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Pharmacology > CNS Part I > Flashcards

CNS Part I Flashcards

1
Q

Describe the blood brain barrier (BBB)

A
  • Highly selective
  • Diffusion: non polar and lipophilic
  • Carrier mediated
  • Efflux systems: transport substances out of the brain
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2
Q

List the excitatory neurotransmitters

A
  • Acetylcholine
  • Glutamate
  • Substance P
  • Enkephalins
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3
Q

List the inhibitory neurotransmitters

A
  • Norepinephrine
  • Dopamine
  • Serotonin
  • GABA
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4
Q

Sites of drug action Slide 8

A
  • re-uptake labeled 6 on image
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5
Q

Basics of sedative hypnotics

A
  • 2 Main categories: Benzodiazepines. and Non-benzodiazepines
  • Main uses: sleep (hypnosis), anxiety, seizures
  • Pharmacokinetics: highly lipid soluble, metabolized via liver; adipose sequestering and active metabolics
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6
Q

Effects of sedative hypnotics Slide 11

A
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7
Q

Describe a GABA receptor

A
  • Ion channel receptor
  • Inhibitory neurotransmitter: GABA binds & allows more chloride ions to enter the cell this causes the cell to be hyper-polarized
  • Sedative hypnotics either mimic GABA or enhance the binding of GABA
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8
Q

Slide 13 for benzodiazepines

A
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9
Q

Describe Benzodiazepines

A
  • MOA: bind to the benzodiazepine receptor & facilitate opening of the GABA receptor
  • SE: anterograde amnesia (memory loss), residual. effects (drowsiness, confusion, psychomotor slowing), tolerance & dependence
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10
Q

Define tolerance and dependence

A
  • Tolerance: more drug is needed to have the same effect over time
  • Dependence: withdrawal symptoms occur. when the drug is stopped; not the same as addiction
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11
Q

Slide 16

A
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12
Q

Describe benzodiazepines and older adults

A
  • Increased body fat leading. to more adipose sequestering
  • Increased susceptibility to side effects
  • Decreased metabolism
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13
Q

Describe barbiturates

A
  • MOA: binding site on the GABA receptor & increase the duration the GABA receptor is open; antagonize glutamate
  • SE: narrow therapeutic index high abuse potential
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14
Q

Slide 19 and 20

A
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15
Q

Describe Z drugs

A
  • MOA: selective agonist of GABA receptor
  • SE: complex sleep behavior (black box), psychomotor slowing (increased in elderly), psychiatric & behavioral effects
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16
Q

Effects on rehabilitation

A
  • Adverse drug reactions: sedation, musculoskeletal, and other somatic effects
  • Decreased arousal or alertness
  • Motor control dysfunction: weakness, increased response time, altered central processing, impaired function ability
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17
Q

Possible therapy solutions to the effects of CNS drugs on rehabilitation

A
  • Explore options with physician regarding the risks & benefits. of the medication
  • Schedule. therapy when drug levels. are the lowest in the system if excessive hangover or sedative effects are problematic
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18
Q

(True/False) Newer hypnotics do not produce excessive hangover effects. Also, for chronic anxiety conditions, antidepressants that are nonsedating like the selective serotonin reuptake inhibitors (SSRIs) may be more appropriate drugs

A
  • True
19
Q

Define depression

A
  • Depressed mood or loss of interest or pleasure in daily activities for more than 2. weeks
20
Q

NIH 2020 drug use and health survey for antidepressants

A
  • 8.4% of all US adults
  • Twice as prevalent in females as males
  • Prevalence decreased with age
21
Q

Pathophysiology of depression

A
  • Complex interaction between genetic, environmental, and biochemical factors
  • Disturbances in neurotransmitters: Serotonin, Norepinephrine, and Dopamine
22
Q

Describe selective serotonin receptor inhibitor (SSRI)

A
  • MOA: inhibit the re-uptake of serotonin into the presynaptic nerve; selective for serotonin synapses
  • SE: nausea, diarrhea, jitteriness, anxiety, headache, sexual dysfunction, withdrawal effects if abruptly stopped, increase suicidal thoughts
23
Q

Slide 28

A
24
Q

Describe selective. serotonin. norepinephrine receptor inhibitor (SNRI)

A
  • MOA: selectively inhibit the re-uptake of serotonin & norepinephrine into the presynaptic nerve, effects vary between the drugs in this class
  • SE: nausea, diarrhea, increased HR/BP/CNS. activation (insomnia, agitation), sweating, sexual dysfunction, increase suicidal. thoughts
25
Q

