ASPIRIN

Mechanism of Action
Description: Aspirin is an analgesic, anti-inflammatory and antipyretic. It inhibits cyclooxygenase, which is
responsible for the synthesis of prostaglandin and thromboxane. It also inhibits platelet aggregation.
Duration: 4-6 hr.
Pharmacokinetics:
Absorption: Rapidly absorbed from the GI tract (oral); less reliable (rectal); absorbed through the skin
(topical). Peak plasma concentrations after 1-2 hr.
Distribution: Widely distributed; crosses the placenta; enters breast milk. Protein-binding: 80-90%.
Metabolism: Hepatic; converted to metabolites.
Excretion: Via urine by glomerular filtration, active renal tubular secretion and passive tubular reabsorption (as
unchanged drug); via haemodialysis; 15-20 minutes (elimination half-life, parent drug).
MIMS Class
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) / Anticoagulants, Antiplatelets & Fibrinolytics (Thrombolytics)

ATROPINE
Mechanism of Action
Description: Atropine is an anticholinergic agent which competitively blocks the muscarinic receptors in
peripheral tissues such as the heart, intestines, bronchial muscles, iris and secretory glands. Some central
stimulation may occur. Atropine abolishes bradycardia and reduces heart block due to vagal activity. Smooth
muscles in the bronchi and gut are relaxed while glandular secretions are reduced. It also has mydriatic and
cycloplegic effect.
Pharmacokinetics:
Absorption: Readily absorbed from the GI tract; also absorbed from mucous membranes, eye, and through
intact skin.
Distribution: Distributes throughout the body and crosses the blood-brain barrier and placenta.
Metabolism: Incomplete metabolism in the liver.
Excretion: Excreted in urine as unchanged drug and metabolites. Half-life reported to be 4 hr.
MIMS Class
Mydriatic Drugs / Antispasmodics / Other Cardiovascular Drugs / Antidotes & Detoxifying Agents

CAPTOPRIL
Mechanism of Action
Description: Captopril competitively inhibits the conversion of angiotensin I (ATI) to angiotensin II (ATII), thus
resulting in reduced ATII levels and aldosterone secretion. It also increases plasma renin activity and
bradykinin levels. Reduction of ATII leads to decreased Na and water retention. This promotes vasodilation
and BP reduction.
Onset: 1-1.5 hr.
Pharmacokinetics:
Absorption: Rapidly absorbed from the GI tract (approx 60-75%). Reduced absorption w/ food. Time to peak
plasma concentration: Approx 1 hr.
Distribution: It crosses the placenta and enters breast milk (approx 1%). Plasma protein-binding: Approx 30%
(mainly albumin).
Excretion: Via urine (40-50% as unchanged drug, the rest as disulfide and other metabolites). Elimination halflife: 2-3 hr.
MIMS Class
ACE Inhibitors/Direct Renin Inhibitors

CLOPIDOGREL
Mechanism of Action
Description: Clopidogrel inhibits adenosine diphosphate (ADP) from binding to its receptor sites on the
platelets and subsequent activation of glycoprotein GP IIb/IIIa complex thus preventing fibrinogen binding,
platelet adhesion and aggregation.
Pharmacokinetics:
Absorption: Rapidly but incompletely absorbed from the GI tract (oral).
Distribution: Protein-binding: Extensive.
Metabolism: Hepatic: Extensive; converted to inactive carboxylic acid derivative and thiol derivative (active).
Excretion: Via urine and faeces (as metabolites and unchanged drug).
MIMS Class
Anticoagulants, Antiplatelets & Fibrinolytics (Thrombolytics)

