FERNANDEZ, KRISTELLE LOUISE I. Mr. Renovo A.

Mirador
BSN 2-Y1-IRR 1 March 28, 2021

Course Task 7
Make a drug study of Drugs for CNS for each drug class using the format below:

Central Nervous System (CNS) Depressants

CLASSIFICATIONS DRUGS PHARMACODYNAMICS PHARMACOKINETICS INDICATIONS SIDE EFFECTS INTERACTIONS NURSING CONSIDERATIONS
SEDATIVES AND Pentobarbital Pentobarbital, a barbiturate, is used Half-Life: 15-50 hr A barbiturate mainly used as a sedative Drowsiness, somnolence, dizziness, Pentobarbital has no known - Monitor V/S. report
HYPNOTICS for the treatment of short term and hypnotic. It has been suggested anxiety, insomnia; hypotension, severe interactions with other irregularities
insomnia. It belongs to a group of Onset: 10-15 min (IM); 3-5 min (IV) that its pharmacologic effect is due to apnoea, resp depression, drugs. Severe interactions of - Observe for withdrawal
medicines called central nervous its property to enhance the activity of bronchospasm, laryngospasm, pentobarbital include: symptoms (N and V,
system (CNS) depressants that induce Duration: 3-4 hr GABA by altering GABA receptor- bradycardia, CNS depression, artemether/lumefantrine. weakness, and headache)
drowsiness and relieve tension or mediated inhibitory synaptic physical and psychological - Monitor for side effects
nervousness. Little analgesia is Protein bound: 45-70% transmissions. dependence, psychiatric - Avoid alcohol consumption
conferred by barbiturates; their use in disturbance, confusion, - Advise not to drive and use
the presence of pain may result in Vd: 0.8 L/kg (children); 1 L/kg (adults) hallucinations, nightmares, hazardous equipment when
excitation. thinking abnormality, syncope, experiencing palpitation,
Metabolism: hepatic microsomal hyperkinesias, ataxia, agitation, nervousness, tremors
enzymes, glucuronidation nervousness, nausea, vomiting, - Instruct client not to
constipation, pain at inj site. discontinue the drug abruptly
Excretion: Mostly urine Potentially Fatal: Stevens-Johnson - Advise not to eat foods with
syndrome. caffeine
- Instruct to eat nutritious
food because drug may cause
anorexic effect
- Teach to report drug side
effects such as tachycardia
and palpitations

ANALGESICS Codeine Codeine is a weak narcotic pain
reliever and cough suppressant that is
similar to morphine and hydrocodone.
A small amount of ingested codeine is
converted to morphine in the body.
Codeine increases tolerance to pain,
reducing existing discomfort. In
addition to decreasing pain, codeine
also causes sedation, drowsiness, and
respiratory depression.
Absorption
Onset: 30-60 min (PO); 10-30 min (IM) pain threshold, alters pain reception
Duration: 4-6 hr
Peak plasma time: 0.5-1 hr
Distribution
Protein bound: 25%
Vd: 3.5 L/kg (PO); 2.6 L/kg (IM)
Metabolism
Prodrug metabolized to morphine by
CYP2D6; demethylated/conjugated in
liver (undergoes O-demethylation, N-
demethylation, and partial
conjugation with glucuronic acid)
Elimination
Half-life: 3-4 hr
a potent opioid analgesic that increases
and inhibits ascending pain pathways
by binding to stereospecific receptors
w/in the CNS.
Reduce pulmonary compliance
and/or apnoea,
bronchoconstriction,
laryngospasm; nausea, vomiting;
bradycardia, oedema, CNS
depression, confusion, dizziness,
drowsiness, headache, sedation,
hypotension, peripheral
vasodilation, increased intracranial
pressure, itching, rash, erythema,
papules, pruritus, exfoliative
dermatitis, pustules, macular rash;
gum bleeding and irritation, taste
perversion, dental caries, tooth
loss, gum line erosion; throat
irritation, nasal ulcers, epistaxis,
rhinorrhoea; coughing; urinary
retention.
Potentially Fatal: Resp depression.
artemether/lumefantrine - Monitor V/S. report
cariprazine irregularities
cobimetinib - Observe for withdrawal
dienogest/estradiol valerate symptoms (N and V,
doravirine weakness, and headache)
elbasvir/grazoprevir - Monitor for side effects
fostemsavir - Avoid alcohol consumption
lonafarnib - Advise not to drive and use
lorlatinib hazardous equipment when
lumacaftor/ivacaftor experiencing palpitation,
lumefantrine nervousness, tremors
lurasidone - Instruct client not to
naloxegol discontinue the drug abruptly
ombitasvir/paritaprevir/ritonavir - Advise not to eat foods with
& dasabuvir caffeine
panobinostat - Instruct to eat nutritious
praziquantel food because drug may cause
regorafenib anorexic effect
roflumilast - Teach to report drug side
vandetanib effects such as tachycardia
and palpitations

