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Pharmacology > CNS Drugs > Flashcards

CNS Drugs Flashcards

1
Q

Train-of Four Pattern (TOF)

A

TOF = 1 (phase 1 of depolarizing block or no drug present)
TOF < 1 (phase 2 of depolarizing block or nondepolarizing block)
*Dantrolene, curare-like drugs, and succinylcholine phase 1 will have TOF < 1

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2
Q

Levodopa

A

MOA: prodrug L-dopa converted to dopamine by dopa decarboxylase (aka aromatic L-amino acid decarboxylase or AAAD), given w/ Carbidopa
Metabolism: food delays absorption
Use: tx sx’s of Parkinson dz
SE: on-off effects (dyskinesia d/t dopamine level fluctuations), psychosis, hypotension
*efficacy decreases as pathology progresses
CI: angle-closure glaucoma

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3
Q

Drugs used as supportive management of Barbiturate withdrawal sx’s?

A

IV Diazepam or Lorazepam for the seizures

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4
Q

Nitrous Oxide

A

MAC is high (so low potency), Blood/Gas is small (fast onset/recovery)
SE: diffusional hypoxia d/t NO displacing O2
steeper arterial tension curve bc decreased solubility so fast onset of action

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5
Q

Fluphenazine (typical)

A

Class: Phenothiazines (sulfa drug)

Exists in depot IM form

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6
Q

Ramelteon

A

MOA: agonist at melatonin receptors MT1 and MT2 in suprachiasmatic nucleus of hypothalamus (Gi coupled receptors)
Use: insomnia (induction only) - has NO dependence issues
SE: drowsiness and dizziness
CI: use w/ Fluvoxamine d/t the CYP-1A2 inhibition

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7
Q

Mesocortical D2 antagonism SE

A

Worsens -ve sx’s (= dysphoria), which decreases compliance

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8
Q

Duloxetine and Milnacipran

A

SNRIs
MOA: decrease reuptake of 5-HT and NE (no ANS SEs)
Use: tx Fibromyalgia (Pregabalin is a voltage-dependent Ca2+ blocker also approved for this condition)

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9
Q

Ketamine

A

MOA: noncompetative antagonist of NMDA glutamate receptor (analog of phencyclidine)
Use: dissociative anesthetic (causes analgesia and amnesia), used in emergent trauma BUT avoid in head trauma bc it increases ICP
SE: vivid dreams, hallucinations, elevated ICP

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10
Q

Thioridazine (typical)

A

Class: Phenothiazines (sulfa drugs)
Strongest antimuscarinic, so most likely to cause torsades - BUT “autotreats” acute EPS
SE: torsade (leading to arrhythmias and sudden death), retinal pigments/deposits

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11
Q

Apomorphine

A

Use: rescue therapy for tx of “off” episodes of akinesia in pt’s on dopaminergic therapy
SE: QT prolongation, dyskinesia, drowsiness, sweating, hypotension

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12
Q

Pramipexole / Ropinirole / Rotigotine

A

MOA: D2 agonists (Pramipexole is also D3 agonist)
Effect: antioxidant properties Katy decrease progression of dz
Use: Parkinson dz, tx restless leg syndrome (RLS), antidepressant effects

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13
Q

Thiopental

A

(Barbiturate)

Anesthetic induction

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14
Q

Lithium

A

MOA: blocks inside 5’-monophosphate, stabilizes inactive forms of Gs and Gi, decreases PKC activity
Metabolism: Vd close to total body water (~60%), really cleared, reabsorbed in PCT like Na+ (Na+ depletion like with increased sweating can cause Li+ toxicity)
Drug interaction: diuretics decrease Li+ clearance and increase toxicity, NSAIDs and ACEIs facilitate PCT reabsorption and cause Li+ toxicity (Triamterene and Amiloride increase clearance of Li+ to decrease toxicity potential)

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15
Q

Carbidopa

A

MOA: irreversible inhibitor of peripheral AAAD
Effect: allows L-dopa to cross BBB before being converted to dopamine
Use: conjunction with Levodopa to tx Parkinson dz

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16
Q

Ziprasidone (atypical)

A

MOA: strong 5-HT blockade at 1, 2, 6, 7 receptors, blocks all subtypes of DA receptors and blocks 5-HT and NE reuptake

