Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm > misc neuro pharm > Flashcards

misc neuro pharm Flashcards

1
Q

CNS organization: integration of sensory relays?

A

thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

CNS organization: temp, appetite, emotional, hormonal regulation?

A

hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

CNS organization: respiration and CV fxn?

A

pons and medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CNS organization: control of consciousness, arousal, alertness?

A

reticular formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

do barbituates & alcohol follow a linear or non-linear slope?

A

linear slope: higher doses need for hypnosis can lead to anesthesia, and can ultimately repress respiratory and vasomotor centers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

are barbituates or benzos safer?

A

benzos; b/c have non-linear slope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

for benzos to be effective sedative-hypnotics, where must the electronegative substituent be?

A

EN substituent must be in the 7 position (ie. halogen or a nitro group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which benzos are not affected by age?

A

lorazepam, oxazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

are eszopicolone and zolpidem considered to be benzos?

A

NO, they are benzo-like

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

which anxiolytic is non-sedating?

A

buspirone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MOA of buspirone?

A

5HTA1 partial agonist

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which benzo is the date rape drug?

A

flunitrazepam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which drugs are contraindicated with benzos?

A

those that create additive CNS depresiion (EtOH, opioids, anticonvulsants, phenothiazine, antihistamines, TCA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

which drug is a melatonin receptor agonist?

A

ramelteon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

main issues with initiation of antidepressants?

A
  1. delay of therapeutic response (can take 2-4 weeks)

2. side effects can limit usage (high risk of AE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the hypotheses of depression?

A
  1. Monoamine/biogenic amine hypotheses

2. Neurotrophic hypotheses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the monoamine/biogenic amine hypothesis?

A

deficiency in the level of 5-HT, NE & DA projecting from pontine & midbrain–>cortical&limbic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the neurotrophic hypothesis?

A

loss of brain derived neurotrophic factor (BDNF)–>loss of brain fertilizer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

MAO-A targets what?

A

tyramine, NE, 5HT, DA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

mAO-B targets what?

A

DA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

which class of antidepressants are termed “hip breakers” of elderly?

A

TCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the early sx of serotonin syndrome?

A

lethargy, restlessness, mental confusion, flushing, diaphoresis, tremor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

if a SSRI is suddenly discontinued, how long may it take serotonin syndrome to present?

A

1-7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

are ssri or snri preferred for tx of chronic pain?

A

snri (specifically, duloxetine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MOA of trazadone?

A

5HTA2 blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

which types of antidepressants must you avoid mixing?

A

MAOI, TCA, SSRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

which antidepressants are potent inhibitors of CYP2D6?

A

paroxetine, fluoxetine, fluvoxamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

definition of a seizure

A

abnormally excessive, synchronous, and rhythmic firing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the 3 main causes of seizures?

A
  1. CNS injury
  2. congenital abnormalities
  3. genetic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

when the underlying cause of epilepsy is unk, what is it termed?

A

primary (idiopathic) epilepsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

majority of seizures fall into what type?

A

complex partial (temporal lobe) & tonic clonic (grand mal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

types of partial (focal) seizures

A

simple partial, complex partial, partial becoming generalized
(they all start in a specific portion of he brain, remain there)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

name that seizure: minimal spread of abnormal neuronal discharge, no LOC

A

simple partial seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

name that seizure: starts in small brain area–>quickly spreads to other ares that affect awarness; altered consciousness, automatisms (lip smacking)

A

complex partial seizure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

name that seizure: partial seizures that spread throughout brain and progresses to a generalized seizure

A

partial becoming generalized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

types of generalized seizures (7)

A
  1. absence (petit mal) 2. tonic clonic (gran mal) 3. tonic 4. atonic 5.clonic and myoclonic 6. infantile spasms 7. status epilepticus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

name that seizure: involve entire brain with global EEG change & bilateral manifestation, sudden onset & abrupt cessation, brief LOC, children

A

absence (petit mal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

name that seizure: tonic spasms and major convulsions of entire body (bilateral), LOC, aura, tonic phase w/ muscle tensing/tremor, clonic phase with convulsions, sleep

A

tonic clonic (gran mal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

name that seizure: continuous or very rapid recurring seizures, usually tonic clonic; medical emergency requiring immediate tx

A

status epilepticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what are the 3 stages of epileptic seizures

A
  1. initiation
  2. synchronization of surrounding
  3. propagation–>recruitment of normal neurons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how successful are antiepileptic meds in eliminating seizures?

A

effective in 2/3 patients; but 20% do not respond

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

anticonvulsant drugs bind to Na channels during which state?

A

inactive state—>prolong Na channel inactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

result of inhibiting VG Na channel?

