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NUR 408 Pharmacotherapeutics > Exam 2 Concepts > Flashcards

Exam 2 Concepts Flashcards

1
Q

dark outer ring of the brain which is Latin for “bark”

A

cortex, roughly the size of a pillow case, which is responsible for human intellect and folded

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2
Q

lobes of the brain (4) and their function

A
  1. frontal: executive function
  2. parietal: sensory information, especially tactile (pressure, touch, pain)
  3. temporal: language and memory
  4. occipital: visualization
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3
Q

mental disorders in which the frontal lobe is at play

A

substance abuse

ADHD

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4
Q

limbic system function

A

controls learning, memory, emotions, and basic drives; hippocampus (memory), hypothalamus (homeostasis), and amygdala (emotion) all part of

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5
Q

how many neurons do we have in our brains?

A

86 billion and none of them touch

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6
Q

neurotransmitters (NTs) function, creation, and storage

A

NTs are signaling chemicals which the cell body of the nueron creates and the axon terminal stores within small vesicles

approximately 50 different types

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7
Q

action potential

A

an electrical charge which travels down the axon between cells of the myelin sheath and causes the release of NTs into the synapse

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8
Q

monoamines (3)

A
  1. Dopamine (DA)
  2. Norepinephrine (NE)
  3. Serotonin (5HT)
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9
Q

dopamine (DA)

A

NT which regulates mood, attention, energy, PLEASURE, MOTIVATION, and MUSCLE movements

ex. meds used to increase in clients with depression or ADHD

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10
Q

norepinephrine (NE)

A

NT involved in mood, attention, energy, and the FIGHT OR FLIGHT response

excessive amounts can cause anxiety or aggitation

ex. meds often used to increase in clients with depression or ADHD

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11
Q

serotonin (5HT)

A

NT which regulates mood, anxiety, SEXUAL DESIRE, and APPETITE

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12
Q

glutamate

A

main excitatory NT

“gas pedal”

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13
Q

GABA

A

main inhibitor NT
“brake pedal”

used in several meds to reduce anxiety, prevent seizures, and induce sleep

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14
Q

acetylcholine

A

NT which aids in regulation of attention and MEMORY

ex. often increased in pt’s w/Alzheimer’s dz

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15
Q

termination of a neuronal signal

A
  1. diffusion
  2. enzymatic degradation
  3. reuptake
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16
Q

NT diffusion

A

NTs float away from the synapse into the cerebrospinal fluid where they cannot activate postsynaptic receptors

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17
Q

NT enzymatic degradation

A

NTs broken apart by enzymes which end in “-ase”

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18
Q

NT reuptake

A

presynaptic terminal “pumps” suck NTs back into presynaptic terminal to be stored for future use

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19
Q

functions of psych medications (3)

A

change release of NTs
change enzymatic regulation
block reuptake

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20
Q

monoamine oxidase inhibitors (MAOIs)

A

prescribed for major depression, but usually not the first choice

think food AND drug interactions

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21
Q

MAOI food interactions

A

must AVOID foods w/tyramine (aged/fermented foods)

ex. cheeses, aged/processed meats, anything pickled, overripe fruit

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22
Q

MAOI drug interactions

A

pts must avoid drugs which increase monoamine NT levels

ex. other antidepressants, cold meds, meperidine (pain med), triptans (migraine meds)

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23
Q

MAOI mechanism of action

A

block monoamine oxidase which breaks down all three monoamines (DA, NE, 5HT) which increases their levels in the brain’s synapses

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24
Q

MAOI adverse effects

A

hypertensive crisis: tyramine or NE levels too high –> increased BP

serotonin syndrome: 5HT too high –> altered mental state, fever, sweating, clonus (involuntary rhythmic muscle contraction…foot test)

orthostatic hypotension

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25
Q

tricyclic antidepressants (TCAs)

A

drugs which help treat major depression, neuropathic pain, and anxiety disorders

ex. diabetes neuropathic pain tx

think LESS selective than SNRIs

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26
Q

TCA mechanism of action

A

block NE and 5HT REUPTAKE pumps which increases NE and 5HT levels in synapses

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27
Q

TCA adverse effects

A

anti-cholinergic: block muscarinic cholinergic receptors –> can’t see, spit, pee, sh*t

cardiotoxicity: fatal cardiac dysrhythmias w/overdose; children and pt w/suicidal ideation at risk

orthostatic hypotension

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28
Q

selective serotonin reuptake inhibitors (SSRIs)

A

first line of drugs for depression and may also be used for anxiety

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29
Q

SSRI mechanism of action

A

serotonin reuptake pumps blocked which increases 5HT

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30
Q

SSRI adverse effects (5)

A

“5 s’s”

  1. S tomach trouble
  2. S lowed metabolism (weight gain)
  3. S exual dysfunction
  4. S uicidal ideation
  5. S edating (EXCEPT fluoxitine)
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31
Q

serotonin norepinephrin reuptake inhibitors (SNRIs)

A

prescribed for major depression; duloxetine for neuropathic pain and venlafaxine for anxiety disorders.

