SSRI

AE: sexual dysfunction

HL: Long (days)

SSRI

AE: sexual dysfunction

SSRI

AE: sexual dysfunction

SSRI

AE: sexual dysfunction

SSRI

AE: sexual dysfunction

SSRI

AE: sexual dysfunction

HCA

5HT2a antagonist (-> 5HT1A stimulation)

AE: sedation, moderate ortho hypotension

MAO-I

irreversible & non-selective

lithium salt

affects PIP2; accumulates in cells via Na/K pump

[] affected by pregnancy, meds (caffeine dec.; ace-i's inc. Li)

AE: narrow TI; slow onset; ton of effects

benzodiazepine anti-anxiety

other effects: long-term sedative, muscle relaxant, grand mal seizures & status epilepticus, EtOH withdrawal

MOA: enhance a2 GABAaR Cl- conductance

dec. anxiety by selectively inhibiting limbic system circuits

all have sedative effects; may have anticonvulsant/muscle relaxant properties

notes: highly protein-bound

tolerance develops if high doses taken for long period; withdrawal symptoms faster if short-acting drugs

AEs: drowsiness, confusion

CI's: liver disease, alcohol/other CNS depressants (additive effect)

benzodiazepine anti-anxiety

other uses: alcohol withdrawal

notes: short-acting

benzodiazepine anti-anxiety

notes: effective short- & long-term, withdrawal reactions in 30% of pts

benzodiazepam anti-anxiety

notes: useful in chronic treatment of epilepsy

benzodiazepine anti-anxiety

notes: EtOH withdrawal

benzodiazepine sedative

notes: short-acting; tolerance/withdrawal

benzodiazepine sedative

notes: intermediate-acting

benzodiazepine sedative

notes: intermediate-acting

benzodiazepine sedative

notes: long-acting

benzodiazepine sedative

notes: long-acting

non-benzo hypnotic

acts on BZ1, no withdrawal effects

Elim: CYP450

HL: 2 hours

non-benzo hypnotic

HL = 1 hour

non-benzo hypnotic

HL = 6 hours

non-benzo anti-anxiety

MOA: 5-HT1AR partial agonist (also D2 & 5-HT2Rs), upregulates presyn 5-HT1A (anxiolytic) & postsyn 5-HT1A (nausea, dizziness)

notes: no dependence, withdrawal, additive symptoms; delayed onset

CYP34 metabolism

non-benzo hypnotic

MOA: binds melatonin R's in SCN (no GABA binding)

notes: approved for long-term use, no abuse potential

non-benzo anti-anxiety

MOA: SNRI (mixed 5-HT/NE reuptake inhib), weak DA reuptake blocker; no adren/hist/chol AEs

notes: inc NE action at inc doses

uses: when selective SSRIs don't work

sleep-inducing via GABA-mediated CNS depression

not often used as sedative b/c of AE's (large tolerance, dependence; CV & resp depression in OD)

barbituate sedative

notes: used more as anti-convulsant

HL: long-acting

barbituate sedative

notes: effective sedative & hypnotic

HL: short-acting

MOA: block D2 receptors

mesolimbic -> dec. positive symptoms

mesocortical -> worsen negative symptoms

nigrostriatal -> EPS symptoms

tubuloinfundibular -> hyperproloactinemia

notes: readily absorbed, HL ~ 20 hours

AEs: weight gain, CV risks

MOA: 5-HT2a & D2 antagonists

5-HT2a blockade -> inhibit DA release -> inc. DA

mesolimbic: D2 > 5-HT2 -> dec. pos. symptoms

mesocortical: 5-HT2 > D2 -> dec. neg. symptoms

nigrostriatal: dec. 5-HT2a inhibition of DA -> avoid parkinsonism

tubuloinfunbidublar pathway: 5-HT & DA cancel out -> normal PRL

MAO: binds autoreceptors of 5HT1&2 neurons in raphe nuclei, thus inhibits cortical inputs

notes: most potent hallucinogen

MOA: stimulates presynaptic release of DA & other catecholamines; also inhibits catecholamine transporter (reuptake)