A

decr in sustained, high frequency, repetitive discharge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

result of reducing activity of Ca channels?

A

reduce Ca influx–>decr NT release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

name the drugs that have interactions with phenytoin

A

barbituates, warfarin, carbamapazine, saliclyates, valproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what is the drug of choice for absence seizures?

A

ethosuximide or valproic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

what is the anti seizure drug of choice for pregnancy?

A

phenobarbital

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what limits the use of lorazepam and diazepam to tx status epilepticus?

A

tolerance, sedative effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

which anticonvulsant can create stevens johnson syndrome?

A

lamotrigine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

what drugs can be used for status epilepticus?

A

phenytoin, benzodiazepines, phenobarbitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what is the triad of anethesia?

A

asleep, pain free, still

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

in addition to CV issues, respiratory disease, and allergies, what hx must you know before doing anesthesia?

A

famhx of malignant hyperthermia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

anesthetics with higher or lower solubility are more affected by ventilation rate?

A

partial pressure of anesthetics with higher solubility are affected by vent rate (ie. halothane vs NO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

what is the ostwald coefficient?

A

blood: gas partiton coefficient (solubility in blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

lower ostwald coefficient = lower solubility in blood = what?

A

more rapid rise in partial pressure of blood–>faster induction, lower potency (ex. NO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

how to determine an anesthetics agents solubility in lipid?

A

brain: blood partition coefficient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

high blood flow/solubility of an anesthetic agent mean what type of induction?

A

low induction–> slower onset (b/c gets more rapidly disseminated everywhere)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

if an anesthetic agent is less soluble, will it be faster or slower to eliminate?

A

faster elimination (faster induction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

lower MAC = what potency anesthetic?

A

more potent anesthetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what type of drugs can decrease the MAC of inhaled anesthetics when admin together/?

A

CNS depressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

why use NO for fast induction with other general anesthetics?

A

decr general induction time, decr req’d conc of primary agent, decr toxicity of primary agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

halogentated inhalables are used for what?

A

maintenance anesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

which anesthetic is assc’d with post-op hepatitis?

A

halothane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

why is enflurane not as popular as other halogenated agents?

A

CNS stimulation effects–>EEG convulsive pattern, jerking, twitching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

which halogenated agent has a lower toxicity and can be used in sick patients with impaired kidneys/liver?

A

isoflurane

66
Q

which halogenated agent has teh fastest onset & recovery?

A

desflurane

67
Q

what is the most commonly used halogenated agent?

A

sevoflurane

68
Q

into what space do you inject a spinal block??

A

subarachnoid space

69
Q

into what space do you inject an epidural block?

A

extradural space

70
Q

all local anesthetics are……..?

A

weak bases

71
Q

what forms can local anesthetics take?

A

cationic form–>active at Na receptor

uncharged form–>lipid penetration of membranes

72
Q

what does a larger fiber size indicate for the minimum anesthetic concentration (Cm)?

A

incr Cm (requires larger amt local anethesia to block)

73
Q

list the order that fibers would be blocked by local anesthesia?

A

B fibers 1st, then C-fibers, A delat, A gamme, A beta, A alpha

74
Q

does a lower or higher pH correlate with a lower Cm?

A

more alkaline will require less LA

75
Q

does a lower or higher Ca conc correlation with a higher Cm?

A

higher Ca concentration = higher Cm

76
Q

what is the most important factor that affects reversal of LA?

A

absorption into circulation

77
Q

what is a potential issue with admins of an ester LA?

A

ppl may be prone to PABA allergic rxn (PABA is what esters is metabolized into)

78
Q

what is the tx for LAST (local anesthetic toxicity)?

A

IV lipid emulsion or intralipid–>forms a lipid sink to absorb circulating lipophilic toxin

79
Q

what would be considered negative sx in schizophrenia?

A

flat affect, socially withdrawn, inattentiveness

80
Q

what is the dopamine hypothesis of schizo?

A

hyperactivity of mesolimbic/mesocortical DA system–>excessive limbic DA activity

81
Q

what is the glutamate hypothesis of schizo?

A

hypofxn of NMDA receptors on GABAergic interneurons

82
Q

what are neuroleptics/direct antipsychotics associated with?

A

extrapyramidal side effects

83
Q

what are some extrapyramidal sx?

A

PD-like syndrome, akathesia, dystonia, tardive dyskinesa

84
Q

besides EPS effects, what are some other anti-D2 effects?

A

antiemetic, hyperprolactemia, weight gain, anticholinergic effects, antihistaminic (Sedation), anti-adrenergic (postural hypotension)

85
Q

metabolic syndrome is higher risk in typical or atypical antipsychotics?

