Brainscape's Knowledge GenomeTM

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


See full index

Boards studying > Neuro-pharmacology > Flashcards

Neuro-pharmacology Flashcards

1
Q

Phenytoin

A

For simple partial and complex partial1st line for tonic clonic1st line prophylaxis for status epilepticusMechanism: Increase Na+ channel inactivationNotes: Fosphenytoin for parenteral use

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

Carbamazepine

A

For both simple and complex partial.1st line for tonic-clonicMechanims: increases Na+ channel inactivationNotes: 1st line for trigeminal neuralgia

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

Lamotrigine

A

For both Simple and complex partial.Used in Tonic clonic.Blocks voltage-gated Na+ channel.

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

Gabapentin

A

For both simple and complex partialTonic clonicDesigned as GABA analog, but primarily inhibits HVA Ca2+ channelsNotes: Also used for peripheral neuropathy; bipolar disorder

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

Topiramate

A

For simple and complex partialFor tonic-clonicMechanism: Blocks Na+ channels and increases GABA action

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

Phenobarbital

A

For simple and complex partial For Tonic-clonicIncreases GABA action1st line in CHILDREN AND PREGNANT WOMEN

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

Valproic acid

A

For simple and complex partial1st line for tonic-clonic generalizedUseful for AbsenceIncrease Na+ channel inactivation and increases GABA concentrationUsed for myoclonic seizures

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

Ethusuximide

A

2st line for Absence seizuresBlocks thalamic T-type Ca2+ channels

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

Benzodiazepines (diazepam or lorazepam)

A

1st line for acute status epilepticusIncreases GABAa actionAlso used for seizures of eclampsia, though first line is MgSO4

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

Tiagabine

A

For simple and complex partial.Inhibits GABA uptake

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

Vigabatrin

A

For simple and complex partial.Irreversibly inhibits GABA transaminase - increases GABA

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

Levetiracetam

A

For simple and complex partial.For generalized tonic-clonic.Unknown mechanism - may modulate GABA and glutamate release

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

What are the 1st line therapies for tonic-clonic

A

Phenytoin, Carbamazepine, and valproic acid

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

Benzodiazepines toxicities

A

Sedation, tolerance, dependenceAlprazolam, Triazolam, Oxazepam, Midazolam (ATOM) (short-acting): high risk of dependence/withdrawalLorazepam, Estazolam, Temazepam (LET) (medium-acting): moderately severe side effectsDrazepam, Flurazepam, Clorazepate, Chlordiazepoxide (DFCC) (long-acting): daytime drowsiness/falls

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

Carbamazepine toxicity

A

Diplopia, ataxia, blood dyscrasias (agranulocytosis, aplastic anemia), liver toxicity, teratogenesis, induction of cytochrome P-450 system, SIADH, Stevens-Johnson syndrome

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

Ethosuximide toxicity

A

GI distress, fatigue, headache, urticaria, Stevens-Johnson syndromeEFGH - ehtosuximide, fatigue, GI, headache

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

Phenytoin toxicity

A

Nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsutism, megaloblastic anemia, teratogenesis *fetal hydantoin syndrome), SLE-like syndrome, induction of cytochrome P-450

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

Valproic acid toxicity

A

GI distress, rare but fatal hepatotoxicity (measure LFTs), neural tube defects in fetus (spina bifida), tremor, weight gain. Contraindicated in pregnancy.

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

Lamotrigine toxicity

A

Steven-Johnson syndrome

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

Gabapentin toxicity

A

Sedation, ataxia

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

Topiramate toxicity

A

SEdation, mental dulling, kidney stones, weight loss

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

Phenytoin: mechanism, clinical use, toxicity

A

Mechanism: Use-dependent block of Na+ channels; increases refractory period; inhibition of glutamate release from excitatory presynaptic neuron.Clinical use: Tonic-clonic seizures. Also a class IB antiarrhythmic.Toxicity: Nystagmus, ataxia, diplopia, sedation, SLE-like syndrome, induction of cytochrome P-450. Chronic use produces gingival hyperplasia in children, peripheral neuropathy, hirsutism, megaloblastic anemia (decreased folate absrption). Teratogenic (fetal hydantoin syndrome)

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

Barbituates (phenobarbital, pentobarbital, thiopental, secobarbital) are contraindicated in?

A

porphyria

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

Barbiturates (phenobarbital, pentobarbital, thiopental, secobarbital) Mechanism, Clinical use, toxicity

A

Mechanism: Facilitate GABAa action by increasing the duration of Cl- channel opening, thus decreasing neuron firing.Clinical use: sedative for anxiety, seizures, insomnia, induction of anesthesia (thiopental)Toxicity: Dependence, additive CNS depression effects with alcohol, respiratory or cardiovascular depression (can lead to death), drug interactions owing to induction of liver microsomal enzymes (cytochrome p-450).Treat overdose with symptom management (assist repiration, increase BP), induces enzymes involved in heme synthesis –> acute intermittant porphyria exacerbation.

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

Benzodiazepines

A

Diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam

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

Short acting benzodiazepines.

A

TOM: Triazolam, oxazepam, midazolam.Highest addictive potential

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

Mechanism of benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)

A

Facilitate GABAa action by increased frequency of Cl- channel opening. Decreased REM sleep.Most have long half-lives and active metabolites.