Excretion: Urine, feces

ANTI- Phenobarbital Depresses sensory and motor cortex, Absorption A long-acting barbiturate. It depresses Bradycardia, syncope, hypotension; artemether/lumefantrine - Monitor V/S. report
CONVULSANTS cerebellum Bioavailability: 70-90% the sensory cortex, reduces motor anxiety, agitation, ataxia, CNS atazanavir irregularities
activity, changes cerebellar function excitation or depression, cabotegravir - Observe for withdrawal
Antiseizure activity occurs primarily Onset: 5 min (IV) and produces drowsiness, sedation and confusion, dizziness, drowsiness, calcium/magnesium/potassium/s symptoms (N and V,
where GABA mediates hypnosis. Its anticonvulsant property is hallucinations, hangover effect, odium oxybates weakness, and headache)
 neurotransmission Duration: 4-6 hr (IV/IM)
Hypnotic effects of barbiturates result Peak plasma time: 8-12 hr
from activity at GABA receptor in the
polysynaptic midbrain reticular Therapeutic plasma concentration:
formation (controls CNS arousal) 10-40 mcg/mL; may require 3-4 weeks
of treatment to achieve therapeutic
Off-label use for hyperbilirubinemia: levels
Phenobarbital induces glucuronyl
transferase and hepatic bilirubin- Distribution
binding Y-protein to lower serum Protein bound: 20-45%
bilirubin concentrations
Metabolism
Metabolized by hepatic oxidative
hydroxylation
Metabolites: Inactive
Enzymes induced: CYP1A2, CYP2B6,
CYP2C19, CYP2C9/10, CYP3A4
Elimination
Half-life: 50-140 hr
Excretion: Urine (major)
ANTI- Chlorpromazine Phenothiazine; antagonizes dopamine Absorption
PSYCHOTICS D2 receptors in brain; depresses Bioavailability: 20%; extensive 1st-
release of hypothalamic and pass metabolism
hypophyseal hormones; may also
depress reticular activating system Onset: 30-60 min
Duration: 4-6 hr; extended release,
10-12 hr
Distribution
Protein bound: 92-97%
Vd: 20 L/kg
Metabolism
Metabolized by hepatic P450 enzyme
CYP2D6
Metabolites: 10-12 different
compounds
Elimination
Half-life: 30 hr
exhibited at high doses.
A neuroleptic that acts by blocking the
postsynaptic dopamine receptor in the
mesolimbic dopaminergic system and
inhibits the release of hypothalamic
and hypophyseal hormones. It has
antiemetic, serotonin-blocking, and
weak antihistaminic properties and
slight ganglion-blocking activity.
headache, hyperkinesias; cariprazine
constipation, nausea, vomiting; cobimetinib
agranulocytosis, darunavir
thrombocytopenia, megaloblastic dienogest/estradiol valerate
anaemia; oliguria; pain at inj site, doravirine
thrombophlebitis (w/ IV use); elbasvir/grazoprevir
laryngospasm, resp depression, elvitegravir/cobicistat/emtricitabi
apnoea (esp w/ rapid IV use), ne/tenofovir DF
hypoventilation; gangrene (w/ etravirine
unintentional intra-arterial inj). fostemsavir
Potentially Fatal: Stevens-Johnson ledipasvir/sofosbuvir
syndrome, toxic epidermal lonafarnib
necrolysis. lorlatinib
lumacaftor/ivacaftor
lumefantrine
lurasidone
naloxegol
ombitasvir/paritaprevir/ritonavir
& dasabuvir
panobinostat
pirfenidone
praziquantel
regorafenib
rilpivirine
roflumilast
sodium oxybate
vandetanib
voriconazole
Tardive dyskinesia (on long-term disopyramide
therapy). Involuntary movements eliglustat
of extremities may also occur. Dry ibutilide
mouth, constipation, urinary indapamide
retention, mydriasis, agitation, metrizamide
insomnia, depression and pentamidine
convulsions; postural hypotension, pimozide
ECG changes. Allergic skin reaction, procainamide
amenorrhoea, gynaecomastia, quinidine
weight gain. Hyperglycaemia and sotalol
raised serum cholesterol.
Potentially Fatal: Agranulocytosis.
Instantaneous deaths associated
with ventricular tachyarrhythmias.
Marked elevation of body
temperature with heat stroke.
Neuroleptic malignant syndrome,
extrapyramidal dysfunction.
- Monitor for side effects
- Avoid alcohol consumption
- Advise not to drive and use
hazardous equipment when
experiencing palpitation,
nervousness, tremors
- Instruct client not to
discontinue the drug abruptly
- Advise not to eat foods with
caffeine
- Instruct to eat nutritious
food because drug may cause
anorexic effect
- Teach to report drug side
effects such as tachycardia
and palpitations
- Monitor V/S. report
irregularities
- Observe for withdrawal
symptoms (N and V,
weakness, and headache)
- Monitor for side effects
- Avoid alcohol consumption
- Advise not to drive and use
hazardous equipment when
experiencing palpitation,
nervousness, tremors
- Instruct client not to
discontinue the drug abruptly
- Advise not to eat foods with
caffeine
- Instruct to eat nutritious
food because drug may cause
anorexic effect
- Teach to report drug side
effects such as tachycardia
and palpitations

Excretion: Urine
ANTI- Amitriptyline Neurotransmitter (especially Absorption Adibenzocycloheptadiene tricyclic Significant: Serotonin syndrome disopyramide - Monitor V/S. report
DEPRESSANTS norepinephrine and serotonin) Peak serum time: 4 hr antidepressant. It inhibits the neuronal e.g. CNS depression, bone dronedarone irregularities
reuptake inhibitor; anticholinergic reuptake of serotonin (5-HT) and/or fractures, bone marrow ibutilide - Observe for withdrawal
Metabolism norepinephrine by the presynaptic suppression, mild pupillary indapamide symptoms (N and V,
Metabolized by hepatic CYP2C19, neuronal membrane, hence increasing dilation, orthostatic hypotension, iobenguane I 123 weakness, and headache)
 CYP3A4 the synaptic concentration in the CNS. QT interval prolongation. isocarboxazid - Monitor for side effects
It also possesses affinity for muscarinic Blood and lymphatic system pentamidine - Avoid alcohol consumption
Metabolites: Nortriptyline and histamine (H1) receptors to varying disorders: Agranulocytosis, phenelzine - Advise not to drive and use
degrees. leukopenia, thrombocytopenia, pimozide hazardous equipment when
Elimination purpura, eosinophilia. procainamide experiencing palpitation,
Half-life: 9-27 hr Cardiac disorders: MI, heart block, procarbazine nervousness, tremors
arrythmias, tachycardia, quinidine - Instruct client not to
Excretion: Urine (18%), small amounts palpitation. safinamide discontinue the drug abruptly
in feces Ear and labyrinth disorders: selegiline - Advise not to eat foods with
Tinnitus. sotalol caffeine
Eye disorders: Mydriasis, blurred tranylcypromine - Instruct to eat nutritious
vision, increased intraocular food because drug may cause
pressure, accommodation disorder. anorexic effect
Gastrointestinal disorders: Dry - Teach to report drug side
mouth, constipation, nausea, effects such as tachycardia
epigastric distress, vomiting, and palpitations
anorexia, stomatitis, peculiar taste,
diarrhoea, parotid swelling, black
tongue.
General disorders and
administration site conditions:
Fever, hyperthermia, ataxia.
Investigations: Increase or
decrease of blood sugar, weight
gain or loss.
Metabolism and nutrition
disorders: Oedema.
Nervous system disorders:
Headache, seizures,
incoordination, tremors, peripheral
neuropathy, numbness,
paraesthesia, extrapyramidal
symptoms (e.g. speech difficulties),
involuntary movements, tardive
dyskinesia, disturbed
concentration, excitement,
insomnia, stroke, restlessness,
drowsiness, agitation, dysgeusia.
Psychiatric disorders: Confusional
states, hallucinations,
disorientation, delusions,
nightmares, dysarthria, anxiety,
delirium, hypomania, mania.
Renal and urinary disorders:
Urinary retention, frequency.
Reproductive system and breast
disorders: Testicular swelling,
gynecomastia, breast enlargement,
galactorrhea, libido decreased,
impotence.
Skin and subcutaneous tissue
disorders: Rash, urticaria,
photosensitivity, alopecia.
Vascular disorders: Syncope,
hypertension, hypotension.
Central Nervous System (CNS) Stimulants