A

atypical

86
Q

tops reasons that ppl stop antipsychotics?

A

lack of efficacy, cannot tolerate SE, weight gain, EPS, sedation, sexual SE

87
Q

how many ppl re affected with PD?

A

1% of ppl >65

88
Q

how many ppl are affected with AD?

A

10% of ppl>65

89
Q

how long does it take for death to ensue after onset of AD?

A

6-12 yrs

90
Q

key pathological findings of AD?

A
  1. neuronal degeneration, cortical atrophy
  2. neuritic plaques
  3. neurofibrillary tangles
91
Q

what is the cholingic hypothesis of AD?

A

degeneration of subcortical cholinergic neurons–>deficiency of Ach–>affects memory formation areas

92
Q

does accumulation of beta amyloid plaques correlation well with neuronal loss?

A

no

93
Q

what is the MT-assc’d tau hypothesis of AD?

A

hyperphosphorylation of tau–>neurofibrillary tangles–>MT disintegration & instability–>collapse of neuronal transport system

94
Q

what are the 3 AchE inhibitors used for AD?

A

donepezil, galantamine, rivastigmine

95
Q

which AchE inhibitor has a long half life (70-80 hrs)?

A

donepezil

96
Q

which AchE inhibitor also inhibits butyrylchlinesterase?

A

rivastigmine

97
Q

which AchE inhibitor is admin via transdermal patch?

A

rivastigmine

98
Q

cholinesterase inhibitors all ave what SE?

A

N/V, diarrhea + SLUDGE (salivation, lacrimation, urinary incontinence, diarrhea, GI cramps, emesis)

99
Q

which AD drug is a non-competitive antagonist of NMDA glutamate receptor?

A

memantine

100
Q

best drugs to give to AD patients with psychosis?

A

atypical antipsychotics

101
Q

best drugs to give to AD patients with depression.anxiety?

A

SSRI (esp setralin, citalopram)

102
Q

which antidepressants should you def avoid in AD?

A

TCA due to anticholinergic effects + orthostatic hypotension

103
Q

aggregation of misfolded proteins is what disease?

A

PD

104
Q

PD can affect what brain regions?

A

basal ganglia, brainstem, hippocampus, cerebral cortex

105
Q

what are the cardinal signs of PD?

A

bradykinesia, muscular rigidity, resting tremor, postural instability

106
Q

pathophysiology of PD?

A
  1. loss of DA neurons in substantia nigra that project to striatum (putamen + caudate nucleus)
  2. incr activity of Ach in basal ganglia
107
Q

what are some of the genetic factors that characterize PD?

A

alpha synuclein accumulation, lewy body formation, incr production of free radicals

108
Q

which motor pathway becomes more dominant in PD?

A

indirect pathway

109
Q

adverse effects of levodopa

A

dyskinesias, response fluctuations, on-off phenomenon, drug holiday, GI disturbance, postural hypotension, tachycardia, behavioral disturbance

110
Q

what class of PD drugs is assc’d with lower incidence of the response fluctuations that are associated with L-dopa?

A

DA-receptor angonists

111
Q

what type of drug can you start a PD patient on once they start having a diminished response to levodopa?

A

rasagiline, selegiline (MAO-B inhibitors)

112
Q

what drug increases DA release?

A

amantidine

113
Q

livedo reticularis

A

SE of amantidine

114
Q

benztropine and trihexyphenidyl have what tx effects for PD?

A

reduces tremor and rigidity

NOT bradykinesia

115
Q

what are opioids generally used for?

A

euphoria, analgesia, sedation, diarrheal relief, cough suppression

116
Q

what are the 2 naturally occuring opioids?

A

morphine + codeine (opium)

117
Q

when a drug is extracted from the exudate of the poppy?

A

opiate

118
Q

which opioids are endogenous?

A

endorphins, enkephalins, dynorphins

119
Q

what are the opioid receptors?

A

mu 1, mu 2, kappa, delta

120
Q

which opioid receptor is located outside the spinal cord?

A

mu 1; central interpretation of pain

121
Q

which opioid receptor is located in the CNS?

A

mu 2

122
Q

what is disinhibition?

A

when opioids block inhibitory GABAergic interneurons–>enhanced inhibition of nocioceptive processing

123
Q

what are the sites of action of opioids?

A
  1. periaqueductal gray area (midbrain)
  2. rostral ventral medulla (brainstem)
  3. locus coerulus (pons in brainstem)
124
Q

what are the analgesic effects of opioids (2)?

A

sensory and affective

125
Q

what do opioids do to respiratory system?