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

Clinical use of benzodiazepines (diazepam, lorazepam, triazolam, temazepam, oxazepam, midazolam, chlordiazepoxide, alprazolam)

A

Anxiety, spasticity, status epilepticus (lorazepam and diazepam), detoxification (especially alcohol withdrawal - DTs), night terrors, sleepwalking, general anesthetic (amnes, muscle relaxation), hypnotic (insomnia)

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

Benzos, Barbs, and EtOh all bind to?

A

GABA(A)-R, which is a ligand-gated chloride channel (increase frequency of channel opening)

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

Toxicity of benzodiazepines

A

Dependence, additive CNS depression effects with alcohol.less risk of respiratory depression and coma than with barbituates.Treat overdose with flumazenil (competitive antagonist at GABA benzodiazepine receptor)

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

Nonbenzodiazepine hypnotics

A

Zolpidem (ambien), zaleplon, eszopiclone

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

Mechanism, clinical use, and toxicities of nonbenzodiazepine hyponotics (Zolpidem (ambien), zaleplon, eszopiclone)

A

Mechanism: Act via BZ1 receptor subtype and is reversed by flumazenilClinical use: insomniaToxicity: Ataxia, headaches, confusion. short duration because of rapid metabolism by liver enzymes.Unlike older sedative-hypnotics, cause only modest day-after psychomotor depression and few amnestic effects.Lower dependence risk than benzodiazepines.

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

Inhaled anesthetics

A

halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide

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

Inhaled anesthetics (halothane, enflurane, isoflurane, sevoflurane, methoxyflurane, nitrous oxide) effects, toxicity

A

mechanism is unknown. (HST150: Isoflurane potentiates GABAa, whereas nitrous oxide xenon, and cyclopropane do not.)Effects: Myocardial depression, respiratory depression, nausea/emesis, increases cerebral blood flow and decreases cerebral metabolic demandToxicity: hepatotoxicity (halothane), nephrotoxicity (methoxyflurane), proconvulsant (enflurane), malignant hyperthermia (rare), expansion of trapped gas (NO)

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

Which inhaled anesthetic is hepatotoxic?

A

halothane

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

Which inhaled anesthetic is nephrotoxic?

A

methoxyflurane

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

Which inhaled anesthetic is a proconvulsant?

A

enflurne

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

Intravenous anesthetics - Barbiturates

A

Thiopental - high potency (because lipid solubility), high lipid solubility, rapid entry into brain.Used for induction of anesthesia and short surgical procedures.Effect terminated by rapid redistribution into tissue and fat.Decreased cerebral blood flow.

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

intravenous anesthetics - benzodiazepines

A

Midazolam most common drugs used for endoscopy; used adjunctively with gaseous anesthetics and narcotics.May cause severe postoperative respiratory depression, decreased BP (treat overdose with flumazenil), and amnesia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Intravenous anesthetics - Arlcyclohexylamines

A

Ketamine - PCP analogs that act as dissociative anesthetics.Block NMDA receptors.Cardiovascular stimulants. Cause disorientation, hallucination, and bd dreams.Increased cerebral blood flow.

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

Intravenous anesthetics - opiates

A

Morphine, fentanyl used with other CNS depressants during general anesthesia

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

Intravenous anesthetics - Propofol

A

Used for rapid anesthesia induction and short procedures.Less postoperative nausea than thiopental. Potentiates GABAa.

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

Local anesthetics: esters and amides

A

Esters - procaine, cocaine, tetracaine.Amides (two I’s) = lidocaine, mepivacaine, bupivacaine

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

Mechanism of local anesthetics - procaine, benzocaine, cocaine, tetracaine, lidocaine, mepivacaine, bupivacaine

A

Block Na+ channels by binding to specific receptors on inner portion of channel.Preferentially bind to activated Na+ channels, so most effective in rapidly firing neurons.Tertiary amine local anesthetics penetrate membrane in uncharged form, then bind to ion channels as charged form.Often norepinephrine is coinjected in order to prolong time to removal from circulation. This has its own problems, as NE is packaged in neurotoxant antioxidants and at a low pH, which impairs anesthetic penetration (many local anesthetics are bases).Sensations from more proximal regions are blocked earlier and recover later than those from more distal segments. This reflects the diffusion of anesthetic through the somatotopically organized peripheral nerve.

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

Local anesthetics - procaine, cocaine, tetracaine, lidocaine, mepivacaine, bupivacaine principles

A

Principles:1) In infected (acidic tissue), alkaline anesthetics are charged and cannot penetrate membrane effectively.More anesthetic needed.2) Order of nerve blockade: small-diameter fibers>large diameter. Myelinated fibers> unmyelinated.Overall, size factor predominates over myelination such that small myelinated fibers > small unmyelinated fibers>large myelinated fibers>large unmyelinated fibers. Order of loss - pain (lost first), > temperature > touch > pressure (lose last)3. Except for cocaine, given with vasoconstrictors (usually epinephrine) to enhance local action (decreases bleeding, increases anesthesia by decreased systemic concentration)

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

Local anesthetics - procaine, cocaine, tetracaine, lidocaine, mepivacaine, bupivacaine clinical use and toxicities

A

Clinical use: minor surgical procedures, spinal anesthesia.if allergic to esters, give amides.Toxicity: CNS excitation, severe cardiovascular toxicity (bupivacaine), hypertension, hypotension, and arrhythmias (cocaine)