ANALEPTICS Doxapram Produces respiratory stimulation in Onset: 20-40 sec Doxapram stimulates respiration Significant: Dysrrhythmias, seizure, benzphetamine - Monitor V/S. report
medulla (which propagates through action on peripheral carotid HTN or hypotension, dyspnoea. desflurane irregularities
 stimulation to other parts of brain & Duration: 5-12 min (single IV chemoreceptors. It also directly Nervous: Confusion, convulsions, dexfenfluramine - Observe for withdrawal
spinal cord) through peripheral injection) stimulates the central respiratory dizziness, hallucinations, headache, dexmethylphenidate symptoms (N and V,
carotid chemoreceptors center in medulla w/ progressive hyperactivity. dextroamphetamine weakness, and headache)
Peak Plasma Time: 1-2 min stimulation of other parts of the brain GI: Diarrhoea, nausea, vomiting. diethylpropion - Monitor for side effects
and spinal cord at higher doses. Resp: Bronchospasm, cough, dobutamine - Avoid alcohol consumption
Half-life: 3.4 hr (2.4-4.1 hr) hiccup, laryngospasm, dopamine - Advise not to drive and use
hyperventilation, rebound ephedrine hazardous equipment when
hypoventilation. epinephrine experiencing palpitation,
Genitourinary: Urinary retention, etomidate nervousness, tremors
urinary bladder stimulation w/ fenfluramine - Instruct client not to
spontaneous voiding. isocarboxazid discontinue the drug abruptly
Musculoskeletal: Muscle isoproterenol - Advise not to eat foods with
fasciculation or spasticity. ketamine caffeine
Dermatologic: Flushing, sweating, linezolid - Instruct to eat nutritious
warm sensation. lisdexamfetamine food because drug may cause
Others: Fever. methamphetamine anorexic effect
methylenedioxymethamphetami - Teach to report drug side
ne effects such as tachycardia
methylphenidate and palpitations
midodrine
norepinephrine
phendimetrazine
phenelzine
phentermine
phenylephrine
phenylephrine PO
propofol
propylhexedrine
pseudoephedrine
sevoflurane
tranylcypromine
xylometazoline
yohimbine
PSYCHOMOTOR amphetamine Sympathomimetic amine that Absorption This combination medication is used to Loss of appetite amphetamine and - Monitor V/S. report
STIMULANTS and promotes release of dopamine and Well absorbed treat attention deficit hyperactivity Headache dextroamphetamine has no irregularities
dextroampheta norepinephrine from their storage disorder - ADHD. It works by changing Insomnia known severe interactions with - Observe for withdrawal
mine sites in the presynaptic nerve Onset of action: 30-60 min the amounts of certain natural Abdominal pain other drugs symptoms (N and V,
terminals; may also block reuptake of substances in the brain. Weight loss weakness, and headache)
catecholamines by competitive Duration: 4-6 hr Anxiety - Monitor for side effects
inhibition Vomiting Nervousness - Avoid alcohol consumption
Vd: 3.5-4.6 L/kg (distributes into CNS; Tachycardia - Advise not to drive and use
mean CSF concentrations are 80% of Fever hazardous equipment when
plasma) Nausea experiencing palpitation,
Infection nervousness, tremors
Peak plasma time: 3 hr (Adderall); 7 hr Emotional lability - Instruct client not to
(Adderall XR) Dizziness discontinue the drug abruptly
Diarrhea - Advise not to eat foods with
Metabolism Fatigue caffeine
Hepatic via glucuronidation and Dry mouth - Instruct to eat nutritious
CYP450 mono-oxygenase Dyspepsia food because drug may cause
anorexic effect
Elimination - Teach to report drug side
Half-life elimination (children) effects such as tachycardia
6-12 years: 9 hr (d-amphetamine); 11 and palpitations
hr (l-amphetamine)
12-18 years: 11 hr (d-amphetamine);
13-14 hr (l-amphetamine)
Half-life elimination (adults)
 d-amphetamine: 10 hr
l-amphetamine: 13 hr
Excretion
Urine; dependent on urinary pH
METHYLXANTHI theophylline Theophylline relaxes smooth muscles Absorption Theophylline is indicated for the Peak serum concentration <20 dipyridamole - Monitor V/S. report
NES of respiratory tract and suppresses Onset: Variable treatment of the symptoms and mcg/mL febuxostat irregularities
STIMULANTS the response of the airways to stimuli reversible airflow obstruction Central nervous system riociguat - Observe for withdrawal
Duration: Variable associated with chronic asthma and excitement, headache, insomnia, symptoms (N and V,
May increase tissue concentration of other chronic lung diseases, e.g., irritability, restlessness, seizure weakness, and headache)
cyclic adenine monophosphate Peak plasma time: 1-2 hr emphysema and chronic bronchitis. Diarrhea, nausea, vomiting - Monitor for side effects
(cAMP) by inhibiting 2 isoenzymes of Diuresis (transient) - Avoid alcohol consumption
phosphodiesterase (PDE III and, to a Peak plasma concentration: 10 Exfoliative dermatitis - Advise not to drive and use
lesser extent, PDE IV), which mcg/mL Skeletal muscle tremors hazardous equipment when
ultimately induces release of Tachycardia, flutter experiencing palpitation,
epinephrine from the adrenal medulla Distribution Hypercalcemia (with concomitant nervousness, tremors
cells Protein bound: 40-55% hyperthyroid disease) - Instruct client not to
Difficulty urinating (elderly males discontinue the drug abruptly
Vd: 0.3-0.7 L/kg with prostatism) - Advise not to eat foods with
Peak serum concentration >30 caffeine
Metabolism mcg/mL - Instruct to eat nutritious
Metabolized in liver by CYP1A2 and Acute myocardial infarction food because drug may cause
CYP3A4 Seizures (resistant to anorexic effect
anticonvulsants) - Teach to report drug side
Metabolites: 1,3-Dimethyluric acid, 1- Urinary retention effects such as tachycardia
methyluric acid, 3-methylxanthine and palpitations

Elimination
Half-life: Nonsmoker, 8 hr; smoker, 4-5
hr

Clearance: 1.45 mL/min/kg

Excretion: Urine
CENTRAL NERVOUS SYSTEM (CNS) HALLUCINOGENS

DELIRIANTS. Diphenhydrami Histamine H1-receptor antagonist of Absorption
ne effector cells in respiratory tract, Bioavailability: PO, 42-62% (drug is
blood vessels, and GI smooth muscle well absorbed but undergoes first-
pass metabolism)
Moderate to high anticholinergic and
antiemetic properties Onset: 15-30 min
Duration: ≤12 hr (histamine-induced
flare suppression); ≤10 hr (histamine-
induced wheal suppression)
Peak serum time: 2 hr (PO)
Distribution
Protein bound: 98.5%
Vd: 22 L/kg (Children); 17 L/kg
(adults); 14 L/kg (elderly)
Metabolism
Metabolized by liver (first-pass)
Elimination
Diphenhydramine is an antihistamine
used to relieve symptoms of allergy, hay
fever, and the common cold. These
symptoms include rash, itching, watery
eyes, itchy eyes/nose/throat, cough,
runny nose, and sneezing. It is also used
to prevent and treat nausea, vomiting
and dizziness caused by motion
sickness.
Frequency Not Defined eliglustat Assessment
Sedation History: Allergy to any
antihistamines, narrow-angle
Confusion glaucoma, stenosing peptic
ulcer, symptomatic prostatic
Anticholinergic effects hypertrophy, asthmatic
attack, bladder neck
May decrease cognitive function in obstruction, pyloroduodenal
geriatric patients obstruction, third trimester
of pregnancy, lactation
Xerostomia Physical: Skin color, lesions,
texture; orientation, reflexes,
Dry nasal mucosa affect; vision examination; P,
BP; R, adventitious sounds;
Pharyngeal dryness bowel sounds; prostate
palpation; CBC with
Thick bronchial sputum differential
Agranulocytosis Interventions
Administer with food if GI
Hemolytic anemia upset occurs.
Administer syrup form if
Thrombocytopenia patient is unable to take