Effects: euphoria, sleeplessness, stereotyped behavior, anorexia

Notes: causes a psychosis similar to that of schizophrenia (paranoia, hallucination)

Toxicity: cardiac arrhythmias, MI, cerebral vasoconstriction, seizure; chronic use: involuntary motor activity, stereotyped behavior

Withdrawal: depression (for extended period), fatigue, bradycardia

Type: narcotic analgesic

notes: more lipid soluble than morphine -> crosses BBB; "speedball" = heroin + cocaine

hallucinogen

notes: properties similar to amphetamines

"ecstasy"

stimulant, as methamphetamine

strong psychdeleic effects

neurotoxic to 5HT neurons

sympathomimetic

Notes: isolated from herb Ma Huang; used for asthma in Chinese medicine

Stimulant (sympathomimetic)

MOA: binds ACh receptors; responsible for reward effect in nucleus accumbens

Withdrawal Treatment: nicotine replacement + psychotherapy; some antidepressants (buproprion)

Stimulant, Local Anesthetic

MOA: inhibitor of DA/NE/5-HT reuptake; inc. HR & BP, arousal & euphoria

Reward effects are from inc. in DA in mesolimbic pathway (VTA, N. Accumbens)

Toxicity: cardiac arrhythmias, MI, seizure; chronic: invol. motor activity, paranoia, psychosis

Withdrawal: depression, fatigue, bradycardia

Long-acting Opiod

Notes: Lacks euphoria of morphine & heroin; useful as therapy for morphine addiction

MOA: Blocks NMDA receptors

Notes: "angel dust", "dissociative anesthetic"

Effects: delirium, hallucination, catatonic posturing, emotional withdrawal, psychotic symptoms similar to schizophrenia

Relaxant; cognitive & motor capabilities impaired; cannabinoid receptors are GPCRs (Gi -> dec. cAMP in cell)

Receptor Distribution: hippocampus (short-term memory deficit), substantia nigra & cerebellum (impaired motor function), and mesolimbic DA circuit (reward)

Possible Therapeutic Value: anti-emetic, dec. intraocular pressure

Endogenous cannabinoids: anandamide (derivative of AA)

AEs: OD produces sensory distortion & hallucination; dec. serum testosterone & sperm count in males

Mechanism: Partial agonist of opiod u-receptor

Used to treat opiate addiction (maximal dose has less effect than full agonists)

Inhalational Anesthetic

Notes: not used alone except for dental procedures; highest MAC, rapid induction, good analgesia, no toxicity

Inhalational Anesthetic

Notes: Used for induction in children; sweet, pleasant odor

Lowest MAC; highest blood:gas partition; highest oil: gas partition; moderate induction; poor analgesia

Effects: Drop in BP, drop in CO, + arrythmias; 15-20% metabolism; hepatic toxicity

Inhalational Anesthetic

Notes: Most widely used inhalational anesthetic

High blood:gas partition; high oil:gas partition; moderate induction; excellent analgesia; no toxicity

Inhalational Anesthetic

Notes: As halothane w/ less hepatotoxicity

Inhalational Anesthetic

Notes: Most widely used for outpatient surgery; bronchial irritant

Lowest blood:gas partition; rapid induction; excellent analgesia; dec. BP; dec. SVR; airway irritant

Inhalational Anesthetic

Notes: Becoming popular in U.S.; outpatient use; induction in children (non-pungent); expensive

Low MAC; rapid induction; excellent analgesia; dec. BP; dec. SVR; low toxicity

IV Anesthetic

Barbituate

Used for induction of anesthesia

Pros: Rapid onset (10-30 secs); highly lipid-soluble (crosses BBB); short duration (20-30 mins) due to redistribution from brain to muscle