😳

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17
Q

Desipramine

A

TCA
Use: cocaine craving and withdrawal
(Safe in pregnancy)

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18
Q

Rasagiline

A

MOA: irreversible inhibitor of MAO type B
Effect: prevents breakdown of dopamine to dihydrosyphenylacetic acid (DOPAC)
SE: (none) no amphetamine metabolites

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19
Q

Bath salts

A

Substituted cathinones w/ cocaine or amphtamine-like pharmacology, produced as “legal substitutes” of Cocaine, Methamphetamine or MDMA
SE: agitation, HTN, tachycardia, hallucinations, sz, rhabdomyolysis, acute renal failure

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20
Q

Lithium Teratogenicity

A

Epstein anomaly (septal tricuspid leaflet displaced downward toward apex of RV), large RA and small RV, assoc. w/ Wolff-Parkinson-White Syndrome

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21
Q

MAOIs

A

MOA: inhibit MAO(A) or MAO(B) in outer membrane of mitochondria
Effect: increase levels of NE, 5-HT, and DA
Interactions: tyramine-rich foods/beverages, α1 agonists cause HTN crisis d/t increased NE, Serotonin Syndrome d/t interaction w/ SSRIs, TCAs, Meperidine, Dextromethorphan and St. John’s wort

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22
Q

Selegiline (Deprenyl)

A

MOA: selective inhibitor of MAO type B (so NO tyramine interactions)
Effect: prevents breakdown of dopamine to dihydrosyphenylacetic acid (DOPAC), enhances effects of Levodopa
Use: adjunct to Levodopa to tx Parkinson Dz
SE: metabolized to amphetamine (sympathomimetic) and can produce +ve amphetamine screen on drug test

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23
Q

Thiopental / Methohexital

A

Barbiturate
MOA: GABA(A) enhancers, prolong the duration of Cl- channel opening
PK: ultra-short acting
Use: induction and maintenance of anesthesia, lowers ICP
SE: severe respiratory depression potential

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24
Q

Benzodiazepines SEs

A 
Drowsiness, sedation, rebound insomnia (worse w/ short-acting agents), anterograde amnesia, anxiolytics are class D for pregnancy and sedatives are class X for pregnancy (except for Quazepam)
Tx: Flumazenil is non-selective benzodiazepines site antagonist used in OD (also used in OD of “Z drug”)
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25
Q

Amoxapine

A

TCA

Use: psychotic depression

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26
Q

Phenytoin

A

MOA: blocks voltage gated Na+ channels, keeping them in an inactivated state (Class 1B antiarrhythmic)
Effect: decreases conduction of APs (enhances refractoriness)
PK: zero-order elimination, inducer of CYP450s, narrow therapeutic range
Use: tx any sz type EXCEPT absence
SE: gingival hyperplasia, hirsurism, folate and Vit D deficiency, SLE-like rxn (acts as hapten), teratogenic

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27
Q

Fluoxetine

A

SSRI
PK: inhibition of CYP 3A4 (and 2D6)
Interactions: increases levels of Alprozolam and Carbamazepine (bc 3A4 metabolizes Benzos)
(Safe in pregnancy)

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28
Q

Olanzapine (atypical)

A

MOA: strong 5-HT2A blockade
Effect: improves -ve sx’s
SE: weight gain, sz

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29
Q

Antidepressants in Pregnancy

A

Safe SSRIs (Fluoxetine, Ser

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30
Q

Temazepam

A

Intermediate-acting sedative benzo w/ few active metabolites

*sudden withdrawal causes rebound insomnia

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31
Q

Alprazolam

A

Use: panic disorder

*only benzo used for anxiety assoc w/ depression

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32
Q

Haloperidol (typical)

A

Class: Butyrophenones
MOA: potent D2 blockade
Use: IV in acute management of psychosis and mania
SE: severe EPS

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33
Q

THC

A

MOA: CB1 > CB2 agonist
Effect: decreased 5-HT release from CTZ = antiemetic, decreased Leptin release in hypothalamus = appetite stimulant

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34
Q

Dronabinol / Nabilone

A

Cannabinoid

Use: tx nausea, and cancer/aids anorexia

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35
Q

Felbamate

A

MOA: NMDA receptor blocker
Use: antiepileptic
SE: aplastic anemia

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36
Q

Sertraline

A

2nd most potent SSRI, 2nd most selective SSRI (👇🏽 likelihood to cause bleeding abnormalities)
(Safe in pregnancy)