DISSOCIATIVES ketamine Produces dissociative anesthesia
Blocks NMDA receptor
Overdose may lead to panic attacks (IM): dissociative state may last >20
and aggressive behavior; rarely min
seizures, increased ICP, and cardiac
arrest
Very similar in chemical makeup to
PCP (phencyclidine), but it is shorter Metabolism
acting and less toxic
Half-life: 5 hr (children); 9 hr (adults); tablets.
13.5 hr (elderly) Convulsions Monitor patient response,
and arrange for adjustment
Excretion: Urine (50-75%), mainly as Tachycardia of dosage to lowest possible
metabolites effective dose.
Hypotension
Teaching points
Nervousness Take as prescribed; avoid
excessive dosage.
Restlessness Take with food if GI upset
occurs.
Blurred vision Avoid alcohol; serious
sedation could occur.
Palpitations These side effects may occur:
Dizziness, sedation,
Constipation drowsiness (use caution
driving or performing tasks
Vertigo requiring alertness);
epigastric distress, diarrhea
Menstrual irregularities or constipation (take drug
with meals); dry mouth (use
Euphoria frequent mouth care, suck
sugarless lozenges);
Anorexia thickening of bronchial
secretions, dryness of nasal
Urinary retention mucosa (use a humidifier).
Report difficulty breathing,
Neuritis hallucinations, tremors, loss
of coordination, unusual
Diplopia bleeding or bruising, visual
disturbances, irregular
Tinnitus heartbeat.
Absorption Anesthesia-induction and maintenance Emergence rxns ketamine has no known severe Monitor patient response to
Onset: 30 sec (IV); 3-4 min (IM) Analgesic for procedure interactions with other drugs therapy (analgesia, loss of
HTN consciousness).
Duration: 5-10 min (IV); 12-25 min Monitor for adverse effects
Increased cardiac output (e.g. respiratory depression,
hypotension, bronchospasm,
Increased ICP skin breakdown, etc).
Peak plasma concentration: 0.75 Evaluate patient
mcg/mL Tachycardia understanding on drug
therapy by asking patient to
Tonic-clonic movements name the drug, its indication,
Liver and adverse effects to watch
Visual hallucinations for.
Elimination Monitor patient compliance
Excretion: Urine (91%), feces (3%) Vivid dreams to drug therapy.
Bradycardia
Diplopia
Hypotension
Increased IOP
Injection-site pain

CENTRAL NERVOUS SYSTEM (CNS) DISSOCIATIVE ANESTHETICS
DISSOCIATIVE Dextromethorp Nonnarcotic derivative of levorphanol.
Absorption
ANESTHETICS han (DXM) Chemically related to morphine but
without central hypnotic or analgesic Onset: 15-30 min
effect or capacity to cause tolerance Duration: ≤6 hr
or addiction. Antitussive activity Time to peak: 2-3hr
comparable to that of codeine but is
Metabolism
less likely than codeine to cause
constipation, drowsiness, or GI Hepatic P450 enzyme CYP2D6
disturbances.
Elimination
Half-life: 2-4hr (extensive
metabolizers); 24 hr (poor
metabolizers)
Excretion: Urine
DISSOCIATIVE Phencyclidine Phencyclidine works primarily as an The N-methyl-D-Aspartate (NMDA)
ANESTHETICS (PCP) NMDA receptor antagonist, which receptor, a type of ionotropic
blocks the activity of the NMDA receptor, is found on the dendrites of
Receptor. neurons and receives signals in the
form of neurotransmitters. It is a
major excitatory receptor in the brain.
Normal physiological function
requires that the activated receptor
fluxes positive ions through the
channel part of the receptor. PCP
enters the ion channel from the
outside of the neuron and binds,
reversibly, to a site in the channel
pore, blocking the flux of positive ions
into the cell. PCP therefore inhibits
depolarization of neurons and
interferes with cognitive and other
functions of the nervous system.
Nystagmus
Anaphylaxis
Cardiac arrhythmia
Depressed cough reflex
Fasciculations
Hypersalivation
Increased IOP
Increased metabolic rate
Hypertonia
Laryngospasm
Respiratory depression or apnea
with large doses or rapid infusions
Dextromethorphan is used to Nausea High risk of excitation,
temporarily relieve cough caused by the Vomiting hypotension, and hyperpyrexia Monitor for dizziness and
common cold, the flu, or other Constipation with MAO INHIBITORS. drowsiness, especially when
conditions. Dextromethorphan will Drowsiness concurrent therapy with CNS
relieve a cough but will not treat the Dizziness depressant is used.
cause of the cough or speed recovery. Sedation
Dextromethorphan is in a class of Confusion
medications called antitussives. It works Nervousness
by decreasing activity in the part of the
brain that causes coughing.
PCP is also known as a dissociative Avoid taking with
drug. It causes you to feel separated  euphoria apraclonidine ophthalmic, Monitor for dizziness and
from your body and surroundings. brexanolone drowsiness, especially when
 sound, image and body concurrent therapy with CNS
, brimonidine ophthalmic depressant is used.
distortion
brimonidine topical
 depersonalization or esketamine
flibanserin
feelings of detachment
ioflupane I 123
 loss of balance and lasmiditan
coordination
 loss of sensation and
inability to feel pain
 acute anxiety, agitation,
and mood swings
  feelings of impending doom

 numbness in the arms and

legs

CENTRAL NERVOUS SYSTEM (CNS) NARCOTIC ANALGESICS

NARCOTIC Opium Description: Opium, obtained from Adverse Reactions
Hypersensitivity. Convulsion (e.g. status epilepticus, Maydiarrhoea
tetanus, strychnine poisoning), cause increased CNS or
ANALGESICS dried latex of unripe Papaver caused by poisoning. Concomitant or within Significant:
14 days ofDrug
MAOIdependence,
use. respiratory depression with  Assess for
somniferum capsules, contains apnoea, hypotension. other narcotic analgesics, general mentioned
morphine, codeine, thebaine and Eye disorders:Miosis. anaesthetics, sedative/hypnotics, cautions and
other alkaloids (e.g. noscapine, Gastrointestinal disorders: Nausea, antihistamines, phenothiazines, contraindications
papaverine). The pharmacologic effect vomiting, constipation, dry mouth. or other CNS depressants. May (e.g. drug allergy,
of opium is mainly due to the General disorders and cause decreased effect or respiratory
morphine content. As an administration site increased withdrawal symptoms dysfunction,
antidiarrhoeal, morphine increases conditions: Asthenia. with other morphine myocardial
gastrointestinal muscle tone and Immune system agonists/antagonist (e.g. infarction and
decreases peristalsis, thereby disorders: Urticaria. buprenorphine, nalbuphine, CAD, hepatorenal
decreasing gastrointestinal Metabolism and nutrition pentazocine). Decreased effect dysfunction, etc.)
propulsion. Morphine is used in disorders: Anorexia. with CYP3A4 inducer (e.g. to prevent
combination with belladonna in Nervous system rifampicin). Increased toxicity of untoward
suppositories for its analgesic effect. It disorders: Lightheadedness, squill with concomitant diuretics. complications.
is also used in combination with squill dizziness, drowsiness, sedation. Potentially Fatal: May cause
 Conduct pain
in cough preparations as it directly Psychiatric disorders:Confusion, serotonin syndrome if used with
assessment with
depresses the cough reflex. euphoria, dysphoria. MAOIs.
patient to establish
Duration: Antidiarrhoeal effect: 3-4 Renal and urinary
baseline and
hours. disorders:Urinary retention.
evaluate
Pharmacokinetics: Respiratory, thoracic and
effectiveness of
Absorption: Variably absorbed from mediastinal
drug therapy.
the gastrointestinal tract. disorders: Bronchospasms.
Distribution: Crosses the placenta and Skin and subcutaneous tissue  Perform thorough
enters breast milk. disorders: Pruritus. physical (CNS, vital
Metabolism: Morphine is metabolised Vascular disorders: Flushing. signs, bowel
in the liver via glucuronidation at the Potentially Fatal:Severe respiratory sounds, urine
3-hydroxyl group; further metabolised depression; increased intracranial output) to
via glucuronidation at the 6-hydroxyl pressure. establish baseline
group into morphine-3,6- status before
diglucuronide. beginning therapy,
Excretion: Via urine (approx 75%; determine drug
mainly as morphine-3-glucuronide, effectiveness and
morphine-3,6-diglucuronide and evaluate for any
unchanged drug). potential adverse
effects.
 Monitor laboratory
results (liver
function, kidney
function) to
determine need
for possible dose
adjustment and
identify toxic drug
effects.

