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NBS > Drugs > Flashcards

Drugs Flashcards

1
Q

MOA
acetominopehn

A

inhbits COX in CNS

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2
Q

MOA
NSAIDS

A

inhibits COX in PNS and CNS

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3
Q

MOA

Opioids

A
  • MOA: GPCR –> reduces cAMP –> activates potassium conductance and inhibits calcium conductance –> hyperpolarization –> decreased NT release –> analgesia
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4
Q

Amides and Esters

MOA

A

binds voltage gated Na channels –> no depolarization –> no AP –> decreased NT release –> no pain signal

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5
Q

Amides

metabolized how? allergic?

A

liver, no

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6
Q

Esters

metabolized how? allergic?

A

PABA, yes

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7
Q

Amide examples

A

Lidocaine, Bupivacaine (toxic), Ropivacaine

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8
Q

Ester examples

A
  • Tetracaine, Chloroprocaine, Procaine, Benzocaine, cocaine
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9
Q

amide and ester SE

A

cns excitation, HTN, hypotension

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10
Q

bupivacaine

A

cardiotoxicity

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11
Q

cocaine SE

A

arrhythmias, causes vasoconstriction too

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12
Q

benzocaine

A

methemoglobinemia

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13
Q

glaucoma tx

A

alpaha agonists, beta blockers, CA inhibotrs, miotics, PG analogs

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14
Q

Shy-drager syndrome tx

A

fludrocortisone

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15
Q

POTS tx

A

fludicortisone

beta blockers, miodrine, methylphenidate/adderall

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16
Q

ischemis stroke tx

A

tPA 3-4.5 hrs

or

IA devices to manually remove clot

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17
Q

ischemic stroke prevention

A

AMCDEFs

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18
Q

Essential tremor

tx

A

propranolol (non selective beta agonsit)

or

primidone (anti-convuslant - decreases GABA)

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19
Q

ICP

tx

A

mannitol, hyperventilation, head elevation

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20
Q

Migraines

tx

acute and prophylaxis

(alot)

A
  • Acute: NSAIDs, triptans, dihydroergotamine, steroids, valproate (MOA : GABA agonist), monoclonal antibodies (anti-CGRP)
    • Prophylaxis: lifestyle changes (sleep, exercise, diet), beta blockers, calcium channel blockers, amitriptyline (MOA: inhibits reuptake of NorEpi/5-HT), topiramate (MOA: Ca+ blocker), valproate, gabapentin (MOA: Ca blocker and GABA agonist)
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21
Q

Triptan MOA:

A
    • Triptan MOA: 5HT1D (trigeminal nerve ending) and 5HT1B (cranial blood vessel) agonists
      *
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22
Q

cluster HA

tx (acute and prophylaxis)

A
  • Acute: sumatriptan, O2
  • Prophylaxis: verapamil
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23
Q

trigeminal nerualgia

tx

A
  • Treatment: carbamazepine (first-line), Baclofen, gabapentin
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24
Q

tension HA

tx (acute chronic)

A
  • Acute: analgesics (NSAIDs, acetaminophen)
  • Chronic: amitriptyline
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25
Q

