Drug MOA Indication CI/ADR Others

Benzodiazepines Bind allosteric site on 1) 1st line for seizure and 1) Tolerance Triazolam, alprazolam, midazolam,
-diazepam GABA-A receptor (Cl delirium associated with (downregulation of oxazepam, lorazepam are short
-chlordiazepoxide channel) potentiate alcohol withdrawal (long GABA) acting- more likely to cause physical
-lorazepam GABA-A transmission in acting preferred due to 2) same withdrawal sx as dependence. Preferred in hepatic
-oxazepam CNS  increased self-tapering effects) alcohol withdrawal insufficiency b/c no active
chloride conductance 2) IV benzo for alcohol 3) addiction; CI in pt metabolites.
due to increased Fq of withdrawal management and with drug abusive hx -All are metabolized by liver
ion channel opening  anesthesia 4) dose related -Long acting (diazepam and
inhibits synaptic 3) status epilepticus IV depression chlordiazepoxide) met in liver but
transmission  benzo) 5) drowsiness, impaired form active metabolites which have
depression. 4) general anesthesia (IV judgement, diminished long half lives
benzo)-muscle relaxation motor skills -Benzos do not substitute GABA;
and amnesia 6) dose related they enhance by binding at a
5) IV benzo to induce anterograde amnesia- different site on GABA-A R.
conscious sedation for minor used for conscious -Alcohol binds GABA-A R at a
procedures(colonoscopy) anesthesia (pt separate allosteric site and enhance
(short acting benzos) cooperative during -Chronic alcohol use results in
6) Insomnia (not 1st line) due procedure but amnestic decreased GABA sensitivity and
to dependence afterwards alcohol tolerance need to increase
7) parasomnia in kids (sleep 7) avoid in elderly due to intake to get same effects
walking and night terror increased risk of falls - elderly are more sensitive to ADR
8) spasticity due to UMN (CNS ataxia) of benzos (confusion, somnolence)
disorders (MS, tetanus, 8) CI other depressants
stroke, SC trauma like EtOH, 1st gen anti- Flumazenil- antidote for benzo
9) GAD (2nd line) histamines, barbs, overdose
10)panic disorder (2nd line) neuroleptic)
Flumazenil Competitive antagonist Reverses benzo induced Precipitates withdrawal Antidote for benzo and non-benzo
at BZD receptor sedation following gen seizures in pts using hypnotics
anesthesia, procedural benzo chronically (those
anesthesia or overdose who developed
tolerance)
Non-benzo hypnotics Bind GABA-A R (same 1)for short term treatment 1) risk for fall in older EtOH binds at a different site of
Zolpidem, Zaleplon, portion as benzos) of insomnia (rapid onset and pts(also confusion, GABA A. Barbs bind at a different
Eszopiclone facilitate GABA R short duration)—for pts delirium, agitation, site as well
increase chloride with diff falling asleep not ataxia in old pts) -Zaleplon and zolpidem haveshort
conductance-> maintaining sleep 2) don’t combine with T1/2 (1-2 hrs) are rapidly
depression - Eszopiclone has longest other depressants, metabolized by liver vyp 450
half-life and is effective EtOH, H1 blockers (1st -half life increased in older pts
for both sleep onset and gen), benzos and barbs -Less likely to cause tolerance
maintenance -Less likely to cause withdrawal and
dependence sx
-due to their specificity, they hv less
anxiolytic and anti-convulsive activity
-Antidote- Flumazenil
Ramelteon, Activates Melatonin Insomnia especially in older -no direct effect on GABA receptor
tazemeltion receptors (MT1 and MT2 pts - safe in old pts
in suprachiasmatic -no rebound insomnia, no withdrawal
nucleus of hypothalamus sx
 maintain circadian
rhythm
Barbiturates Bind GABA-A R 1)IV Thiopental- for 1)phenobarb- not 1st line -Longer half life than benzos
-Thiopental-short allosteric site separate induction during rapid b/c causes sedation, hangover effects
acting from benzo and alcohol sequence intubation hypoventilation, -Thiopental rapid onset and short
-Phenobarbital binding sites increased (induction of anesthesia) hypotension duration (lipid soluble)-due to drug
-Primidone flow of chloride and seizure management 2)significant sedation distribution to muscles and fat not
ionsincrease channel Decreases cerebral blood 3)profound cardiac and metabolism
opening duration of Cl flow resp depression, CNS
channel opening 2)Phenobarb- seizures but depression
hyperpolarization not first line in adults 1st 4) always avoid in old
line in neonates. pts. Can cause coma 1)rapid decay in plasma thiopental due
3)Primidone- 1st line along 5) don’t use with other to redistribution
with beta blocker for depressants 2)rapid accumulation of thiopental in
essential tremor. Also tx 6) cause tolerance, brain & redistribution
seizure physical dependence, 3)accumulation of thiop in skm and
withdrawal sx adipose (recovery from anesthesia)