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37
Q

Citalopram

A

Most selective SSRI w/ 👇🏽 likelihood to cause bleeding abnormalities (indicated if pt has bleeding disorder, or if pt is taking Warfarin or Aspirin)
PK: NO inhibition of CYP 450
(Safe in pregnancy)

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38
Q

Esters (local Anesthetics)

A

“x-caine”
Procaine (short-acting) / Cocaine / Tatracaine (long-acting)
SE: HS rxn d/t PABA (allergen)

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39
Q

Malignant Hypethermia

A

SE of Succinylcholine and Chlorofluorocarbons
ROS: contractions d/t prolonged Ca2+ release, 👆🏽ETC activity leads to 👆🏽heat produced from ETC, stress of the heat 👆🏽SANS activity; lactic acidosis as anaerobic processes attempt to make ATP too

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40
Q

Fetal Hydantoin Syndrome

A

Cause: Phenytoin taken by mother during pregnancy
ROS: cleft lip/palate, microcephaly, epicalthal folds, broad nasal bridge, absent nails, hypoplasia of distal phalanges, congenital heart defects (VSD, pulmonary stenosis, transposition)

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41
Q

SNRIs

A

Venlafaxine / Desvenlafaxine / Duloxetine / Milnacipran

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42
Q

Cannabinoid Receptors

A

CB1 (neuronal) and CB2 (peripheral) are Gi coupled = CNS depressants

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43
Q

Sevoflurane

A

Chlorofluorocarbon, least likely to cause respiratory irritation (ok to use for induction)

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44
Q

Local Anesthetics MOA

A

Inhibit voltage-gated Na+ channels

  1. Cross cell membrane: drugs are weak bases so require alkaline pH to be unionized to cross the membrane
  2. Bind w/ in the Na+ channel: the cationic form is active drug
  3. Stabilize the inactivated state of the Na+ channel once bound
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45
Q

Cocaine

A

MOA: blocks DA, NE and 5-HT reuptake; also blocks voltage-dependent Na+ channels (NO effect on mobile pool, unlike amphetamines)
Use: local anesthetic (does not require epinephrine bc it has intrinsic sympathomimetic activity d/t the NE reuptake inhibition)
SE: vasoconstriction, hypertension, ischemia
*#1 cause of ED visits involving elicit drugs

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46
Q

Toparamate

A

MOA: blocks AMPA/kainate receptors, CA inhibitor
Use: migraine prophylaxis, tx obesity when used in combination w/ Phentermine

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47
Q

Desflurane

A

Chlorofluorocarbons w/ small Blood/Gas, most likely to cause respiratory irritation so avoid in induction

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48
Q

”Z drugs”

A

Zolpidem / Zaleplon / esZopiclone
MOA: strong affinity for GABA(A) receptors w/ α1 subunits
PK: Zapelon t1/2 is 1h, esZopiclone t1/2 is 6h
SE: Class C in pregnancy, drowsiness and motor impairment, parasomnia (somnambolism)
OD tx: Flumazenil

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49
Q

Midazolam

A

Use: pre-operative sedation (bc it’s so short-acting)
SE: respiratory depression/arrest (usually nbd tho bc you’re in a pre-op hospital sorta setting)

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50
Q

Selegiline

A

MOA: selective MAO(B) inhibitor
Effect: increases DA primarily
Use: available as skin patch, tx for Parkinson Dz

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51
Q

Benzodiazepines approved for EtOH withdrawal

A

Chlordiazepoxide, Clorazepate, Diazepam, Oxazepam

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52
Q

Tolcapone and Entacapone

A

MOA: COMT inhibitors —> prevent conversion of dopamine to 3-O-methyldopa (3OMD)
Effect: increases t1/2 of L-dopa, increased fraction of L-dopa reaching CNS
Use: add to Levodopa-Carbidopa as pathology of Parkinson dz progresses
SE: hepatotoxic (Tolcapone only)

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53
Q

Perioral Tremor (EPS)

A

Timeline: weeks-months
ROS: “rabbit syndrome” (muscle movement of mouth)
Antidote: antimuscarinics

54
Q

Tardive Dyskinesia (EPS)