levertiracetam

use, mOA, SE

A

USE: partial, toninc clonic

MOA: unknown

SE: fatigue, HA, psych issues

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26
Q

lamotrigine

use, mOA, SE

A

USE: all seizure types

MOA: blocks Na, decreases glutamate

SE: SJS

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27
Q

topiramate

use, mOA, SE

A

USE: partial,tonic clonic, migraine prophylaisis

MOA: increases GABA

SE: sedation, kidney stones

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28
Q

gabapentin

use, mOA, SE

A

USE:partial, pheripheral neuropathy

MOA: blocks Ca, GABA analog

SE: sedation, ataxia

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29
Q

valproic acid

use, mOA, SE

A

USE: tonic clonic

MOA: blocks Na, increasea GABA

SE: GI distress, hepatotoxicity, pancreatitis, trmor, weight gain

tertogenissi: neural tube defects

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30
Q

carbamenzapine

use, mOA, SE

A

USE: partial

MOA: blocks Na, decreases glutamate

SE: SJS, SIADH, diplopia, ataxia, agranucytosis

tertogenissi: cleft palate

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31
Q

phenytonin

use, mOA, SE

A

USE: gran-mal, status epilepticus

MOA: blocks Na

SE: SJS, SLE, diplopia, ataxia, mregloblastic anemia

tertogenissi: fetal hydantoin syndrome

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32
Q

phenbarbital

use, mOA, SE

A

USE: partial, gran-mal

MOA: increase GABA

SE: sedation, tolerance/dependence, resp. depression

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33
Q

BZDs

use, mOA, SE

A

USE: status elipticas

MOA: increase GABA

SE: sedation, tolerance/dependence, resp. depression

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34
Q

ethosuxide

use, mOA, SE

A

USE: absences seizures

MOA: blocks thalamic Ca channels

SE: SJS, fatgiue, GI distress, HA, itiching

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35
Q

Meningitis

tx by age

A
  • Newborn: Ampicillin + gentamicin/cefotaxime
  • 2 – 50 y/o: Vancomycin + ceftriaxone/cefotaxime
  • >50 y/o: Ampicillin + vancomycin + ceftriaxone/cefotaxime
  • Dexamethasone is indicated in bacterial meningitis
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36
Q

brain abcess tx

A

Abx (vancomycin/naficillin + ceftriaxone/cefotaxime + metronidazole) + drainage

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37
Q

HIV

A

antiretroviral therapy (ART)

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38
Q

neurosphyilis tx

A

penicillin

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39
Q

cryptococcal memoinigitis tx

A

Amphotericin B + fluconazole

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40
Q

CMV

A
  • Treatment: ganciclovir, valganciclovir, foscarnet
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41
Q

PML tx

A

antiretroviral treatment for HIV

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42
Q

HSV tx

A

acyclovir

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43
Q

MS acute sx tx

A

steriods

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44
Q

MS

first line tx

provde MOA (5)

A
  • Glatiramer acetate: decreases Th1 cells via Th reg cells
    • category B
  • IFN-beta: prevents T-cell migration
    • SE: flu
  • Fingolimod: prevents T-cell migration to CNS by holding lymphocytes in lymph nodes
  • Teriflunomide: decreased T-cell synthesis
  • Dimethyl fumarate: decreases inflammatory response via activation of Nrf2 pathway
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45
Q

MS

2nd line tx

provde MOA (2)

A
  • Natalizumab: binds integrin preventing T-cell migration
    • Risk of PML
  • Mitoxantrone: causes breakage in DNA à immunosuppression
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46
Q

cervical dystonia tx

A

botulin

SE: dysphagia

47
Q

MG tx

A
  • Treatment: pyridostigmine (AchE inhibitor), prednisone, IVIG, plasmapharesis
48
Q

plymyositis or dermatomyostisis

tx

A

steriods

49
Q

DMD

A

expondys 51

50
Q

carpal tunnel tx

A
  • Treatment: splints at nighttime (avoid flexion of wrist), steroid injection (outside of tunnel), surgery to open tunnel
51
Q

GBS

A
  • Treatment: supportive, mechanical ventilation if needed, plasmapheresis/IVIG (attacks ABs), NO steroids
52
Q

Amyotrophic Lateral Sclerosis (ALS)

A
  • Treatment: Riluzone, Edavarone
53
Q

parkinsons tx

MOA and SE

explin why carbidopa is used and why it works

A
  • Dopamine precursor (Levodopa)
    • MOA: Dopamine precursor given orally à absorbed in duodenum
      • Bypasses rate-limiting step of dopamine synthesis
    • Side effects: dyskinesia (abnormal involuntary movements) after long-term use, nausea, GI upset, lowers BP
      • Carbidopa (prevents peripheral breakdown of Levodopa into dopamine) is now given in combination to minimize these side effects
54
Q

Huntingtons tx

A

MOAI

55
Q

SSRI

MOA SE

A
  • MOA: inhibits serotonin reuptake by serotonin transporters –> increased serotonin in terminal
  • SE (fewer than TCAs): GI distress (most common 1st), SIADH, sexual dysfunction, suicidal thoughts (not contraindication)
56
Q

P450 reactions with SSRIs

A
  • P450 reactions: fluoxetine, fluvoxamine paroxetine (less metabolism of drugs like Tamoxifen, TCAs, etc)
57
Q
  • Serotonin Syndrome
A
  • Etiology: Due to excess serotonin secondary to SSRIs, stoppage of MAOI, combos of sertotnergic drugs (i.e. Tramadol, linezolid)
  • Signs/sx: AMS, GI sx, diaphoresis, myoclonus/hyperreflexia
58
Q
  • Discontinuation Syndrome
A
  • Suspect after: use of short-life drug (i.e. Paroxetine)
  • Sx: dizziness, HA, N/V, anxiety, paresthesias
59
Q

