ADRENERGIC DRUGS

AGONISTS
DESC also called sympathomimetic
GENERAL
DIRECT-ACTING AGONISTS INDIRECT-ACTING AGONISTS DUAL-ACTING AGONISTS
CLASSIFICATION
MOA Bind to & activate a1, a2, B1 and B2 Produce NE-like actions by Act as direct & indirect adrenergic agonists.
receptors then producing effects. stimulating NE release and
preventing its reuptake and
produces activation.
E.g. Adr & NA Isoproterenol* Tyramine Ephedrine
Isoproterenol Metaproterenol Amphetamine Metaraminol
Phenylephrine Methoxamine Cocaine Pseudoephedrine
Albuterol Phenylephrine Amphetamine
Clonidine Piruterol Mephenteramine
Dobutamine* Salmeterol
Dopamine* Terbutaline
Formoterol Xylometazoline

THERAPEUTIC ↑BP Ionotropic Central Muscle Muscle Allergic Local Appetite

CLASSIFICATION (vasoconstrictors) action of stimulants relaxants stimulant reactions vasoconstrictors suppressor
heart
E.g. NA Dopamine Benzedrine Adr (Epi) Salbutamol Adr Adr Fenfluramine
Metaraminol Dobutamine Isoprenaline Ephedrine Phenylephrine Phentermine
Xamoterol Isoxsuprine Naphazoline Amphetamine
selective β2

CHEMICAL
STRUCTURE CATECHOLAMINES NONCATECHOLAMINES
CLASSIFICATION
DESC Orally Orally
Duration of action: short (t1/2) Duration of action: longer (t1/2)
Polar molecules: cannot pass BBB ↑ lipid solubility: can cross BBB
Contain 3,4-dihydroxybenzene group Lacking catechol hydroxy groups
High potency
EXAMPLES Adr Isoprenaline Amphetamine Naphazoline Isosupurine
NA Dobutamine Ephedrine Metaraminol Nylidrine
Dopamine Isoproterenol Phenylephrine Salbutamol
ANTAGONIST
DESC Also called adrenergic blockers.
Bind to adrenoreceptors but NO RESPONSE triggered. (blockade)
 Selective or non-selective.
Reversible or irreversible.
Alpha receptor antagonist Beta receptor antagonist
MOA Enter the bloodstream thru GIT.
Prevent adr from attaching to receptor (heart) cells.
Effector (HR) stays normal = NO fight & flight.
Non-selective α1 α2 Non-selective β11 Non-selective β1
E.g. Phenoxybenzamine Prazosin* Yohimbine Nadolol Acebutolol Carteolol Betaxolol
Phentolamine Terazosin Penbutolol Atenolol* Carvedilol* Celiprolol
Doxazosin* Pindolol Bisoprolol Bucindolol Nebivolol
Alfuzosin Propranolol* Esmolol Labetalol*
Tamsulosin Timolol Metoprolol
Indoramin Sotalol *
Urapidil Levubunolol
Bunazosin Metipranolol
SIDE EFFECTS Orthostatic hypotension Hypotension
Tachycardia Bradycardia
Vertigo Symptoms of CHF
Sexual dysfunction Drowsiness
Depression
CHOLINERGIC DRUGS

also called parasympathomimetic/cholinomimetic

AGONIST ANTAGONIST
CLASSIFICATION DIRECT-ACTING CHOLINERGIC INDIRECT-ACTING CHOLINERGIC (Anti-ChE)
mainly for nicotinic effects at NMJ.
Treatment: myasthenia gravis
Reverse the effects of competitive muscle
relaxants used in surgery.
E.g. Choline esters: Cholinomimetic alkaloids: Reversible cholinesterase Irreversible
inhibitors: cholinesterase
inhibitors:
Acetyl choline Pilocarpine Physostigmine (eserine) Pralidoxime
Methacholine Muscarine Neostigmine (pristigmine) Ecothiopate
Carbachol Arecoline Pyridostigmine (mestinon) Malathion
Bethanechol Edrophonium Isfluorphate
Ambenonium (mytelase) Parathion
Demecarium (humorsol)
Distigmine (ubretid)

CLASSIFICATION NICOTINIC
BASED ON (Ganglionic stimulator) MUSCARINIC MUSCARINIC
RECEPTOR TYPE
DESC Simulate nicotinic receptors Directly activate muscarinic Block the effect of Ach
on para & sympa ganglionic receptors (excitatory effects). released from
neurons. postganglionic para nerve
terminals.
EFFECTS Salivary secretion
Bronchial secretion
Sweat glands secretion
E.g. Nicotine (tobacco) Muscarine (amanita muscarina) Atropine
Lobeline (Indian tobacco) Arecoline (betel nut, areca catechu)
Dimethylphenylpiperazinium Pilocarpine (pilocarpus jaborandi)
(DMPP) Carbachol + methacholine (lab
Epibatidine (from frog skin) purposes)
Bethanechol + pilocarpine (clinical
purposes)
CLINICAL USES
 ADVERSE Asthma
REACTIONS Hyperthyroidism
Coronary incapacity
Peptic ulcer disease
DOSAGE FORMS

SOLID
ADVANTAGES Stability > liquid
Easy handling
No preservation required
Accurate dosage (single dose)
DISADVANTAGES Need time for preparation.
Preparation needs complicated n expensive machines.
Not suitable for dispensing many unpleasantly tasting, hygroscopic & deliquescent drugs.
POWDERS GRANULES TABLETS CAPSULES SUPPOSITORIES
DESC Mixture of finely Powdered particles A compressed OR 1≥ medicinal n inert Intended for
divided drugs/ that hv been molded uniform ingredients are enclosed in insertion into body
Chemicals in a aggregated to form volume of particles. small shell/container orifices where they
dry form. larger particles Single dose of 1≥ (hard/soft) made of gelatin. melt/soften/dissolve
(usually 2-4mm). active ingredients. and exert local
Prepared as: bulk Larger than powder effects.
or divided Irregular shape
powder. Excellent flow

ADMINISTRATION internal (orally) Placed on tongue Oral, Oral Rectally/vaginally

External and swallowed with Sublingual/buccal Rectally/vaginally Urethrally
(topical/dusting) water. Vaginal
Dissolved in water.
ADVANTAGES Stability > powder Low manufacturing Easily administered (masked Easily administered
cost taste n odor) Convenient mode of
Easy to package n Attractive appearance administration for
ship. Easy to swallow (slippery drugs which irritates
Easy to identify when moist) the GIT.
Physiologically inert Faster onset of
(easy/quick to digest) action
Easy to handle n carry Produce local action
Shells can be colored (TiO2) for
protection from light.
DISADVANTAGES Poor bioavailability Hygroscopic drugs aren’t Stringent storage
May cause local suitable → brittle conditions
irritation in GIT Leaking prob →
mucosa. embarrassment.
Difficult to swallow: Proctitis in some
pediatrics & geriatrics cases.
 E.g. Dusting powder Effervescent Disintegrating tablet Hard gelatin capsule (gelatin + Rectal suppositories
Dentifrice granules Effervescent tablet sugar + H2O) Bullet/torpedo
powder Coated tablet shaped.
Insufflation Chewable tablet Soft gelatin capsule (gelatin + Relieves
powder Sublingual & buccal H2O + polyhydric alcohol + constipation,
Oral powder tablet preservatives) irritation n itching.
Douche powder Lozenges (troches) Polyhydric alcohol:
glycerol/sorbitol + propylene Vaginal suppositories
glycol (pessaries)
Preservative: Globular, oviform,
methylparaben/propylparaben cone shaped.
Contraceptives n
antiseptics.

Urethral
suppositories
(bougies)
Slender, pencil
shaped.
Antibcaterial, local
anaesthetic.

LIQUID
DEFIN Consists of 2≥ active ingredients in liquid vehicle (solvent).
SOLUTIONS DISPERSIONS
SUSPENSIONS EMULSIONS
(solid in liquid dispersions) (liquid in liquid dispersion)
DESC Homogenous mixture of 2≥ substances; btwn Heterogenous fluid of insoluble solid Liquid preparation containing 2
solute & solvent. particles with/without suspending agent. immiscible liquids - one disperses
as globules in the other liquid with
help of emulsifying agent.
CHAR Uniform (homogenous) particles distribution. Heterogenous 2-phase systems:
Extremely small particles (naked eye ) Relatively large particles (naked eye ) - Oil-in-water emulsion (O/W)
Stable mixture (doesn’t separate on standing n dissolve - Water-in-oil emulsion (W/O)
remain suspended) > dispersions. Separate on standing Unstable → doesn’t form
filter filter spontaneously.
Transparent (may be colored). Murky/opaque
Orally Orally Topically
 Orally
IM
ADV Easy to swallow. Ease swallowing Facilitates administration of water
Quick absorption > tablets/capsules Insoluble substances can be administered immiscible substances
Homogenous → no need to shake. in liquid form. Mask unpleasant taste
Cover disagreeable taste.
DISADV Bulky → difficult to transport. Physical instability – tends to settle over -
Difficult to mask its taste/odor. time → lack of uniformity of dose.
Needs accurate spoon to measure the dose.
Stability < solids (color changes, precipitation, Packaging & storage:
microbial growth, chem gas formation) - Hv adequate spacing above the
liquid. (for shaking)
- Tight containers (protected from
freezing n excessive heat/light)
- “Shake b4 use” → uniform
distribution → uniform n proper
dosage.
E.g. Douches Antacids oral suspension Mineral oil emulsion
Enemas (rectal) Antibacterial oral suspension Castor oil emulsion
Mouth gargles Dry powders for oral suspension Simethicone emulsion
Mouthwashes (antibiotics)
Nasal solutions Analgesic oral suspension
Otic solutions (ear) Anthelmintic oral suspension
Liniments (minyak panas) Anticonvulsant oral suspension
Antifungal oral suspension