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32
Q

SNRIs mechanism of action

A

blocked reuptake of NE and 5HT; MORE selective than TCAs

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33
Q

SNRI adverse effects

A

similar to SSRIs plus HTN, especially if dose is high

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34
Q

bupropion

A

prescribed for depression, smoking cessation, and ADHD

inhibits NO and DA reuptake (NE 5HT effect!!!–>no weight gain)

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35
Q

trazadone

A

prescribed for depression, but mainly used for insomnia

weak SRI w/ strong sedative and anticholinergic effects

36
Q

important note about anti-depressants

A

takes 2-3 weeks for them to kick into action

black box warning for suicidal thoughts, especially pts <18yo

37
Q

mood stabilizer challenges

A

treating from above and below
medication adherence, esp w/mania
self-medication w/other substances

38
Q

mood stabilizer medications

A

lithium
anti-epileptic
atypical anti-psychotics

39
Q

lithium benefits and difficulty

A

pro: highly effective, lowers suicide risk
con: NARROW therapeutic index of 1.5mEq/L

40
Q

signs of lithium toxicity

A

A taxia
C oarse tremors
N ausea/vomiting
E ars ringing “tinnitus”

HOLD the drug and call provider

41
Q

client teaching w/lithium

A

take w/food to prevent GI upset
maintain fluid and salt intake
avoid strenuous exercise
knows signs of toxicity

42
Q

normal side effects of lithium

A

mild nausea/diarrhea
fine hand tremors
polyuria/polydipsia (frequent urination and thirst)
weight gain

43
Q

anti-anxiety “anxiolytic” medications

A 
benzodiazepines
buspirone
anti-depressants
beta blockers
certain anti-histamines
44
Q

uses of benzodiazepines

A 
anxiety
insomnia
muscle spasms
seizures
alcohol w/drawal
45
Q

benzodiazepine mechanism of action

A

increase GABA activity “break pedal” which decreases neuronal firing, similar to alcohol

EXTREMELY addictive d/t rapid onset and short half life

46
Q

benzodiazepine side effects

A

ataxia
sedation
impaired memory

47
Q

benzodiazepine precautions

A

hx of drug abuse
liver dz
elderly d/t possible fall risk

pt must be weaned off benzos after long term use

48
Q

buspirone mechanism of action

A

not entirely understood, but binds strongly to 5HT and loosely to DA

49
Q

benefits and difficulty w/buspirone

A

pros: no abuse potential, not CNS depressant, no major w/drawal sx
con: long period of onset (weeks)

50
Q

buspirone food interactions

A

must AVOID grapefruit juice b/c it is a cyp inhibitor which increases drug levels in the blood–> toxicity

51
Q

anti-psychotic medications

A

FGAs “typical”

SGAs “atypical”

52
Q

uses of FGAs

A

schizophrenia
aggitation/aggression
nausea/vomiting
intractable hiccups

53
Q

signs of schizophrenia

A 
"4 D's"
D istress
D anger
D eviant
D ysfunction
54
Q

schizophrenia symptoms

A

positive: hallucinations, delusions, disorganized speech, bizarre behavior
negative: flat affect, alogia (absence of thought), avolition (lack of motivation), anhedonia (no pleasure), social isolation

55
Q

FGA mechanism of action

A

block all dopamine receptors to reduce dopamine activity in the brain

56
Q

dopamine pathways (4)

A

mesolimbic: positive sx
mesocortical: negative sx
nigrostriatal: extrapyramidal sx
tuberoinfundibular: endocrine issues

ex. gynecomastia, galactorrhea, amenorrhea

57
Q

FGA side effects

A 
anticholinergic
EPS
orthostatic hypotension
sedation
neuroendocrine
photosensitivity
58
Q

extrapyramidal symptoms d/t FGA

A

acute dystonia
akathisia
parkinsonism
tardive dyskinesia

59
Q

neuroleptic malignant syndrome

A 
F ever
E levated WBCs and CPK
V ital signs unstable
E ncephalopathy
R igidity

extremely fatal

60
Q

uses of SGAs

A

schizophrenia
bipolar disorder
late stage dementia w/psychotic features

61
Q

SGA mechanism of action

A

block all dopamine AND serotonin receptors to reduce dopamine activity in the brain in areas w/too much and increases dopamine in areas w/too little