Slide 30

A
26
Q

Serotonin Syndrome

A
  • Anxiety, agitation/restlessness, and disorientation
  • Ocular clonus, muscle rigidity, tremor, hyper-reflexia, muscle clonus, bilateral babinski reflex
  • Hyperthermia, dilated pupils, dry mucus membranes, tachycardia, sweating, diarrhoea, vomiting
  • Potentially life threatening
27
Q

Describe tricyclic antidepressants. (TCA)

A
  • MOA: inhibit the re-uptake of serotonin & norepinephrine into the presynaptic nerve; effect many other receptors resulting in more side effects & toxicity
  • SE: dry mouth, blurred vision, constipation, sedation, confusion, delirium (elderly), orthostatic hypotension, cardiac toxicity
28
Q

Slide 33

A
29
Q

Describe monoamine oxidase inhibitor (MAOI)

A
  • MOA: breaks down NTs (MAOa and MAOb); MOAI prevent the breakdown of NTs resulting in an increase in NTs in the nerve ending
  • SE: orthostatic hypotension, restlessness, agitation, insomnia, confusion, delirium, constipation, hypertensive crisis (food interaction)
30
Q

MAOIs interaction with tyramine and tyramine foods

A
  • Tyramine stimulates release of endogenous catecholamines
  • MAO metabolizes catecholamines
  • Foods: red wines, fermented cheese, pickled foods
31
Q

Slide 36

A
32
Q

Basics of antipsychotics

A
  • Psychosis is a severe form of mental illness that encompasses several disorders
  • Inability to distinguish b/w. reality & what is not (delusions, hallucinations, disorganized thoughts)
  • Historically tranquilizers were used as primary treatment
33
Q

Neurotransmitter Hypothesis of Schizophrenia

A
  • Dopamine hypothesis: ↑ DA (dopamine activity) limbic system (positive symptoms) and ↓ DA mesocortical system (negative and cognitive symptoms)
  • Serotonin hypothesis: ↑ 5HT2A (serotonin) cortex and limbic systems (hallucinations)
  • Glutamate hypothesis
34
Q

Mechanism of antipsychotics

A
  • Dopamine antagonist: Block postsynaptic dopamine receptors; Newer agents also block serotonin receptors
  • First generation high affinity for D2
  • Second generation inhibit serotonin receptors and have weak affinity for D2
35
Q

Extrapyramidal effects of antipsychotics

A
  • Akathisia: feeling of restlessness
  • Dystonia: happens more is face/neck
  • Psuedoparkinsonism: Tremor and Bradykinesia
  • Tardive dyskinesia: Irreversible, Involuntary movements of mouth, tongue, and jaw, Dystonia of neck and truck,
    Choreoathetosis
  • Dopamine activity decreased in nigrostriatal pathway
  • Acetylcholine activity increased in nigrostriatal pathway
36
Q

Slide 45 and 46

A
37
Q

Intramuscular antipsychotics short. versus long acting

A
  • Short: acute psychosis; onset is minutes & last a few hours
  • Long: improve adherence leading to decreased hospitalizations & relapses; traditional side effects in addition to injection related side effects
38
Q

Slide 48

A
39
Q

Describe older adults and antipsychotics

A
  • Agitation or aggression treatment: black box warning associated with death & treatment of dementia psychosis
  • Increased side effects: anticholinergic, sedation, hypotension
40
Q

When might you notice increased participation with therapy in a patient started on an SSRI for depression?

A
  • SSRI’s take a while to show effect and may not immediately participate in therapy when started on an SSRI
41
Q

Effects of antidepressants on rehabilitation

A
  • Depression & side effects of antidepressants can impact participation of clients
  • Improvement in symptoms can take several weeks to months
  • Watch for increased thought of suicide (
42
Q

Sedative hypnotics effects on rehabilitation

A
  • Adverse effects: sedation, confusion, and weakness
  • Possible solutions: discussion with provider about risk/benefit, scheduling of sessions, and nonpharmacologic sleep interventions
43
Q

Antidepressant effects on rehabilitation

A
  • Depression and side effects of antidepressants can impact participation of clients
  • Improvement in symptoms can take several weeks to months
  • Watch for increased thought of suicide (most common at the start)
  • These medications can also be used to improve pain
  • May help to improve outcomes of therapy
  • Be mindful of dangerous side effects or possible overdose situation
44
Q

Antipsychotic effects on rehabilitation

A
  • Side effects: Cognitive and psychomotor slowing, sedation, orthostatic hypotension, movement related, and metabolic
  • Possible solutions: Extra monitoring, use of pictures, timing of therapy, physical activity programs, and fall prevention

Pharmacology (12 decks)

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