Brainscape's Knowledge GenomeTM

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


See full index

My cards > CNS Drugs 1 > Flashcards

CNS Drugs 1 Flashcards

0
Q

Triazolam

A

Benzodiazepine

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

Diazepam

A

Sedative-hypnotic, benzodiazepine
*PROTOTYPICAL
“valium” “mother’s little helper”

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

Lorazepam

A

Benzodiazepine, Sedative hypnotic/anxiolytic

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

Estazolam

A

Benzodiazepine, sedative-hypnotic/anxiolytic

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

Flumazenil

A

Benzodiazepine Antagonist
*Mainly used in combined EtOH/BZD OD.
MOA: direct acting competitive antagonist that binds to the BZD receptor site on GABAa receptors, prevents increase in GABA activity.

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

Pentobarbital

A

Barbituate

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

Phenobarbital

A

Barbituate

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

Benzodiazepines (BZDs)

A

Long acting (Anxiety disorders and waking frequently at night): Diazepam
Intermediate acting (Long-term sedation and cannot stay asleep): Estazolam, Lorazepam
Short acting (For difficulty falling asleep, assoc. with retrograde amnesia): Triazolam
MOA: Increases the affinity of GABA for the GABA-A receptor which increases the FREQUENCY at which the Cl- channel opens in response to GABA. Binds to benzodiazepine receptor site on GABAa between alpha and gamma-2 subunit– changes tertiary structure
Effects: Increases Cl- conductance which shunts depolarization = CNS depression. Since they are agonist at the site, but inhibit NT effect, they are INVERSE AGONISTS
“State-dependent action”: BZD action dependent on the status of GABA release. As the drug depresses CNS fxn, GABA release is reduced. Therefore BZDs have a ceiling effect, = little respiratory depression.
Toxicity: Very hard to kill a patient by OD = ceiling effect through CNS depression/GABA release reduction. IV use can have significant respiratory depression at very high doses. *Characteristic signs of CNS depression. Dirrahea, epigastric distress, bitter taste, nausea, vomitting, rare hallucination.
Withdrawal is mild, can have rebound insomnia, anxiety, increased reflexes, excessive motor activity, headache.
Can induce drug hang-over (reduced alertness, groggy feeling)

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

Benzodiazepine antagonist

A

Flumazenil

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

Barbituates

A

Pentobarbital (induces coma in status epilepticus)
Phenobarbital (Managing generalized seizures)
*Risk of respiratory depression HIGH
“drug automatism”: patient awakens, takes another pill, and this cycles until fatal consequences occur, originated with this drug class.
Commonly causes drug hangover.
MOA: binds to the Cl ionophore site independent of GABA binding site.
Increases time the gate is open in presence of GABA. *Opposite of BZDs, barbs can open Cl gate in ABSENCE of GABA (at high dose)
*no ceiling effect, dose-dependent increase in Cl conductance.
Toxicity: Easily produce coma/death, at high dose, can block Ca channels No ceiling effect. *potent CYP450 enzyme inducers, biotransformation increased = complication of therapy w/ other drugs
*Differential rates of tolerance, respiratory depression=antiepileptic efficacy in tolerance, «sedation tolerance

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

Other sedatives/hypnotics

A

Zolpidem (least likely to produce rebound insomnia with little muscle relaxant effects)
Meprobromate (older agent with greater potential for toxicity in OD)
Eszopiclone (For chronic use sedation with less tolerance)
Remelteon (Melatonin agonist with no adverse side effects seen with other drugs in same class. Not as good of a sedative)

MOA: all work on Cl channel.

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

Sedative/Anxiolytics

A

Buspirone (no dependence, no sedation, no anti-epileptic activity)
Propranolol
*All have anxiolytics, but are not anxioselective

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

Situational Anxiety drugs

A

Propranolol

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

Anti-spastic Drugs

A

Baclofen

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

Propranolol

A

Sedative-hypnotic and Antitremor drug
MOA: beta adrenergic non-specific antagonist
Anxiolytic may be due to increased activity of the locus ceruleus, blocking the action of NE reduces locus ceruleus activation of central nucleus of the amygdala
Use: preferred for situational anxiety– stage fright *can also use for essential tremor

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

Buspirone

A

Anxiolytic
Use: reduced anxiety with absence of sedation w/ few other actions
MOA: 5HT-1A partial agonist with small anti-dopaminergic component, reduces firing of raphe nucleus
Effects: do not have typical sedative-hypnotic effects, are without tolerance/cross-tolerance with BZDs
Toxicity: headache, dizziness, and nervousness
*not effective in management of panic attacks, where SSRIs are.