NARCOTIC Morphine As morphine sulfate: Dosage is Pharmacokinetics: Indications and Dosage Adverse Reactions Drug Interactions
ANALGESICS individualised based on the severity of Absorption: Well absorbed from the Intraspinal Significant: CNS depression, Increased depressant effects  Assess for
pain, patient response and prior gastrointestinal tract (oral) and into Moderate to severe pain orthostatic hypotension, severe with other CNS depressants (e.g. mentioned
analgesic experience. Initially, 5 mg the blood (SC/IM). Increased hypotension,
Adult: As morphine sulfate: Dosage is individualised syncope
based on theconstipation. sedatives,
severity of pain, patient hypnotics, general cautions and
epidural inj, if desired pain relief is not bioavailability with food. response and prior analgesic experience. Initially, 5 mg epidural inj, if desired pain relief is notphenothiazines,
Blood and lymphatic system anaesthesia, contraindications
achieved within 1 hour, incremental
doses of 1-2 mg may be given up to 10 peak plasma concentration: 1 hour
mg/24 hour.
Bioavailability: 17-33 % (oral). Time to achieved within 1 hour, incremental doses disorders:
of 1-2 mg Anaemia.
may be given up to 10 mg/24 tranquilisers).
hour. May enhance the
Cardiac disorders: Bradycardia, neuromuscular blocking action of (e.g. drug allergy,
(conventional tab, epidural); 3-4 hours Intraspinal palpitation, tachycardia. skeletal muscle relaxants. respiratory
(extended-release tab); 20-60 minutes Postoperative pain Eye disorder: Blurred or double Reduced analgesic effect with dysfunction,
(supp); 50-90 minutes (SC); 30-60 vision, miosis.
Adult: As morphine sulfate liposomal inj: Dosage mixed agonist/antagonist
is individualised based on the severity of pain, opioid myocardial
minutes (IM); 20 minutes (IV). Gastrointestinal
patient response and prior analgesic experience. 10-20 mg for lumbar administration analgesics
only (e.g. buprenorphine, infarction and
Distribution: Widely distributed disorders: Abdominal
depending on the type of surgery. Dose adjustments pain, according nalbuphine,
may be required to individualpentazocine). CAD, hepatorenal
throughout the body mainly in the response. constipation, delayed gastric Increased plasma concentrations dysfunction, etc.)
kidneys, liver, lungs and spleen, with emptying, diarrhoea, dyspepsia, with cimetidine. Reduced plasma to prevent
lower concentrations in the brain and Intrathecal flatulence, nausea, vomiting, concentration with rifampicin, untoward
muscles. Crosses the blood-brain Moderate to severe pain xerostomia, dry mouth, anorexia. ritonavir. Decreased therapeutic complications.
barrier and placenta; enters breast General
Adult: As morphine sulfate: 0.2-1 mg as single dosedisorders
for up toand
24 hours. Dosage iseffect of diuretics. Increased
individualised
 Conduct pain
milk. Volume of distribution: 1-6 L/kg. administration
based on the severity of pain, patient response site
and prior analgesic experience. plasma concentration with
assessment with
Plasma protein binding: Approx 35%. conditions: Asthenic conditions, cisapride. Increased risk of
patient to establish
Metabolism: Metabolised in the liver Intravenous hyperhidrosis, withdrawal orthostatic hypotension with
baseline and
and gut via glucuronidation to syndrome.
Moderate to severe pain, Pain associated with myocardial infarction, Postoperative antihypertensive
pain, agents.
evaluate
produce morphine-3-glucoronide and Severe cancer pain Hepatobiliary disorders: Biliary Increased risk of severe
effectiveness of
morphine-6-glucoronide; undergoes colic, hypoesthesia,
Adult: As morphine sulfate: Dosage is individualised hypokalemia.
based on the constipation
severity of pain, patient and CNS depression
drug therapy.
extensive first-pass metabolism. Metabolism and nutrition
response and prior analgesic experience. As Patient-Controlled Analgesia (PCA): Loadingwith antidiarrhoeal
dose: agents
Excretion: Via urine [approx 60% disorders:
1-10 mg (Max 15 mg) via IV infusion over 4-5 minutes, Anorexia.
then 1 mg on demand with Potentially Fatal: Enhanced
5-10 minutes  Perform thorough
(oral); approx 90% (parenteral)]; lockout time. Musculoskeletal and connective depressant effect with MAOIs. physical (CNS, vital
faeces (10%, as conjugates). Elderly: Dose reduction needed. tissue disorders: Back pain. signs, bowel
Elimination half-life: Approx 2 hours Nervous system sounds, urine
(morphine); 2.4-6.7 hours (morphine- Oral disorders: Dizziness, headache, output) to
3-glucoronide). Moderate to severe pain paresthesia, paralytic ileus, establish baseline
myoclonus.
Adult: As morphine sulfate: Dosage is individualised based on the severity of pain, patient status before
response and prior analgesic experience. AsPsychiatric
conventionaldisorders: Anxiety,5-20 mg 4 hourly. As
preparation: beginning therapy,
confusion, dependence,
extended-release tab/cap: Recommended initial dose: 1 or 2 (10 mg) insomnia
tab 12-24 hourly. determine drug
hallucination,
Child: As morphine sulfate: Dosage is individualised basedeuphoria, agitation,
on the severity of pain, patient effectiveness and
response and prior analgesic experience. Asmood altered. preparation:
conventional evaluate for any
Renal and
(Max: 30 mg daily); 6-12 years 5-10 mg 4 hourly (Max: urinary
60 mg daily); potential adverse
dose. disorders: Bladder spasm, oliguria, effects.
urinary retention.
 Monitor laboratory
Parenteral Reproductive system and breast
results (liver
Severe pain disorders: Decreased libido or
function, kidney
potency (long
Adult: As morphine sulfate: Dosage is individualised term
based on use).
the severity of pain, patient
function) to
Respiratory, thoracic
response and prior analgesic experience. Recommended dose: 10-20 and mg 4-6 hourly (dose may
determine need
vary from 5-20 mg) via SC, IM or IV inj. mediastinal disorders: Dyspnea,
for possible dose
Elderly: Dose reduction needed. hypoxia, rigors, bronchospasm,
adjustment and
pulmonary oedema.
identify toxic drug
Parenteral Skin and subcutaneous tissue
effects.
Acute pulmonary oedema, Premedicationdisorders:
in surgeryPruritus, skin rash,
Adult: As morphine sulfate: Dosage is individualisedsweating.
urticaria, based on the severity of pain, patient
Vascular disorders:
response and prior analgesic experience. Recommended dose:Hypertension,
10 mg 4 hourly if necessary
(dose may vary from 5-20 mg) via SC or IMfacial flushing.
inj. May also be given via IV infusion at a dose
corresponding to ¼ - ½ of the IM dose not more than 4Fatal:
Potentially Hypersensitivity.
hourly.
Elderly: Dose reduction needed. Respiratory depression.
Parenteral
Severe cancer pain, Severe pain
Adult: As morphine tartrate: 5-20 mg 4-6 hourly via SC/IM inj. If rapid onset of action is desired,
may give 2.5-15 mg via slow IV inj over 4-5 minutes. As IV Patient-controlled analgesia (PCA): 1
mg/hour administered with a lockout interval of 6-10 minutes and 0.5 (Max of 1.5 mg) demand
doses.
Child: As morphine tartrate: 0.1-0.2 mg/kg 4-6 hourly via SC/IM inj. Max dose: 15 mg. If rapid of
onset is desired, 0.05-0.1 mg/kg via slow IV inj, may titrate dose incrementally over 5-15
minutes.
 Rectal
Severe pain
Adult: As morphine sulfate: Dosage is individualised based on the severity of pain, patient
response and prior analgesic experience. 10-20 mg 4 hourly.
Renal Impairment
Oral
Moderate to severe pain: Dose reduction needed.