Cons: Not analgesic; dec. BP (venodilation); dec. RR & TV

IV Anesthetic

Uses: Induction in high-risk pts w/ CV problems; sedation or general anesthesia in children

Pros: CV stimulant; bronchodilator; complete IV anesthetic

Cons: Emergence reactions (not in children < 15; uncommon in adults > 65)

IV Anesthetic

Uses: Induction in pts w/ CV problems

Pros: Rapid induction; ultra-short-acting (5 mins); no CV depression; minimal respiratory depression

Cons: Pain on injection, involuntary muscle movement, n/v, hiccups, not analgesic

IV Anesthetic

Uses: Combined w/ fentanyl to produce neuroleptic analgesia for diagnostic or minor surgical procedures; sedation

Pros: Anti-emetic, anti-convulsant, safe & simple procedure

Cons: No amnesia, dec. BP, respiratory depression

IV Anesthetic

Uses: Anesthesia for short procedures

Pros: Rapid onset & recovery (even after repeated injections), antiemetic

Cons: Pain on injection, involuntary muscle movement, respiratory depression, dec. BP (drop in TPR)

IV Anesthetic

Uses: Anti-anxiety agent preoperatively; sedation

Pros: Rapid onset, causes amnesia, little CV effect, anti-convulsant

Cons: Not analgesic, causes respiratory depression, long-acting

IV Anesthetic

Uses: Analgesia; General Anesthesia (in high doses w/ N2O in cardiac surgery)

Pros: Profound analgesia, relative CV stability, high potency, short duration of action, reduces emergence phenomenon, reversible by opiod antagonists

Cons: Nausea, slow gastric emptying, respiration depression at high doses (assisted ventilation required)

IV Anesthetic

Uses: As fentanyl; 1000x potency of morphine

Opiate Antagonist

Notes: Rapidly displaces bound opiods from receptors w/in 30 seconds of IV injection

Reverses respiratory depression & coma of heroin OD

Competitive antagonist at u, d, & k w/ 10-fold inc. affinity for u than k

Opiate Antagonist

Notes: Longer duration of action than naloxone

Single oral dose blocks the effects of injected heroin for 48 hours

Opiod Analgesic; Opiate

Notes: Strong agonist @ u receptor; HL = 4 hours

Uses: Acute & Chronic pain

AEs: Sedation, respiratory depression, constipation, n/v, itching (hist release), tolerance/dependence, euphoria

Opiod Analgesic; Opiate-like

Notes: Long-acting strong agonist @ u receptor

HL = 24 hours

Uses: Chronic pain and/or maintenance in opiod addicts

AEs: Less euphoria, sedation, resp. depression, constipation, n/v, itching, tolerance/dependence

May accumulate b/c of long HL

Opiod Analgesic; Opiate-like

Notes: Strong agonist @ u receptor, binds d & k as well

HL = 2 hours

Opiod Analgesic; Opiate-like

Notes: Strong agonist @ u receptor

HL = 5-45 minutes

Uses: Anesthetic or for acute pain

Opiod Analgesic; Opiate

Notes: moderate agonist (binds u, d, & k w/ same affinity)

Uses: Mild pain

Opiod Analgesic; Opiate-like

Notes: strong agonist @ u receptor (like fentanyl)

HL = 5-45 mins

Uses: Anesthetic or acute pain (more potent than fentanyl)

Opiod Analgesic

Notes: Mixed agonist-antagonist; agonist on k; weak antagonist on u & d

Uses: Acute pain

AE: u-antagonist effect might precipitate morphine withdrawal syndrome

Opiod Analgesic

Notes: Moderate agonist

Strong agonists: morphine, meperideine, methadone, heroin, fentanyl

Moderate agonists: propoxyphene, codeine

Mixed agonists-antagonists: pentazocine, nalbuphine, buprenorphine

Angatonists: naloxone, naltrexone

u, k, d receptors: G-proteins; inc. K+ efflux (hyperpol), reduce Ca entry

CNS actions: Analgesia, sedation, euphoria, mental clouding, resp depression, n/v, cough reflux, miosis

