PHARMACOLOGY OF

RIGHT LOW BACK PAIN

Diclofenac (NSAIDs)
Indications Dosage Administration contraindications
Acute pain, Pain Oral : Should be taken if the patient is
and inflammation Adult: 75-150 mg with food. Take unable to tolerate
associated with daily in divided immediately after diclofenac or has
musculoskeletal doses. meals. an increased
and joint disorders, cardiovascular risk.
Pain and Injetions : Diclofenac is
inflammation Adult: 75 mg once contraindicated in
associated with daily via deep patients who have
periarticular intragluteal inj. If had a myocardial
disorders, Pain and necessary, may give infarction in the
inflammation another 75 mg at previous 12
associated withsoft alternate site Max: months.
tissue disorders, 150 mg daily. Max
Postoperative duration:2 days.
inflammation,
Postoperative pain.
• pharmacodynamics
Diclofenac sodium binds to and chelates both isoforms of the cyclooxygenase 1 (COX-1) and 2 (COX-2) enzymes.
This blocks the conversion of arachidonic acid to prostaglandins. Diclofenac sodium's inhibition of COX-2 will
relieve pain and inflammation, and the drug's inhibition of COX-1, may have adverse gastrointestinal effects.
Diclofenac sodium may be more active against COX-2 than some other non-steroidal anti-inflammatory drugs
containing carboxylic acids.

• pharmacokinetics
Absorption: Rapidly absorbed from the gastrointestinal tract, skin. Decreased absorption rate with food.
Bioavailability : 55%. Time to peak plasma concentration (under fasted conditions): Approx 1 hour, (conventional
tab or cap, supp); approx 4-5 hours (extended-release tab or cap, supp); approx 0.25 hour (powder fororal
solution); approx 20 minutes (IM);10-20 hours (transdermal). Distribution: Penetrates the synovial fluid. Crosses
the placenta, enters breast milk. Volume of distribution: Approx 1.3-1.4 L/kg (oral). Plasma protein binding:
>99%,mainly to albumin. Metabolism: Undergoes first-pass metabolism in the liver and metabolised via
hydroxylation and methoxylation into 4'-hydroxydiclofenac, 3'-hydroxydiclofenac, 5-hydroxydiclofenac, 4’, 5-
dihydroxydiclofenac and 3'-hydroxy-4'-methoxydiclofenac; further metabolised via glucuronidation orsulfation.
Excretion: Mainly via urine (approx 60%as glucuronide and sulfate conjugates)bile (approx 35%). Terminal
eliminationhalf-life: Approx 1-2 hours; approx 12hours (transdermal).
• Adverse Reactions
Significant: Kounis syndrome; Na and fluid retention, new-onset or exacerbation of hypertension, decreased platelet
adhesion and aggregation, prolonged bleeding time; rarely, severe blood dyscrasias (e.g. agranulocytosis,
thrombocytopenia, aplastic anaemia); increased transaminase, increased risk of hyperkalaemia, renal
papillarynecrosis and other renal injury (systemic long-term use); increased risk of gastrointestinal anastomotic leak;
Quincke's oedema or urticaria; masks signs and symptoms of infection; rarely increased risk of aseptic meningitis;
keratitis, sight-threatening complication(e.g.corneal perforation) (ophthalmic).
Ciprofloxacin (fluoroquinilones)
Indications Dosage Administration contraindications
Infeksi contohnya Adult: Patients with Should be taken Hypersensitivity to
pyelonephritis uncomplicated with food. Take ciprofloxacin or
cases: 500 mg immediately after other quinolones.
bid(2x1) for 7 days meals. History or risk of QT
prolongation;
known history of
myasthenia gravis.
Concomitant use
with tizanidine.
• pharmacodynamics
Ciprofloxacin is a second generation fluoroquinolone that is active against many Gram negative and Gram positive
bacteria. It produces its action through inhibition of bacterial DNA gyrase and topoisomerase IV. Ciprofloxacin
binds to bacterial DNA gyrase with 100 times the affinity of mammalian DNA gyrase. There is no cross resistance
between fluoroquinolones and other classes of antibiotics, so it may be of clinical value when other antibiotics are
no longer effective. Ciprofloxain and its derivatives are also being investigated for its action against malaria,
cancers, and AIDS.