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

Neuromuscular blocking drugs- use

A

Used for muscle paralysis in surgery or mechanical ventilation.Selective for motor (vs. autonomic) nicotinic receptor

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

Neuromuscular drugs - depolarizing

A

Succinylcholine (complications include hypercalcemia and hyperkalemia). Reversal of blockade:Phase I (prolonged depolarization) - no antidote.Block potentiated by cholinesterase inhibitors.Phase II (repolarized but blocked) - antidote consists of cholinesterase inhibitors (e.g. neostigmine)

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

Neuromuscular blocking drugs-nondepolarizing

A

Tubocurarine, atracurium, mivacurium, pancuronium, vecuronium, rocuroniumCompetitive blockage - compete with nicotonic Ach for receptors (nAChRs). Reversal of blockage - neostigmine, edrophonium, and other cholinesterase inhibitors

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

Depolarizing effects - organophosphate - inhibit AchE.Treatment?

A

Common cause of poisoning - treat with atropine, pralidoxime

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

Dantrolene

A

Used in the treatment of malignant hyperthermia, which is caused by inhalation anesthetics (except nitric oxide) and succinylcholine.Also used to treat neuroleptic malignant syndrome (a toxicity of antipsychotic drugs).Mechanism: prevents the release of Ca2+ from the sarcoplasmic reticulum of skeletal muscle

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

Dopamine receptor agonists for Parkinson’s

A

Bromocriptine, pramipexole, ropinirole (non-ergot); non-ergots are preferred

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

Drugs for increasing dopamine in Parkinson’s

A

Amantadine (may incrase dopamine relase); also used as an antiviral against influenza A and rubella.Toxicity = ataxiaLevo-dopa with carbidopa (converted to dopamine in CNS. Carbidopa inhibits peripheral conversion to dopamine)

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

Drugs for parkinson’s: preventing dopamine breakdown

A

Selegiline (selective MAO type B inhibitor); entacapone, tolcapone *COMT inhibitors - prevents L-dopa degradation, thereby increasing dopamine availability)

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

Parkinson’s drugs: curb excess cholinergic activity

A

Benztropine (antimuscarinic; improves tremor and rigidity but has little effect on bradykinesia)

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

How to treat essential or familial tremors?

A

Beta-blocker (e.g. propranolol)

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

L-dopa can cross the blood-brain barrier and is changed into dopamine by?

A

dopa decarboxylasecarbidopa keeps this from happening peripherally

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

Toxicity of Levodopa

A

Arrhythmias from peripheral conversion to dopamine.Long-term use can lead to dyskinesia following administration, akinesia between doses.Carbidopa, a peripheral decarboxylase inhibitor, is giving with L-dopa to increase bioavailbility of L-dopa in the brain and decrease peripheral effects

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

Selegiline - Mechanism, Clinical use, toxicity

A

Mechanism: Selectively inhibits MAO-B, which preferentially metabolizes dopamine over NE and 5-HT, thereby increasing the availability of dopamine.Clinical use: Adjunctive agent to L-dopa in treatment of Parkinson’s diseaseToxicity: May enhance effects of L-dopa

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

Alzheimer’s drugs

A

MemantineMechanism - NMDA receptor antagonist; helps prevent excitotoxicity (mediated by Ca2+)Toxicity - Dizziness, confusion, hallucinationsDonepezil, galantamine, rivastigmineMechanism: Acetylcholinesterase inhibitorsToxicity: Nausea, dizziness, insomnia

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

Huntington’s drugs

A

Disease: Increase dopamine, decreased GABA + AChReserpine + tetrabenazine = amine depletingHaloperidol = dopamine receptor antagonist

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

Sumatriptan

A

Mechanism: 5-HT agonist.Causes vasoconstriction, inhibition of trigeminal activation and vasoactive peptide release.Half-life < 2 hours. Clinical use: Acute migraine, cluster headache attacksToxicity: Coronary vasospasm (contraindicated in patients with CAD or Prinzmetal’s angina), mild tingling

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

Treatment for ADHD

A

methylphenidate (Ritalin), amphetamines (Dexedrine), atomoxetine (nonstimulate SNRI)

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

Treatment for Tourette’s syndrome

A

antipsychotics (e.g., haloperidol)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Treatment for bipolar disorder

A

Lithium, valproic acid, carbamazepine, atypical antipsychotics (use of antidepressants lead to increased mania)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Depressants - Intoxication and withdrawal

A

Intoxication - nonspecific: mood elevation, decreased anxiety, sedation, behavioral disinhibition, respiratory depressionWithdrawal - nonspecific: anxiety, tremor, seizures, insomnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Alcohol (depressant)

A

Intoxication: Emotional lability, slurred speech, ataxia, coma, blackouts. Serum gamma-glutamyltransferase (GGT) - sensitive indiator of alcohol use.Lab AST is twice ALT value.Treatment: NaltrexoneWithdrawal: Symptoms similar to other depressants.Severe alcohol withdrawal: Delerium tremens- delirium, tremors, autonomic instability.Treatment: Benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Opioids (e.g. morphine, heroin, methadone) (depressant)

A

Intoxication: CNS depression, nausea, vomiting, constipation, pupillary constriction (pinpoint pupils), seizures (overdose is life-threatening).Treatment: Naloxone, naltrexoneWithdrawal: Sweating, dilated pupils, piloerection (cold turkey), fever, rhinorrhea, nausea, stomach cramps, diarrhea (fluelike symptoms). Treat symptomatically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Barbiturates (depressant)