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

Baclofen

A

Anti-spastic drug
MOA: works on presynaptic terminals in spinal cord to ease spasticity. inhibits transmission of both monosynaptic and polysynaptic reflexes, possibly by hyperpolarization of primary afferent fiber terminals = antagonism of the release of excitatory NTs. *Hence, reduces the afferent reflexes that mediate spasticity. B/c of GABAb specificity, it produces less sedation than BZDs at doses that = anti-spasticity effects.
Toxicity: High doses can still be sedating, withdrawal can = hyper-spastic symptoms and seizure.
*For high doses that would = sedation, pumps are used intrathecally, allows for high levels of baclofen in spine w/o significant sedation

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

Eszopiclone

A

Other sedative/hypnotic “Lunesta”

BZD-like agent, “safe for chronic use”

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

Remelteon

A

Other sedative/hypnotic

New type of sedative, works at melatonin agonist at MT-1 receptor

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

Zeleplon

A

Other sedative/hypnotic “Sonata”
Short duration effect for those who have problems falling asleep, but not used for staying asleep.
*clears system rapidly, no drug hangover

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

Drugs for Parkinson’s

A

Carbidopa/Levadopa (indirect-acting DA agonists)

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

Indirect-acting DA Agonists

A 
Benztropine
Selegiline
Rasagiline
Tolcapone
Entacapone
Stalevo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Anti-muscarinic agents

A

Trihexyphenidyl

Benztropine

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

Direct-acting DA Agonists

A

Pramipexole

Ropinirole

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

Other drugs used

A

Clozapine

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

Huntington’s and Tourette’s Drugs

A

Haloperidol

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

Antitremor Drugs

A

Propranolol

Ethanol

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

Dystonia Drugs

A

Antimuscarinics
Benzodiazepines
BoTox

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

AD/HD Drugs

A

Methylphenidate
Adderall
Atomoxetine

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

Benztropine

A

Indirect-acting DA agonist/Antimuscarinic, Antipsychotic
DAT inhibitor and ACh antagonist
Use: other PD drug also Antipsychotic
Effects: Dual action- DA uptake inhibitor (DAT) and antimuscarinic mixes actions and enhances effect, both effectively overcome the deficiency of DA in the striatum at two locations in the pathway
Toxicity: produces unwanted side effects when used to treat PD, secondary to treatment with antipsychotic drugs anticholinergic properties produce sedation and other antimuscarinic effects including memory clouding/constipation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Selegiline

A

Indirect-acting DA agonist
converted to amphetamine and methamphetamine
MOA: MAO-B selective at normal doses, reuptake inhibitor. Contributes to effects by inducing DA release. Increases synaptic DA pool, and overall DA tone. *Normal DA release, extends duration
Toxicity: Can be a problem in working PD patients due to conversion to amphetamine (drug testing) Blocks MAO-A at high doses, but no tyramine effect.

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

Rasagiline

A

Indirect-acting DA agonist
MOA: MAO-B preferring with MAO-A blocking at normal doses, higher concentrations (pressor amine effect).
*Does not convert to amphetamine
Toxicity: MAO-A1 effect at high dose (NE neurons)

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

Tolcapone

A

Indirect-acting DA agonist
MOA: blocks COMT in peripheral and central CNS
Effect: increases bioavailability of levodopa to brain, and increases duration of levodopa action (reduced catabolism) *Crosses BBB
Toxicity: liver toxic!