A

Timeline: months-years
Mechanism: upregulation and sensitization of D2 receptors after long-term tx
ROS: oral and facial dyskinesia w/ chorea and athetosis
NO TX (Diazepam may help)
*less likely to occur w/ Atypical Antipsychotics

55
Q

Suvorexant

A

MOA: orexin receptor antagonist
Use: tx insomnia (induction and maintenance of sleep)
CI: narcolepsy

56
Q

Blood-Gas Partition Coefficient

A

Measures solubility of anesthetic in the blood, so smaller blood-gas ratio indicates faster onset as more of the drug is reaching the CNS (bc it’s not as soluble in blood)
*the more soluble an anesthetic is in the blood, the longer it takes to get to the CNS

57
Q

Lamotrigine

A

MOA: blocks voltage-gated Na+ channels
Effect: inhibits glutamate release
Use: adjuvant for sz, tx BP disorder
SE: rash, Class C in pregnancy

58
Q

Fluvoxamine

A

SSRI
PK: inhibition of CYP 1A2 (which metabolizes TCAs)
Interaction: increased levels of TCAs (so dont combine)

59
Q

Lamotrigine

A

MOA: inhibits voltage-sensitive Na+ channels and inhibits release of glutamate
Use: Bipolar disorder
SE: skin rashes, sz w/ abrupt withdrawal, teratogenic (cleft lip/palate)

60
Q

Pentobarbital

A

(Barbiturate)

Drug-induced coma for severe brain trauma

61
Q

Lithium SEs

A

GI sx’s (take w/ food), tremors (add Propranolol to tx if needed), polyuria (d/t decreased response to ADH Gs-coupled receptor in collecting duct), thyroid dysfunction (d/t decreased TSH response), teratogenicity**

62
Q

Benztropine and Trihexyphenidyl

A

MOA: muscarinic antagonist that cross BBB
Effect: potentiate dopamine effect in basal ganglia
SE: Atropine-like (dry mouth, eyes, mydriasis, cycoplegia, tachycardia, constipation, urine retention, BPH)

63
Q

Ethosuximide

A

MOA: blocks T-type Ca2+ channels (T = transient) in the thalamus
Effect: burst of thalamic neuron activity
Use: only tx absence sz

64
Q

Akathisia (EPS)

A

Timeline: days/weeks/months
ROS: restlessness
Antidote: dose-reduction of antipsychotic, benzodiazepines, non-selective β-blockers, antimuscarinics (Clonazepam or Propranolol)

65
Q

Chlorofluorocarbons (Halothane fam)

A

MAC is low (so high potency), Blood/Gas is higher (slower onset)
SE: malignant hyperthermia risk (tx w/ Dantrolene), respiratory irritation (coughing), hepatotoxic
more flat arterial tension curve bc increased solubility so slow onset of action

66
Q

General Anesthetics MOA

A

Ehnance GABA(A) activity

67
Q

Amides (local Anesthetics)

A

“x-i-x-caine”

Prilocaine (short-acting) / Lidocaine / Buvicaine (long-acting)

68
Q

Benzodiazepines approved for status epilepticus

A

Diazepam and Lorazepam (bc they are long-acting and are available IV)

69
Q

Pregabalin

A

Use: chronic pain

70
Q

Acute Dystonic Reaction (EPS)

A

Timeline: within days
ROS: muscle spasms of upper body (tongue, face, neck, back) = spasmodic torticollis
Antidote: antimuscarinics (Benztropine, Trihexyphenidyl,Diphenhydramine)

71
Q

Local anesthetic effect on fiber type over time (fast to slow)

A

C-fibers (pain), Aδ (temp), Aγ and Aβ (touch), Aα (motor)

fast to slow - and small diameter to larger diameter

72
Q

SSRIs

A

MOA: block 5-HT reuptake (less anticholinergic activity)
use: first-line agents for chronic depression, panic, generalized anxiety disorders, bulimia, OCD, PTSD
SE: GI upset (diarrhea), sexual dysfunction (anorgasmia, 👇🏽libido, 👇🏽arousal), stimulant effect (anxiety, agitation), bleeding abnormalities (caution w/ Aspirin or Warfarin)

73
Q

Minimal Alveolar Concentration (MAC)