FUROSEMIDE
Mechanism of Action
Description: Furosemide inhibits reabsorption of Na and chloride mainly in the medullary portion of the
ascending Loop of Henle. Excretion of potassium and ammonia is also increased while uric acid excretion is
reduced. It increases plasma-renin levels and secondary hyperaldosteronism may result. Furosemide reduces
BP in hypertensives as well as in normotensives. It also reduces pulmonary oedema before diuresis has set in.
Pharmacokinetics:
Absorption: Fairly rapidly absorbed from the GI tract (oral).
Distribution: Crosses the placenta and enters breast milk. Protein-binding: 99%.
Excretion: Via urine (as unchanged); 2 hr (elimination half-life), may be prolonged in neonates and renal and
hepatic impairment.
MIMS Class
Diuretics

DIPHENHYDRAMINE
Mechanism of Action
Description: Diphenhydramine blocks histamine H1-receptors on effector cells of the GI tract, blood vessels
and respiratory tract. It also causes sedation and has some anticholinergic action.
Pharmacokinetics:
Absorption: Absorbed well from the GI tract (oral); peak plasma concentrations after 1-4 hr.
Distribution: Widely distributed, CNS; crosses the placenta and enters breast milk. Protein-binding:Highly
bound.
Metabolism: Extensive first-pass metabolism.
Excretion: Via urine (as metabolites, small amounts as unchanged drug); 1-4 hr (elimination half-life).
MIMS Class
Antihistamines & Antiallergics

HYDROCORTISONE
Mechanism of Action
Description: Hydrocortisone is a corticosteroid used for its anti-inflammatory and immunosuppressive effects.
Its anti-inflammatory action is due to the suppression of migration of polymorphonuclear leukocytes and
reversal of increased capillary permeability. It may also be used as replacement therapy in adrenocortical
insufficiency.
Pharmacokinetics:
Absorption: Readily absorbed from the GI tract (oral); sodium phosphate and sodium succinate esters are
rapidly absorbed but the free alcohol and its lipid soluble ester are slowly absorbed (IM); Acetate is slowly
absorbed (intra-articular inj); absorbed from the skin (denuded areas).
Distribution: Crosses the placenta. Protein-binding: >90%.
Metabolism: Hepatic (metabolised to hydrogenated and degraded forms).
Excretion: Via urine (as conjugates and glucuronide, with small portion as unchanged drug).
MIMS Class
Corticosteroid Hormones / Eye Corticosteroids / Topical Corticosteroids

HYOSCINE
Mechanism of Action
Description: Hyoscine competitively blocks muscarinic receptors and has central and peripheral actions. It
relaxes smooth muscle and reduces gastric and intestinal motility.
Onset: Oral, IM: 0.5-1 hr; IV: 10 min.
Duration: Oral, IM: 4-6 hr; IV: 2 hr.
Pharmacokinetics:
Absorption: Tertiary salts: Readily absorbed. Quaternary salts: Poorly absorbed.
Distribution: Reversibly bound to plasma proteins.
Metabolism: Hepatic.
Excretion: Via urine (as metabolites); 4.8 hr (elimination half-life).
MIMS Class
Mydriatic Drugs / Muscle Relaxants / Antivertigo Drugs / Antispasmodics

METOCLOPRAMIDE
Mechanism of Action
Description: Metoclopramide enhances the motility of the upper GI tract and increases gastric emptying
without affecting gastric, biliary or pancreatic secretions. It increases duodenal peristalsis which decreases
intestinal transit time, and increases lower oesophageal sphincter tone. It is also a potent central dopaminereceptor antagonist and may also have serotonin-receptor (5-HT3) antagonist properties.
Pharmacokinetics:
Absorption: Rapidly and almost completely absorbed from the GI tract (oral); peak plasma concentrations
after 1-2 hr.
Distribution: Widely distributed; crosses the blood-brain barrier and placenta; enters breast milk.
Metabolism: Extensively hepatic.
Excretion: Via urine (as unchanged drug, sulfate or glucuronide conjugates and metabolites), faeces; 4-6 hr
(terminal elimination half-life).
MIMS Class
Antiemetics / GIT Regulators, Antiflatulents & Anti-Inflammatories