Parenteral
Acute pulmonary oedema; Premedication in surgery; Severe pain; Severe cancer pain:
reduction needed.

Intravenous
Moderate to severe pain; Pain associated with myocardial infarction; Postoperative pain;
Severe cancer pain: Dose reduction needed.
Hepatic Impairment
Oral
Moderate to severe pain: Dose reduction needed.

Parenteral
Acute pulmonary oedema; Premedication in surgery; Severe pain; Severe cancer pain:
reduction needed.

Intravenous
Moderate to severe pain; Pain associated with myocardial infarction; Postoperative pain;
Severe cancer pain: Dose reduction needed.
CENTRAL NERVOUS SYSTEM (CNS) INHALANTS

INHALANTS Atrovent Adult (including elderly) &
adolescent >12 yr Maintenance
treatment 40 drops tds-qds. Acute
attacks 40 drops/dose, repeat
administration until the patient is
stable. Childn 6-12 yr Maintenance
treatment 20 drops tds-qds. Acute
attacks 20 drops/dose, repeat
administration until the patient is
stable. <6 yr Maintenance
treatment 8-20 drops tds-qds. Acute
attacks 8-20 drops/dose, repeat
administration until the patient is
stable.
Following administration by oral
inhalation from a metered-dose
inhaler, the majority of the delivered
dose is deposited in the
gastrointestinal tract and, to a lesser
extent, in the lung, the intended site
of action. Ipratropium bromide is a
quaternary amine and hence is not
readily absorbed into the systemic
circulation either from the surface of
the lung or from the gastrointestinal
tract as confirmed by blood level and
renal excretion studies.
The half-life of elimination is about 2
hours after inhalation or intravenous
administration. Ipratropium bromide
is minimally bound (0% to 9% in vitro)
to plasma albumin and α1-acid
glycoprotein. It is partially
metabolized to inactive ester
hydrolysis products. Following
intravenous administration,
approximately one-half of the dose is
excreted unchanged in the urine.
Bronchodilator for maintenance
treatment of bronchospasm associated
w/ COPD including chronic bronchitis &
emphysema. Acute bronchospasm
associated w/ COPD including
bronchitis & asthma, in combination w/
inhaled β-agonists.
Adverse Reactions
Headache, throat irritation, cough,
dry mouth, GI motility disorders
(including constipation, diarrhoea
& vomiting), nausea & dizziness.
Not recommended for chronic
co-administration w/ other anti- Contraindicated in patients
cholinergics. Bronchodilatory with renal and hepatic
effect may be intensified by β- insufficiency
adrenergics & xanthine prep.
Precipitation may occur in Antidote for anticholinergic
concurrent administration w/ poisoning: physostigmine
diNa cromoglycate nebuliser
soln. May increase risk of acute
glaucoma in patients w/ narrow-
angle glaucoma history.
Absorption: The therapeutic
effect of ATROVENT is produced
by a local action in the airways.
Time courses of bronchodilation
and systemic pharmacokinetics
do not run in parallel.
Following inhalation 10 to 30% of
a dose is generally deposited in
the lungs, depending on the
formulation and inhalation
technique. The major part of the
dose is swallowed and passes the
gastro-intestinal tract.
The portion of the dose
deposited in the lungs reaches
the circulation rapidly (within
minutes). Cumulative renal
excretion (0-24 hrs) of the parent
compound is approximated to
46% of an intravenously
administered dose, below 1% of
an oral dose and approximately 3
to 13% of an inhaled dose. Based
on these data the total systemic
bioavailability of oral and inhaled
doses of ipratropium bromide is
estimated at 2% and 7 to 28%
respectively.
Taking this into account,
swallowed dose portions of
ipratropium bromide do not
relevantly contribute to systemic
exposure.
Distribution: The drug is
minimally (less than 20%) bound
to plasma proteins. Nonclinical
data indicate that quaternary
amine ipratropium does not
cross the placental or the blood-
brain barrier. The known
metabolites show very little or
no affinity for the muscarinic
receptor and have to be
regarded as ineffective.
Biotransformation: After
intravenous administration
approximately 60% of a dose is
metabolised, mainly by
conjugation (40%), whereas after
inhalation about 70% of the
systemically available dose is
metabolised by ester hydrolysis
(41%) and conjugation (36%).
The known metabolites, are
formed by hydrolysis,
dehydration or elimination of the
hydroxy-methyl group in the
tropic acid moiety.
Elimination: Ipratropium has a
total clearance of 2.3 L/min and
a renal clearance of 0.9 L/min.
In an excretion balance study
cumulative renal excretion (6
days) of drug-related
radioactivity (including parent
compound and all metabolites)
accounted for 72.1% after
intravenous administration, 9.3%
after oral administration and
3.2% after inhalation. Total
radioactivity excreted via the
faeces was 6.3% following
intravenous application, 88.5%
following oral dosing and 69.4%
after inhalation. Regarding the
excretion of drug-related