SEMISOLID
USES Emollient – soothes/softens the skin/mucous membrane.
Protective – protects injured/exposed skin.
Occlusive – promotes water retention by forming hydrophobic barrier.
Humectant – retains water due to hygroscopic properties.
OINTMENTS CREAMS GELS
CHAR Opaque/translucent Opaque Transparent
Viscous Viscous Non-greasy
Greasy Greasiness: none to mild Excellent spreading properties
 Softens but melt upon application. evaporated Cooling effect
evaporated absorbed
absorbed Vanishing (invisible)
W/O preparation
Retained at skin → prevents moisture loss.
→ longer duration of drug release.
Stains clothes
E.g. Classification on penetration: Crotamiton – Eurax cream Clobetasol propionate gel
Epidermic Endodermic Diadermic (anti-allergic, anti-itching) (antipruritic)
Acts on skin surface. Penetrates skin. Pass thru skin. Fluorouracil – Efudex cream
Local effect Partially absorbed. Systemic effects. (anti-neoplastic)
Poor penetration Emollients & - Nitroglycerine
Protective, stimulants. ointment
antiseptics & - Lanolin
parasiticides.
- Whitfield’s
ointment
- Petrolatum

INHALATION
DESC Most rapid administration due to rich blood supply of resp tract.
Rapid absorption.
Sprays, powders & liquids.
DEVICE METERED-DOSE INHALER (MDIs) DRY POWDER INHALERS (DPIs) NEBULIZER
CHAR Hand-held Deliver dry powder formulations Deliver liquid form → mist of
Disperse medication into airway n lungs. into lungs. small droplets.
Most common Main factor of delivery: Inhaled thru mask/mouthpiece.
Consists of canister (contain solvent + liquid propellant; inspiratory volume n flows For severe attacks,
CFCs) & chamber (mouthpiece + protective cover). generated by patient. Commonly for children/elderly
Metering valve – dispense constant/measured vol/dose coordination required. with asthma/lung disease.
of drug thru pressurized spray (fine mists). propellants required. Also, for:
Contained in capsule. - Patients are unable to use
other type of inhalation
devices due to
physical/cognitive deficits.
- Severe dyspnea (need high
doses of medication n O2).
E.g. - Rotahaler Diskus -
 Aerolizer HandiHaler
Turbuhaler Twisthaler
Diskhaler Flexhaler
ADV Portable Portable Therapy for patients who can’t
Multidose delivery capability Breath-actuated use other devices.
Suitable in emergency situations spacer Allow large doses of meds.
Short treatment time need to hold breath after coordination
Low risk of bacterial contamination inhalation CFC release
propellant
Lung deposition > MDI
DISADV Needs correct actuation n inhalation coordination. Need adequate inspiratory flow. ↓ portability
Difficult for children n elderly. May hv high pharyngeal Long setup & administration
Oropharyngeal drug deposition. deposition. time.
Requires propellant. Humidity → may cause clumping. ↑ cost
→ reduced dispersal of fine
particles.
INHALATION ACCESORY DEVICES (IAD)
ADV Enhanced drug delivery.
Compensate poor technique/coordination of MDI.
Reduced oropharyngeal drug deposition.
DISADV Large
Possible bacterial contamination.
Electricity charges may reduce drug delivery to the lung.
Antidepressant drugs

Name of Symptoms Mechanism of Action Example drugs Adverse effect

antidepressant drug
Tricyclic • Anxiety • Inhibit reuptake Amitriptyline • Blurred vision
antidepressants (TCA) • Bed-wetting mechanism responsible Amoxapine • Constipation
• Chronic nerve-related pain for the termination of Clomipramine • Disorientation/confusion
• Migraine prevention the synaptic action. Desipramine • Dry mouth
• Panic attacks • of both NE and 5-HT. Doxepin • Excessive sedation
• PTSD • Involves two Imipramine • Tachycardia, agitation
mechanisms: Nortriptyline • Sweating
By blocking the major route Protriptyline • ECG abnormalities
of neurotransmitter Trimipramine • Sexual dysfunction
removal, the TCAs increased • TCA drug-drug
• concentrations of interaction
monoamines in the • Tremor
synaptic cleft. • Urine retention
• 2) TCAs also block • Weight loss/gain
serotonergic, adrenergic,
histaminic & muscarinic
receptors
Selective Serotonin • Low mood • The acute effect of SSRI Fluoxetine • Blurred vision
Reuptake Inhibitors • Irritability is highly selective action Escitalopram • Dizziness
(SSRI) • Feelings of worthlessness on the serotonin Fluvoxamine • Drowsiness
• Restlessness transportation (SERT). Paroxetine • Dry mouth
• Anxiety • SSRI inhibit the Sertraline • GIT upset
• Sleeping difficulty transporter for binding Citalopram • Headache
at a receptor to enter • Sexual dysfunction
postsynaptic neuron.

Monoamine Oxidase • (typically used when other • Increase brain amine Phenelzine • Dizziness
Inhibitors (MAOI) antidepressants have proven levels by Tranycypromine • Drowsiness
ineffective) • Interfering with NE and Selegiline • Insomnia
• Sadness 5-HT metabolism in • Nausea
• Anxiety nerve ending
• Worry • Neuronal activity Long-term theraphy:
discharges the vesicles, • Edema
increased amount of the • Muscle pains
amine is released. • Myoclonus
 • Enhance the action of • Paresthesias
neurotransmitters. • Sexual dysfunction
• Weight gain

Heterocyclics- • Major depression disorder • Inhibit the reuptake of Duloxetine • Sexual dysfunction
Serotonin- • Anxiety, phobic features, both serotonin and Venlafaxine • Cardiovascular effects
Norepinephrine hypochondriasis, sleep norepinephrine. Diazepam • Headache
Reuptake inhibitors disturbances, poor appetite • contribute to mood • Insomnia
(SNRI) and Stabilization and
• weight loss. symptom relief.
• Panic attacks, phobic disorders
and bipolar affective disorders
• Attention deficit hyperkinetic
disorder and chronic pain
states.
Sedative hypnotics drugs

Name of the • Symptoms • Mechanism of Action Example drugs • Adverse effect

class
Benzodiazepine • insomnia and • Target receptor: GABAA Estazolam • Respiratory
reports increased receptors Flurazepam depression
stress and anxiety • Opens chloride channels & Triazolam • Respiratory arrest
at work.
leads to an increase in Alprazolam • Drowsiness
chloride conductance. Clonazepam • Confusion
• Small hyperpolarization. Diazepam • Headache
• Inhibits formation AP. Lorazepam • Syncope
• Nausea/vomiting
• Diarrhea
• Tremor
Barbiturate • Seizure disorder • Target receptor: GABA Phenobarbital • Respiratory
• Neonatal receptor but different sites Amobarbital (Amytal) depression.
withdrawal from benzodiazepines. Secobarbital (Seconal) • Acute intermittent
• Insomnia • Increases duration of GABA Butalbital porphyria
• Preoperative mediated chloride channel • Hypotension
anxiety opening. • Coma
• Anesthesia • May also block excitatory
glutamic acid.
• Leads to decreased neuronal
activity.
Miscellaneous • Anxiety • Exert CNS effects via Buspirone • Respiratory
Anxiolytics • Panic attack • interaction with certain Chloral hydrate depression
Sedatives & • Insomnia benzodiazepines receptors. Eszopiclone • Angiodema
Hypnotics Ramelteon • Shortness of breath
Zaleplon • Nausea/vomiting
Zolpidem
 SKELETAL MUSCLE RELAXANTS

TYPE SUBTYPE MOA E.g. Desc Therapeutic use Pharmacokinetics Adverse Effects
Competitive Tubocurarine 1st muscle relaxant Adjuvant in Injection Histamine release
antagonists Long acting surgical Not metabolized ↓BP
Block Ach anesthesia. (eliminated/excreted) Bronchospasms
receptors. Skin wheals
Pancuronium Aminosteroid compound - Elimination: Hypertension
Drug Onset: 3-5 mins -kidney (85%) Tachycardia
interactions: Duration: 60-90 mins -liver (15%) Dysrhythmia
Cholinesterase Long acting
inhibitors: ↓ Vecuronium Analogue of pancuronium - Elimination: Few, prolong
effectiveness Duration < pancuronium -kidney (40%) paralysis
NEUROMUSCULAR BLOCKERS (NMBD)

Aminoglycoside Onset: 3-5 mins -liver (60%)

antibiotics: ↑ Duration: 20-35 mins
action Intermediate acting
NONDEPOLARIZING

Ca channel Rocuronium Analogue of vecuronium - Elimination: -

blockers: ↑ Onset: 1-2 mins (similar to -kidney (slightly)
action succinylcholine) -liver (primarily)
Inhalational Duration: 20-35 mins
anesthetics: Intermediate acting
enhance Atracurium Onset: 3-5 mins - Hepatic metabolism Histamine release→
neuromuscular Duration: 25-35 mins (ester hydrolysis). hypotension,
blockade by Intermediate acting Hofmann elimination (in tachycardia,
drugs. plasma/tissue at normal bronchospasm.
body pH/temp) into Laudanosine toxicity
laudanosine. → seizures
Renal failure
Cisatracurium Onset: 3-5 mins - Hofmann elimination Laudanosine toxicity
Duration: 20-35 mins
Mivacurium Short acting - Clearance: by plasma Larger dose →
Larger dose to ↑spd of cholinesterase hypotension,
onset flushing,
No longer in clinical use. bronchospasm.
 Phase I block: Succinylcholine The only depolarizing Adjunct to GA Rapidly metabolized by When administered
Depolarization NMBD. Facilitate plasma cholinesterase (so with halothane:
- Nicotinic Ultra-short acting tracheal need to be administered • Malignant
receptor Onset: 60s intubation. continuously) hyperthermia
- Open Duration: 3-6 mins • ↑ intraocular
channels & ↑ pressure
ionic • ↑ intragastric
conductance. pressure (emesis)
- Depolarization • Muscle pain
of motor • Bradycardia
endplate → • Hyperkalemia
contraction
- Depolarization
persists (not
metabolized) n
depolarized
DEPOLARIZING

membranes
remain
unresponsive to
subsequent
impulses.