A

Measure of anesthetic potency defined as concentration of gas in lungs that is able to prevent movement in 50% of pt’s (analogous to ED50)
*higher MAC = lower potency (so they are inversely related)

74
Q

Succinylcholine

A

MOA: nicotenic agonist; phase 1 - depolarization, phase 2 - desensitization and channel blockade (can be antagonized by AChE inhibitors)
Effect: depolarizes the NMJ, stimulates ANS ganglia and muscarinic receptors (could reduce HR)
Metabolism: rapidly metabolized by liver and plasma cholinesterases
CI: pt w/ poor cholinesterase metabolism

75
Q

Chlorpromazine (typical)

A

Class: Phenothiazines (sulfa drug)

Prominent ANS SEs, and deposits in cornea/lens

76
Q

Trazodone (and Nefazodone)

A

SARIs
MOA: 5-HT(2A) antagonist and reuptake inhibitors, also block α1 receptors
SE: hypotension, arrhythmias and priapism (d/t α1 blockade)
*Trazodone blocks H1 receptors and acts as sedative

77
Q

Buspirone

A

MOA: partial agonist at 5-HT(1A) receptors
Use: anxiolytic (takes several wks to work)
SE: drowsiness and dizziness
CI: use w/ MAOIs (can cause HTN crisis)

78
Q

TCAs

A

MOA: block NE and 5-HT reuptake, also block α1, M and H1 receptors
Metabolism: metabolized by CYP450
Interactions: additive anticholinergic effects, additive sympathomimetic effects, antagonism w/ α2 agonists*

79
Q

Antiepileptic rx in Pregnancy

A

PK: inducers of CYP enzymes can decrease efficacy of oral contraceptives
*Supplement folate @ 4mg/day, check maternal AFP (α-fetoprotein) levels during pregnancy to monitor for neural tube defects

80
Q

DOC in Bipolar Disorder?

A

Lithium

*Lamotrigine (anticonvulsant) indicated for maintenance during pregnancy

81
Q

Nondepolarizing NM Blockers MOA

A

Competitive antagonist at skeletal muscle Nm (nicotenic) ACh receptor
*reversed using AChI - Neostigmine

82
Q

Pimozide (typical)

A

Class: Diphenylpiperidines
Use: Tourette syndrome and tic disorders

83
Q

Bromocriptine

A

MOA: D2 receptor agonist
Effect: inhibition of indirect pathway (👇🏽cAMP)
Use: adjunct or alt therapy to Levodopa for Parkinson,m hyperprolactinemia and acromegaly
SE: dyskinesia, hallucination, psychosis

84
Q

Valproate

A

MOA: anticonvulsant that enhances GABA activity, decreases degradation of GABA in CNS
Use: Bipolar Disorder
SE: sedation, GI upset, hepatotoxicity, agranulocytosis, neural tube defects

85
Q

Neuroleptic Malignant Syndrome (EPS)

A

Timeline: weeks-months
ROS: Catalonia, high fever, rhabdomyolysis (myoblobinemia), stupor, CV instability
Antidote: Dantrolene + Bromocriptine (and STOP antipsychotic immediately)

86
Q

Phencyclidine

A

MOA: antagonist of NMDA glutamate receptor and binds nicotenic receptors
SE: violence, agitation, rhabdomyolysis

87
Q

Aripiprazole (atypical)

A

MOA: 5-HT2A antagonist, 5-HT1A partial agonist, partial D2 agonist
Use: mania, Autism spectrum

88
Q

Propofol

A

PK: poorly water soluble
Use: induction and maintenance of anesthesia
SE: propofol infusion syndrome (metabolic acidosis, hyperkalemia, rhabdomyolysis, retail failure, CV collapse)

89
Q

Benzodiazepines

A

MOA: binds GABA(A) receptor at allosteric site distinct from GABA (cannot open Cl- channels w/o GABA = potentiation)
Effect: increases frequency of Cl- ion channels opening —> hyperpolarization of cell which inhibits APs
Use: α1 mediates sedation and α2 mediates anxiolysis
PK: most have active metabolites through CYP3A4 metabolism (except Lorazepam and Oxazepam)

90
Q

Paroxetine

A

Most potent SSRI and strong anticholinergic (more likelihood for cardiotoxic SEs)
PK: NO active metabolite, inhibitor of CYP 2D6
SE: weight gain

91
Q

Batrachotoxin

A

MOA: prevents inactivation, prolongs Na+ entry
SE: hallucinations
*frog toxin

92
Q

Phenelzine and Tranylcypromine

A

Nonselective MAOIs

93
Q

What drugs have life-threatening withdrawal sx’s?