Sedatives
 Anesthetics and Analgesics

Drug MOA Indication CI/ADR Others

Propofol Potentiates chloride IV anesthetic for induction Profound Anesthesia inducing agents are
current through GABA and maintenance vasodilation(arterial and lipophilic
A receptor complex venous) decreased
preload and afterload
-hypotension more
prominent than other
anesthetics
Etomidate Potentiates chloride IV anesthetic for induction -decreases cerebral Alternative to propofol
current through GABA Use in pts with compromised blood flow cerebral Preserves CVS stability after
A receptor myocardial contractility hypoxic injury injection
Minimal changes to CVS

Ketamine Inhibits NMDA -IV anesthetic for induction Hallucinations-vivid Analgesia, bronchodilation, minimal
receptor complex -Dissociative anesthesia- colorful dreams, out of resp depression
eyes open with slow body experience, -sympathomimetic
nystagmic gaze euphoria -increases cerebral blood flow
-useful for mentally Sig increase in BP, HR - Drugs for induction of
challenged and and CO due to SNS anestheis
uncooperative pediatric pts stimulation  increased 1. Propofol
contractility and HR 2. Etomidate
3. Ketamine
4. Benzo (midazolam)
5. Barb (thiopental)

Inhaled Anesthetics

Drug MOA Indication ADR others

N2O (Nitrous Oxide) gaseous anesthetics To deepen anesthesia CVS- myocardial -taken up via gas exchange b/n alveoli
depressiondecreased and capillaries
CO and increase in -less soluble (low partition
arterial and ventricular coefficient) in bloodfaster
pressures. saturation of blood with the
-NOT respiratory anestheticfaster onset and faster
depressant recovery. Low potency

Volatile anesthetics unknown General anesthesia -CVS- myocardial -are fluorinated

-Enflurane depressiondecreased -taken up by gas exchange
- Isoflurane CO and increase in -Highly soluble in blooddelayed
-Halothane arterial and ventricular saturationslower onset
-Methoxyflurane pressures. -highly soluble (more gas partition
-decrease in CO coefficient) easily
hypotension in volatile absorbedlarger amount must be
anesthetics absorbed before blood becomes
-All inhaled anesthetics saturatedslower onset and slower
except N2O are resp recovery AND longer duration, high
depressantsdecrease potency
TV, Minute ventilation
and hypercapnia,
suppress mucocilliary
clearancepost-op MAC (Minimal Alveolar concentration)
atelectasis Percentage of anesthetics in the
-decrease vascular inspired gas mixture that renders
resistanceincreased 50% of pts unresponsive to painful
cerebral blood flow stimuli. Corresponds to ED50.
increased ICP -Potency is inversely proportional to
-Halothane- severe MAC. Low MAC increased potency
 liver damage including - Malignant hyperthermia- - due to
hep necrosis (presents defect in Ryanodine receptors in SR
2 days to 4 wks after of SKM. RyR are on surface of SR
exposure)-increased and act as Ca channels during
LFT, tenderness muscle contraction. Abnormal RyR
LM- centrilobular release large amount of Ca after
necrosis exposure to anesthetics+ ATP
Enflurane- nephrotoxic dependent reuptake by SR. Excessive
and seizure consumption of ATPheatloss of
-Malignant hyperthermia ATP and increased heatmuscle
(MH)- AD disorder due damagerhabdomyolysis. Increased
to hypersensitivity of K, CK, myoglobin
SKM to volatile - fever and muscle rigidity
anesthetics. Only (contraction) after surgery under gen
occurs with volatile anesthesia, tachycardia, HTN
anesthetics (not N2O). Tx with Dantrolene- blocks
Succinylcholine also RyRprevents further release of Ca
causes MH. into cytoplasm of muscle fibers
Methoxyflurane-
nephrotoxic

