockers (neruomuscular)

A

Nondepol last longer by acting as competitive antagonists of post synaptic recetor ro prevent ACh from binding whereas depol is more short term since it acts like ACh and binds and stimulates receptor to depol it so it cant contract

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20
Q

What are the rehab concerns of general anesthesia

A
  • lingering effects (woozy, confused) esp in older adults
  • bronchial secretions in lungs
  • LT effects on mem and cognition in older adults and those w/cognitive disorders
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21
Q

What is the goal of local anesthesia

A

To block afferent NT along the periph nerve

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22
Q

What are some advantages of local anesthesia

A
  • rapid recovery
  • lack of residual effects
  • does not interfere w/CV, pulm, or renal function
  • beneficial for childbirth
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23
Q

What are some disadvantages of local anesthetics

A
  • takes longer to achieve effects and there is a risk that analgesia will be incomplete or insufficient
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24
Q

What are the two main categories of local anesthetics

A

esters and amides

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25
Q

What drug is often co-administered w/local anesthetics and why

A

A vasoconstrictor so that the anesthetic does not travel out of the target tissue

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26
Q

What is the pharmacokinetics of local anesthetics

A
  • metabolized in liver and blood stream

- excreted in the kidneys

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27
Q

what are the clinical uses of anesthesia (list)

A 
topical
transdermal
infiltration anesthesia
peripheral nerve block
central nerve block
sympathetic block
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28
Q

What is topical anesthetic

A

A local anesthetic applied directly to the skin surface, mucous membrane or cornea to allow for symptomatic relief of minor irritations and injury and can reduce pain before minor surgical procedures

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29
Q

What is transdermal anesthetic

A

A local anesthetic applied to the surface of the skin via patches that can be enhanced w/ionto or phonophoresis to treat tendons, bursae or soft tissue

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30
Q

What is infiltration anesthetic

A

A local anesthetic where the drug is injected directly into the select tissue and diffuses to sensory nerve endings w/in that tissue –> good for suturing lacerations

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31
Q

What is peripheral nerve block anesthetic

A

a local anesthetic injected close to the nerve trunk of a peripheral nerve so that transmission is interrupted-> can sometimes be a continuous nerve block where they insert a catheter near the nerve

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32
Q

What is central nerve block anesthetic

A

A local anesthetic that is injected w/in the spaces surrounding the SC or win the SC but there is a higher risk of Neurotoxicity

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33
Q

What is sympathetic blockade anesthetic

A

a local anesthetic that selectively interrupts sympathetic efferent DC w/the goal to disrupt outgoing sympathetic signals

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34
Q

What is sympathetic blockade anesthetic useful for

A

complex regional pain syndrome (CRPS)

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35
Q

What is the mechanism of action of local anesthetics

A

Disrupt the Na+ channels along the periph nerve so that the message cannot be transferred down further

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36
Q

What are the systemic effects of local anesthesia

A

CNS toxicity (ringing in ears, agitation, dec sensation) or cardiac toxicity (bradycardia, fatigue, dizziness)

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37
Q

What are the rehab concerns of local anesthetics

A
  • keep a lookout for transdermal patches as you don’t want to heat it (will infuse too fast)
  • if continuous nerve block will lack sensation and possible motor control
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38
Q

What are sedative hypnotics

A

Drugs that promote sleep, esp in acute or ST situations

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39
Q

What are the two categories of sedative hypnotics

A

Benzodiazepines and non-benzodiazepines

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40
Q

List some other uses of sedative-hypnotics

A
  • anti-anxiety
  • sedation and amnesia
  • seizure treatment
  • control of withdrawal
  • mm relax
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41
Q

What are affective disorders

A

characterized by marked disturbances in a person’s mood - very common in society

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42
Q

What are two types of affective disorders

A

Depression

Bipolar Disorder

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43
Q

What is depression

A

General dysphoric mood and lack of interest in previously pleasurable activities that can lead to recurrent thoughts of death and suicide

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44
Q

How can depression be classified

A
  • type
  • duration
  • intensity of symptoms
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45
Q

What are the 3 factors that contribute to depression

A

Environmental, biochemical, and genetic

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46
Q

What is the pathophysiology of depression

A

Disturbance in amine neurotransmitters (serotonin, norepinephrine, and DA)

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47
Q

What are the amine NTs

A
  • serotonin
  • norepinephrine
  • dopamine
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48
Q