A

Barbiturates and EtOH d/t the life-threatening seizures caused by withdrawal

94
Q

Valproic Acid

A

MOA: inhibits GABA-transferase (👆🏽GABA), inhibits T-type Ca2+ channels, inhibits voltage-gated Na+ channels, inhibits histone deacetylases
PK: inhibits CYP2C9 (no induction of CYP450s)
Use: tx all type of sz including absence, prophylaxis of migraine, tx mania in BP disorder
SE: alopecia, pancreatitis (fatal), thrombodytopenia (w/ 👆🏽BT), teratogenic (neural tube defects)

95
Q

Bupropion

A

MOA: increase DA and NE (blocks reuptake and enhances release
Use: smoking cessation (Varenicline is alternative tx)
SE: potent inhibitor of CYP 2D6
(Safe in pregnancy)

96
Q

Pancuronium

A

MOA: competitive antagonist at Nm receptor and antimuscarinic
Longer-acting

97
Q

Carbamazepine

A

MOA: blocks inactivated Na+ channel
Effect: prevents propagation of APs
PK: inducer of CYP (induces its own metabolism so tolerance develops)
Use: DOC for trgeminal neuralgia, tx mania in BP disorder
SE: SIADS (at high doses), rashes (including SJS👺), aplastic anemia of WBCs mainly, teratogenicity (neural tube defects and urinary tract defects)

98
Q

Clomipramine

A

TCA

Use: tx OCD

99
Q

Serotonin Syndrome

A

SSRI SE
ROS: rigidity, hyperthermia, ANS instability, myoclonus (pathognomonic)
Tx: Benzos for sedation, consider Cyproheptadine or Chlorpromazine

100
Q

Baclofen

A

MOA: GABA(B) agonist, activates the Gi receptor
Effect:👇🏽 cAMP, activates PKA,👆🏽 K+ conductance
Use: tx spasticity (UMN lesions, MS)

101
Q

Atomoxetine

A

MOA: selective NE reuptake inhibitor (NRI)
SE: SI (no abuse potential and no withdrawal)

102
Q

Dantrolene

A

MOA: binds to ryanodyne receptor channel RyR1 inhibiting Ca2+ release from SR inside skeletal muscle cell
Use: antidote to malignant hyperthermia (caused by Succinylcholine, or chlorofluorocarbons), and used tp tx neuroleptic malignant syndrome

103
Q

Amantadine

A

MOA: antiviral that increases synthesis and release of DA, blocks reuptake of DA, and blocks muscarinic receptors
SE: livedo retidularis (mottling pattern of skin)

104
Q

Tetrodotoxin

A 
MOA: blocks activated Na+ channel (similar to class 1A)
Use: identifies fast Na+ channels in physio
*puffer fish toxin
105
Q

Clozapine (atypical)

A

MOA: strong D4 and 5-HT2A blockade
SE: agranulocytosis, weight gain, sz (antimuscarinic), hypersalivation (5-HT blockade in mouth)

106
Q

Nigrostriatal D2 antagonism SE

A

Causes EPS (= dyskinesias), which decreases compliance

107
Q

Mivacurium

A

Shortest duration of action w/ slow onset of action
PK: metabolized by plasma cholinesterase
SE: histamine release (red-man like sx’s)

108
Q

Local Anesthetics SEs

A

CNS toxicity: can induce life-threatening sz, to avoid when giving high doses you co-administer IV benzo (Diazepam / Lorazepam)
CV toxicity: vasodilation, bradycardia, CV collapse

109
Q

Imipramine

A

TCA

Use: enuresis (but Desmopressin is DOC)

110
Q

Treatment of Bipolar Disorder during pregnancy

A

Lamotrigine alternative to Lithium for maintenance, Babapentin and Clonazepam (benzos) safe as anti-panic or acute mania tx during pregnancy (Class D), or Atypical antipsychotics can be used (Class C)

111
Q

Amitriptyline

A

TCA
Use: neuropathic pain, migraine
(Safe in pregnancy)