A

Intoxication: Low safety margin, marked respiratory depression. Treatment: symptom management (assist respiration, increase BP)Withdrawal: Delirium, life-threatening cardiovascular collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Benzodiazepines (depressant)

A

Intoxication:Greater safety margine. Ataxia, minor respiratory depression.Treatment: Flumazenil (competitive GABA antagonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Stimulants: Intoxication and withdrawal

A

Intoxication: Nonspecific: mood elevation, psychomotor agitation, insomnia, cardiac arrythmias, tachycardia, anxietyWithdrawal: Nonspecific: post-use “crash”, including depression, lethargy, weight gain, headache

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Amphetamines (stimulants)

A

Intoxication: Impaired judgment, pupillary dilation, prolonged wakefulness and attention, delusions, hallucinations, fever Withdrawal: Stomach cramps, hunger, hypersomnolence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Cocaine (stimulant)

A

Intoxication: Impaired judgment, pupillary dilationf, hallucinations (including tactile), paranoid ideations, angina, sudden cardiac death.Treatment: benzodiazepines.Withdrawal: Suicidality, hypersomnolence, malaise, severe psychological craving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Caffeine (stimulants)

A

Intoxication: Restlessness, increased diuresis, muscle twitching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Nicotine (stimulant)

A

Intoxication: RestlessnessWithdrawal: irritability, anxiety, craving.Treatment: nicotine patch, gum, lozenges.Bupropion/varenicline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

PCP (Hallucinogen)

A

Intoxication: Belligerence, impulsiveness, fever, psychomotor agitation, vertical and horizontal nystagmus, tachycardia, homicidality, psychosis, deliriumWithdrawal: Depression, anxiety, irritability, restlessness, anergia, disturbances of thought and sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

LSD (hallucinogens)

A

Intoxication: Marked anxiety or depression, delusions, visual hallucinations, flashbacks, pupillary dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Marijuana (hallucinogen)

A

Intoxication: Euphoria, anxiety, paranoid delusions, perception of slowed time, impaired judgment, social withdrawal, increased appetite, dry mouth, hallucinationsWithdrawal: Irritability, depression, insomnia, nausea, anorexia.Most symptoms peak in 48 hours and last for 5-7 days.Can detected in urine for up to 1 month after use.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Heroin addiction

A

Users at increased risk for hepatitis, abscesses, overdose, hemorrhoids, AIDS, and right-sided endocarditis.Look for track marks (needlesticks in veins). Methadone - long-acting oral opiate; used for heroin detoxification or long-term maintenance (prevent withdrawal symptoms)Suboxone - naloxone + buprenorphine (partial agonist); long acting with fewer withdrawal symptoms than methaodone. naloxone is inactive when administered orally, but will induce withdrawal when injected.Pentazocine - partial agonist; can parcipitate withdrawal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is given to condition patients not to abuse alcohol

A

disulfiram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Treatment for alcohol withdrawal

A

Benzodiazepines

83
Q

Treatment for Anorexia/Bulimia

A

SSRIs

84
Q

Treatment for Anxiety Disorder

A

Benzodiazepines, buspirone, SSRIs

85
Q

Treatments for ADHD

A

Methylphenidate (Ritalin)Amphetamines (Dexedrine)

86
Q

Treatment for atypical depression

A

MAO inhibitors SSRIs

87
Q

Treatments for Bipolar disorder

A

Mood stabilizers: Lithium, Valproic acid, Carbamazepine

88
Q

Two drugs that work in absence seizures

A

Ethosuximide (1st line), valproic acid

89
Q

Treatment for depression

A

SSRIs, SNRIs, TCAs

90
Q

Treatment for depression with insomnia

A

Mirtazapine

91
Q

Treatment for OCD

A

SSRIs, Clomipramine

92
Q

Treatment for Panic disorder

A

SSRIs, TCAs, Benzodiazepines

93
Q

Treatment for PTSD

A

SSRI

94
Q

Schizophrenia treatment

A

Antipsychotics

95
Q

Treatment for Tourette’s

A

Antipsychotics (haloperidol)

96
Q

Treatment for social phobias

A

SSRIs

97
Q

CNS stimulants

A

Methylphenidate, dextroamphetamine, mixed amphetamine salts.Mechanism: Increased catecholamines at the synaptic cleft, especially NE and dopamineClinical use: ADHD, narcolepsy, appetite control

98
Q

Antipsychotics (neuroleptics)

A

Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine (haloperidol + -azine’s)

99
Q

Mechanism of antipsychotics (Haloperidol, trifluoperazine, fluphenazine, thioridazine, chlorpromazine)

A

All typical antipsychotics block dopamine D2 receptors (increase cAMP1)

100
Q

High potency antipsychotics

A

Neurologic side effects (extrapyramidal effects are greater)Haloperidol, trifluoperazine, fluphenazineEPS symptoms:4h acute dystonia (muscle spasm, stiffness, oculogyric crisis)4 d akinesia (parkinsonian symptoms)4 wk akathisia (restlessness)4 mo tardive dyskinesia

101
Q

Low potency antipsychotics

A

Thioridazine, chlorpromazineNon-neurologic side efects (anticholinergic, antihistamine, alpha blockade effects)Thioridazine - reTinal depositsChlorpromazine - Corneal depositsblock Muscarinic - dry mouth, constipationblock alpha - hypotensionblock histamine - sedation

102
Q

Which low potency antipsychotic can lead to corneal deposits?