List the two theories of how the pathology of depression occurs

A

Receptor sensitivity theory

neurogenesis theory

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49
Q

What is the receptor sensitivity theory

A
  1. Depression causes a supersensitivity to amine NT
  2. Antidepressants enhance the stimulation of pre and postsynaptic receptors
  3. Receptor sensitivity decreases to a more balanced level (takes about 2-3 weeks)
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50
Q

What is the neurogenesis theory

A
  • When people are depressed, they grow less neurons and receptors
  • Drugs promote regrowth so there is increased influences of the amines
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51
Q

List some anti-depressant drugs

A
  • SSRI (selective serotonin reuptake inhibitors)
  • SNRI (serotonin-norepinephrine reuptake inhibitors)
  • tricyclics
  • MAOI
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52
Q

What are Selective Serotonin Reuptake Inhibitors (SSRIs)

A

Antidepressant that block enzyme responsible for the re-uptake of serotonin back into the presynaptic terminal so that more remain in the synaptic cleft –> people are happier

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53
Q

What is the most common antidepressant

A

SSRI

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54
Q

What are Serotonin-norepinephrine reuptake inhibitors (SNRI)

A

Antidepressant that decreases serotonin and norepinephrine reuptake without effecting dopamine synapses
- also treat pain conditions (fibromyalgia, chronic, etc)

55
Q

What are the adverse effects of SSRI and SNRI

A
  • GI: N/V, diarrhea, constipation

- serotonin syndrome

56
Q

What is serotonin syndrome

A

a serious and potentially fatal condition of elevated serotonin that causes sweating, agitation, restless, shivering, tachycardia, and neuromuscular excitability that can lead to coma and death

57
Q

What are tricyclics

A

Antidepressants that block the reuptake of amine NTs into the presynaptic terminal nonselectively (leading to more interactants with other drugs)

58
Q

Who are tricyclics used for

A

Those who have failed w/other antidepressant treatments

59
Q

What are some of the adverse events from tricyclics

A
  • sedation
  • arrhythmias and OH
  • increase in seizure
  • anticholinergic prop (block ACh to cause confusion and delirium)
60
Q

Which antidepressant has the highest potential for fatal OD

A

Tricyclics because of the risk of cardiac arrhtymias

61
Q

What is Monoamine oxidase

A

An enzyme in the CNS that breaks down NT in the synapses

62
Q

What are monoamine oxidase inhibitors (MAOI)

A

Antidepressants that inhibit MAO allowing more NTs to remain in the amine synaptic cleft, which can lead to changes in receptor sensitivity - BUT have a lot of interactions with food and other drugs

63
Q

What are some of the adverse events of MAOI

A
  • They produce CNS excitation (restlessness, irritability)
  • increase BP including hypertensive crisis
  • central and peripheral anticholinergic effects
  • interactions w/foods and tyramine
64
Q

What are other mechanisms for antidepressants

A
  • block serotonin receptors and inhibit serotonin reuptake

- DA and norepinephrine reuptake inhibitor

65
Q

What are the pharmacokinetics of antidepressants

A
  • administered orally
  • cross BBB to exert effects
  • metabolized in liver
  • eliminated in the kidneys
66
Q

Can antidepressants treat chronic pain

A

Yes BUT only Cymbalta is FDA approved to treat it

  • tricyclics have been used
  • SSRI & SNRI are used in fibromyalgia and neuropathies
67
Q

What is Bipolar Disorder

A

An affective disorder characterized by mood swings from one extreme (mania) to the other (depression) - but the exact cause is unknown

68
Q

What is Lithium (Li+)

A

A monovalent cation from the alkali metal group of the periodic table that competes w/other cations (Na+, K+, and Ca+) and has neuroprotective effects and limits neuronal damage

69
Q

What are the pharmacokinetics of lithium

A
  • It is administered orally and readily absorbed in GI tract
  • LITHIUM IS NOT METABOLIZED
  • whole drug is eliminated by excretion in urine
70
Q

When is a higher dose of lithium needed in bipolar disorder

A

In an acute mania

71
Q

What are some adverse effects of lithium

A

Lithium toxicity

- Early on mild symptoms, but can progress (in the: CNS, GI, CV, Renal)

72
Q

What are drugs that treat bipolar disorder

A
  • Lithium
  • Anti-seizure meds (stabilize mood and limit manic symptoms)
  • Antipsychotic meds (anti-mania)
73
Q

Which affective disorder medications cause sedation

A

Tricyclics and lithium

74
Q

What is the most common side effect of affective disorders

75
Q

What are the rehab concerns of affective disorders

A
  • other non-pharmacological treatments can be helpful as well
  • exercise increases brain derived neurotropic factor - which is good for brain health
  • drug therapy can increase depression
76
Q

What is the main way affective disorder medications exert their effects

A

By modifying synaptic transmission and neuronal growth and function in the CNS

77
Q

What is psychosis

A

A term that describes a more severe form of mental illness that is characterized by marked thought disturbance and an impaired perception of reality

78
Q

What is the most common type of psychosis

A

Schizophrenia

79
Q

What are neuroleptics and why are the important?