Phase II block:
Desensitization
- Endplate
eventually
repolarizes
-
Succinylcholine
continues to
occupy Ach
receptor to
desensitize the
endplate → no
formation of
further AP.
 Inhibit Neostigmine Reversal of neuromuscular Antidote for - Bradyarrhythmia
acetylcholinest Edrophonium blockade. nondepolarizing ↑ salivary secretion

Acetylcholinesterase inhibitor
erase from Pyridostigmine blockers. ↑ GI secretion &
breaking down peristalsis
Ach → Treatment for Stimulate urination
↑lvl/duration myasthenia Miosis
of action → gravis Bronchoconstriction
freer Ach in (neostigmine).
synaptic cleft at
NMJ, will knock
off the NMBD.
(competitive)

GABAB agonist Baclofen Centrally acting ↓ hyperreflexia Oral, intrathecal Weakness

(pre- & ↓ painful spasm Sedation
postsynaptic ↓ anxiety Hypotonia
receptors) → Ataxia
hyperpolarizati Confusion
on Fatigue
Nausea
Liver toxicity
SPASMOLYTICS

Alpha-2- Tizanidine & Centrally acting ↓ hyperreflexia Oral, transdermal patch Drowsiness
CHRONIC USE

receptor Clonidine ↓ muscle tone Dizziness

agonist Relieve spasm Dry mouth
(reinforces Orthostatic
presynaptic hypotension
inhibition in
spinal cord)
GABAA Diazepam Centrally acting ↓ hyperreflexia Oral, intravenous, rectal Sedation
receptors on (benzodiazepine) Brand name: Valium ↓ painful spasm Weakness
spinal cord & Abuse potential ↓ anxiety Hypotension
CNS Memory impairment
Ataxia
Confusion
Depression
 Ryanodine Dantrolene Peripherally acting ↓ body temp - Significant muscle
receptor. Indications: Restore weakness but less
Interferes with - muscle spasticity electrolyte & sedation <
Ca release thru - malignant hyperthermia acid-base bal. diazepam.baclofen
sarcoplasmic
reticulum
channel.
- Cyclobenzaprine Used along with rest & - - Drowsiness
physical therapy. Dizziness
ACUTE USE

Interfering with Dry mouth

polysynaptic reflexes that Constipation
maintain muscle tone. Tiredness
Marked sedative & Fast/irregular hb
antimuscarinic actions. Mental/mood
changes
 ANESTHETICS

TYPE SUBTYPE MOA E.g. Desc PK Therapeutics use Adverse Effects

Halothane Oxidatively metabolize POTENT anaes Cardiac eff:
into tissue-toxic WEAK analgesic - vagomimetic →
hydrocarbons. → co-administered atropine-sensitive
with bradycardia.
May cause toxicity: NO/opioids/local - cardiac arrhythmias
-symptoms: fever, anaes. - concentration-
anorexia, nausea, dependent
vomiting → signs of Relaxes skeletal & hypotension (if
hepatitis uterine muscle. excessive
hypotension, give
Not hepatoxic in with phenylephrine)
paeds.
Malignant
hyperthermia:
• circulatory collapse
GENERAL ANAESTHETICS

& death.
• syndrome: muscle
INHALED

rigidity,
hyperthermia, rapid
onset of tachycardia
& hypercapnia,
hyperkalemia,
metabolic acidosis.
• Susceptible
patients: burn
victims, Duchenne
dystrophy,
myotonia,
osteogenesis
imperfecta, central
core disease.
• ↑in free cytosolic
Ca2+ in skeletal
muscle cells
• - Treatment:
Dantrolene
 Enflurane Potency < halothane Excretion: kidney Greater Fewer arrhythmias
Rapid induction & (contraindication: potentiation of Less sensitization of
recovery kidney failure) muscle relaxants heart to
Excites CNS at lower (curare-like effects) catecholamines
dose → seizure
Isoflurane Very stable - ↑ blood flow & O2 Conc dep hypotension
Tissue toxic consumption by
Cardiac myocardium
arrhythmias (beneficial for
ischemic heart
disease)
Nitrous Oxide Depress respiration Excretion: rapid (poor WEAK anaes Diffusion hypoxia (due
Muscle relaxation solubility in blood & POTENT analgesic its spd of movement
↑ cerebral blood tissue) (but not enough for causing O2 uptake
flow surgery, need to retardation during
Least hepatotoxic combine with more recovery)
= safest anaes potent agent)
Desflurane Very rapid onset & Metabolism: minimal ↓vascular res Toxicity: rare
recovery (low blood Stimulates respi
solubility) reflexes (but not
Low volatility (need inhalation
special heated induction)
vaporizer)
Expensive
Sevoflurane Rapid onset & Metabolism: liver - Nephrotoxic (if fresh
recovery. gas too low)
LOW pungency →
rapid induction
without airways
irritation
Suitable for paeds.
Often for RAPID Thiopental Ultra short acting Metabolism: liver (15% POTENT anaes Minor effects on CVS
INDUCTION (Barbiturate) Highly soluble in lipid per hour) WEAK analgesic (severe hypotension
Depress CNS function in hypovolemic/shock
Must be injected in <1 min. patients)
IV

slowly Contraindication: Apnea

acute intermittent or Coughing
variegate porphyria Chest wall spasm
Laryngospasm
 Bronchospasm
Ketamine Short acting Metabolism: liver Sedation ↑BP
N-methyl-D-aspartate (unconscious but ↑CO
receptor. appear to be awake Hallucinations (adults)
Contraindication: & no pain)
hypertension & stroke. Amnesia
Lipophilic Immobility
Midazolam Used adjunctively with - - Severe post-operative
(Benzodiazepine) inhaled anaes & IV respi depression
opioids,
Onset < thiopental
Duration > thiopental
Its receptor antagonist
(flumazenil) →
accelerate recovery.
Etomidate Imidazole derivatives - - May cause pain,
Rapid induction Myoclonus,
Short duration Nausea
For patient with Adrenal suppression
limited cardiac/respi (prolong
reserve. administration)
Propofol Rapid anaes - Antiemetic action Hypotension (↓
Rapid recovery peripheral res)
As component of
balance anaes & anaes
in OP surgery.
fospropofol Prodrug broken down - - Paresthesia
by alkaline Sensation of skin
phosphatase → (tingling, pricking,
propofol. chilling, burning,
SLOWER onset & numbness)
recovery
Less pain at injection
site

Opioids
(morphine &
fentanyl)
TYPE Adverse Effects
CNS effects:
PK Light-
Metabolism: headedness/sedation
Esters – by plasma Restlessness
cholinesterase Nystagmus
(pseudocholinesterase) Tonic clonic
Amides – by convulsions
SUBTYPE MOA NAME OF DRUGS Desc Therapeutics use
cytochrome P450 Coma
isozymes in liver
CVS effects:
Injection, topical Vasodilators (exc
(localized effect) cocaine)
Heart block
Cardiac electrical
function
• Block Na+ Tetracaine Long action Less dependent on • Pain reducer – IV Antibody formation in
channels → ↓Na Surface action vasoconstrictor (perioperative some patients →
influx → administration. period) allergic response
depolarization POTENCY: high Metabolism: very slow • Weak skeletal Neurotoxic action
→ AP conduction ONSET: slow muscle blocker.
DURATION: long • Minor surgical
• LA is weak base. (spinal) procedures
LOCAL ANAESTHETICS

• pH of infected Procaine Short action Duration of action: • Spinal anesthesia

tissue= 6.4 Readily absorbed limited (to produce
→ so blood flow needs autonomic
ESTERS