SNRIs
MOA and SE

A
  • MOA: inhibits serotonin and norepinephrine reuptake by serotonin transporters à increased serotonin and norepinephrine in terminal
  • SE: HTN
60
Q

Venlafaxine, Duloxetine (used for pain), Desvenlafaxine

what are these

A

SNRIs

61
Q

TCAs

MOA and SE

A
  • MOA: inhibits 5-HT and NE reuptake in CNS
  • SE: anticholinergic effects, antihistaminergic effects (sedation), alpha blockage (hypotension)
62
Q

Secondary TCAs

name some

A

Nortriptyline, Desipramine, Maprotiline

63
Q

Tertiary TCAs

name some

A

Imipramine, Amitriptyline)

64
Q

TCA

toxicity

A
  • Toxicity: cardiac arrhythmias/convulsions/coma (3 Cs) secondary to Na blockade, wide QRS (administer bicarb)
65
Q

MAOIs

MOA and SE

A
  • MOA: Inhibits monoamine oxidase located on mitochondria –> increases [NT]
  • SE: CNS stimulation, hypertensive crisis w/ ingestions of tyramine (a.a. in wine, cheese, and preserved meats)
66
Q
  • Phenelzine, Tranylcypromine, Selegiline

what are these

A

MAOIs

67
Q

What drugs are indicated for the following

  • OCD
  • Long half life
  • QTC
  • Short half life
  • Less interactions
A
  • Indications
    • OCD: Fluvoxamine, Sertraline
    • Longest half-life: Fluoxetine (if non-compliant pt)
    • QTC prolongation: citalopram
    • Short half-life: Fluvoxamine, paroxetine
    • Less interactions: Citalopram
68
Q

What is the MOA, SE, and use (if applicable) for the following drugs:

  • Bupropion
  • Mirtazapine
  • Trazodone
  • Nefazodone
A
  • Atypical antidepressants
    • Bupropion
      • MOA: inhibits reuptake of NE and dopamine
      • SE: seizures (people w/ eating disorders), tachycardia, insomnia
      • Uses: smoking cessation, sexual dysfunction
    • Mirtazapine
      • MOA: alpha-2 antagonist → increase release of NE and 5HT
        • Blocks 5HT2/3 and H1 receptors
      • SE: sedation, increased appetite/weight gain, dry mouth
    • Trazodone
      • MOA: blocks 5HT2, alpha1, and H1 receptors and inhibits 5HT reuptake
      • SE: sedation, priapism (traZZZobone)
      • Uses: insomnia
    • Nefazodone
      • MOA: blocks 5HT2, alpha1, and H1 receptors and inhibits 5HT reuptake
      • SE: hepatotoxicity
69
Q

What is the MOA, SE, and use (if applicable) for the following drugs:

  • Varenicline
  • Vilazodone
  • Vortioxetine
A
  • Varenicline
    • MOA: nicotinic Ach agonist
    • SE: sleep disturbance, depress mood
    • Uses: smoking cessation
  • Vilazodone
    • MOA: inhibits 5HT reuptake + 5HT1A agonist
    • SE: HA, GI issues, weight gain, anticholinergic effects
  • Vortioxetine
    • MOA: inhibits 5HT reuptake + 5HT1A agonist
    • SE: nausea, sexual dysfunction, abnormal dreams, anticholinergic effects
70
Q
A
71
Q

For typical antipscyhotics (1st gen)

  • What do they typically end with?
  • Basic MOA (secondary actions too)
  • Storage
A

Typical Antipsychotics (-azine)

  • MOA: block D2 receptor and secondary M1/H1/alpha-1 blockade
  • Storage: body fats (lipid soluble) – slowed to be removed
72
Q

What typical antipsychotics have a high potency? Low potency?

A
  • Potency:
    • High (Effects: EPS): trifluoperazine, fluphenazine, haloperidol (Try 2 Fly High)
    • Low (Effect: anticholinergic/antihistamine/anti-alpha): chlorpromazine, thioridazine
73
Q

What are EPS sx of typical antipyschotics? Define based on onset and provide treatments for each!