A

Antipsychotic drugs that treat the disorder instead of simply sedating the patient (like before they came out)

80
Q

What occurs in schizophrenia

A
  • (primarily) Overactivity of DA pathways
  • Increased serotonin
  • defect in GABA
  • decreased sensitivity to ACh
81
Q

What is the mechanism of action of first generation antipsychotics

A

Strong dopamine antagonists (D2 receptor)

- BUT can increase incidence of movement disorders and motor side-effects

82
Q

What is the mechanism of action of second generation antipsychotics

A

Weak antagonists at the D2 receptor but strong antagonists of serotonin
- w/less side effects than the 1st gen

83
Q

What are other uses of antipsychotics

A
  • decrease N/V
  • control agitation and aggression in Alzheimer’s patients
  • combo w/lithium in acute mania for bipolar
84
Q

What are the pharmacokinetics of antipsychotics

A
  • metabolized in liver
    (over t can lead to enzyme induction//less effective)
  • excreted in kidneys
85
Q

When are higher doses of antipsychotics given

A

During acute episodes w/lower maintenance doses

86
Q

What are some problems and adverse effects of antipsychotics

A
  • extrapyramidal symptoms (PD like)
    tardive dyskinesia, akathisia, dyskinesia
  • nonmotor effects
87
Q

What is tardive dyskinesia

A

involuntary and fragmented mvmts, particularly in the mouth, tongue, and jaw that are often irreversible as a side effect of antipsychotic medicatiosn

88
Q

How does pseudoparkinsonism develop w/antipsychotic use

A

they block DA receptors in the BG leading to resting tremor, bradykinesia, and rigidity

89
Q

What is akathisia

A

Sensations of motor restlessness caused by an inability to sit or lie still that can be improved w/lower doses of antipsychotics

90
Q

What is neuroleptic malignant syndrome (NMS)

A

Lack of DA leading to catatonia, stupor, rigidity, tremors, and fever and can lead to death if untreated

91
Q

What are the metabolic effects of antipsychotics

A

mostly seen w/atypical antipsychotics

  • weight gain
  • increased plasma lipids
92
Q

T or F: Sedation is beneficial in antipsychotic medications

93
Q

What are some anticholinergic effects (seen w/antipsychotics)

A
  • blurred vision
  • dry mouth
  • constipation
  • urinary retention
94
Q

T or F: OH is more of a long-term concern with anti-psychotics

A

False - it occurs only in the first few days of taking a medication

95
Q

What are some rehab concerns of antipsychotics

A
  • be on the alert for new extrapyramidal symptoms and report to MD
96
Q

What is the primary means of controlling epilepsy and seizures

A

Drug therapy

97
Q

What happens in epilepsy

A

some cerebral neurons are hyperexcitable and discharge spontaneously causing seizures

98
Q

What are the goals of antiseizure drugs?

A
  1. Increase the activity of CNS inhibitory neurons
  2. Decrease the activity of CNS excitatory neurons
  3. Stabilize Na+/Ca+ channels
  4. Suppress excitability of neurons that initiate the seizures
99
Q

What are some first gen antiseizure drugs

A
  • barbiturates
  • benzodiazepines
  • hydantoins
  • iminostilbenes
  • succinimides
  • valproates
100
Q

why use second gen antiseizure drugs

A

Better pharmacokinetic profile w/milder side effects allowing for better LT use

101
Q

What are some second gen antiseizure drugs

A

gabapentin
pregabalin
lacosamide

102
Q

How do anti-seizure meds treat chronic pain

A

Reduce excitation in pathway responsible for chronic pain –> most effective in neuropathic pain

103
Q

What are the pharmacokinetics of anti-seizure meds

A
  • CAN cross BBB
  • metabolized in liver
  • excreted in kidneys
104
Q

What are some side effects of anti-seizure meds

A 
sedation
tolerance
ataxia
GI
confusion
dizzy
cardiac arrhythmias
105
Q

How are seizures categorized

A

according to clinical and electrophysiological manifestation that occur during the seizure

106
Q

T or F:

Some people can be withdrawn from their antiseizure meds if specific criteria has been met

A

True - under medical supervision

107
Q

What is PD

A

A movement disorder from slow, progressive degeneration of certain DA-secreting neurons in the BG causing resting tremor, bradykinesia, rigidity, and postural instability

108
Q

Normal vs Parkinsonism: what chemical is more dominant in the brain?