GI actions: constipation, biliary tract spasm

CIs: Dec. resp reserve (COPD, obesity, asthma), biliary colic, head injury, reduced BV, hepatic insufficiency, convulsant states

Tolerance: to analgesia, euphoria, sedation, lethal dose, nausea; NOT to miosis, constipation, resp. depression (partial)

Antitussive: Codeine, dextromethorphan

Anesthetic: Fentanyl, sufentanil

B2-Agonist AntiAsthmatic

Use: Inhaled on "as needed" basis

Notes: Effective bronchodilation w/o cardiac effects; not a substrate for COMT (longer DOA)

AEs: (unusual w/ inhalation), muscle tremor, inc. FFAs, glucose, lactate, hypokalemia, V/Q mismatching

Inhaled Corticosteroid AntiAsthmatic

Uses: Severe episodes; prophylaxis; little effect on early response but will suppress late response to allergen challenge.

Notes: Used to dampen the inflammatory aspects of asthma pathogenesis (esp. late phase). 

MOA: Reduces # & activity of inflammatory cells in airway; inhibits release of AA metabolites, prevents inc. vascular permeability, suppresses IgE binding, increases B-adrenergic responsiveness

AEs: Few; dysphonia, oropharyngeal candidiasis

Goal: To use lowest possible dose concurrently w/ B2-agonist or methyxanthine

Leukotriene Antagonist AntiAsthmatic

MOA: Cysteinyl-leukotriene receptor antagonist (receptor for LTC4, LTD4, LTE4)

Notes: Prevents aspiring-sensitive & exercise asthma; dec. early and late response to allergen asthma; relax airways in mild asthma; dec. sputum eosinophilia

Use: Add-on therapy for mild-to-moderate asthma not controlled by "as needed" B2 agonist + corticosteroid

AntiAsthmatic

MOA: Inhibits PDE & adenosine receptor; relaxes bronchial SM, dec. mast cell mediator release, inc. mucociliary clearance, prevents microvascular leakage

Anti-Asthmatic

Not a good choice, side effects due to B1 cardiac effects, a-agonistic bronchoconstriction

Muscarinic Antagonist Anti-Asthmatic

MOA: Relaxes bronchoconstriction caused by PS stimulation, particularly in irritant-stimulated asthma; inhibits augmentation of mucus secretion and may inc. mucociliary clearance

Notes: no effect on late phase

Cholinergic Antagonist Anti-Asthmatic

Notes: Similar to ipratropium, but less clinically relevant

Anti-Asthmatic

MOA: Mast cell stabilization via dec. Ca++ influx into cells; inhibition of degranulation, LT production; suppresses release of chemoattractants that recruit eosinophils, neutrophils, & monocytes; reverses inc. receptor expression on leukocytes

Uses: Primarily prophylactic; when administered before challenge inhibits response to exercise, allergens, cold air. Long-term treatment prevents early & late responses to allergens & dec. bronchial responsiveness.

Notes: No bronchodilator or antihistamine activity

B-Agonist Anti-Asthmatic

Note: Long-acting b/c not a COMT substrate; moderately selective B-agonist

Anti-Asthmatic

MOA: 5-Lipoxygenase Inhibitor

Inhibits generation of bronchoconstrictive LTs

Barbituate Anti-Seizure Med

MOA: Enhances binding of GABA to receptors and inc. open time of Cl- channels in presence of synaptically-released GABA

Uses: One of most widely used & effective anti-seizure drugs; 

Generalized & Partial Tonic-Clonic seizures

Metabolism: Up to 25% excreted unchanged; major hepatic metabolite is p-hydroxyphenyl derivative (inactive); HL = 100 hours

Toxicity: Sedation (partial tolerance develops); altered behavior (children: irritability & hyperactivity; elderly: agitation & confusion)