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

Entacapone

A

Indirect-acting DA agonist
MOA: Block COMT in periphery only. *Does not cross BBB
Use: increases the bioavailability of Levodopa

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

Trihexyphenidyl

A

Antimuscarinic / Antipsychotic
Clean antimuscarinic, with typical anticholinergic side effects
MOA: very little inhibition of DAT, primarily antimuscarinic

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

Pramipexole

A

Direct-acting DA agonist
Use: used in early stage monotherapy, delays the requirement of levadopa.
MOA: Synthetic full intrinsic activity agonist (D2 and D3 agonist) with no D1 activity.
Effects: neuroprotective: may slow progression of PD. Similar efficacy to levadopa in early stage, but not as effective in late stage. Antidepressant action work against “amotivational” stage.
Toxicity: more hallucination, less dyskinesias. Associated with sleep attacks (all DA agonists), associated with OCDs (gambling, hypersexuality, risk taking

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

Ropinirole

A

Direct-acting DA agonist
effects: neuroprotective
Toxicity: more hallucinations, less dyskinesias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Clozapine

A

Other drug (PD) and 2nd generation Antipsychotic (atypical)
Use: drug of choice for hallucinations in PD patients, Antipsychotic
MOA: has little affinity for D-2 receptors in striatum, more potent D4 antagonists. Also potent antimuscarinic
Effects: produces agranulocytosis, peridoxical wet pillow due to high antimuscarinic activity,
Toxicity: Very low EPSE, no TDs, high sedation and orthostasis. High weight gain

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

Haloperidol

A

Use: HD and Tourette’s
High TI
Effects: decreases DA = treatment for movement disorder AND psychosis

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

Antimuscarinic drugs

A

Uses: generalized dystonia

40
Q

Benzodiazepines

A

Uses: generalized dystonia

41
Q

BoTox

A

Uses: Focal dystonia
MOA: inhibits release of ACh by interfering with release mechanism.
*long duration

42
Q

Methylphenidate

A

Use: ADHD management
MOA: Indirect-acting DA agonist. DA selective slightly greater than NE, with fewer NE side effects than amphetamines
Effects: decreased hyperactivity, increased focus
Toxicity: psychomotor stimulation, headaches, appetite suppression, insomnia, nausea

43
Q

Adderall

A

Use: ADHD management
MOA: Longer duration of action, greater dependence liability. Combination of amphetamine and dextroamphetamine –replaces DA in DAT and MAOI
Slightly prefers NE over DA.
Toxicity: increased insomnia

44
Q

Atomoxetine

A

Use: ADHD management
MOA: NE»>DA, no dependence liability. Works on ventral attention system (many have dorsal deficits)
*non-amphetamine
Toxicity: fewer side effects

45
Q

Levodopa

A

Indirect-acting DA agonist
*PROTOTYPICAL drug for PD treatment
Use: late stage PD treatment
MOA: immediate precursor to DA converted by aromatic amino acid decarboxylase (AAAD). “precursor load strategy” DATs and recycling of DA by terminals extend the effective duration of levadopa.
Effects: Increases precursor for DA production, as PD progresses, fewer DA terminals exist, there will be less recycling of DA thereby decreasing the effective duration of levadopa. “End of dose wearing of Effect”
*Does not occur at non-target sites, which decreases the TI as PD progresses. Thus frontal cortex terminals are significantly less damaged and as levodopa dosage is increased to compensate for striatal DA terminal loss, frontal cortex become hyperstimulated = psychosis.

46
Q

Carbidopa

A

Indirect-acting DA antagonist (periphery)
Use: administered with Levodopa in the treatment of PD
MOA: Inhibits AAAD in the periphery (does not cross BBB). Decreased conversion of levodopa to DA in periphery reduces peripheral side effects of increased DA. Also results in increased bioavailability and availability to brain and increases CNS side effects (epigastric distress, nausea vomiting, orthostasis, +inotropy)
Toxicity: CNS side effects. Dyskinesias, dystonia, psychosis/hallucinations, hypoprolactinemia, hyperthermia, myoclonus

47
Q

Stalevo

A

PD treatment, combination of Levodopa, Carbidopa, and Entacapone

48
Q

First Generation Antipsychotics

A

Chlorpromazine*
Thioridazine
Fluphenazine
Haloperidol

49
Q

Second Generation Antipsychotics

A 
Clozapine
Risperidone
Olanzapine
Quetiapine
Aripiprazole
Ziprasidone
50
Q

Antimuscarinic Antipsychotics

A

Benztropine

Trihexyphenidyl

51
Q

Other Antipsychotic

A

(usually for dyskinesias)

Reserpine

52
Q

Chlorpromazine

A

Antipsychotic 1st gen
*PROTOTYPICAL
Toxicity: Orthostasis, weight gain, moderate EPSE, sedation, moderate TD.