A
  • D2 blockade: EPS, endocrine changes, sexual dysfunction
    • EPS
      • Hours to days: Dystonic reactions
        • Description: uncoordinated spastic movements of muscle groups (i.e. trunk, tongue, face)
        • Tx: benztropine
      • Days to months: Akathisia, Parkinsonism
        • Akathisia: extreme restlessness and pacing; may lead to insomnia
          • Tx: beta blockers
        • Parkinsonism: tremors of extremities
          • Tx: Oral antiparkinsonian drugs
      • Months to years: Tardive dyskinesia
        • Description: involuntary and potentially irreversible movements around oral area
        • Dx: Abnormal Involuntary Movement Scale (AIMS)
        • Tx: benztropine; change dosage of meds
74
Q

What is a syndrome that can occur with D2 blockade with typical antipscyhotics? Explain signs and sx (mnemonic). Provide treatment!

A
  • Neuroleptic malignant syndrome (life-threatening)
    • Signs/sx (Malignant FEVER): Myoglobinuria (breakdown of muscles from movement), Fever, Encephalopathy, Vitals unstable, Enzymes increased, Rigidity of muscles
    • Tx: discontinuation of antipsychotic, Dopamine agonists (bromocriptine/dantrolene)
75
Q

Provide other SE of tpyical anti-pscyhotics based on the receptors the meds block. Provide other SE

A
  • H1 blockade: sedation, drowsiness, weight gain, hypotension
  • Alpha-1 blockade: postural hypotension, reflex tachycardia, dizziness
  • M1 blockade: blurred vision, dry mouth, sinus tachycardia, constipation, urinary retention, memory dysfunction
  • Other: corneal deposits (chlorpromazine), retinal deposits (thioridazine), QT prolongation
76
Q

For atypical antipscyhotics/second-gen

  • What do the names end with?
  • MOA?
A

Atypical Antipsychotics/Second-Generation (-apine, -peridone, -idone)

  • MOA: post-synaptic blockade of D2 receptor and secondary 5HT-2A blockade
    • Equal efficacy as first-generation; less side effects
77
Q

What is a special type of atypical antispsyhcotic? What is its MOA?

A
  • **Aripiprazole: partial D2 agonist
    • Hyperdopaminergic areas (mesolimbic area) → antagonist →+ sx
    • Hypodopaminergic areas (mesocortical area) → agonist → - sx
78
Q

What are the side effects of atypical antipsychotics? General benefits? General SE?

A
  • Benefits: rare EPS, rare increase in prolactin, reduced negative sx
  • Side effects: prolonged QT
79
Q

For the following atypical antipsychotics provide SE:

  • -Apines
  • Clozapine
  • Risperidone
  • Olanzapine
  • Ziprasidone
  • Quetiapine
A
  • -Apines: Metabolic syndrome
  • Clozapine: agranulocytosis, seizures, reduced risk of suicide, must monitor CBC
  • Risperidone: increased prolactin (only second gen), less weight gain
  • Olanzapine: weight gain
  • Ziprasidone: prolongs QT interval, dizziness, somnolence
  • Quetiapine: lenticular opacities, HA, increased AST
80
Q

clozapine

tx for?

A

resistent pyshcosis.. when no other drug works

81
Q

OCD tx

A

SSRi, clomipramine

82
Q

PTSD tx

A

SSRIs, and venlafaxine are first line. Prazosin can reduce nightmares.

83
Q

bipolar meds

A

lithium, valporate, carbamazepine, oxcarbazepine, lamotrigine

84
Q

lithium

MOA SE

A
  • Proposed MOAs:
    • Interactions with cation transport process by substituting for Na+ à direct effect on NTs (i.e. serotonin, dopamine, NE, Ach) OR inhibits PIP3 pathway
  • Side Effect
    • Teratogenicity (cardio malformations: Ebstein’s anomaly), goiter, hypotonia, CNS depression
    • SE: tremor, hypothyroidism (weight gain, GI distress, fatigue), nephrogenic diabetes insipidus (ADH inhibited à polyuria), metallic taste
85
Q

anxiety tx

A

Antidepressants, BZDz, Z drugs, beta agonists, buspirone

86
Q

Benzodiazepines

MOA SE

A
  • MOA: enhance the effect of GABA by binding on GABA A receptor –> increased rush of chlorine into post-synaptic
  • SE: tolerance (increased dose to produce effect), sedation, ataxia, anterograde amnesia, confusion, muscle weakness, withdrawal (anxiety, insomnia, muscle twitches/tremors, etc)
87
Q

name some BZds

short v long half life

A
  • Short half-life: alprazolam (Xanax), Triazolam, Lorazepam (Ativan)
  • Long half-life: diazepam (Valium), Chlordiazepoxide (Librium)

orazepam has slowest absorption

88
Q

“Z” Compounds (Zolpidem, Zopiclone)