Anti-Epileptics- broad spec

Drug MOA Indication ADR Others

VA 1)Binds inactivated vol Focal and generalized GI distress(N+V)
(broad spec) gated Na seizures Appetite increase and
channelsprevents Juvenile myoclonic epilepsy weight gain
sustained firing of AP (type of generalized) fatal hepatotoxicity
2)inhibits GABA Migraine prophylaxis
transaminaseincrease Absence
GABA conc
Topiramate Blocks Na channel and Focal seizure and tonic- Somnolence and fatigue
(broad spec) increased GABA by clonic (generalized) (dose related)
directly binding GABA A Juvenile myoclonic Confusion and cognitive
receptor slowing, weight loss
Kidney stone, acute
myopia and acute angle
closure glaucoma
Lamotrigine Blocks voltage gated Na Focal, tonic clonic, absence 10% benign Skin rash
(broad spec) channels , inhibits 1% life threatening SJS
release of or TEN
diplopia
Levetiracetam 1)SV2A receptor blocker Partial and tonic clonic and Somnolence
(broad spec) 2)Modulates GABA and juvenile myoclonic Neuropsych
glutamate release sx(personality change)
directly
3)Inhibit vol gates Ca
channels

Anti-epileptics- narrow spec

Drug MOA Indication ADR Others

Carbamazepine Blocks vol dependent Na 1)Focal seizures 1)diplopia and ataxia Avoid in absence and juvenile or other
(narrow) channels after they 2)trigeminal neuralgia (v2 2)SIADH due to generalized seizures.
changed from activated and V3) increased -P450 inducer
to inactivated responsiveness of CD to
stateextends the ADHdose related
inactivated hyponatremia
stateblocks sustained 3)Leukopenia in 12%
high fq of neurons 4)SLE
 4)Aplastic anemia and
agranulocytosis
4)drug rxn with
eosinophilia and DRESS
syndrome (after 8 wks,
fever, gen
lymphadenopathy, facial
edema, diffue skin rash
5)teratogen (NTD) spina
bifida
6)SJS and TEN during
first 8 wks- more
common in HLA B1502 in
Asians
Phenytoin Blocks sodium channels 1)focal seizure 1)ataxia, diplopia, Avoid in absence and other generalized
prolongs inactivation of 2)status epilepticus nystagmus like JME
Na channels 2)meg anemia Zero order kinetics
3)gingival -Status epilepticus: single episode of
hyperplasia(increased seizure with LOC for more than 30 min
expression of PDGF) OR series of seizures within 30 min
Hirsutism w/o gaining consciousness
4)drug induced SLE Now- it is seizure for more than a few
5) Dress syndrome and min w/o gaining consciousness in b/n
eosinophilia Give IV benzo then phenytoin for
6) SJS/TEN first 8 wks maintenance . If pt not responding to
Asian pt HLA B1502 phenytoin start IV phenobarb
7)teratogenic
8)CYP inducer
9)decreased bone
density
Gabapentin Inhibit voltage gated Ca Refractory focal seizure Dose dependent Does not bind GABA receptors
pregabalin channel inward Ca add ons dizziness, sedation and
current Neuropathic pain including ataxia more common in
diabetic neuropathy and elderly
postherpetic neuralgia
fibromyalgia
Vigabatrin Irreversibly inhibit Adjunct for focal seizures Permanent visual loss
GABA
transaminasesincrease
in GABA due to
decreased degradation
Tiagabine Inhibits GABA Adjunct for focal seizures
uptakeprolonging
synaptic GABA
Ethosuximide Blocks T-type Ca Gi distress Absence seizures are visible on EEG
channels in thalamic Lethargy or fatigue 3 Hz spike wave complex on EEG
nucelus -VA also effective
-pt with absence seizure and
occasional tonic clonic , tx with VA