Interactions:

MOA: Slows reactivation of Na+ channels fr. inactivation

Uses: Partial seizures (esp. psychomotor); generalized tonic-clonic

Metabolism: Converted to 10,11 epoxide then to inactive glucuronide; HL = 10-20 hours in chronic therapy; much longer after single dose

Toxicity: More toxic than most anti-seizure drugs; drowsiness, dizziness, ataxia, nausea

Interactions: Induces hepatic drug metabolizing enzymes

Obsolete Barbituate Anti-Seizure Med

MOA: As phenobarbitol

Uses: As phenobarbitol

Metabolism: HL = 5-15 hours, converted to phenobarbitol & phenylethylmalonamide (both active), 40% excreted unchanged

Toxicity: Similar to phenobarbitol but can be more severe when therapy begins; acute feeling of intoxication reported immediately after administration

Interactions: Induces hepatic drug metabolizing enzymes; phenytoin can inc. conversion to phenobarbitol

Anti-Seizure Med

Mechanism: Absence seizures (blocks T-type Ca channels in thalamus); tonic-clonic seizures (dec. reactivation of Na channels which inc. absolute & relative refractory periods of neurons)

Metabolism: Essentially complete; major metabolite is ester glucuronide; HL = 15 hours

Uses: Absence seizures; generalized & partial seizures, myoclonic seizures, atonic seizures

Toxicity: Very low acute toxicity; GI symptoms (n/v, anorexia) common; idiosyncratic hepatotoxicity (fulminant hepatitis, very rare), high doses may inhibit platelet function & produce bruising & gingival bleeding

Interactions: Inhibits hepatic metabolism of phenobarbitol; high degree of plasma protein binding may displace other drugs; can cause absence status epilepticus when given w/ clonazepam (rare)

Anti-Seizure Med

MOA: Slows rate of recovery of Na channels fr. inactivation; inhibitory effects on NMDA Receptor

Uses: Add-on or monotherapy in partial & generalized seizures; only for pts uncontrolled by other agents, withdrawn from general use b/c of risk of aplastic anemia

Metabolism: Metab. by liver; HL = 20 hours

Toxicity: GI disturbances, HA, & insomnia initially; weight loss & anorexia in prolonged use; aplastic anemia, hepatic failure

Benzodiazepine Anti-Seizure Med

MOA: As clonazepam

Uses: Status epilepticus, control seizures induced by local anesthetic injection

Metabolism: HL = 1-2 days; major metab. is N-desmethyl-diazepam

Toxicity: As clonazepam

Anti-Seizure Med

MOA: Lipophilic GABA agonist (inc. promoted release of GABA by unknown mechanism; does not interact w/ GABA Rs, no effect on GABA reuptake or synthesis)

Uses: Primarily add-on drug for control of partial & tonic-clonic that arise from partial seizures

Metabolism: None, excreted in urine unchanged

Toxicity: Very low, few AEs, transient sedation, dizziness, GI disturbances

Interactions: None

Anti-Seizure Med

MOA: Slows rate of recovery of voltage-gated Na channels fr. inactivation; inc. absolute & relative refractory period of neurons

Uses: Broad spectrum; add-on or monotherapy in partial & secondarily generalized tonic-clonic seizures; may be useful in absence seizures

Metabolism: Mainly metab. by glucuronidation; HL = 1 day; dec to 15 hours in presence of phenytoin, carbamazepine or barbituates; inc. to 50 hours in presence of valproic acid

Toxicity: Dizziness, ataxia, blurred/double vision, GI symptoms, rash

Interactions: Rash more prevalent when given w/ valproic acid; use with carbamazepine inc. metabolite which can result in greater toxicity

Anti-Seizure Med

MOA: Slows rate of recovery of inactivated Na channels, enhances GABA activity, blocks action of glutamate

Uses: Add-on therapy for partial seizures; may be of use in generalized tonic-clonic seizures