A
  • MOA: same as benzodiazepines
  • SE: less than benzos (no tolerance, no physical dependence, no sleep disturbance)
89
Q

buspirone

A
  • MOA: partial agonist for 5-HT1A receptors in brain
  • Disadvantages: Slow onset of action; short half-life (needed 2-3x per day)
  • Advantages: no physical dependence, no abuse potential, less sedation, less interaction with alcohol
90
Q

Delrium tx

A
  • First line: haloperidol (typical psychotic)
  • Benzos for withdrawal from alcohol/benzos/barbiturates or seizures
  • Cholinergic meds are only indicated in cases caused by anticholinergics or antihistamines (may have secondary anticholinergic effects)
  • Avoid anticholinergic drugs in treatment
91
Q

Alzhiemers dementia tx

A
  • Cholinesterase inhibitors (Donepezil, Galantamine, Rivastigmine)
    • MOA: block cholinesterase à increased ACh
    • SE: GI sx (diarrhea), leg cramps, vivid dreams, bradycardia
  • Memantine
    • MOA: NMDA receptor antagonist
  • Anti-Amyloid-beta Antibody
92
Q

opioids

examples, MOA for euphoria and analgesia

A
  • Examples: morphine/codeine, oxycodone (semi-synthetic opioids), fentanyl (synthetic opioid)
    • Demerol (Meperidine) dilates pupils (exception)
    • Tramadol: can cause serotonin syndrome (careful with SSRI); less addiction potential
  • MOA (euphoria): binds to Mu receptor → ↓ release of GABA → lack of GABA stimulation → dopamine release from neighboring neuron (Opioid = dope)
    • Acts at nucleus accumbens (reward)
  • MOA (analgesia): binds to Mu-GPCR→ hyperpolarization → ↓ NT → analgesia
    • Acts at anterior cingulate cortex, thalamus, periaqueductal gray (pain areas)
93
Q

opioid

toxidrome and withdrawal

tx for each

A
  • Toxidrome (all decreases): ↓ HR/BP, ↓ RR (overdose risk), ↓ temp, ↓ pupil size (constriction), ↓ bowel sounds, ↓ sweating, euphoria
    • Tx: naloxone (opioid antagonist)
  • Withdrawal (opposite of toxidrome): dilated pupils, tachycardia/HTN, V/D, insomnia, sweating, craving for drug, dysphoria, piloerection (goosebumps), myalgia
    • Tx (not life-threatening)
      • Methadone (long-acting opioid full agonist)
      • Buprenorphine (partial opioid receptor agonist)
      • Naltrexone (competitive opioid antagonist)
94
Q

cocaine

MOA, toxidrome, withdrawal

tx and complications

A
  • MOA: dopamine reuptake inhibitor
  • Toxidrome (all increases): ↑HR/BP, ↑RR, ↑Temp, ↑pupil size (dilation), ↑bowel sounds, ↑sweating
    • Complications: arrhythmias, MI, respiratory distress
    • Acute management for agitation: benzodiazepines or anti-psychotics (severe)
  • Withdrawal (opposite of toxidrome): constricted pupils, malaise, fatigue, hypersomnolence, depression, vivid dreams, psychomotor agitation
    • Tx: supportive (not life-threatening)
95
Q

Amphetamines

classic MOA and designer MOA

examples for each

A
  • Classic MOA: blocks reuptake → facilitates release of dopamine and NE from nerve endings → stimulant
    • Examples: methamphetamine (“speed”, “meth”), Ritalin, Dexedrin
    • Use: ADHD, narcolepsy, depression
  • Substituted (designer) MOA: release of dopamine, NE, and serotonin from nerve endings → stimulant, hallucinogen
    • Examples: MDMA (Ecstasy)
96
Q

amphetamines

toxidrome

chronic complications

A
  • Toxidrome (all increases): ↑HR/BP, ↑RR, ↑Temp, ↑pupil size (dilation), ↑bowel sounds, ↑sweating
    • Chronic use can lead to tooth decay (meth mouth)
97
Q