53
Q

Thioridazine

A

Antipsychotic 1st gen
Original Atypical drug choice (no longer considered atypical)
MOA: Antimuscarinic activity breaks the pattern of depolarization blockade = reduced EPSEs
Effects: potent antimuscarinic effect and DA antagonist
Toxicity: less TD, low EPSE,

54
Q

Fluphenazine

A

Antipsychotic 1st gen

Toxicity: High EPSE, low weight gain, sedation, orthostasis, and low antimuscarinic effect. High TD

55
Q

Haloperidol

A

Antipsychotic 1st gen
*High TI
Toxicity: high EPSE, low orthostasis and antimuscarinic effect, low weight gain, not sedating. High TD

56
Q

Risperidone

A

Antipsychotic 2nd gen (atypical)
MOA: some DA receptor affinity, potent 5HT antagonist
Toxicity: Moderate EPSE, and less TD. Moderate orthostasis and sedation

57
Q

Olanzapine

A

Antipsychotic 2nd gen/ Other drug (PD)
Use: used for treatment of PD hallucinations
Effects: Does have some D-2 blocking effects, more potent D4 antagonist and can aggravate PD symptoms but reduces hallucinations. Potent antimuscarinic
Toxicity: Low EPSE and TD, high weight gain and sedation, low orthostasis

58
Q

Quetiapine

A

Antipsychotic 2nd gen

Toxicity: Low EPSE and TD, high weight gain, orthostasis, and sedation

59
Q

Aripiprazole

A

Antipsychotic 2nd gen (atypical)
Use: rapid cycle bipolar disorder and antipsychotic
MOA: high levels of occupation of the D2 receptors. (partial agonist)
Toxicity: Low EPSE and TD, low weight gain, not sedating with little orthostasis.

60
Q

Ziprasidone

A

Antipsychotic 2nd Gen (atypical)
MOA: potent antagonist at D2, D3, 5HT-1D, 5HT-2A, 5HT-2C, and 5HT-7. 5HT-1A agonist may alleviate anxiety and depression. Has moderate inhibitory effects on neuronal transport inactivation of 5HT similar to SSRIs (antidepressant)
Toxicity: Low EPSE and TD, CONTRAINDICATED in patients with history of arrhythmias.

61
Q

Reserpine

A

Other antipsychotic

Use: treats dyskinesias

62
Q

SSRIs

A

Fluoxetine*
(paroxetine, sertraline, fluvoxamine, citalopram)
-All can produce 5HT syndrome, when used with another drug (meperidine, tramadol, or MAOIs) or St. John’s Wort
Some weight gain, sexual dysfunction, nausea/vomiting, insomnia

63
Q

5HT and NE reuptake inhibitors (SNRIs)

A

Venlafaxine* NE>5HT
(Desvenlafaxine - metabolite of venlafaxine NE=5HT, Duloxetine - DAT inhibition and NE/5HT)
- Nausea, constipation, somnolence, anorexia, abnormal ejaculation/orgasm, dose-dependent increase in diastolic BP.

64
Q

Tricyclic antidepressants (TCAs)

A

Imipramine* - NE=5HT
(Amitriptyline -5HT>NE, Desipramine - almost pure NET inhibitor, Clomipramine - 5HT>NE)
-Some alpha antagonism (orthostasis), antimuscarinic action (sedation, increased HR, dry mouth, constipation, blurred vision, urinary retention)
weight gain, nausea, and highly toxic in OD (arrhythmias)

65
Q

5HT-2A Antagonists

A

Trazodone*
(Nefazodone)
-Paradoxical antidepressant due to 5HT antagonism, down regulate 5HT-1A autoreceptors which increases 5HT release, mild alpha-1 antagonism (some orthostasis), potent H-1 antagonism (somnolence), priapism

66
Q

Atypical Antidepressants (uni/heterocyclics)

A

Bupropion* -DAT and NET inhibitor, also used in craving reduction
(Mirtazapine (similar to trazodone), Maprotiline, Amoxipine

67
Q

Monoamine Oxidase Inhibitors (MAOIs)

A

Phenelzine*
(Isocarboxazid, Tranylcypromine)
-Hypertensive crisis with foods high in tyramine (protein high), Orthostatic hypotension chronically from DA-beta-hydroxylase inhibition and false NT octopamine, Blurred vision, constipation