A

Chlorpromazine

103
Q

Which low-potency antipsychotic can lead to retinal deposits?

A

Thioridazine

104
Q

Toxicity of antipsychotics

A

Other than EPS of high potency and anti muscarinic, anti alpha, anti-histamine of low potency-Highly lipid soluble and stored in body fat - slowly removed from body-Endocrine effects - dopamine receptor antagonism - hyperprolactinemia leading to galactorrhea-Neuroleptic malignant syndrome (NMS) - rigidity, myoglobinuria, autonomic instability, hyperpyrexia. Treatment: dantrolene, agonists (bromocriptine)-Tardive dyskinesia

105
Q

Neuroleptic malignant syndrome, an adverse effect of antipsychotics, can be treated how (has ridigity, myoglobinuria, autonomic instability, hyperpyrexia)

A

Dantrolene, agonists (bromocriptine)

106
Q

Atypical antipsychotics

A

Olanzapine, colzapine, quetiapine, risperidone, aripiprazole, ziprasidone

107
Q

Clinical use of antipsychotics

A

Schizophrenia (primarily positive symptoms, psychosis, acute mania, Tourette’s syndrome)

108
Q

Atypical antipsychotics (olanzapine, clozapine, quetiapine, risperidone) mechanism

A

Block 5-HT2, dopamine, alpha, and H1 receptors

109
Q

Clinical use for atypical antipsychotics: olanzapine, clozapine, quetiapine, risperidone, aripiprazole, ziprasidoneMechanism: Block 5-HT2, dopamine, alpha, and H1

A

Schizophrenia - both positive and negative symptoms. Olanzapine is also used for OCD, anxiety disorder, depression, mania, Tourette’s syndrome

110
Q

Toxicities of atypical antipsychotics

A

Fewer extrapyramidal and anticholinergic side effects than traditional antipsychotics.Olanzapine/zclozapine may cause significant weight gain.Clozapine may cause agranulocytosis (requires weekly WBC monitoring)

111
Q

Which of the atypical antipsychotics cause weight gain?

A

Olanzapine/clozapine

112
Q

Which atypical antipsychotic may cause agranulocytosis (WBC monitoring)

A

clozapineWatch clozapine clozely

113
Q

Lithium

A

Mechanism: Not established, possibly inhibition of phosphoinositol cascadeClinical use: Mood stabilizer for bipolar disorder; blocks relapse and acute manic events.Also SIADHToxicity: Tremor, sedation, edema, heartblock, hypothyroidism, polyuria (ADH antagonist causing nephorgenic diabetes insipidus), teratogenesis.Fetal cardiac defects include Ebstein anomaly and malformation of great vessel.Narrow therapeutic window requires close monitoring of serum levels.Almost exclusively excreted by the kidneys; most is reabsorbed at the proximal convoluted tubules following Na+ reabsorption

114
Q

Lithium side effects

A

MNOPMovement (tremor)Nephrogenic diabetes insipidusHypOthyroidismPregnancy problems

115
Q

Buspirone

A

Mechanism: Stimulates 5-HT1A receptorsClinical Use: Generalized anxiety disorder. Does not cause sedation, addiction, or tolerance. Does not interact with alcohol (vs. barbituarates, benzodiazepines)I’m always anxious if the BUS will be ON time, so I take BUSpirONe.

116
Q

Tricyclic antidepressants

A

Imipramine, amitriptyline, desipramine, nortriptyline, clomipramine, doxepin, amoxapine Mechanism: Block reuptake of NE and serotonin

117
Q

Mechanism and clinical use, toxcity of TCAs (Imipramine, amitriptyline, desipramine, nortriptyline, comipramine, doxepin, amoxapine)

A

Mechanism: Block reuptake of NE and serotoninClinical use: Major depression, bedwetting (imipramine), OCD (clomipramine), fibromyalgiaSide effects: Sedation, alpha-blocking effects, atropine-like (anticholinergic) side effects (Tachycardia, urinary retention).Tertiary TCAs (Amitriptyline) have more anticholinergic effects than do secondary TCAs (nortriptyline). Desipramine is least sedating and has lower seizure threshold.Toxicity: Tri-C’s: Convulsions, Coma, Cardiotoxicity (arrythmias); also respiratory depression, hyperpyrexia, confusion, hasslucinations in elderly due to anticholinergic effects (use nortriptyline).Treatment: NaHCO3 for CV toxicity.

118
Q

Which TCA (blocks reuptake of NE and serotonin) can be used to treat bedwetting?

A

imipramine

119
Q

Which TCA (blocks reuptake of NE and serotonin) can be used to treat OCD?