(normal=7.4)
• Degree of POTENCY: low to be reduced. How? → blockade in
ionization ONSET: rapid administer ischemic
(function of pKa) DURATION: short vasoconstrictor: agonist conditions)
of drugs varies → sympathomimetic • Postoperative
the nearer the Metabolism: very rapid analgesia
pKa of LA to (t½: 1-2 min) (repeated
tissue pH, the Benzocaine Surface action (Ability injection →
more rapid the to reach superficial tachyphylaxis)
onset time. nerves when applied • Neuropathic pain
to mucous membrane (orally &
surface) parenterally)
 • (near=more Cocaine Surface action Has intrinsic Mood elevation CV toxicity:
unionized, lipid- sympathomimetic Severe hypertension
soluble form) action. (vasoconstrict) Cerebral hemorrhage
Inhibit NE reuptake into Cardiac arrythmias
UNIONIZED: to nerve terminals. Myocardial infarction
cross lipid Metabolism: slow
membrane. Bupivacaine Long action Less dependent on • Pain reducer – IV Severe CV toxicity:
IONIZED: to block Ropivacaine vasoconstrictor (perioperative Arrhythmias
the receptor. POTENCY: high administration. period) Hypotension
ONSET: slow-moderate Metabolism: t½: 3.5 & • Weak skeletal
High extracellular DURATION: long 4.2 hrs muscle blocker. Levobupivacaine –
K+ → enhances LA • Minor surgical less cardiotoxic
action. Lidocaine Medium action t½: 1.5 hrs procedures
Surface action • Spinal anesthesia
High extracellular (to produce
Ca2+ → antagonize POTENCY: low autonomic
LA. ONSET: rapid blockade in
DURATION: ischemic
AMIDES

intermediate conditions)
Prilocaine Metabolism: to o- • Postoperative Decompensation in
toluidine (converting analgesia patients with
agent of Hb → metHb) (repeated cardiac/pulmonary
injection → disease
tachyphylaxis)
• Neuropathic pain
(orally &
parenterally)
Articaine ONSET: fastest

Convulsions – Bupivacaine toxicity –

diazepam (IV) or difficult to treat.
thiopental (short-
Toxicity
acting barbiturate)
treatment
Hyperventilation –
O2
 OPIOID ANALGESICS & ANTAGONISTS

INTRO Natural OR synthetic compounds that produce morphine-like effects.

Bind to specific opioid receptors in CNS → produce effects mimic the action of endogenous peptide NT (endorphins, enkephalins, dynorphins)
Main uses: relieve pain & anxiety.
Euphoric.
RECEPTORS All three receptors are G protein coupled receptors and inhibit adenylyl cyclase.
Associated with ion channels:
- Increasing postsynaptic K+ efflux (hyperpolarization)
- Reducing presynaptic Ca2+ influx → impeding neuronal firing & transmitter release.
Distribution:
CNS:
- Brainstem: influence respiration, cough, nausea, vomiting, BP, pupillary diameter & stomach secretions.
- Medial thalamus: mediates deep pain.
- Spinal cord: attenuation of painful afferent stimuli.
- Hypothalamus: affects neuroendocrine secretion.
- Limbic system: influence emotional behavior.
Periphery: inhibit Ca2+-dependent release of excitatory, proinflammatory substance (substance P).
Immune cells: role of bounding site is unknown.
μ (mu) κ (kappa) δ (delta)
Mediate analgesic properties of opioids. In dorsal horn. Enkephalins
NAME OF THERAPEUTIC
TYPE SUBTYPE ACTION MOA PK ADVERSE EFFECTS
DRUGS USE
 Morphine Major analgesic drug Hyperpolarization Administration: Analgesia Severe respi depression
Analgesia of nerve cells → GIT absorption: Diarrhea Vomiting
Respiration AP → inhibit slow (1st -pass treatment Dysphoria
Depression of cough presynaptic NT metabolism ) Cough relief Allergy-enhanced
reflex release. IM, IV & Acute pulmonary hypotensive effects
Miosis Acts at κ receptors subcutaneous disease ↑cerebral & spinal
Emesis (vomiting) in Lamina I & II → ischemia
GIT ↓substance P Distribution: Acute urinary retention
CV release → Rapid into all body
Histamine release modulates pain. tissues (& fetus)
Hormonal actions Inhibit excitatory
▶️labor
Labor NT release carrying
Infants show phys
nociceptive stimuli.
Repeated use dependent to
→tolerance opiates & exhibit
withdrawal
Death: very rare
symptomps.
BBB: small% (least
Drug interactions:
lipophilic)
Depressant actions –
phenothiazines,
Fate:
monoamide oxidase Conjugated in liver
inhibitors & tricycclic
into glucuronic acid
antidepressants
Morphine-6-
↑analgesia –
glucuronide (very
amphetamine &
OPIOID ANALGESICS

potent analgesic)
STRONG AGONISTS

hydroxyzine
Excreted in urine.
Duration of action:
4-6 hrs
Meperidine Synthetic opioid Binds to opioid Orally Acute pain Large doses:
Depression of respi receptors (μ & κ) Parenterally (analgesia) Anxiety
⬇️peripheral res & Duration: 2-4 hrs Cough Tremors
peripheral blood flow N-demethylated to Diarrhea Muscle twitches
⬆️smooth muscle normeperidine in Urinary Convulsions (rare)
contraction liver retention: less Hyperactive reflexes
Dilate cerebral effect
vessels Excreted in urine Uterine muscle Severe hypotension
⬆️ CSF pressure contraction: less (postoperatively)
Pupil dilation effect
Antimuscarinic action:
Common in Dry mouth
obstetrics Blurred vision

Convulsions &
hyperthermia (if taken
with MAOI)
Methadone Synthetic opiod μ receptor Orally Analgesic Physical dependence
POTENCY = morphine, Accumulates in Heroin &
but less euphoria tissues ▶️bound to morphine
DURATION < substitute
protein & slowly
morphine released
t½: 24 hrs Biotransformed in
liver.
⬆️biliary pressure & Excreted in urine.
constipation
Milder withdrawal
syndrome but
protracted than other
opioids.
Fentanyl Chemically related to Metabolized to IV: Analgesia Similar to other μ receptor
meperidine. inactive -Epidural agonistsx
POTENCY 100x> metabolites by (postoperatively &
morphine cytochrome during labor)
Highly lipophilic P4503A4 system. -Intrathecal
ONSET: rapid Oral transmucosal
DURATION: short (cancer patients)
action [15-30 min] Transdermal patch
(may cause death
Anesthesia from
Often for cardiac hypoventilation due
surgery (negligible to creation of drug
effect on myocardial reservoir & its onset
contractility) is delayed & offset
Muscular rigidity of is prolonged)
chest wall
Pupillary Eliminated in urine.
constrictiction

Contraindication:
Management of acute
& postoperative pain
(bcos of
hypoventilation)
Sufentanil/ Related to fentanyl - - - -
Alfentanil/ All 3 hv diff potency &
remifentanil metabolic disposition.

POTENCY:
Sufentanil > fentanyl
Alfentanil &
remifentanil < fentanyl

DURATION
Alfentanil &
remifentanil < fentanyl
Heroin Synthetic (produced Lipid soluble (cross No accepted
by diacetylation of BBB rapidly than medical use in
morphine (▶️3x morphine → USA.
exaggerated
increase in potency)
euphoria when
injected

Converted to
morphine.
Oxycodone Semisynthetic Orally active Analgesic
derivative of Metabolized to (moderate-
morphine products with lower severe pain)
Sometimes analgesic activity.
formulated with Excretion: kidney
aspirin or
acetaminophen.
Many properties =
morphine.
Abuse of the
sustained-released
preparation (ingestion
of crushed tablest) →
many deaths.
 Codeine Present in crude Oral effectiveness > Analgesic
opium in lower [] & morphine Antitussive
less potent. Converted to effects (higher
POTENCY: < morphine morphine effects at doses
Abuse potential < that doesn’t
morphine cause analgesia)
Less euphoria Euphoria
Dependence: rare
Often used with
aspirin or
acetaminophen.

*most nonprescription
for antitussive →
replaced by
MODERATE AGONISTS

dextromethorphan
(synthetic & non
analgesic & low abuse
potential)
Propoxyphene Derivative of Metabolism: liver Well absorbed Analgesic (mild- Nausea
methadone Peak plasma levels: orally moderate) – Anorexia
Analgesic < codeine occurs in 1 hr. dextro isomer Constipation
(require twice the
dose) or Antitussive – levo Toxicity:
Used with isomer Respi depression
acetaminophen. Convulsions
Hallucinations
Confusion
Cardiotoxicity
Pulmonary edema
 Drugs that stimulate one receptor but block another.
Effects depend on previous exposure of opioids:
- If not recently received opioids → agonist effect & analgesic
- If has opioid dependence → blocking effects (withdrawal symptoms)
Pentazocine Less euphoria Agonist receptor: κ Analgesic Respi depression
In angina, ↑mean Antagonist (moderate) ↓ GIT activity
aortic pressure & receptor: μ & δ ↑ BP
pulmonary arterial Hallucinations
pressure. Activate receptors Nightmares
MIXED AGONIST-ANTAGONIST & PARTIAL AGONIST

↓renal plasma flow in spinal cord. Dysphoria

Tachycardia
Due to multi adverse Dizziness
eff→ decreased usage.
Repeated usage led to
tolerance &
dependence.
Can precipitate
withdrawal syndrome
of a morphine abuser.
Buprenorphine Partial agonist Receptor: μ Sublingually Opiate Little sedation
Acts like morphine in Parenterally detoxification Respi depression
naïve patients but can Metabolism: liver Hypotension
precipitate withdrawal Excretion: bile & Nausea
in morphine users. urine Dizziness
Withdrawal Tablet: for opioid
symptoms: severity & dependence
duration < methadone Injected form:
DURATION: long moderate-severe
analgesic
Nalbuphine/ Limited role in chronic Receptor: κ Oral use Psychotomimetic effects
Butorphanol pain treatment. (of psychosis)
Psychotomimetic
effects < pentazocine Heart & hypertension
(in contrast to pentazocine
& butorphanol)
Tramadol Receptor: μ Analgesic Respi depression
ANALGESIC