A

inhibits brainstem respiratory mechanisms–>less sensitive to pCO2 tension

126
Q

what can occur in opioid OD when brainstem not responsing to incr pCO2?

A

reflexive cerebral vasodilation

127
Q

how do opioids suppress the cough center?

A

via the brainstem chemoreceptor trigger zone

128
Q

how do opioids stimulate emesis?

A

via the brainstem chemoreceptor trigger zone

129
Q

how do opioids stimulate constipation?

A

decr gut motility, incr tone of intestinal smooth muscle

130
Q

CV effects associated with opioids?

A

hypotension, bradycardia

131
Q

receptor down regulation and desensitization is what type of tolerance?

A

physiological tolerance

132
Q

what is cross tolerance?

A

tolerance to one drug produces tolerance to another drug (ie. someone tolerant to morphine will also be toelrant to fentanyl)

133
Q

how is the reward pathway activated by opioids?

A

they inhibit GABAergic inhibitory interneurons–>incr activation of dopaminergic neurons

134
Q

withdrawal sx for opioids? onset of sx when?

A

muscular aches, chills, diarrhea, N/V, fever, insomnia, sweating, anxiety, hostility

occurs within 6-10 hrs

135
Q

which stimulant is a resp stimulant used to counteract postanesthetic resp depression?

A

doxapram

136
Q

are methylxanthines bronchodilators or bronchoconstrictors?

A

bronchodilators

137
Q

what is the primary tx for apnea of prematurity?

A

caffeine

138
Q

what type of stimulant can you use to tx COPD and asthma?

A

theophylline

139
Q

what is teh main drug used to tx narcolepsy?

A

modafinil

140
Q

what drug is used as adjunctive tx for obesity?

A

amphetamine

141
Q

what are amphetamines approved to tx?

A

narcolepsy, ADHD, short term weight loss

142
Q

what area of the brain does cocaine affect?

A

reward circuitry–>the ventral tegmental area (VTA)

143
Q

which CNS stimulant has an incr risk for suicide risk?

A

atomoxetine; esp in children

144
Q

what are the % for each subtype of ADHD?

A
  1. impusivity/hyperactivity: 10%
  2. inattention: 30-40%
  3. impulsivity/hyperactivity/inattention: 50-60%
145
Q

sx of childhood ADHD

A

motoric hyperactivity
aggressiveness
low frustration tolerance
impulsiveness

146
Q

children with ADHD have deficits in what part of brain?

A

frontal lobe:

  1. dorsolateral prefrontal cortex
  2. dorsal anterior cingulate cortex
  3. caudate + putamen
147
Q

adults with ADHD present how?

A

shift activities, easily bored, impatient, restlessness

148
Q

when incr drug metabolism results in decr in amt of available drug or duration of drug at target site?

A

pharmacokinetic tolerance

149
Q

when CNS responds and adapts to presence of drug, resulting in desensitization, down regulation, or internalization of receptors?

A

pharmacodynamic tolerance

150
Q

is addiction psychological or physical dependence?

A

psychological dependence

dependence is physical

151
Q

what CNS mechanisms account for addiction?

A

incr synaptic plasticity and DA release in the mesolimbic reward pathways

152
Q

why is it that you get more drunk when drinking on an empty stomach?

A

drinking on an empty stomach reduces the time EtOH is susceptible to 1st pass metabolism—>incr BAC

153
Q

metabolism of alcohol includes?

A
  1. alcohol dehydrogenase (ADH)
  2. microsomal ethanol-oxidizng system (MEOS)
  3. aldehyde dehydrogenase (ALDH)
154
Q

is rate of elimination of alcohol dependent on time and concentration of alcohol?

A

no it is independent.

constant amt eliminated per unit time

155
Q

what does disulfuram inhibit?

A

aldehyde dehydrogenase (step 2 of alcohol metabolism)

156
Q

chronic alcohol use leads to upregulation of what type of receptor?

A

glutamate NMDA receptors–>responsible for withdrawal sx

157
Q

what is a benzodiazepine receptor antagonist used to tx benzo OD?

A

flumazenil

158
Q

what is the date rape drug used to induce amnesia (not flunitrazepam)?

A

GHB

159
Q

what sympathomimetic effects can amphetamines induce?

A

mydriasis, tachycardia, HTN

due to vesicular release of NE

160
Q

MOA of MDMA?

A

inhibs SERT to release 5HT from presynaptic terminals–>depletes 5HT

161
Q

what are the most commonly abused opioids?

A

codeine, morphine, heroin, oxycodone

162
Q

what can be used to tx nicotine addiction

A

transdermal nicotine patch, buproprion, vareniclin

Pharm (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions