Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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
Other drugs used
Clozapine
25
Huntington's and Tourette's Drugs
Haloperidol
26
Antitremor Drugs
Propranolol | Ethanol
27
Dystonia Drugs
Antimuscarinics Benzodiazepines BoTox
28
AD/HD Drugs
Methylphenidate Adderall Atomoxetine
29
Benztropine
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
30
Selegiline
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.
31
Rasagiline
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)
32
Tolcapone
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!
33
Entacapone
Indirect-acting DA agonist MOA: Block COMT in periphery only. *Does not cross BBB Use: increases the bioavailability of Levodopa
34
Trihexyphenidyl
Antimuscarinic / Antipsychotic Clean antimuscarinic, with typical anticholinergic side effects MOA: very little inhibition of DAT, primarily antimuscarinic
35
Pramipexole
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
36
Ropinirole
Direct-acting DA agonist effects: neuroprotective Toxicity: more hallucinations, less dyskinesias
37
Clozapine
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
38
Haloperidol
Use: HD and Tourette's High TI Effects: decreases DA = treatment for movement disorder AND psychosis
39
Antimuscarinic drugs
Uses: generalized dystonia
40
Benzodiazepines
Uses: generalized dystonia
41
BoTox
Uses: Focal dystonia MOA: inhibits release of ACh by interfering with release mechanism. *long duration
42
Methylphenidate
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
Adderall
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
Atomoxetine
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
Levodopa
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
Carbidopa
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
Stalevo
PD treatment, combination of Levodopa, Carbidopa, and Entacapone
48
First Generation Antipsychotics
Chlorpromazine* Thioridazine Fluphenazine Haloperidol
49
Second Generation Antipsychotics
``` Clozapine Risperidone Olanzapine Quetiapine Aripiprazole Ziprasidone ```
50
Antimuscarinic Antipsychotics
Benztropine | Trihexyphenidyl
51
Other Antipsychotic
(usually for dyskinesias) | Reserpine
52
Chlorpromazine
Antipsychotic 1st gen *PROTOTYPICAL Toxicity: Orthostasis, weight gain, moderate EPSE, sedation, moderate TD.
53
Thioridazine
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
Fluphenazine
Antipsychotic 1st gen | Toxicity: High EPSE, low weight gain, sedation, orthostasis, and low antimuscarinic effect. High TD
55
Haloperidol
Antipsychotic 1st gen *High TI Toxicity: high EPSE, low orthostasis and antimuscarinic effect, low weight gain, not sedating. High TD
56
Risperidone
Antipsychotic 2nd gen (atypical) MOA: some DA receptor affinity, potent 5HT antagonist Toxicity: Moderate EPSE, and less TD. Moderate orthostasis and sedation
57
Olanzapine
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
Quetiapine
Antipsychotic 2nd gen | Toxicity: Low EPSE and TD, high weight gain, orthostasis, and sedation
59
Aripiprazole
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
Ziprasidone
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
Reserpine
Other antipsychotic | Use: treats dyskinesias
62
SSRIs
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
5HT and NE reuptake inhibitors (SNRIs)
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
Tricyclic antidepressants (TCAs)
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
5HT-2A Antagonists
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
Atypical Antidepressants (uni/heterocyclics)
Bupropion* -DAT and NET inhibitor, also used in craving reduction (Mirtazapine (similar to trazodone), Maprotiline, Amoxipine
67
Monoamine Oxidase Inhibitors (MAOIs)
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
Lithium
Myo-inositol-1 phosphatase inhibitor | Toxicity: headache, diarrhea, dose-dependent tremor, confusion, polyuria, polydipsia, ataxia, slurred speech
69
Other drugs for Bipolar disorder
Carbamazepine Valproate Aripiprazole
70
Fluoxetine
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
Venlafaxine
5HT and NE Reuptake Inhibitor (SNRI) *PROTOTYPICAL NE>5HT Toxicity: Nausea, constipation, somnolence, anorexia, abnormal ejaculation/orgasm, dose-dependent increase in diastolic BP
72
Imipramine
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
Trazodone
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
Bupropion
Atypical antidepressants (Uni/hetero-cyclic) *PROTOTYPICAL MOA: DAT and NET inhibitor facilitates release of catecholamines Use: craving reduction
75
Phenelzine
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
Lithium
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
Carbamazepine
Anti-epileptic (treatment of bipolar) *PROTOTYPICAL | Use: bipolar *especially rapid-cycle
78
Valproate
Use: bipolar
79
Full Opioid Agonists
``` Morphine Codeine Heroin Hydromorphone Oxymorphone Hydrocodone Methadone Meperidine Fentanyl Oxycodone ```
80
Other Morphine-like drugs (no analgesic)
Dextromethorphan Diphenoxylate Loperamide
81
Partial Opioid agonist/antagonist
Pentazocine | Buprenorphine
82
Full Opioid Antagonist (non-analgesic)
Naloxone | Naltrexone
83
Morphine
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
Naloxone
Opioid Antagonist | Use: treats respiratory depression (regardless of the cause -- rules out opioid OD) IV or nasally, short acting
85
Naltrexone
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
Clonidine
alpha-2 agonist | Use: treat anxiety and dysautonomia associated with opioid withdrawal.
87
Heroin-Diacetylmorphine
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
Codeine
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
Meperidine
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
Fentanyl
*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
Diphenoxylate
``` 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
Loperamide
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
Methadone
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
Dextromethorphan
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
Buprenorphine
semi-synthetic partial Mu agonist | Use: analgesic in non-tolerant patients, or as management of opioid-dependency
96
Tramadol
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
Pentazocine
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.
© 2025 Bold Learning Solutions. Terms and Conditions