Weakly inhibits (moderate- (<morphine)

OTHER

reuptake of NE & 5- moderately Seizures (especially in

HT severe) patients taking SSRI)
 Bind to opioid receptors BUT doesn’t activate any response (or reverse the effects of opioid agonists).
Precipitate the withdrawal symptoms of opioids.
Naloxone Reverse coma & respi Competitive IV (30 seconds None (but
depression antagonist at: onset → patient precipitates
t½: 60-100 mins μ (higher affinity), revived & alert) withdrawal
κ& symptoms in
δ receptors opioid abusers)

Rapidly displaces all

receptor-bound
ANTAGONISTS

opioid molecules &

reverse the effects
of overdosage.
Naltrexone Similar to naloxone - Orally (blocks the Opioid detox Hepatotoxic
DURATION > naloxone effect of injected (when combined
heroin up to 48 hrs) with clonidine &
buprenorphine)

Treating chronic
alcoholism
Nalmefene Similar actions to Parenteral
naloxone & IV
naltrexone. IM
t½: 8-10 hrs Subcutaneous
ANTISEIZURE DRUGS

MOA SODIUM CHANNEL BLOCKADE GABA-RELATED TARGETS CALCIUM CHANNEL BLOCKADE

1. Block voltage-gated Na channels in GABA receptor Inhibits low threshold (T-type) Ca2+
neuronal membranes. Frequency of Cl- channels ↑ currents.
Action is rate dependent. Influx of Cl- → small hyperpolarization Especially in thalamic neurons that act
2. Results in prolong inactivation state → inhibit AP formation. as pacemakers to generate rhythmic
of Na+ channel & refractory period cortical discharge.
of the neuron. E.g.:
E.g.: - benzodiazepines E.g.:
- Phenytoin - phenobarbital - ethosuximide
- Carbamazepine - felbamate - gabapentin
- Lamotrigine - topiramate - pregabalin
- Zonisamide - valproic acid
CLINICAL USES - Generalized tonic-clonic seizures ~VA, carbamazepine, phenytoin
- Partial seizures ~felbamate, phenobarbital, topiramate, VA
- Absence seizures ~ethosuximide, VA, clonazepam
- Myoclonic & atypical absence syndrome ~topiramate, zonisamide, clonazepam
- Status epilepticus ~diazepam, lorezepam
TOXICITY - Teratogenicity: risk of congenital malformations, craniofacial anomalies & spina bifida.
- Overdose toxicity: CNS/respi depressions
- Life threatening toxicity: skin rashes & Steven-Johnson Syndrome
- Withdrawal syndrome
TYPE NAME OF DRUGS ACTION MOA PK USES
TONIC-CLONIC & Carbamazepine 1st line treatment Induces formation Complex partial seizures
PARTIAL of liver-drug
SEIZURES metabolizing
enzymes →
↑drug itself &
↑clearance of
other anti-seizure
drugs.
Lamotrigine 1st line treatment Focal onset seizures
for focal seizures.
Phenytoin Oral
bioavailability

Metabolism: non-
linear
 Elimination:
-kinetic shift from
1st order to zero
order at
moderate to high
dose lvl.
-enhanced in
presence of
inducers
Valproic acid Inhibit
metabolism of
Carbamazepine,
Ethosuximide,
Phenobarbital &
Lamotrigine.
ABSENCE SIZURES Ethosuximide
Clonazepam
Valproic acid
MYOCLONIC Clonazepam
SEIZURES Lamotrigine
Valproic acid
BACK-UP & Felbamate
ADJUNCTIVE Gabapentin
DRUGS Lamotrigine
Levetiracetam
Phenobarbital
Tiagabine
Topiramate
Vigabatrin
Zonisamide
 RESPIRATORY DRUGS

CHAR - Rapid administration & absorption

- Due to rich-blood supply tract thru the alveolar-capillary network
- Forms: gases, sprays, powders, & liquids.
DISEASES Chronic obstructive pulmonary
Asthma Bacterial pneumonia
disease (COPD)
Smoking history some 90% of sufferers Inflammation of lungs due to bacterial infection (S.
Chronic cough & Not common Common pneumoniae)
sputum Can occur in both lungs, one lung or one section of the lung.
production Treatment: antibiotic
Shortness of infrequent Often
breath
Symptoms often Not common
worse at night
Onset Children & young adults Usually > 35 yrs old
INHALATION ACTIVE BRAND
DESC ADVANTAGES DISADVANTAGES
DEVICES INGREDIENTS NAME
Hand-held device ▪ Portable ▪ Needs correct
Medication is dispersed in lungs. Salbutamol Asthalin ▪ Multidose delivery capability actuation & inhalation
Consists of: ▪ Lower risk of bacterial coordination
- Pressurized canister Albuterol Ventolin contamination ▪ Oropharyngeal drug
(contains medications, deposition
solvent & liquid propellant
METERED DOSE
[CFC}) Levalbuterol HCl Xopenex
INHALERS (MDI)
- Chamber outfitted with
mouthpiece & cap.
Dispense constant vol of Fluticasone 50μg Flixotide
solution/suspension per puff
thru pressurized spray. Formoterol
-
Fine mists are produced. fumarate 12mcg
INHALATION A chamber that can be attached to MDI. ▪ Overcome difficulties of using MDI ▪ Large size
ACCESSORY DEVICE Have a one-way valve that holds the medication in the chamber (due to coordination problems, ▪ Needs to be cleaned
(IAD): Spacer before it is inhaled → so u can inhale one or many breaths. physical/mental handicaps, etc) periodically.
▪ ↑medication delivery directly to ▪ Electrostatic charges
airways. may ↓ drug delivery
▪ Prevents candidiasis (yeast to the lungs.
infection) in the mouth.
▪ Prevents dysphonia (hoarse voice)
 A portable inspiratory flow- Terbutaline Bricanyl ▪ Breath-actuated ▪ Adequate inspiratory
driven device. 0.25mg ▪ Spacer not necessary flow (IF) required for
Deliver dry powder ▪ No need to hold breath after delivery
formulations. Beclometasone Becloforte inhalation ▪ May result in high
Drug is formulated in a filler & diproprionate ▪ Portable pharyngeal
contained in a capsule. 250mg ▪ No propellant deposition
No gas Fluticasone Flixotide ▪ Humidity potentially
No propellants. propionate causes powder
DRY POWDER Drug delivery is determined by clumping → reducing
INHALER (DPI) inspiratory volume & the flows Salbutamol Salbutamol dispersal of fine
generated by the patient. dry powder particle mass
Doesn’t require coordination. capsules
Ipratropium ATEM
bromide 20mcg

Xinafoate Seretide
evohaler

ROTAHALER Deliver measured dose of powdered form drug.

Drug form: capsule
Consist of 2 chambers: mouthpiece & reservoir (separated by an
integrated mesh)
Indication: Albuterol Proventil ▪ Substitute for other inhalation ▪ Decreased portability
- Unable to use other types of Ventolin devices ▪ Longer setup &
inhalation devices. Ipratropium Atrovent ▪ Allow administration of large administration time
(phys/cognitive deficits) bromide doses. ▪ Higher cost
NEBULIZER - Severe dyspnea Ipratropium & DuoNeb ▪ Coordination not required
- When high doses of albuterol
medication or O2 must be Acetyl cysteine Mucosil
administered.
Cromolyn sodium Intal
 RENAL PHARMACOLOGY (DIURETICS)

SUBTYPE MOA E.g. PK ADVERSE EFFECTS INDICATION CONTRAINDICATION

Osmotic effect in PCT Mannitol IV Extracellular water ▪ Glaucoma (intraocular
Hydrophilic compound Orally → expansion & dehydration pressure)
DIURETICS
OSMOTIC

that easily filtered with diarrhea Hypernatremia ▪ Cerebral edema

little reabsorption→ Hyperkalemia (Intracranial pressure)
↑urinary output via ▪ Acute renal failure
osmosis. ▪ Acute drug poisoning
Acetazolamide Orally
▪ Sedation ▪ Acute mountain
↑urine pH (HCO3)
▪ Drowsiness sickness
CARBONIC ANHYDRASE INHIBITOR

ONSET: 30-120 Cirrhosis:

▪ Paresthesia ▪ Epilepsy
mins - ↓excretion of NH3
▪ Hypersensitivity ▪ Hyperphosphatemia
Inhibit carbonic DURATION: 12 hrs → hyperammonemia
▪ Renal stone ▪ Metabolic alkalosis
anhydrase in the brush Excretion: PCT S2 & hepatic
(phosphaturia & ▪ CSF leakage
border system & segment* encephalopathy
Dorzolamide Ocular (topical) hypercalciuria)
cytoplasm in all tissues
* ▪ Metabolic acidosis
→ interferes with
▪ Hyperchloremia
NaHCO3 reabsorption →
(metabolic acidosis
diuresis Open-angle glaucoma
▪ Hyponatremia
Brinzolamide Ocular (topical) Ocular hypertension
▪ Hypokalemia
*
▪ Hypophosphatemia
(potassium wasting)

Inhibit sodium-potassium- Furosemide Orally Ototoxicity (imbalanced of Acute pulmonary

chloride co-transporter in Bumetanide IV fluids & salts in inner ear → edema
THICK ASCENDING LoH. Torsemide ONSET: fast tissue swelling → influence Heart failure
Ethacrynic acid DURATION: short nerve signals transmission) Hypertension
Hence, ↓Na, K, Cl
Excretion: active Hyponatremia & Edema
LOOP DIURETICS

reabsorption→ water is
drawn into the nephron &
tubular secretion hypokalemia Pt with hypercalcemia
↑urine vol. Interferes with uric Hypocalcemia & or hyperkalemia
acid secretion hypomagnesemia Acute renal failure
Also ↓Ca & Mg →hyperuricemia Sulfonamide
reabsorption. (due to the hypersensitivity
+ve charged lumen is lost Hyperuricemia
then Ca & Mg will not be Hypovolemia
repelled into the body)
 Inhibit Na/Cl co- Chlorothiazide Orally Ototoxicity 1° Hypertension
transporter on the Hydrochlorothia ONSET: slow Hyponatremia & Refractory edema
luminal membrane of zide DURATION: long hypokalemia Calcium nephrolithiasis
THIAZIDES

DCT. (40hrs) Hypomagnesemia & Nephrogenic diabetes

Excretion: active hypercalcemia insipidus
↑NaCl excretion tubular secretion Hyperlipidemia & Osteoporosis
↑ K excretion Interferes with uric hyperglycemia Calcinuria
Mg excretion acid secretion Hypokalemic metabolic
↓Ca excretion →hyperuricemia alkalosis
Metolazone
↑Ca reabsorption Hypovolemia
THIAZIDE-

Indapamide
Hyperuricemia
LIKE

Chlorthalidone
Sulfa allergy

Aldosterone antagonist Spironolactone ONSET: slow

POTASSIUM SPARING DIURETICS

Antagonize cytoplasmic DURATION: 24-48

aldosterone receptors in hrs
CD.
Na+ channels inhibitors Triamterene Hyperkalemia Hypertension
Inhibit Na influx via Na Hyperkalemia
Metabolic acidosis Prevent hypokalemia
channels in the luminal Liver disease (need
Gynecomastia Pt with hepatic cirrhosis
membrane adjustment)
GIT upset & peptic ulcer 2° hyperaldosteronism
Amiloride Orally
DURATION: 24 hrs
 BLOOD PHARMACOLOGY

INTRO Platelet response to vascular injury: Coagulation factors: ada 13

- Resting platelets INTRINSIC: 12, 11, 9. 8
- Platelet adhesion EXTRINSIC: 7
- Platelet activation COMMON: 10, Prothrombin, Fibrinogen, 13
- Platelet aggregation
- Clot formation
- Fibrinolysis
MAJOR SUBGROUP E.g. MOA PK USES ADVERSE EFFECTS
GROUPS
Heparin Combines with IV ↑bleeding
antithrombin III → Subcutaneous - Protamine can
Deep vein
heparin-ATIII complex. Bioavailability: 20% lessen the risk.
thrombosis
Complex irreversibly Moderate transient
Pulmonary
inactivates thrombin thrombocytopenia
Direct thrombin embolism
by binding to it & (heparin)
inhibitors Acute MI
factor Xa. Immune-mediated
LMWH Affect factor Xa but IV thrombocytopenia
Fondaparinux not thrombin. Subcutaneous Pregnancy
(less likely)
Bioavailability: 90% Osteoporosis
> DURATION (heparin)
ANTICOAGULANT
Vitamin K Warfarin Inhibits Vit K epoxide • Orally Chronic Bleeding disorders
Inhibit
antagonist reductase (VKOR) → • Food: no effect anticoagulation
action/synthesis
reduced Vit K • 99% bound to Cytochrome P450-
of coagulation
regeneration → γ- plasma albumin. Pregnancy inducing drugs:
factors.
carboxylation of Vit K- • Can cross placenta → ↑warfarin
dependent clotting → bone defect & clearance
factors (factors 2, 7, 9 hemorrhage in → ↓anticoagulant
ANTICLOTTING DRUGS

& 10) fetus. effect

• Metabolism:
Reversal agent: products are Cytochrome P450
- Vit K (slow) inactive. inhibitors:
- Fresh/frozen • Excretion: → ↓warfarin
plasma (rapid) conjugated to clearance
glucuronic acid in → ↑anticoagulant
urine & stool. effect
 Tissue Alteplase • Directly convert IV • Deep vein Bleeding
plasminogen (normal plasminogen to thrombosis Cerebral hemorrhage
activators (t.PA human plasmin. • Serious Hypersensitivity
derivatives) plasminogen) • Selectively to pulmonary (streptokinase)
plasminogen that has embolism
Reteplase bounded to fibrin. • Acute myocardial
THROMBOLYTICS/ (mutated) infarction
PLASMINOGEN ONSET: faster • Peripheral arterial
ACTIVATORS/ DURATION: thrombosis &
FIBRINOLYTICS longer emboli
Dissolve blood
clots by activating Tenecteplase
plasminogen. (mutated)
t½: longer
Streptokinase Forms complex with IV
(protein from streptococci) endogenous
plasminogen.
NOT selective.
Cyclooxygenase Aspirin • Inhibit thromboxane ▪ Myocardial ▪GIT irritation
-1 (COX-1) A2 synthesis by infarction ▪Bleeding risks
inhibitors irreversible prevention in ▪Hypersensitivity
acetylation of COX-1 coronary ▪↓kidney function
ANTIPLATELET → ↑ bleeding time. thrombosis ▪Reye’s syndrome
DRUGS • Used In low doses ▪ Prevent ▪Platelet dysfunction
- ↓Platelet (100-325mg/day) coronary ▪Asthma
aggregation ∴low doses thrombosis in exacerbation
triggered by unstable ▪ Tinnitus
selectively inhibit
endogenous angina
TXA2
mediators: ▪ Prevent
∴ high doses inhibit transient
(prostaglandin,
both TXA2 & PGI2 → ischemic
thromboxane,
can reverse the attacks (TIA) &
ADP, thrombin beneficial effects. recurrent of
& fibrin)
ischemic
TXA2: potent stroke.
aggregation inducer
PGI2: potent
aggregation inhibitor
Glycoprotein Abciximab Reversibly block ▪ Prevent ▪ Bleeding
IIb/IIIa IIb/IIIa receptor restenosis after ▪ Thrombocytopenia
inhibitors Eptifibatide complex. coronary
∴receptor for angioplasty.
Tirofiban fibrinogen, ▪ Acute coronary
vitronectin, syndromes
fibronectin & von
Willebrand factor.
(Glanzmann’s
thrombasthenia: xde
receptor ni)
ADP inhibitors Clopidogrel Irreversibly inhibit • Food interferes Prevent TIA &
Ticlopidine binding of ADP to with absorption ischemic stroke.
P2Y12 receptors on of ticlopidine but
platelet. not clopidogrel. Stent insertion
• Both bound to during myocardial
Interfere other pp. infarction.
drugs: • Metabolism:
Phenytoin, hepatic by
tolbutamide, cytochrome P450
warfarin, • Elimination: renal
fluvastatin, & fecal
tamoxifen
 PDE/adenosine Dipyridamole Dual MOA: • Prophylaxis for Headaches
uptake 1. Inhibit angina pectoris Bleeding risk
inhibitors Cilostazol phosphodiesterase • Adjunct to
enzyme esp. PDE3 & warfarin in CONTRAINDICATION:
PDE5 which prevention of Congestive heart
responsible for thrombosis in failure (cilostazol)
degradation of cAMP cardiac valve
& cGMP. replacement.
2. Inhibit adenosine • Combine with
uptake by aspirin for 2°
endothelial cells & prevention of
erythrocytes → ischemic stroke.
↑[adenosine] • Intermittent
claudication
*cAMP: platelet (cilostazol)
aggregation inhibitor
by ↓ intracellular Ca2+
*cGMP: vasodilator
*adenosine: ↑platelet
cAMP
VITAMIN K Phytonadione (vit K1) Oral • Vit K deficiency -
Parenteral • Reverse
anticoagulant of
excess warfarin
Fresh plasma Factor 8 (hemophilia Hemophilia Immunologic
& purified A) reactions risk
HEMOSTATIC AGENTS

human blood Factor 9 (hemophilia Possible infection

clotting factors B)
REPLACEMENT
FACTORS
Clotting factors Desmopressin • ↑plasma [] of Hemophilia A Thrombosis
acetate von Von Willebrand Hypotension
(vasopressin Willebrand disease Myopathy
V2 receptor factor & factor Diarrhea
agonist) 8
ASNTIPLASMIN Aminocaproic acid Inhibit fibrinolysis Orally Prevention/
DRUGS Tranexamic acid management of
acute bleeding
episodes in
hemophilia pt.
 ANTISEPTICS & DISINFECTANTS

INTRO
CLASS E.g. DESC MOA PK INDICATIONS & SIDE EFFECTS
CONTRAINDICATIONS
ALCOHOLS
ALDEHYDES
BIGUANIDE
HALOGENS
PHENOL
DERIVATIVES
OXIDIZING
AGENTS
ACIDS
METALLIC SALTS
QUARTERNARY
AMMONIUM
DYES
FURAN
DERIVATIVES