A

Normal: DA
PD: ACh

109
Q

List some drugs used in PD

A 
Carbidopa (DOPA decarboxylase inhibitor)
Levadopa (Dopamine precursor)
DA Receptor agonists
MAO inhibitors
COMT inhibitors
Antimuscarinic Agents (Anticholinergic Agents) 
Amatadine (symmetrel)
110
Q

How does Levadopa work

A

It is a DA precursor that is converted to DA after crossing the BBB that then improves all symptoms of PD

111
Q

T or F: Ldopa is equally effective over time

A

False - it becomes less effective due to side effects

112
Q

What converts Ldopa to dopamine

A

Dopa decarboxylase

113
Q

What is carbidopa

A

A peripheral decarboxylase inhibitor that is given w/Ldopa to prevent early conversion to DA in the periphery

114
Q

What are the possible Carbidopa-Levidopa ratios?

A

1:4 or 1:10

115
Q

What are the adverse effects of Ldopa

A
  • OH
  • Psychotic symptoms
  • GI problems
  • dyskinesias
116
Q

What is the On-Off phenomenon and why is this important

A
  • OFF = effectiveness of Ldopa decreases –> worsening symptoms
    ON = remission of symptoms after taking dose of Ldopa
    Dosing schedule to maximize On time
117
Q

List the fluctuations seen w/taking LDopa

A

On-Off
End-of-dose akinesia
Freezing gait

118
Q

What is end-of-dose akinesia and how to we fix it

A

Drug’s effectiveness wears off prior to next dose.

- give smaller doses more frequently

119
Q

What do DA receptor agonists do and side effect

A

Smooth out the On-Off phenomenon, given alone or w/levadopa or antimusc drugs BUT may cause impulse control disorders

120
Q

What are some DA receptor agonists

A

bromocriptine (Parlodel)

ropinirole (Requip)

121
Q

What do MAO-B inhibitors do

A

As an adjunct to Ldopa, it inhibits MAO-B so that DA is not metabolized in the BG and stays active for a longer time

122
Q

What do COMT Inhibitors do

A

As an adjunct to Ldopa-Cdopa to inhibit COMT so that Ldopa is not broken down in the periphery so more can reach the brain

123
Q

What do antimuscarinic drugs do

A

They act as antag at cholinergic muscarinic receptors to inhibit excessive ACh influence on cells in the striatum to improve tremor and rigidity (NOT BRADYKINESIA)

124
Q

What are the side effects of antimuscarinic drugs

A

PERIPHERAL

  • sedation
  • urinary retention
  • constipation
  • confusion
125
Q

What is amantadine (symmetrel)

A

An antagonist at glutamate NMDA receptors to create anticholinergic actions that either increases syn/releas of DA or inhibits its reuptake

126
Q

Which DA drug is also an anti-viral agent

A

amantadine (Symmetrel)

127
Q

When should you initiate pharmacotherapy for PD patients?

A

No clear answer

128
Q

What are the rehab concerns of drug therapy in PD

A
  • Monitor BP since OH is a common side effect
129
Q

What is MS

A

focal areas of demyelination w/reactive gliosis in the white matter (Brain, SC, optic nerves) w/an autoimmune component

130
Q

What is the presentation of MS

A
  • wewakness, numbness, tingling, spasticity
  • unsteadiness, dyscoord
  • visual changes
  • sphincter disturbances
131
Q

What do MS meds seek to do?

A
  • reduce frequency of exacerbations
  • slow disease progression
  • treat acute exacerbations
  • symptomatic treatment
132
Q

What meds reduce frequency of exacerbations in MS

A
  • Interferons (immune enhancers)
  • Immunomodulators
  • Antineoplatsics/Antimetabolites
133
Q

What drugs slow disease progression in MS

A

Monocolonal antibody

Sphingosine 1-phosphate receptor modulator

134
Q

What drugs are used in an acute exacerbation in MS

A

Corticosteroids

UM - Pharmacology (4 decks)

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