KETOROLAC
Mechanism of Action
Description: Ketorolac inhibits prostaglandin synthesis by decreasing the activity of the cyclooxygenase
enzyme.
Onset: 30-60 min (oral); 10 min (IM).
Duration: 6-8 hr (oral/IM).
Pharmacokinetics:
Absorption: Well absorbed (oral/IM); peak plasma concentrations after 30-60 min.
Distribution: Protein-binding: 99%. Crosses the placenta; enters breast milk; poorly penetrates into CSF.
Metabolism: Hepatic via glucuronic acid conjugation.
Excretion: Via urine (90%, as unchanged drug and metabolites); via faeces (remaining dose). Terminal
elimination half-life: 4-6 hr; 6-7 hr (elderly); 9-10 hr (renal impairment).
MIMS Class
Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) / Ophthalmic Decongestants, Anesthetics, AntiInflammatories

METOCLOPRAMIDE
Mechanism of Action
Description: Metoclopramide enhances the motility of the upper GI tract and increases gastric emptying
without affecting gastric, biliary or pancreatic secretions. It increases duodenal peristalsis which decreases
intestinal transit time, and increases lower oesophageal sphincter tone. It is also a potent central dopaminereceptor antagonist and may also have serotonin-receptor (5-HT3) antagonist properties.
Pharmacokinetics:
Absorption: Rapidly and almost completely absorbed from the GI tract (oral); peak plasma concentrations
after 1-2 hr.
Distribution: Widely distributed; crosses the blood-brain barrier and placenta; enters breast milk.
Metabolism: Extensively hepatic.
Excretion: Via urine (as unchanged drug, sulfate or glucuronide conjugates and metabolites), faeces; 4-6 hr
(terminal elimination half-life).
MIMS Class
Antiemetics / GIT Regulators, Antiflatulents & Anti-Inflammatories

NOREPINEPHRINE
Mechanism of Action
Description: Norepinephrine is a direct-acting sympathomimetic which stimulates 1- and -adrenergic
receptors. Its -agonist effects cause vasoconstriction, thereby raising systolic and diastolic BP with reflex
slowing of heart rate.
Onset: Rapid.
Duration: Short; stops within 1-2 min after discontinuing the infusion.
Pharmacokinetics:
Absorption: Oral: Destroyed in the GI tract; SC: Poorly absorbed.
Distribution: Mainly localises in sympathetic nervous tissue; crosses the placenta but not the blood-brain
barrier.
Metabolism: Metabolised in the liver and in other tissues by the enzymes catechol-O-methyltransferase
(COMT) and monoamine oxidase (MAO).
Excretion: Via urine (mainly as metabolites).
MIMS Class
Vasoconstrictors

PARACETAMOL
Mechanism of Action
Description: Paracetamol exhibits analgesic action by peripheral blockage of pain impulse generation. It
produces antipyresis by inhibiting the hypothalamic heat-regulating centre. Its weak anti-inflammatory activity is
related to inhibition of prostaglandin synthesis in the CNS.
Onset: Oral: <1 hr. IV: 5-10 min (analgesia); w/in 30 min (antipyretic).
Duration: 4-6 hr (analgesia). IV: 6 hr (antipyretic).
Pharmacokinetics:
Absorption: Readily absorbed from the GI tract. Time to peak plasma concentration: Approx 10-60 min (oral).
Distribution: Distributed into most body tissues; crosses the placenta and enters breast milk. Plasma protein
binding: Approx 25%.
Metabolism: Hepatic via glucuronic and sulfuric acid conjugation. N-acetyl-p-benzoquinoneimine (minor
hydroxylated metabolite), is usually produced in very small amounts by CYP2E1 and CYP3A4 isoenzymes in
the liver and kidneys.
Excretion: Mainly via urine (as glucuronide and sulfate conjugates, <5% as unchanged drug). Elimination halflife: Approx 1-3 hr.
MIMS Class
Analgesics (Non-Opioid) & Antipyretics