62
Q

SGA benefit and difficulties

A

pro: lower extrapyramidal sx
cons: metabolic syndrome, expensive (2-3 times more so than FGAs) while equally effective

63
Q

metabolic syndrome

A

may lead to diabetes

central obesity, HTN, high blood sugar, dyslipidemia (bad cholesterol)
mainly caused by clozapine (also causes destrcution of WBCs) and olanzapine

64
Q

uses of CNS stimulants

A

ADHD

narcolepsy

65
Q

CNS stimulants mechanism of action

A

block reuptake of NE and DA to increase levels at the synapses to increase executive function

66
Q

CNS stimulant side effects

A

A ddiction/abuse
A norexia
A rrhythmias
A wake at night (insomnia)

*do NOT combine w/alcohol–>increased BPx2

67
Q

atomoxetine benefits and risks

A

pros: NE reuptake inhibitor ONLY, low abuse potential
cons: long period of onset, increased risk of suicide, weight loss, liver toxicity
* not as effective as other CNS stimulants, but option fo pts w/hx of abuse

68
Q

alcohol cessation medication uses

A

to help facilitate withdrawal

maintain abstinence

69
Q

alcohol withdrawal

A 
w/in hrs of last drink:
INCREASE all vital signs
hallucination
illusion
N/V
seizures
tremors

d/t brain compensation for constant GABA increase–> overstimulation w/glutamate

70
Q

delirium tremens

A 
rare, 2-3 days after last drink:
severe disorientation
hallucinations
severe HTN
cardiac dysrhythmias
71
Q

seizure precautions

A

pad bedrails
have O2 ready
have suction regulator in case pt begins vomiting; prevent aspiration

72
Q

disulfiram

A

causes N/V, sweating, hypotension, headache, palpations w/ANY alcohol ingestion to decrease alcohol temptation

must avoid hidden alcohol in sauces, cough syrup, etc

contraindicated for pts w/CV issues

73
Q

naltrexone

A

opioid antagonist which reduces the pleasure derived from alcohol

reduced cravings, reduced buzz

74
Q

opioid toxicity

A

C oma
P inpoint pupils
R espiratory depression !!!!

75
Q

naloxone

A

powerful opioid antagonist which reverse opioid toxicity

short half life, pain/withdrawal
MUST monitor pt, usually given multiple doses

76
Q

opioid withdrawal sx

A 
N/V/D
yawning
rhinorrhea
sweating
irritability
tremor
goosebumps
muscle spasms/kicking movements "kicking the habit"
77
Q

methadone

A

opioid agonist

doses gradually reduced to aid w/withdrawal sx

78
Q

buprenorphine

A

PARTIAL opioid agonist

doses gradually reduced to aid w/withdrawal sx

79
Q

nicotine addiction

A

HIGHLY lipid soluble so it reaches brain instantaneously and binds to nicotinic N acetylcholine receptors

80
Q

nicotine N receptors

A

CV: increased BP and cardiac work
GI: increase motility
CNS: increased alertness, memory, cognition, decreased appetite, pleasure activated

81
Q

nicotine withdrawal

A

begins w/in 24h and can last months
abrupt discontinuation best tolerated

cravings, irritability, insomnia, impaired concentration, weight gain

82
Q

nicotine patches

A

slower, steadier release of nicotine ONLY which is not carcinogenic itself

CAUTION: increased absorption w/inflammed skin, open wounds, heating pad

83
Q

varenicline

A

partial nicotinic agonist to decrease reward of nicotine

side effects: N, mood changes, suicidal ideation!!

84
Q

activated charcoal mechanism of action

A

binds to certain drugs to prevent absorption of the drug and allow them to be excreted

lipid soluble drugs such as TCAs, benzos, opioids, NSAIDs, antihistamines, etc

85
Q

activated charcoal administration

A

pt must be awake and alert to avoid aspiration
give anti-nausea beforehand !!
mix in 6-8oz water can be w/juice or chocolate to improve taste
NEVER milk

*must be taken w/in 1 hr of drug ingestion

NUR 408 Pharmacotherapeutics (22 decks)

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