A

clomipramine

120
Q

What TCA should be used in the elderly (because they encounter confusion and lassucination due to anticholinergic)

A

nortriptyline - less cholinergic effects

121
Q

SSRIs

A

Fluoxetine, paroxetine, sertraline, citalopramTakes 2-4 weeks to work. Mechanism: Serotonin-specific reuptake inhibitors Clinical use: Depression, OCD, bulimia, social phobiasToxicities: Fewer than TCAs. GI distress, sexual dysfunction (anogasmia). “Serotonin syndrome” with any drug that increases serotonin (e.g. MAO inhibitors) - hyperthermia, muscle rigidity, cardiovascular collapse, flushing, diarrhea, seizures.Treat with cyproheptadine

122
Q

Serontonin syndrome and treatment

A

Caused by SSRIs, MAO inhibitors : any drug that increases serotoninHyperthermia, muscle rigidity, cardiovascular collapse, flushing, diarrhea, seizuresTreat: Cyproheptadine (5-HT2 receptor antagonist)

123
Q

SNRIs

A

Venlafaxine, duloxetineMechanism: Inhibit serotonin and NE reuptakeClinical use: Depression. Venlafaxine is also used in GAD; duloxetine is also indicated for diabetic peripheral neuropathy. Duloxetine has greater effet on NE.Toxicity: Increased BP most common, stimulant effects, sedation, nausea

124
Q

SNRI’s (Venlafaxine, duloxetine) work how?

A

Inhibit serotonin and NE reuptake

125
Q

Which SNRI is used in GAD?

A

Venlafaxine

126
Q

Which SNRI is used in diabetic neuropathy?

A

Duloxetine (greater effect on NE)

127
Q

Monoamine oxidase inhibitors (MAO)

A

Phenelzine, tranylcypromine, isocarboxazid, selegiline (selective MAO-B inhibitor)Mechanism: Nonselctive MAO inhibition, increase levels of amine neurotransmitters (NE, serotonin, dopamine)

128
Q

MAO inhibitors - phenelzine, tranylcypromine, isocarboxazid, selegiline (MAO-B selective) used in? Toxicity?

A

Atypical depression, anxiety, hypochondriasisToxicity: Interact with indirect sympathomimetics, e.g. hypertensive crisis with tyramine ingestion (in many foods such as wine and cheese) and Beta-agonists; CNS stimulation. Contraindicated with SSRIs or meperidine to prevent serotonin syndrome

129
Q

Atypical antidepressants - Bupropion

A

Also used for smoking cessation.Increased NE and dopamine via unknown mechanisms. Toxicity: stimulant effects (tachycardia, insomnia), headache, seizure in bulimic patients. No sexual side effects

130
Q

Atypical antidepressants - Mirtazapine

A

Alpha-2 antagonist (Increase release of NE and serotonin) and potent 5-HT2 and 5-HT3 receptor antagonist.Toxicity: Sedation, increased appetite, weight gain, dry mouth

131
Q

Atypical antidepressant - Maprotiline

A

Blocks NE reuptake. Toxicity: sedation, orthostatic hypotension

132
Q

Atypical antidepressant - Trazodone

A

Primarily inhibits serotonin reuptake. Used for insomnia, as high doses are needed for antidepressant effects.Toxicity: sedation, nausea, priapism (continuous erection), postural hypotension.

133
Q

What is scopolamine used for?

A

Muscarinic cholinergic antagonist.Used in motion sickness.

134
Q

What is phenoxybenzamine used for?

A

Non-selective alpha-adrenergic antagonist used to treat pheochromacytoma

135
Q

Carbachol and pilocarpine

A

cholinergic agonists used to lower intraocular pressure in glaucoma.Cholinergic-associated miosis causes the iris to move further from the cornea, widening the anterior chamber angle and allowing better outflow of the aqueous humor.

136
Q

Drugs whose co-administration increase risk of lithium toxicity.

A

Thiazide diuretics, ACE inhibitors, NSAIDs

137
Q

Treatment of acute lead and mercury poisoning.

A

CaNa2EDTA - chelating agent; forms complexes with mono, di- and trivalent ions

138
Q

Carbamazepine - what is it used for, how does it work?

A

Blocks voltage-taged Na channels in cortical neurons-Used for the management of generalized tonic-clonic seizures, as a mood stabilizer in bipolar disorder, and to treat trigemanl neuralgia Side effects: Bone marrow suppression, hepatoxicity, and increase in ADH

139
Q

Hemicholinium

A

Blocks the entry of choline into the neuron to make it into acetylcholine.

140
Q

Vesamicol

A

Blocks uptake of AcH into vesicles (anticholinergic).

141
Q

Botulinum

A

Blocks release of Ach on presynaptic terminal

142
Q

Metyrosine

A

Blocks conversion of tyrosine to dopa (blocks synthesis of dopamine and NE)

143
Q

Guathedine

A

Blocks relesae of Ne at presynaptic nerve terminal

144
Q

Cocaine, Amphetamines, TCAs

A

Block NE reuptake

145
Q

Bethanechol

A

Ach action. Postoperative and neurogenic ileus and urinary retention. Activates bowel adn bladder smooth muscle.Resistant to AChE.

146
Q

Carbachol

A

Ach action. Glaucoma, pupillary contraction, and relief of intraocular pressureCarbon copy of Ach

147
Q

Pilocarpine

A

Ach agent.Potent stimulator of sweat, tears, salivaContracts ciliary muscle of eye (open angle), pupillary sphincter (narrow angle); resistant to AchE. PILE on the sweat and tears.

148
Q

Methacholine

A

Muscarinic ACh agonistChallenge test for diagnoises of asthma - Muscarnic receptors in airway when inhaled.