68
Q

Lithium

A

Myo-inositol-1 phosphatase inhibitor

Toxicity: headache, diarrhea, dose-dependent tremor, confusion, polyuria, polydipsia, ataxia, slurred speech

69
Q

Other drugs for Bipolar disorder

A

Carbamazepine
Valproate
Aripiprazole

70
Q

Fluoxetine

A

Selective Serotonin Reuptake Inhibitor (SSRI)
*PROTOTYPICAL
MOA: heterocyclic that binds to allosteric regulatory site on the SERT and reduces binding of 5HT to SERT. 5HT»>NE

71
Q

Venlafaxine

A

5HT and NE Reuptake Inhibitor (SNRI)
*PROTOTYPICAL
NE>5HT
Toxicity: Nausea, constipation, somnolence, anorexia, abnormal ejaculation/orgasm, dose-dependent increase in diastolic BP

72
Q

Imipramine

A

Tricyclic Antidepressant
*PROTOTYPICAL
NE=5HT
MOA: competitive reuptake inhibitor, also have affinity for other receptors, muscarinic, alpha, and histamine
Toxicity: Some alpha antagonism, orthostasis, antimuscarinic: sedation, dry mouth, constipation, blurred vision, urinary retention
weight gain, nausea, Toxic due to arrhythmias

73
Q

Trazodone

A

5HT-2A Antagonist
*PROTOTYPICAL
MOA: bind 5HT-2A receptors (apical dendrites of pyramidal cells in layer V of cortex) *Modulate cognitive processes by enhancing glutamate release. Enhancing glutamate release increases activity and reduces depression. *Weak, but selective SERT inhibitor, metabolite has high affinity for 5HT-2A receptors
Effects: paradoxical antidepressant due to 5HT antagonism, down regulation of 5HT-1a autoreceptor = increased 5HT release
Toxicity: alpha-1 antagonism: orthostasis, somnolence, priapism

74
Q

Bupropion

A

Atypical antidepressants (Uni/hetero-cyclic)
*PROTOTYPICAL
MOA: DAT and NET inhibitor facilitates release of catecholamines
Use: craving reduction

75
Q

Phenelzine

A

Monoamine Oxidase Inhibitor (MAOI)
*PROTOTYPICAL
MOA: pressor amines (tyramine) build up due to MAO-A inability to convert it to an inactive product and accumulation occurs = hypertensive crisis.
Toxicity: hypertensive crisis with food intake high in tyramine, orthostatic hypotension due to DA-beta-hydroxylase and false NT octopamine, blurred vision, constipation

76
Q

Lithium

A

myo-inositol-1 phosphatase inhibitor
USE:
MOA: block myo-inositol-1 phosphatase and reduces the cycling of DAG and inositol-triphosphate. Stabilizes production of NTs 5HT and DA preventing mood swings. IP3 reduction = ^5HT release which resets circadian clock
Toxicity: headahe, dirrahea, dose-dependent tremor, confusion, polyuria, polydipsia, ataxia, slurred speech *increased with exercise (ADH unresponsiveness) –> diuresis, water loss, increased reabsorption. Can lead to diabetes insipidus
*Tremor is give away to lithium toxicity. Treated with dialysis

77
Q

Carbamazepine

A

Anti-epileptic (treatment of bipolar) *PROTOTYPICAL

Use: bipolar *especially rapid-cycle

78
Q

Valproate

A

Use: bipolar

79
Q

Full Opioid Agonists

A 
Morphine
Codeine
Heroin
Hydromorphone 
Oxymorphone
Hydrocodone
Methadone
Meperidine
Fentanyl
Oxycodone
80
Q

Other Morphine-like drugs (no analgesic)

A

Dextromethorphan
Diphenoxylate
Loperamide

81
Q

Partial Opioid agonist/antagonist

A

Pentazocine

Buprenorphine

82
Q

Full Opioid Antagonist (non-analgesic)