112
Q

Gabapentin

A

Use: management of chronic pain

113
Q

Mirtazapine

A

NaSSA
MOA: α2 antagonist, blocker of 5-HT(2A), 5-HT(2C), 5-HT(3) and H1
Effect: increased NE synthesis and release, and increased 5-HT release (d/t the α2 antagonism via α1 receptors at raphe nucleus)
Use: anorexia nervous (weight gain via 5-HT(2C) and H1 blockade), anxiolytic
SE: sedation (d/t H1 blockade)

114
Q

Atypical Antipsychotics

A

MOA: strong 5-HT2A blockers, and weak D2 antagonists
Effect: improve -ve sx’s, decrease +ve sx’s
Use: first-line therapy for Schizophrenia
SE: few EPS and few hyperprolactinemia sx’s

115
Q

Opioids used as Anesthetics

A

Fentanyl / Meperidine / Tapentadol

116
Q

Tuberoinfundibular D2 antagonism SE

A

Increased prolactin leads to gynecomastia and menstrual irregularities, increased eating = obesity (long-term use has increased death rates d/t obesity related complications)

117
Q

Atracurium

A

Not metabolized, can be spontaneously inactivated via Hofmann degradation resulting in byproduct Laudanosine which causes seizures

118
Q

Cannabinoid SEs

A

Hypotension (d/t vasodilation) causing dizziness and then palpitations from reflex tachycardia, conjunctival injection (d/t vasodilation), additive CNS depression (opioids and EtOH), additive CV toxicity (Amphetamines, antimuscarinics, TCAs, antipsychotics), opposes effects of β-blockers (increased risk of ischemic CV dz)

119
Q

Typical Antipsychotics

A

MOA: D2 (and D1) antagonists in mesolimbic pathway (antimuscarinic, α1 antagonism, H1 antagonism)
Effect: improve/decrease +ve sx’s, worsen -ve sx’s by causing dysphoria
SE: extrapyrimidal sx’s (EPS), hyperprolactinemia, lower sz threshold (antimuscarinic), orthostatic hypotension (α1 antagonism), weight gain (H1 antagonism)

120
Q

Quazepam

A

Long acting sedative benzo that is only Class D (not X)

121
Q

Etomidate

A

Use: induction of anesthesia, off-label use in Cushing Syndrome (bc it blocks steroidogenesis)
*not analgesic

122
Q

Fosphenytoin

A

Water-soluble prodrug of Phenytoin

Use: can be rapidly infused w/o SEs assoc w/ the highly alkaline IV soln of Phenytoin

123
Q

Drug-induced Parkinsonism (EPS)

A

Timeline: weeks
ROS: bradykinesia, rigidity, resting remor
Antidote: antimuscarinics (Benztropine, Diphenhydramine, Amantadine)

124
Q

Phenobarbital and Primidone

A

(Barbiturate)

Anticonvulsants

125
Q

Amphetamine / Methylphenidate / Dexmethylphenidate

A

MAO: increase fleas of DA, NE and 5-HT from MOBILE POOL and block reuptake of these amines
Use: ADHD, Narcolepsy, obesity, sleep apnea
SE: assoc w/ increased NE (anxiety, palpitations, HTN, hydriasis, loss of appetite), high abuse potential

126
Q

Risperidone (atypical)

A

MOA: strong 5-HT2A blockade, some α1 blockade
SE: hypotension (reflex tachycardia)

127
Q

IV Anesthetics

A

Midazolam or Dexmedetomidine (α2 agonist) to sedate the pt and Atropine-like drugs to dry up secretions

128
Q

Vigabagrin

A

MOA: inhibitor of GABA transaminase

*assoc w/ weight gain

129
Q

Quetiapine (atypical)

A

MOA: strong H1 and α1 antagonism (NO antimuscarinic activity)
SE: hypotension (reflex tachycardia), weight gain, sexual dysfunction

130
Q

Barbiturates

A

MOA: bind allosteric site on GABA(A) receptor than benzos; GABA-mimetic @ high doses annnd block Complex I of ETC
Effect: increase duration of Cl- ion channel opening —> prolonged hyperpolarization which decreases the # of APs
PK: CYP450 inducers (except Secobarbital)
SE: powerful CNS and respiratory depression, OD can lead to coma and death

Pharmacology (27 decks)

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