DRUGS FOR WOUND HEALING

INTRO
CLASS E.g. DESC MOA PK INDICATIONS & SIDE EFFECTS
CONTRAINDICATIONS
DEBRIDING
AGENTS
ANTIBIOTICS
TRIPEPTIDE-
COPPER
COMPLEX (TPP)
NATURAL
PRODUCTS
 ANTIHELMINTIC DRUGS

HELMINTHS E.g. DESC MOA PK INDICATIONS & SIDE EFFECTS

CONTRAINDICATIONS
NEMATODES Mebendazole Synthetic Interferes with the Chew → Swallow Whipworm (Trichuris Short-term:
• Elongated benzimidazole assembly of the (↑surface area) trichiuria) Mild nausea
roundworms compound. parasites’ <10% absorbed (↑with Pinworm (Enterobius Vomiting
• Hv complete Low incidence of microtubules/tubulin high fat meals) vermicularis) Diarrhea
digestive AE. & ↓ glucose uptake. Highly protein bound Hookworms (Necator Abdominal pain
system Parasites expelled americanus &
(mouth – with feces. Metabolism: Ancylostoma High dose: (rare)
anus) Efficacy: depends on Rapid (during 1st pass duodenale) Hypersensitivity
• Infects: GIT transit time, effect) Roundworm (Ascaris Agranulocytosis
intestine, infection intensity, t½: 2-6 hrs lumbricoides) Alopecia
blood, tissues. strain of parasite. ↑liver enzymes
Excretion: Alt for trichinosis
Urine (Trichinella spp.)
Bile
Feces
Ivermectin Semisynthetic Intensifies GABA Orally (rapid) Nematodes, insects, Dizziness
macrocyclic lactone mediated t½: 16 hrs acarine (mites & Rash
Mixture of transmission in PNS ticks)
ivermectin B1a & Hyperpolarisation Excretion: Fever
B1n derived from Paralyzes the muscle Feces Onchocerciasis (river Headache
Streptomyces of nematodes & blindness – Drowsiness
avermitilis arthropods. microfilaria Weakness
Onchocerca volvulus) Pruritus
No paralytic action Strongyloidiasis Diarrhea
on mammals (due to (threadworm – Joint&muscle pains
BBB & GABA Strongyloides Hypotension
mediated stercoralis)
transmission occurs Fatigue
only in CNS) Nausea
Vomiting
Abdominal pain
Piperazine Heterocyclic ring (2 Block Ach at Orally Alt for ascariasis & Nausea
nitrogen atom at myoneural junction Max plasma lvls: 2-4hrs enterobiasis Vomiting
opp position) of parasite Diarrhea
Muscle paralysis Excretion: CI: Abdominal pain
Dislodgement Urine (2-6hrs) Pregnant Dizziness
 Impaired Headache
renal/hepatic
History of Rare:
epilepsy/chronic Neurotoxicity
neurologic disease Allergic reactions

Pregnant

TREMATODES Praziquantel ↑permeability to Orally Schistosomiasis Common:

Ca2+ t½: 0.8-1.5 hrs (blood flukes – S. Headache
↑muscle activity mansoni, S. Dizziness
Paralysis & Bioavailability haematobium, S. Drowsiness
dislodgement ↓ phenytoin, japonicum, S. Lethargy
carbamezepine& mekongi)
corticosteroids Less common:
↑cimetidine & high Clonorchiasis (C. Nausea
carbohydrate meal sinensis) Vomiting
Abdominal pain
80% bound to protein Paragonimiasis (P. Loose stools
Westermani) Pruritus
Metabolism: Urticaria
1st pass effect to inactive Opisthorchiasis (O. Arthralgia
mono&polyhydroxylated Viverrini) Myalgia
products Low-grade fever
Taeniasis (T. saginata
Excretion: & T. solium) Mild & transient
Kidney (60-80%) elevation of liver
Bile (15-35%) Hymenolepiasis enzymes
(Hymenolepis nana)
Common in pt without
Diphyllobothriasis corticosteroids:
(Diphyllobothrium Headache,
latum) nausea,vomiting
Hyperthermia
Cysticercosis (T. Arachnoiditis
solium) ↑ICP
Mental changes
CI: seizures
Pregnancy
(↑abortion)
 Oxamniquine Semisynthetic Schistosome Orally (with food) S. mansoni infections 3hrs after dose:
tetrahydroquinoline esterificated the t½: 2.5 hrs (praziquantel res) Dizziness
Some treatment drug Katayama syndrome Headache
fails due to serum. Alkylates parasite’s Metabolism: Drowsiness
DNA to inactive 6-carboxyl S. haematobium, S.
Interrupts nucleic metabolites japonicum (NOT Common:
acid & protein EFFECTIVE) Nausea vomiting
synthesis Excretion: urine Diarrhea
Death Colic
CI: pregnancy Pruritus
Urticaria

Infrequent:
Low-grade fever
Urine discoloration
Proteinuria
Haematuria
↓leukocytes

Rare: seizures
CESTODES Niclosamide Chlorinated Inhibit Not absorbed in GIT Taenia saginata (beef Nausea
salicylamide phosphorylation of Not found in tapeworm) Vomiting
True derivative ADP in parasite’s blood/urine. T. solium (pork Diarrhea
tapeworms mitochondria (NO tapeworm) Abdominal discomfort
Flat, segmented ATP) Diphyllobothrium
body Detachment of latum (fish
Intestine scolex from tapeworm)
NO mouth & intestinal wall
digestive tract Dislodged Alt for fasciolopsis
buski, Heterophyes
ONLY affects adult heterophyes &
worm not the ova. Metagonimus
yokogawai
Can inhibit in
mammalian cells but Cysticercosis &
with much higher hydatid disease (NOT
doses EFFECTIVE)
Albendazole A benzimidazole Same as other Absorption: GIT nematodes &
carbamate benzimidazoles. <5% orally, ↑with fatty cestodes
meal. ↑corticosteroids
 Better than GIT parasites (on
mebendazole & Metabolism: empty stomach)
pyrantel pamoate. Rapid 1st pass hepatic Tissue parasites (with
to albendazole fatty meal)
sulfoxide
Ascariasis
t½: 8-12 hrs
Trichuriasis
Hookworm
Excretion: urine
Pinworm
Hydatid disease
(Echinococcus
granulosus – dog
tapeworm)

ANTIVIRAL DRUGS

TYPE OF
VIRUS E.g. DESC MOA PK USES RES AE
DRUG
NEURAMINID Oseltamivir Sialic acid analogs Inhibit viral Orally Uncomplicate Mutations: Common:
ASE Effective against neuraminidase Prodrug: rapidly d acute Neuraminidase Nausea
INHIBITORS type A & B No release of new hydrolyzed influenza (pt Haemagglutinin Vomiting
influenza viruses. virions ≥1 yo) but, mutants Abdominal cramp
Do not interfere No spread from cell Distribution: are LESS
with immune to cell Low plasma Prophylaxis infective & LESS Prophylactic use:
response to protein binding (>13) virulent. Headache
influenza A Widely Fatigue
vaccine. distributed Diarrhea
throughout body.
Rare:
Metabolism: Rash
INFLUENZA VIRUS STRAIN

t½: 6-10 hrs Transient

neuropsychiatric
Excretion: kidney Bronchitis
Insomnia
Vertigo

Dosage
adjustment for
renal insufficiency
 Zanamivir Inhaled Uncomplicate Nasal & throat
Bioavailability: d acute discomfort
<5% orally influenza A & Angioedema (rare)
B (pt >7 yo) Bronchospasm (pt
Distribution: with
Limited pp Effective asthma/COPD)
binding prophylaxis
but not FDA
Metabolism: not approved
significant
VIRAL Amantadin Adamantane Inhibit M2 protein Absorption: Influenza A M2 protein
UNCOATING e derivatives (H+ channel) of the GIT (rapid & infections mutation
INHIBITORS Inhibit replication virus completely) Developed
of 3 antigenic I. Prevention of rapidly in ~50%
subtypes of acid-mediated Distribution: treated ind.
influenza A dissociation of Throughout body Cross res to
(H1N1, H2N2, ribonucleoprotein + CNS each other
H3N2) complex → Cross res to
Doesn’t interfere inhibits virus Metabolism: oseltamivir &
with influenza A replication. Not extensively zanamivir
vax. II. ↑pH →alter t½: 12-18hrs
Useful during haemagglutinin (young), 29hrs
endemic/non- →inhibit virus (elderly)
vaccinated pt) assembly
Excretion:
90% excreted
unchanged.
Rimantadin Absorption:
e GIT (rapid &
completely), but
slower

Distribution:
BBB

Metabolism:
Extensively
t½: 25hrs
(young), 36hrs
(elderly)
 Excretion:
<25% excreted
unchanged
Ribavirin Synthetic Not fully elucidated Orally, IV & Aerosol: Rhinovirus & Aerosol:
guanosine analog (only studied in inhalation RSV infection enterovirus (hv Dec respinfunction
Hv broad antiviral influenza virus) Oral (bronchiolitis preformed (esp pt with COPD)
activity to RNA & Bioavailability: & pneumonia) mRNA – no Rare-
DNA viruses. Converted to 5’- 64%. ↑with fatty -infants & need syntehsis) Rash
phosphate meal, ↓with young Conjunctivitis
derivatives: antacids. children Bronchospasm
Ribavirin
monophosphate – Distribution: Oral: Oral & iV:
inhibits GTP Minimally enter + INF-alpha Haemolytic
synthesis & its systemic (HCV) anemia
pathways. circulation
Ribavirin In tissues exc IV: Oral + INF:
triphosphate – CNS Hantaan virus Fatigue
inhibit 5’ capping of Crimean & Nausea
viral mRNA with Metabolism: congo virus Insomnia
GTP. Phosphorylated haemorrhagic Rash
to triazole fever Depression
carboxylic acid Lassa fever Anemia
derivative in Severe Pancreatitis
liver. adenovirus
t½: 12.5 days infection