A

Naloxone

Naltrexone

83
Q

Morphine

A

Direct-acting agonist
*PROTOTYPICAL ANALGESIC
MOA: affect pain threshold at dosages that do not affect conciousness.
*inhibit the release of sub P in the substantia gelatinosa as well as activation of the descending pain suppressing pathways from PAG.
Acts through Mu system.
Effects: pain remains detectable, but affective component is reduced “don’t care about it”.
Toxicity (Side effects): Dependence (increase DA in n. accumbens), Euphoria, Respiratory Depression, Mild antitussive effect, nausea/vomiting, rigidity, increased ADH (increased smooth muscle contraction can make catheterization difficult), Constricted pupils, Histamine release (morphine flush), constipation,
Contraindications: closed head injury (increases cerebral pressure from respiratory depression which increases CO2 levels, induces vasodilation, which increases possibility of a brain bleed. Productive cough patients (antitussive). Reduced Renal Function (recirculated as metabolite if not excreted = toxicity RD

84
Q

Naloxone

A

Opioid Antagonist

Use: treats respiratory depression (regardless of the cause – rules out opioid OD) IV or nasally, short acting

85
Q

Naltrexone

A

Opioid Antagonist
*similar to Naloxone, not as widely used.
Orally available.
Toxicity: Can trigger withdrawal symptoms in dependent individuals, reduces pain threshold in normal individuals.

86
Q

Clonidine

A

alpha-2 agonist

Use: treat anxiety and dysautonomia associated with opioid withdrawal.

87
Q

Heroin-Diacetylmorphine

A

Effects: highly euphoric and analgesic
MOA: hydrolyzed to monacetylmorphine (MAM) and then to morphine
Crosses BBB (lipid soluble)
Toxicity: greater dependence and liability than morphine due to rapid CNS entry, withdrawal

88
Q

Codeine

A

full, direct agonist
“methylmorphine”
MOA: same as morphine, analgesic effect is due to CYP2D6 conversion to morphine. Greater oral efficacy, renal excretion
Effects: less sedating and analgesic, but more antitussive.
Toxicity: same as morphine, less severe. Potent antitussive effect and HIGH constipation

89
Q

Meperidine

A

Use: pre-anethetic, obstetric analgesic
Effects: analgesic, sedation, euphoria, respiratory depression, and others (morphine effects).
Toxicity: Constipation, urinary retention, increased biliary pressure (less than morphine) less miosis and antitussive power. W/ high dose or patient with decreased renal fxn, metabolites accumulate and excite CNS. *With MAOI can =serotonin syndrome b/c of effects on inhibiting serotonin transporter.

90
Q

Fentanyl

A

*HIGHLY POTENT
Use: widely used in surgery as part of balance anesthesia
CONTRAINDICATED: in patients with no tolerance to opioid treatment quickly produces respiratory depression

91
Q

Diphenoxylate

A 
non-analgesic drug
Meperidine congener
*does not cross BBB
no morphine-like effect at normal doses
Use: anti-diarrheal. Formulated with atropine = lomotil. Atropine is anti-muscarinic (constipation)
92
Q

Loperamide

A

non-analgesic
derivative of haloperidol *can cross BBB but generally does not due to p-glycoprotein
Toxicity: when consumed with large amounts of grapefruit juice (naringin) p-glycoprotein is inhibited and drug can enter CNS causing morphine-like effects.

93
Q

Methadone

A

MOA: similar to morphine equi-effective by oral route
Use: analgesia, narcotic abstinence syndrome: reduces but elongated withdrawal symptoms from morphine dependence. Methadone treatment program: orally active and has easier withdrawal *switch from heroin to methadone and then ween off methadone.

94
Q

Dextromethorphan

A

non-narcotic centrally active antitussive
MOA: glutamate antagonistic effects, increases the threshold for coughing
Rare drowsiness or GI disturbances
Toxicity: high doses= glutamate antagonist and PCP effects

95
Q

Buprenorphine

A

semi-synthetic partial Mu agonist

Use: analgesic in non-tolerant patients, or as management of opioid-dependency

96
Q

Tramadol

A

Synthetic
MOA: metabolite efficacy at Mu receptor (contributes to analgesia, and some respiratory depression). reuptake inhibitory properties at NE and 5HT terminals, potentiating pure opioid actions of drug.
Effects: reinstates dependence. drug interaction with SSRIs and MAOIs = serotonin syndrome

97
Q

Pentazocine

A

Partial agonist
Use: can precipitate withdrawal in full agonist users. Formulated with naloxone to prevent IV abuse
Effects: respiratory ceiling, low dependence liability.

My cards (54 decks)

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