Sedatives

BZDs an barbituates

MOA and examples

A
  • Benzodiazepine (BDZs) MOA – gamma unit: increases Cl- channel opening → more Cl- in post-synaptic cell → GABA potentiator
    • BZDs are not lethal alone
    • Examples: Diazepam (Valium), alprazolam (Xanax), Chlordiazepoxide (Librium), lorazepam (Ativan)
  • Barbiturate MOA - beta unit: increases Cl- channel opening → more Cl- in post-synaptic cell → GABA potentiator
98
Q

Sedatives

toxidrome and withdrawal

tx for each

A
  • Toxidrome (all decreased – except eyes): ↓HR/BP, ↓RR, ↓Temp, ↓Bowel sounds, ↓Sweating, drowsiness, slurred speech, ataxia,
    • Tx:
      • BDZ: Flumazenil (short-acting BDZ antagonist)
      • Barbiturate: Na-HCO3 (promotes renal excretion)
  • Withdrawal (life threatening): HTN/tachycardia (medical emergency), hand tremor, psychomotor agitation, N/V, anxiety, irritability, sweating
    • Complications: tonic-clonic seizure
      • Tx: phenobarbital, clonazepam (anti-epileptics)
99
Q

ETOH

MOA, metabolism and toxidrome

A
  • MOA: activates GABA (alpha) and serotonin receptors in CNS → depressant
  • Metabolism: alcohol → acetaldehyde (via alcohol dehydrogenase) → acetic acid (via aldehyde dehydrogenase)
    • Asian glow: lack aldehyde dehydrogenase (less susceptible to dependence)
  • Toxidrome
    • <50 mg/dL: impairment in skilled tasks, increased talkativeness, relaxation
    • >100 mg/dL: ataxia, hyperreflexia, impaired judgement, lack of coordination, nystagmus, slurred speech
    • >200 mg/dL: amnesia, diplopia, N/V, hypothermia, dysarthria
    • >400 mg/dL: respiratory depression, coma, and death
100
Q

ETOH

withdrawal sx and complications

tx for some

A
  • Delirium Tremens (DT): peaks 2-4 days after last drink; characterized autonomic hyperactivity (tachycardia/HTN, tremors, sweating, anxiety, etc)
    • Tx: BZDs (Chlordiazepoxide – Librium, Lorazepam, Diazepam) → taper
  • Wernicke’s encephalopathy: encephalopathy, oculomotor dysfunction, ataxia
  • Korsakoff’s syndrome (chronic dz from untreated Werkicke’s):
    • Pathophysiology: necrosis of mamillary bodies (often irreversible)

Sx: Retrograde/anterograde amnesia, confabulation, unaware of illness

101
Q
  • Chronic Tx for alcohol dependence

disulfiram, naltrexone, acamprosate, topiramate, gabapentin

MOA and uses

A
  • Disulfiram
    • MOA: blocks aldehyde dehydrogenase (Asian glow – flushing, N/V)
    • Contraindicated in cardiac disease, pregnancy, LFTs must be monitored, adherence is low
  • Naltrexone
    • MOA: opioid receptor antagonist → decreases cravings and high associated with alcohol
  • Acamprosate
    • MOA: GABA-like agonist
    • Use: post-detox; indicated in patients with liver disease
  • Topiramate
    • MOA: GABA potentiator
    • Use: reduces cravings
  • Gabapentin (only if vital signs are stable)
102
Q

Weed

MOA and toxidrome

A
  • MOA: THC → binding to cannabinoid receptors on presynaptic neuron → inhibition of adenyl cyclase → release of inhibitory NT (GABA)
  • Toxidrome: impaired motor coordination, euphoria, anxiety, sensation of slowed time, impaired judgement, conjunctival injection (red eyes), increased appetite, dry mouth, tachycardia
    • These symptoms cannot be explained by another substance or mental disorder
    • Complications: Cyclic vomiting syndrome (daily vomiting relieved by showering)
      • Dx: Stop marijuana use for two weeks to see if causal
103
Q