Excretion:
Urine

Interferon Natural occuring Antiviral, IM, IV, SC, IFN-a-2a: Flu-like symptoms
HEPATIC VIRAL INFECTION

(IFN) glycoprotein of immunoregulatory intralesion Chronic HCV, GI distress

cytokines. & antiproliferative. hairy cell Neurotoxicity
Classified Pegylated IFN - leukemia,
according to their Type I (IFN-a, IFN-B): delayed AIDS’ Kaposi’s Myelosuppression
origin of cell type: potent antiviral. absorption, sarcoma Granulocytopaenia
IFN-a (leukocytes Type II (IFN-y): duration of Malignant Anaemia (rare)
IFN-B (fibroblast) immunomodulatory. action, clearance melanoma
IFN-y (NK cells & (1wk) Follicular Rare:
T-lymphocyte) lymphoma Thyroiditis
 Bind to cell surface Non-pegylated Condyloma Alopecia
Pegylated IFN: receptor. -remains in acuminata Heart failure
conjugate of Initiates JAK-STAT plasma (16- (genital wart) Hypersensitivity
recombinant IFN- signal transduction 36hrs) Hepatic failure
a & polyethylene pathway iFN-a-2b +
glycol (PEG). Halt virus replication Elimination: ribavirin: High dose:
& its release within Cellular uptake & chronic HCV Dec fertility
infected cells. catabolism in Miscarriage
liver&kidney IFN-a-n3:
Induce production genital wart CI:
of cytokines & thru AID
oxidants intralesion Heart prob
Inc host immune injection Myelosuppression
response. drug
IFN-B-1a & Neurology
IFN-B-1b: disorder
multiple Children
sclerosis Pregnancy

IFN-y-1b:
prevent/delay
malignant
osteopetrosis
Lamivudine Synthetic Prodrug: Rapidly absorbed HIV Mutation of Typically mild &
cytosine analog phosphorylated by (GIT) – not food <doses for HIV viral enzymes, well tolerated
Inhibitor of HBV cellular enzymes. dependent indicated for drug efficacy
DNA polymerase Inhibit viral enzymes HBV. Headache,
& HIV reverse at low [] Distribution: Discontinuatio Resistance in dizziness, fatigue,
transcriptase. Widely n of drug HIV-1 seen insomnia, GI
Protein binding →relapse within 12 discomfort,
Lamivudine ↑ 36%. weeks of fever, URTI
level of treatment,
zidovudine Metabolism: while HBV in 6 ↑ALT, lipase &
Bioavailability: month or > creatinine kinase
85-90%
t½: 5-9 hrs

Excretion:
Kidney >70%
 Co-
administration
with
trimethoprim
sulfamethoxazole
: ↓ clearance of
lamivudine
Adefovir Analog of Prodrug: Lamivudine- Not developed Dose-dependent
adenosinemonop phosphorylated to Distribution: resistance after 1 nephrotoxicity
hosphate adefovir Protein binding < HBV year of Lactic acidosis
diphosphate → than 4% treatment Hepatomegaly
inhibits HBV’s DNA
polymerase → chain Bioavalibility:
termination of viral 59%, (unaffected
DNA. by food)
Ibuprofen ↑
bioavalibility

Excretion:
glomerular
filtration &
tubular
secretion, 45% as
active compound
HSV-1 Aciclovir/Ac Prototype of Converted to active Incomplete oral Oral: Natural res: Common:
HSV-2 yclovir antiherpevirus metabolite via 3 absorption. HSV-1 & HSV-2 CMV lacks headache, nausea,
VZV drugs phosphorylation infections: a specific viral diarrhoea
EBV A guanine analog steps: Distribution: herpes thymidine
CMV 1) Viral thymidine 20% plasma genitalis, kinase Topical: local
Effects of aciclovir kinase converts protein bound. herpes irritation
Effective to human DNA aciclovir to Widely encephalitis, Acquired res:
• Mutation of
HERPESVIRUS INFECTION

during acute synthesis is much aciclovir-PO4 distributed. herpes Less frequent: skin
phase (not < than viral’s. (Viral thymidine kinase Significant keratitis, viral thymidine rash, fatigue, fever,
latent phase) has > affinity to amount found in herpes kinase hair loss,
aciclovir compared to amniotic fluid, labialis, • Cross depression
human’s: acyclovir- placenta, neonatal resistance to
PO4 accumulated in
breast milk. herpes. antiviral agents Dose-limiting of IV:
infected cells)
that require. neurotoxicity
Metabolism: IV: • thymidine (tremor, seizure,
kinase delirium)
 2) Human enzymes t½: 3-4 hours HSV infection activation: & nephrotoxicity
converted aciclovir– (normal kidney). in famciclovir, (azotemia)
PO4 to acyclovir- immunocomp • ganciclovir, (Slow infusion &
(PO4)2 then to Excretion: romised valacyclovir good hydration
acyclovir-(PO4)3 Unchanged via Patients • Rare: mutation risk of
3) Aciclovir (PO4)3 glomerular nephrotoxicity)
(↓ affinity) of
competed with filtration & Ointment: viral
dGTP to be tubular secretion initial herpes • DNA
incorporated into genitalis, not polymerase
viral DNA → chain effective for
elongation recurrent
terminated. disease

Ophthalmic:
herpes
keratoconjunc
tivitis

Higher doses:
prophylaxis of
VZV (in high
risk
immunocomp
romised pt)

CI:
hypersensitivit
y
Valacyclovir an acyclovir Same as acyclovir Oral absorption Same as Same as High doses:
prodrug is > completed acyclovir acyclovir GI problems &
compared to thrombotic
less dose acyclovir. thrombocytopenic
required than purpura in AIDS
acyclovir. Bioavailability: patients.
3-4X than IV
acyclovir

Esterified to
acyclovir in
 human body in
intestine &
first pass
metabolism

Other PK same
as acyclovir
Penciclovir Guanosine analog Same as acyclovir Topical herpes labialis Same as
Active against & herpes acyclovir
HSV-1, HSV-2, Metabolism: genitalis
VZV t½: 20–30X >
than acyclovir
Cidofovir phosphonate Phosphorylation IV, intravitreal, Treatment & - Nephrotoxicity
cytosine analog doesnt depend on topical. prophylaxis of
viral enzymes. CMV retinitis Rare:
CMV, HSV-1, HSV- ▪ Similar level of Bioavailability: in AIDS Neutropenia,
2, VZV, human cidofovir-(PO4)2 Extremely low Patient metabolic acidosis
herpesvirus seen in infected & & ocular hypotony
(HHV)-6, HHV-8, uninfected cells. Metabolism: acyclovir (↓ intraocular
adenovirus, ▪ cidofovir-(PO4 Not significant resistant HSV pressure)
poxviruses, )2 competes with t½: 84 hours infection
polyomaviruses & deoxcycytidine-
human (PO4)3 (dCTP) for Excretion: CI:
papillomavirus viral DNA Unchanged Renal
polymerase → by glomerular impairment
inhibits DNA chain filtration Pt taking
elongation Probenecid concurrent
↓tubular nephrotoxic
secretion drugs (eg:
NSAIDS)
Ganciclovir analog of 1) CMV protein Absorption: IV: Mutation of myelosuppression,
acyclovir, a kinase IV • CMV retinitis viral protein particularly
guanosine analog phosphotransferase Intraocular (immunocom kinase pUL97 neutropenia
UL97 & implant promised pt)
20X > against HSV thymidine Orally (poor) • CMV colitis & Mutation of neurotoxicity
CMV kinase converts esophagitis pUL97 not
acyclovir to Distribution: • CMV- cross- fever, rash,
Probenecid aciclovir-PO4 Body, CNS, immunoglobul resistance to abnormal liver
CMV

↑level of (CMV lacks vitreous humor in to treat cidofovir & function, retinal
ganciclovir. thymidine kinase). foscarnet detachment
Ganciclovir 2) Human enzymes Metabolism: CMV
↑level of converted Not extensive pneumonitis. mutation
didanosine ganciclovir–PO4 t½: 3-4 hrs (↓affinity) of
to Oral: viral DNA
ganciclovir-(PO4)2 Excretion: Prevention & polymerase
then to ganciclovir- glomerular maintenance (UL54)
(PO4)3 filtration & therapy of
3)Ganciclovir (PO4)3 tubular secretion CMV retinitis Mutation of
competed with (immunocom UL54 is cross-
dGTP to be promised pt) resistance to
incorporated into cidofovir &
viral DNA → chain Intraocular: lesser extent,
elongation. CMV retinitis foscarnet
terminated.

▪Ganciclovir (PO4)3
concentrated 100X >
in infected
cells, but bone
marrow cells
sensitive to this
drug.