INHALANTS Clenbuterol Clenbuterol is a direct-acting
sympathomimetic with predominantly
β-adrenergic activity and has selective
action on β2-receptors.
CANNABIS Marijuana Cannabis is an herbal drug that is made
from the Cannabis plant. It contains
radioactivity after intravenous
administration, the main
excretion occurs via the kidneys.
The half-life for elimination of
drug-related radioactivity (parent
compound and metabolites) is
3.6 hours.
The pharmacokinetics of clenbuterol Inhalation/Respiratory Adverse Reactions Drug Interactions
(CLB) following a single intravenous Bronchodilator Fine tremor of skeletal muscle, Increased risk of cardiac  Assess for
(i.v.) and oral (p.o.) administration Adult: 20 mcg tid. palpitations, tachycardia, nervous arrhythmias when used with mentioned
twice daily for 7 days were tension, headaches, peripheral potassium-depleting drugs e.g. cautions and
investigated in thoroughbred horses. vasodilatation, muscle cramps thiazide or loop diuretics, contraindications
The plasma concentrations of CLB (rare), hypokalaemia (large doses), amphotericin B, corticosteroids. (e.g. drug allergy,
following i.v. administration declined hypersensitivity reactions. Increased risk of hypokalaemia respiratory
mono-exponentially with a median and tachycardia when used with dysfunction,
elimination half-life (t(1/2k)) of 9.2 h, high-dose theophylline. myocardial
area under the time-concentration infarction and
curve (AUC) of 12.4 ng.h/mL, and a CAD, hepatorenal
zero-time concentration of 1.04 dysfunction, etc.)
ng/mL. Volume of distribution (V(d)) to prevent
was 1616.0 mL/kg and plasma untoward
clearance (Cl) was 120.0 mL/h/kg. The complications.
terminal portion of the plasma curve
 Conduct pain
following multiple p.o.
assessment with
administrations also declined mono-
patient to establish
exponentially with a median
baseline and
elimination half-life (t(1/2k)) of 12.9 h,
evaluate
a Cl of 94.0 mL/h/kg and V(d) of
effectiveness of
1574.7 mL/kg. Following the last p.o.
drug therapy.
administration the baseline plasma
concentration was 537.5 +/- 268.4  Perform thorough
and increased to 1302.6 +/- 925.0 physical (CNS, vital
pg/mL at 0.25 h, and declined to 18.9 signs, bowel
+/- 7.4 pg/mL at 96 h. CLB was still sounds, urine
quantifiable in urine at 288 h output) to
following the last administration establish baseline
(210.0 +/- 110 pg/mL). The difference status before
between plasma and urinary beginning therapy,
concentrations of CLB was 100-fold determine drug
irrespective of the route of effectiveness and
administration. This 100-fold evaluate for any
urine/plasma difference should be potential adverse
considered when the presence of CLB effects.
in urine is reported by equine forensic
 Monitor laboratory
laboratories.
results (liver
function, kidney
function) to
determine need
for possible dose
adjustment and
identify toxic drug
effects.
CENTRAL NERVOUS SYSTEM (CNS) CANNABIS
The pharmacokinetics of THC vary as a Pregnancy: Cannabis is UNSAFE when When taken by mouth: Cannabis Major InteractionDo not take The National Council of State
function of its route of administration. taken by mouth or smoked during is POSSIBLY UNSAFE when taken by this combination Boards of Nursing has
chemicals called cannabinoids.
Cannabinoids affect the central
nervous system, which includes
the brain and nerves. Cannabinoids are
found in the highest levels in the leaves
and flowers of cannabis. These are the
parts of the herb that are used to make
medicine.
Pulmonary assimilation of inhaled
THC causes a maximum plasma
concentration within minutes,
psychotropic effects start within
seconds to a few minutes, reach a
maximum after 15-30 minutes, and
taper off within 2-3 hours. Following
oral ingestion, psychotropic effects set
in with a delay of 30-90 minutes,
reach their maximum after 2-3 hours
and last for about 4-12 hours,
depending on dose and specific effect.
At doses exceeding the psychotropic
threshold, ingestion of cannabis
usually causes enhanced well-being
and relaxation with an intensification
of ordinary sensory experiences.
pregnancy. Cannabis passes through
the placenta and can slow the growth
of the fetus and increase the risk for
premature birth. Cannabis use during
pregnancy is also associated with
stillbirth, childhood leukemia,
abnormalities in the fetus, and the
need for intensive care after birth.
Cannabis use during pregnancy has also
been linked with lower intelligence and
increased emotional problems in
children when they grow up. Also,
cannabis use is associated with an
increased risk for anemia and high
blood pressure in the mother.
Breast-feeding: Using cannabis, either
by mouth or by inhalation is LIKELY
UNSAFE during breast-feeding. The
chemicals in cannabis pass into breast
milk. Too much of these chemicals
might slow down the development of
the baby.
Bipolar disorder: Using cannabis might appetite, sweating, headache, and
make manic symptoms worse in people depressed mood. There isn't
with bipolar disorder.
Heart disease: Cannabis might cause
fast heartbeat and high blood pressure. time.
It might also increase the risk of a
having heart attack. However, in many
cases, people who experienced these
events after smoking cannabis had
other risk factors for heart-related
events such as smoking cigarettes or
being overweight.
A weakened immune system: Certain
chemicals in cannabis can weaken the
immune system. This might make it
more difficult for the body to fight
infections.
Allergies to fruits and vegetables:
Cannabis might increase the risk of an
allergic reaction in people with allergies Smoking or vaping cannabis can
to foods like tomatoes, bananas, and
citrus fruit.
Depression: Cannabis use, especially
frequent use, might increase the
chance of getting depression. It can also cavities can cause symptoms such as marijuana while taking warfarin
worsen symptoms of depression and
increase thoughts about suicide in
those that already have depression.
mouth in large amounts or for a identified six principles of
long time. Cannabis containing large Sedative medications essential knowledge about
amounts of THC (50 mg or more) (Barbiturates) interacts with cannabis for nurses, advance
has been linked with anxiety, CANNABISMarijuana might practice nurses, and nursing
psychosis, heart attack, and cause sleepiness and drowsiness. students.
irregular heart rhythm. Regularly Medications that cause
taking large amounts of cannabis sleepiness are called sedatives. 1 The nurse shall have a
over a long period of time might Taking marijuana along with working knowledge of the
cause a disorder called cannabinoid sedative medications might current state of legalization
hyperemesis syndrome, or CHS. CHS cause too much sleepiness. of medical and recreational
leads to severe, repeated bouts of Sedative medications (CNS cannabis use.
nausea and vomiting that don't depressants) interacts with
respond to typical anti-nausea CANNABISMarijuana might
medicine. In a few reports, CHS has cause sleepiness and drowsiness. 2 The nurse shall have a
been linked to severe complications Medications that cause working knowledge of the
that caused death. sleepiness are called sedatives. jurisdiction’s medical
Taking marijuana along with marijuana program.
Using cannabis for at least 1-2 sedative medications might
weeks can also lead to dependence. cause too much sleepiness.Some 3 The nurse shall have an
People with cannabis dependence sedative medications include understanding of the
might experience withdrawal after clonazepam (Klonopin), endocannabinoid system,
stopping cannabis use. Symptoms of lorazepam (Ativan), cannabinoid receptors,
withdrawal include nervousness, phenobarbital (Donnatal), cannabinoids, and the