Metabolism: 50-80% of dose is excrete by kidney unchanged, ~ 20% metabolized; HL = 20-30 hrs

Toxicity: Dizziness, somnolence, ataxia, blurred/double vision, GI disturbance, inc. risk of kidney stones; inhibition of [carbonic anhydrase]

Interactions: Inc. phenytoin concentration by 25%, phenytoin co-admin dec. topiramate by 50%; carbamazepine co-admin dec. topiramate by 40%

Anti-Seizure Med

MOA: Inhibits GAT-1, a GABA reuptake transporter; inc. inhibitory synpatic currents

Uses: Add-on therapy for partial & secondarily generalized tonic-clonic seizures; efficacy for monotherapy is not established

Metabolism: Extensively bound to plasma protein, metab. by CYP3A in liver; HL = 8 hrs; only 2-3 hrs when co-admin w/ enzyme inducing drugs

Toxicity: Mild-to-moderate somnolence, dizziness, tremor; may be CI for absence seizures (facilitates "spike and wave" discharge)

Anti-Seizure Med

MOA: Inhibits T-type Ca channels; prolongs inactivation state of Na channels

Uses: Add-on therapy for partial seizures; small studies suggest possible use in absence seizures & generalized tonic-clonic seizures

Metabolism: 40% bound by plasma protein; 85% excreted as mixture of unchanged & glucuronidated metab

Toxicity: Generally well-tolerated, somnolence, ataxia, anorexia, nervousness, fatigue, maybe renal calculi

Interactions: None known, does not affect metabolism of other anti-seizure meds

Anti-Seizure Med

MOA: Unknown

Uses: Add-on therapy for partial & secondarily generalized tonic-clonic seizures

Metabolism: 65% excreted unchanged, 25% metab. by hydrolysis of acetamide; not a substrate for P450 nor does it induce enzymes

Toxicity: Generally well-tolerated; somnolence, asthenia, dizziness

Interactions: None known

Anti-Alzheimer Drug

MOA: Centrally acting anticholinesterase (compensate for degradation of cholinergic neurons)

Notes: Can be administered orally, only small improvements reported

AEs: Liver toxicity, nausea

Anti-Alzheimer Drug

MOA: Centrally acting anticholinesterase (compensate for degradation of cholinergic neurons)

Notes: Can be administered orally; longer-lasting than tacrine

AEs: Liver toxicity, nausea

Anti-Parkinson

MOA: Immediate precursor of DA (can cross BBB)

Notes: Oral administration improves symptoms rapidly; given in combo w/ decarboxylase inhibitor to decrease peripheral inactivation

AEs: N/V, hypotension, arrhythmias, involuntary movements, hallucinations, paranoia, depressive states

Anti-Parkinson

MOA: Anti-influenza agent, inc. DA by unknown mechanism; may inhibit DA reuptake

Notes: Not as effective as levodopa but less AEs

Anti-Parkinson Drug

Notes: Decarboxylase inhibitor given w/ levodopa to increase potency

Anti-Parkinson Agent

MOA: D2 agonist, semi-synthetic ergot alkaloid

Notes: used as supplement to levodopa & in pts not controlled by levodopa

AEs: N/V, hypotension (avoid in pts taken anti-HTNs), hallucinations

Anti-Parkinson Agent

MOA: MAOb-I, thought to slow down DA degradation thus enhance DAergic influence

Anti-Parkinson Agent

MOA: Ergot derivative; potent D1 & D2 agonist

Anti-Parkinson Agent

MOA: Ergot Derivative; D2 & D3 agonist

MOA: DA antagonist; 1st gen anti-psychotic

Notes: Used to treat symptoms of excessive DA influence (Huntington Chorea)

Anti-Parkinsonian

Uses: Reduce cholinergic influence on indirect pathway

Notes: Anticholinergic

AEs: Similar to other anticholinergics (cycloplegia, constipation, dry mouth, urinary retention)