149
Q

Neostigmine

A

Anti-AchEPostoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockage (postoperative).Increases endogenous ACh, no CNS penetration

150
Q

Pyridostimine

A

Myasthenia gravis (long acting); does not penetrate CNS). Endogenous Ach, increases strength.

151
Q

Edrophonium

A

Diagnosis of myasthenia gravis (extremely short acting)Also helps to distinguish overdose vs underdose of acetylcholinesterase inhibitors.

152
Q

Physostigmine

A

AchE inhibitorGluacoma (crosses blood-brain barrier–> CNS) and atropine overdose Increases AchPHYS is for the eyes

153
Q

Echothiophate

A

AchE inhibitor for glaucoma(HST150: noncompetitive)Increases endogenous Ach

154
Q

Cholinesterase inhibitor poisoning

A

Often due to organophosphates, such as parathion & malathion (insectisides) and soman (nerve agent used in chemical warfare, more potent), that irreversibly bind AchE. Causes DUMBBELSS.Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle adn CNS, Lacrimation, Sweating, and Salivation. Antidote: Atropine + Prolidoxime (regenerates active AchE)

155
Q

Benzotropine

A

Muscarinic antagonist used in Parkinson’s disease

156
Q

Scopolamine

A

Muscarinic antagonist used for CNS - motion sickness

157
Q

Oxybutynin, glycopyrrolate

A

Muscarinic antagonist used for the genitourinary system.Reduce urgency in mild cystitis and reduce bladder spasms.

158
Q

Methscopolamine, pirenzepine, propantheline

A

Muscarinic antagonist used in the GI system.Peptic ulcer treatment.

159
Q

Atropine

A

Muscarinic antagonistHot as a hare, Dry as a bone, red as a beet, blind as a bat, mad as a hatter.increases pupil dilation, cycloplegia, decreases airway secretion, decreases acid secretion and intestine mobility, decreases urgency in cystitis.Toxicity: Increased body temperature due to decrease in sweating, rapid pusle, dry mouth, dry, flushed skin, cycloplegia, constipation, disorientation.Acute angle-closure in glaucome, urinary retention in prostatic hyperplasia, and hyperthermia in infants.

160
Q

Hexamethonium

A

Nicotinic antagonistPut a Hex on smokers to help them quit. Clinical use: Ganglionic blocker (preganglionic sympathetic & parasympathetic neurons release ACh to bind to postganglionic nAChRs). Used in experimental models to prevent vagal reflex responses to changes in blood pressure: prevents reflex bradycardia caused by NE.Toxicity: Severe orthostatic hypotension, blurred vision, constipation, sexual dysfunction

161
Q

Epinephrine

A

Alpha1, Alpha2, Beta1, Beta2 (low dose selects for Beta1). Alpha2 receptors are presynaptic (feedback inhibition).Applications: Anaphylaxis, glaucoma (open angle), asthma, hypotension

162
Q

NE

A

alpha1, alpha2> Beta1. Used in hypotension, but decreases renal perfusion.

163
Q

Isoproterenol

A

Beta-adrenergic agonist. Beta1 = Beta2.Used in AV block (rare).

164
Q

Dopamine

A

D1 = D2 > Beta adrenergic > alpha adrenergic (BP goes up, then down with higher doses), positive ionotropic and chronotropic. Used in shock (to increase renal perfusion), heart failureHypotension is a side effect of L-dopa.

165
Q

Phenylephrine action

A

Alpha-1 adrenergic agonist.Alpha1 > Alpha2Pupillary dilation, vasoconstriction, nasal congestion

166
Q

Metaproterenol, albuterol, salmeterol, terbutaline

A

Selective Beta2 agonists Beta2 > Beta1.

167
Q

Amphetamine

A

Indirect sympathomimetic, releases stored catecholamines Narcolepsy, obesity, ADD

168
Q

Ephedrine

A

Indirect sympathomimetic, releases stored catecholamines. Nasal decongestion, urinary incontinence, hypotension

169
Q

Cocaine

A

Indirect general agonist, reuptake inhibitor. Causes vasoconstriction and local anesthesia

170
Q

Clonidine, alpha methyldopa

A

Centrally acting alpha2-agonists, decrease central adrenergic outflow.alpha2 receptors are presynaptic (negative feedback)used in hypertension, espeically with renal disease (no decrease in blood flow to the kidney)

171
Q

Phenoxybenzamine (irreversible)Phentolamine (reversible)

A

Alpha-blockers. Used for pheochromacytoma (use phenoxybenzamine before surgery).Toxicity: Orthostatic hypotension, reflex tachycardia

172
Q

-zosin endingPrazosin, terazosin, doxazosin

A

Alpha1 blocker. Used in hypertension, urinary retention of BPH (relax smooth muscle around bladder neck).Toxicity: 1st dose orthostatic hypotension, dizziness, headaches

173
Q

Mirtazapine

A

Alpha2 selective blockerused in depression.Toxicity: Sedation, increase in serum cholesterol, increase in appetite

174
Q

Opioids toxicity treatment

A

Naloxone/naltrexone

175
Q

Benzodiazepines toxicity treatment

A

Flumazenil

176
Q

TCAs toxicity treatment

A

NaHCO3(Plasma alkalinization)

177
Q

Drugs that cause cinchonism (headache, tinitus)

A

quinidine, quinine

178
Q

Drugs that cause diabetes inspidus

A

Lithium, demeclocycline

179
Q

Drugs that cause parkinson-like syndrome

A

Haloperidol, chlorpromazine, reserpine, metoclopramide

180
Q

Drugs that cause seizures

A

Bupropion, imipenem/cilastatin, isoniazid

181
Q

Drugs that cause tardive dyskinesia

A

antipsychotics

182
Q

Guanethidine

A

Guanethidine, prevents the release of NE – another kind of chemical sympathectomy. Its side effects, especially postural hypotension and diarrhea, can be severe.