RANITIDINE
Mechanism of Action
Description: Ranitidine competitively blocks histamine at H2-receptors of the gastric parietal cells which
inhibits gastric acid secretion. It does not affect pepsin secretion, pentagastrin-stimulated intrinsic factor
secretion or serum gastrin.
Pharmacokinetics:
Absorption: Readily absorbed from the GI tract. Bioavailability: Approx 50%. Time to peak plasma
concentration: Approx 2-3 hr (oral); approx 15 min (IM).
Distribution: Widely distributed; enters breast milk, crosses the placental barrier. Volume of distribution:
Approx 1.4 L/kg. Plasma protein binding: Approx 15%.
Metabolism: Hepatically metabolised. Small portion is converted to N-oxide (major metabolite, approx 4-6% of
a dose), S-oxide and desmethylranitidine.
Excretion: Via urine (oral: Approx 30%, IV: 70%) as unchanged drug and in the faeces. Elimination half-life:
Approx 2-3 hr.
MIMS Class
Antacids, Antireflux Agents & Antiulcerants

SALBUTAMOL
Mechanism of Action
Description: Salbutamol is a direct-acting sympathomimetic with -adrenergic activity and selective action on
2 receptors, producing bronchodilating effects. It also decreases uterine contractility.
Onset: Inhalation: 5-15 min; oral: 30 min.
Duration: Inhalation: 3-6 hr; oral: 8 hr; modified-release preparation: 12 hr.
Pharmacokinetics:
Absorption: Readily absorbed from the GI tract.
Metabolism: Hepatic and in the gut wall.
Excretion: Via the urine as metabolites and unchanged drug. Some excretion in the faeces.
MIMS Class
Drugs Acting on the Uterus / Antiasthmatic & COPD Preparations

TRAMADOL
Mechanism of Action
Description: Tramadol inhibits reuptake of norepinephrine, serotonin and enhances serotonin release. It alters
perception and response to pain by binding to mu-opiate receptors in the CNS.
Onset: Approx 1 hr.
Duration: 9 hr.
Pharmacokinetics:
Absorption: Readily absorbed from the GI tract. Bioavailability: Approx 70-75% (oral); 100% (IM).
Distribution: Widely distributed. Crosses the placenta and enters breast milk.
Metabolism: Extensive hepatic first-pass metabolism. Converted to O-desmethyltramadol (active) via Nand O-demethylation by CYP3A4 and CYP2D6 isoenzymes and also via glucuronidation or sulfation.
Excretion: Via urine (as metabolites). Elimination half-life: Approx 6 hr.
MIMS Class
Analgesics (Opioid)

TRANEXAMIC ACID
Mechanism of Action
Description: Tranexamic acid is an antifibrinolytic agent that competitively inhibits breakdown of fibrin clots. It
blocks binding of plasminogen and plasmin to fibrin, thereby preventing haemostatic plug dissolution.
Pharmacokinetics:
Absorption: Absorbed from the GI tract; peak plasma concentrations after 3 hr (oral). Bioavailability: 30-50%,
unaffected by food intake.
Distribution: Widely throughout the body. Protein-binding: Very low. Crosses the placenta and distributed into
breast milk.
Excretion: Urine (as unchanged drug); 2 hr (elimination half-life).
MIMS Class
Haemostatics

IPRATROPIUM BROMIDE + SALBUTAMOL

Mechanism of Action
Description: Ipratropium bromide is an anticholinergic agent that inhibits vagally-mediated reflexes by
antagonising the action of acetylcholine. It prevents the increases in intracellular concentration of cyclic
guanosine monophosphate (cyclic GMP) which are brought about by interaction of acetylcholine with the
muscarinic receptors on bronchial smooth muscle. Salbutamol is a direct-acting 2-adrenergic agent. It acts on
the airway smooth muscle resulting in bronchodilation.
Pharmacokinetics:
Distribution: Ipratropium: Minimally bound to plasma proteins.
Excretion: Ipratropium: Elimination half-life: About 2 hr (after IV or inhalational admin). Plasma half-life of
salbutamol: About 4-6 hr.
MIMS Class
Antiasthmatic & COPD Preparations