shaking, trouble sleeping, decreased zolpidem (Ambien), and others. interactions between them.
Theophylline interacts with
CANNABISTaking marijuana 4 The nurse shall have an
enough information to know if might decrease the effects of understanding of cannabis
cannabis is safe to use in theophylline. But there isn't pharmacology and the
moderation for short periods of enough information to know if research associated with the
this is a big concern. medical use of cannabis.
Moderate InteractionBe cautious
When sprayed into the mouth: A with this combination
specific cannabis extract spray 5 The nurse shall be able to
(Sativex, GW Pharmaceuticals) Disulfiram (Antabuse) interacts identify the safety
is POSSIBLY SAFE when applied with CANNABISDisulfiram considerations for patient use
under the tongue. Side effects may (Antabuse) might interact with ofcannabis.
include headache, dizziness, marijuana. Taking marijuana
drowsiness, dry mouth, nausea, and along with Disulfiram can cause 6 The nurse shall approach
paranoid thinking. This cannabis agitation, trouble sleeping, and the patient without judgment
extract spray is available as a irritability. regarding the patient’s choice
prescription-only product in the U.K. Fluoxetine (Prozac) interacts of treatment or preferences
and Canada. It has not been with CANNABISTaking marijuana in managing pain and other
approved as a prescription product with fluoxetine (Prozac) might distressing symptoms.
in the U.S. cause you to feel irritated,
nervous, jittery, and excited.
When inhaled: Cannabis Doctors call this hypomania.
is POSSIBLY UNSAFE when inhaled. Minor InteractionBe watchful
with this combination
cause various breathing problems
such as wheezing and coughing. Warfarin (Coumadin) interacts
Some reports suggest that smoking with CANNABISUsing marijuana
cannabis might cause air-filled might increase the effects of
cavities in the lungs. These air-filled warfarin (Coumadin). Smoking
chest pressure, soreness, and (Coumadin) might increase the
difficulty breathing. Use of e- chance of bruising and bleeding.
cigarettes and other vaping
products containing THC has been
 Diabetes: Cannabis use might make it
harder to control blood sugar levels. It
might also increase the risk for long-
term complications from diabetes. Until
more is known, be cautious using
cannabis.
Liver disease: It is unclear if cannabis
worsens chronic liver disease. While
some weak evidence suggests that
there might be a link, other evidence
has not found a link. Until more is
known, be cautious using cannabis.
Multiple sclerosis: Taking cannabis by
mouth might make symptoms of
multiple sclerosis worse.
Lung diseases: Cannabis can make lung
problems worse. Regular use over a
period of years might increase the risk
of lung cancer. Some people develop a
type of lung disease called emphysema.
Schizophrenia: Using cannabis might
make symptoms of schizophrenia
worse.
Quitting smoking: Using cannabis might
make it harder to quit smoking. Early
research suggests that people who use
cannabis and want to quit smoking
cigarettes are less likely to quit smoking
after 6 months than people who don't
use cannabis.
Stroke: Using cannabis after having a
stroke might increase the risk of having
a second stroke.
Surgery: Cannabis affects the central
nervous system or the brain and nerves.
It might slow the central nervous
system too much when combined with
anesthesia and other medications
during and after surgery. Stop using
cannabis at least 2 weeks before a
scheduled surgery.
CANNABIS Cannabidiol The CB1 receptor is present at a high Absorption: Extent of absorption
density on the presynaptic level of the unknown. High fat/high calorie meals Seizures associated with Lennox-
neuronal synapses, where its increase extent of absorption. Gastaut syndrome or Dravet syndrome.
stimulation activates potassium Distribution: Extensively distributed
channels and on the contrary, inhibits to tissues.
calcium-dependent channels, what Protein Binding: >94%.
results in inhibition of the Metabolism and Excretion: Primarily
neurotransmitter release. Concerning metabolized in the liver by the
this mechanism of action mentioned, CYP2C9 and CYP3A4 isoenzymes to an
linked to serious lung injury in some
people. Smoking cannabis can also
cause headache, dizziness,
drowsiness, dry mouth, nausea, and
paranoid thinking. Smoking
cannabis might also increase
appetite, increase heart rate,
change blood pressure, and impair
mental functioning. Some reports
suggest that smoking cannabis may
also increase the risk of heart
problems such as heart attack and
abnormal heart rhythm. Regularly
smoking large amounts of cannabis
for a long time may cause CHS. It
might also lead to dependence.
People with cannabis dependence
might experience withdrawal after
stopping cannabis use. Symptoms of
withdrawal include nervousness,
shaking, trouble sleeping, decreased
appetite, sweating, headache, and
depressed mood.
CNS: SUICIDAL Drug-Drug  Assess location,
THOUGHTS/BEHAVIORS, drowsines  Concurrent use of duration, and
s, fatigue, insomnia, aggressive valproic acid or characteristics of seizure
behavior, agitation clobazam ↑ risk of activity. Institute seizure
Derm: rash hepatotoxicity. precautions.
EENT: dry mouth  Moderate or strong  Monitor closely for
GI: HEPATOTOXICITY, ↓ CYP2C9 or CYP3A4 notable changes in
appetite, diarrhea, ↑ liver
inhibitors may ↑ levels and behavior that could
enzymes, abdominal pain, ↓
risk of toxicity; consider ↓ indicate the emergence or
 endocannabinoids are also called as active metabolite (7-OH-CBD). weight cannabidiol dose. worsening of suicidal
the “Retrograde Synaptic Primarily excreted in feces. GU: ↑ serum creatinine  Strong CYP2C9 or thoughts or behavior or
Messengers” Half-life: 56–61 hr. Hemat: anemia CYP3A4 inducers may ↓ depression.
TIME/ACTION PROFILE (plasma Neuro: ataxia levels and effectiveness;  Monitor for signs and
concentrations) Misc: hypersensitivity reactions consider ↑ cannabidiol dose. symptom of
ROUTE ONSET PEAK DURATION (angioedema, pruritus), infection,  May ↑ levels and risk of hepatotoxicity
physical dependence, psychological
PO unknow 2.5–5 unknown toxicity of CYP2C8, CYP2C9, (unexplained nausea,
dependence (high doses or
n hr or CYP2C19 substrates ; vomiting, right upper
prolonged therapy)
consider ↓ dose of CYP2C8, quadrant abdominal pain,
* CAPITALS indicate life-
threatening. CYP2C9, or CYP2C19 fatigue, anorexia, jaundice
Underline indicate most frequent. substrate. and/or dark urine). If signs
 May ↑ or ↓ levels of and symptoms occur,
CYP1A2 or CYP2B6 promptly measure serum
substrates ; consider ↓ dose transaminases and total
of CYP1A2 or CYP2B6 bilirubin and interrupt or
substrate. discontinue treatment
 Additive CNS depression with cannabidiol.
with alcohol, antihistamines,  Monitor for signs and
barbiturates, benzodiazepine symptoms of
s, muscle relaxants, opioid hypersensitivity reactions
analgesics, (pruritus, erythema, and
tricyclic antidepressants, angioedema) during
and sedative/hypnotics. therapy. Discontinue
cannabidiol if symptoms
occur.
Lab Test Considerations:
Obtain serum transaminases
(ALT, AST) and total bilirubin
levels before starting therapy.
Elevations usually respond to
decreased dose or
discontinuation of therapy.
Monitor levels at 1, 3, and 6
mo after starting therapy,
within 1 mo following dose
changes, and as needed
thereafter. Discontinue
cannabidiol if transaminase
levels >3 times upper limit of
normal (ULN) and bilirubin
levels >2 times ULN. Also
discontinue therapy if
transaminase persistently >5
times ULN.

REFERENCES:
• An article from IACP website entitled: 7 Drug Category/Classification of CNS
 Medscape by WebMD LLC.
 MIMS