Anti-cholinergics

examples, MOA, toxidrome, SE

A
  • Examples: antihistamines (Benadryl). TCAs (Amitriptyline)
  • MOA: inhibition of Ach receptor
  • Toxidrome: ↑HR/BP, ↑Temp, ↑pupil dilated, ↓Bowel sounds, ↓Sweating, confusion, agitation
  • SE: Hot, dry, blind, red, mad
104
Q

hallucinogens

LSD PCP MOAs

other examples

A
  • LSD MOA: believed to act on serotoninergic receptors
    • Toxidrome: VS stable, perceptual distortion, depersonalization, anxiety, paranoia
  • PCP MOA: NMDA glutamate receptor antagonist → activates dopamine release
    • Toxidrome: anesthetic, dissociative, violence, impulsivity, tachycardia/HTN. Seizures
    • Tx: BZDs, rapid-acting anti-psyhotics
  • Other example: K2/synthetic marijuana, magic mushrooms, ketamine (anti-depressant effects), MDMA
105
Q

caffeine

MOA, toxidrome, withdrawal

split toxidrome by amount

A
  • MOA: adenosine antagonist → increase in cAMP → stimulant effect via dopaminergic system
  • Toxidrome
    • 250 mg (2 cups): anxiety, insomnia, muscle twitching, GI problems, tachycardia
    • > 1 g: tinnitus, agitation, cardiac arrhythmias
    • >10 g: death secondary to seizures/respiratory failure
  • Withdrawal: headache, nausea, vomiting, depression, irritability
106
Q

nicotine

epidemiology, MOA. toxidrome, withdrawal

A
  • Epidemiology: smoking common in patients with mental illness
    • Known to increase chronic pain
  • MOA: stimulates nicotinic receptors and autonomic ganglia of the SNS/PNS
    • Highly addictive via the dopaminergic system
  • Toxidrome: restlessness, insomnia, anxiety, increased GI motility
  • Withdrawal: cravings, dysphoria, anxiety, decreased HR, increased appetite, insomnia
107
Q

nicotine tx

(4) if applicable provide MOA

A
  • Nicotine replacement therapy (patches, gums, sprays)
  • Bupropion: antidepressant (partial agonist of nAChR & inhibits dopamine reuptake → reduces withdrawal sx)
  • Varenicline: antidepressant (partial agonist of nAChR → mimics nicotine → reduces withdrawal sx)
  • Nortriptyline: antidepressant
108
Q
  • Etomidate (induction) –> anesthesia, no analgesia

MOA, kinetics, SE

A
  • MOA: modulates GABA à blocks neuroexcitation
  • Pharmacokinetics: rapid onset and metabolism
  • Organ system effects: respiratory depression, decreases cerebral flow à decreased ICP, suppresses cortisol synthesis (adrenal insufficiency), increases seizure risk
109
Q
  • Ketamine (induction) –> analgesia, amnesia

MOA, kinetics, SE

A
  • MOA: NMDA glutamate antagonist
  • Pharmacokinetics: rapid onset/short duration; lipid soluble (crosses BBB); liver excretion
  • Organ system effects: dissociation (disconnection from thoughts/memories); increased BP/HR; increased ICP
    • SE: hallucinations/dreams, disorientation
110
Q
  • Propofol (induction) –> sedation/amnesia

MOA, kinetics, SE

A
  • MOA: activates GABA-A receptors à Cl influx à hyperpolarization
  • Pharmacokinetics: rapid onset; eliminated through liver
  • Organ system effects: myocardial depression; hypotension; respiratory depression, decreased ICP, decreases seizures
111
Q
  • Succinylcholine

what type of drug, MOA

A

depolarizing

  • MOA: Ach agonist –> sustained depolarization –> desensitization –> prevents muscle contraction
112
Q

name some non-depolaring agents

MOA

A
  • Examples (-cur-): Rocuronium, Atracurium, Pancuronium
  • MOA: competitive Ach antagonist
113
Q

reversal of blockade

what drugs are used

A
  • Neostigmine given (cholinesterase inhibitor – causes bradycardia)
  • Atropine/glycoprolate (anti-muscarinics to counteract bradycardia)
114
Q
  • Fentanyl (100x more potent)/Morphine

MOA, SE

A
  • MOA: opioid agonist at mu-GPCR in CNS à increases K efflux à hyperpolarization à less pain transmission
  • SE: addiction, respiratory depression, hypotension, constipations, miosis

NBS (8 decks)

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