183
Q

Acetylcholine receptors

A

nicotinic acetylcholine (ACh) receptors in muscle, neurons, and glia are strongly activated (agonized) by acetylcholine and nicotine (an alkaloid from tobacco), and less so by muscarine (an alkaloid from Amanita muscaria mushrooms), whereas muscarinic ACh receptors in smooth and cardiac muscle are strongly activated by acetylcholine and muscarine, but weakly by nicotine. nAChRs are released by motor neurons and by preganglionic sympathetic and parasympathetic nerve terminals.

184
Q

alpha-Bungarotoxin

A

One class of very slowly reversible (days to unbind) antagonists of nAChR are small proteins (6-8000 mol wt) in venoms of certain snakes (Formosan Krait, cobra). These molecules called bungarotoxins bind to the a subunits of the receptor from the extracellular surface and were essentially for the original isolation and purification of the receptor

185
Q

Latrotoxin (Black Widow venom)

A

Causes release of acetylcholine from presynaptic terminal, leading to cholergic stimulation followed by block. Symptoms include hypertension, generalized muscle pain, abdominal cramps, extreme sweating and tachycardia. Also works on many other kinds of presynaptic terminals.

186
Q

Carbon Monoxide Toxicity (Mechanism, Symptoms,Treatment)

A

Mechanism: CO displaces O2 from hemoglobin and binds to cytochrome oxidase (electron transport inhibitor).Symptoms: Headache, seizures, ventilatory depression, deathTreatment: 100% (possibly hyperbaric) oxygen, and possibly barbituate-induced coma to decrease Oxygen utilization.

187
Q

Methanol Toxicity (Mechanism, Symptoms, Treatment)

A

Mechanism: methanol is converted to formic acid by alcohol dehydrogenase, which is toxic to the retina. Symptoms: blindnessTreatment: fomepizole, which inhibits alcohol dehydrogenase

188
Q

Cyanide Toxicity (Mechanism, Symptoms, Source, Treatment)

A

Mechanism: binds tightly to Fe3+ in hemoglobin and also inhibits cytochrome oxidase (preventing electron transport). Symptoms: lactic acidosisSource: pesticide (for infestation), gold mining –> artificial lakes, fruit pitsTreatment: nitrites (intentional methemoglobinemia b/c cyanide binds better to methemoglobin than hemoglobin), sodium thiosulfate, 100% oxygen

189
Q

Lead Toxicity (Mechanism, Symptoms, Source, Treatment)

A

Mechanism: after GI absorption, circulates bound to hemoglobin and redistributes to bone (remains there chronically until treated)Symptoms: anorexia, constipation, metallic taste, proteinuria, hematuria, anemia, peripheral neuropathySource: old paint, batteries, acidic fruitsTreatment: CaEDTA, dimercaprol, succimer, penicillamine

190
Q

Codeine

A

Codeine is O-demethylated by CYP2D6 to morphine in the liver. There are mutations that make patients poor metabolizers, or conversely, extensive metabolizers.Morphine is also metabolized to a more active metabolite.

191
Q

Latanoprost

A

Topical medication used to control glaucoma or ocular hypertension by reducing intraocular pressure. It’s a prostaglandin analog that works by increasing the outflow of acqueous fluid from the eyes.

192
Q

Leflunomide

A

Inhibits the mitochondrial enzyme dihydroorotate dehydrogenase, which plays a role in de novo pyrimidine synthesis. Lymphocyte expansion is inhibited. Used treat rheumatoid arthritis and psoriatic arthritis.

193
Q

Potassium Iodide

A

-For hyperthyroidism; high amounts suppress secretion of thyroxine from the thyroid gland-Topical treatment for sporotrichosis

194
Q

Remifentanil

A

An opioid analgesic which undergoes rapid esterase breakdown in the blood, allowing quick dissipation even after very long infusions.

195
Q

slow acetylator mutation (pertinent drugs)

A

Inability to detoxify sulfapyridine from sulfasalazine. Inability to metabolize procainamide to active N-acetylprocainamide. Decreased clearance of isoniazid and hydralazine.

196
Q

Palivizumab

A

Monoclonal antibody used against paramyxoviruses (parainfluenza, RSV, measles, mumps). Binds to surface F (fusion) protein.

197
Q

Nimodipine

A

Calcium channel blocker used to treat vasospasm, a complication of blood breakdown products after subarachnoid hemorrhage.

198
Q

Beta blockers (glaucoma)

A

Work by decreasing aqueous humor production by ciliary epithelium.

199
Q

Primidone

A

Antiepileptic that is metabolized to phenobarbitol and phenylethylmalonamide (PEMA)

200
Q

Which TCA has strong anti-cholinergic properties?

A

Amitriptyline

201
Q

How do you distinguish between amides and esters for local anesthetics?

A

Amides have two i

Esters have one i

Boards studying (5 decks)

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