• pharmacokinetics
Absorption: Rapid and well absorbed from the gastrointestinal tract. Bioavailability: Approx 70-80% . Time to
peak plasma concentration: 0.5-2 hours (conventional tab); 1-2.5 hours (extended-release tab).
Distribution: Widely distributed in the tissues. Crosses placenta, enters breast milk, bile (high concentrations), and
CSF (10% noninflamed meninges; 14-37% inflamed meninges). Volume of distribution: 2.1-2.7 L/kg. Plasma
protein binding: 20-40%.
Metabolism: Partially metabolised in the liver to desthyleneciprofloxacin (M1), sulphociprofloxacin (M2),
oxociprofloxacin (M3), and formylciprofloxacin (M4) in low concentrations.
Excretion: Via urine [approx 40-50% as unchanged drug, approx 15%, as metabolites (oral); 70% as unchanged
drug, 10% as metabolites (parenteral)]; faeces [20-35% (oral), 15% (IV)]. Elimination half-life: Approx 3-5 hours.
• Adverse Reactions
Significant: Irreversible tendinitis, tendon rupture, peripheral neuropathy, CNS effects (e.g. seizures, increased
intracranial pressure), QT interval prolongation, torsades de pointes, psychiatric reactions (e.g. depression, psychosis,
suicidal ideation), aortic aneurysm ruptures or dissection (long-term use), photosensitivity reactions, haemolytic
reactions (in G6PD deficiency patient), hyperglycaemia; delayed corneal healing (ophth). Rarely, crystalluria. Blood
and lymphatic system disorders: Jaundice.
Tamsulosin (alpha-blocker)
Indications Dosage Administration contraindications
benign prostatic Adult: 400 mcg Should be taken History of
hyperplasia, once daily. with food. Take 30 orthostatic
ureteral stones, min following the hypotension.
prostatitis, and same meal daily. Severe renal
female voiding Swallow whole, do impairment (CrCl
dysfunction not <10 mL/min).
open/chew/crush. Severe hepatic
impairment.
• pharmacodynamics
Tamsulosin is an alpha adrenoceptor blocker with specificity for the alpha-1A and alpha-1D subtypes, which are
more common in the prostate and submaxillary tissue. The final subtype, alpha-1B, are most common in the aorta
and spleen. Tamsulosin binds to alpha-1A receptors 3.9-38 times more selectively than alpha-1B and 3-20 times
more selectively than alpha-1D. This selectivity allows for a significant effect on urinary flow with a reduced
incidence of adverse reactions like orthostatic hypotension.

• pharmacokinetics
Absorption: Rapidly absorbed from the gastrointestinal tract. Bioavailability: 30% increase in fasting state. Food
reduces rate and extent of absorption. Time to peak plasma concentration: Approx 1 hour (immediate-release);
approx 6 hours (prolonged-release).
Distribution: Volume of distribution: Approx 0.2 L/kg (prolonged-release); 16 L (immediate-release). Plasma
protein binding: Approx 99%, mainly to α1-acid glycoprotein.
Metabolism: Extensively metabolised in the liver by CYP3A4 and CYP2D6 to metabolites and further undergoes
extensive conjugation to glucuronide or sulfate.
Excretion: Via urine (76%, <10% as unchanged drug); faeces (21%). Elimination half-life: 5-7 hours (immediate-
release); 9-13 hours (prolonged-release).
• Adverse Reactions
Significant: 1st dose orthostatic hypotension, syncope, floppy iris syndrome in cataract and glaucoma surgery,
hypersensitivity reactions, MI exacerbations.
Cardiac disorders: Dyspnoea, palpitations.
Drotaverine (antiphasmodik)
Indications Dosage Administration contraindications
cholecystitis and Adult: 40-80 mg tid May be taken with Severe
gallbladder (3 x 1) or without food. renal/hepatic/cardi
disorders. ac dysfunction.
Porphyria.
• pharmacodynamics
Elevated cAMP levels lead to relaxation of smooth muscle cells. This effect is particularly significant in the
gastrointestinal tract, blood vessels, and the reproductive system.

• pharmacokinetics
Absorption: Drotaverine is well-absorbed after oral administration. Its absorption is not significantly affected by
food intake.
Distribution: The drug is distributed widely in the body, and it can cross the blood-brain barrier. It has a relatively
short half-life.
Metabolism: Drotaverine undergoes extensive metabolism in the liver, primarily through the cytochrome P450
system. The major metabolite is the active N-desethyl metabolite.
Elimination: The metabolites are primarily excreted in the urine. The elimination half-life of drotaverine is
relatively short, contributing to its dosing frequency.

• Adverse Reactions
Vertigo, nausea, vomiting, dry mouth.
Methocarbamol
Indications Dosage Administration contraindications
pain associated Adult: 40-80 mg May be taken with Brain damage;
with muscle spasm tid. or without food. epilepsy;
May be taken with myasthenia gravis,
meals to reduce GI coma or pre-coma
discomfort. states.
• pharmacodynamics
Methacarbamol is a skeletal muscle relaxant with an unknown mechanism of action. Methacarbamol has been
shown to block spinal polysynaptic reflexes, decrease nerve transmission in spinal and supraspinal polysynaptic
pathways, and prolong the refractory period of muscle cells. Methocarbamol does not act as a local anesthetic upon
injection. In animal studies, methocarbamol also prevents convulsions after electric shock.

• pharmacokinetics
Absorption: Rapidly and almost completely absorbed from the gastrointestinal tract. Time to peak plasma
concentration: 1-2 hours (oral).
Distribution: Plasma protein binding: 46-50%.
Metabolism: Metabolised in the liver via dealkylation and hydroxylation.
Excretion: Via urine (mainly as metabolites). Elimination half-life: 1-2 hours.

• Adverse Reactions
Significant: CNS depression.
Blood and lymphatic system disorders: Leucopenia.
Cardiac disorders: Bradycardia.
Ear and labyrinth disorders: Vertigo.
Eye disorders: Blurred vision, nystagmus, diplopia, conjunctivitis.
Gastrointestinal disorders: Dyspepsia, nausea, vomiting, metallic taste.
References :
• Anon. Ciprofloxacin (Ophthalmic) . Lexicomp Online. Hudson, Ohio.
Wolters Kluwer Clinical Drug Information, Inc.
• Anon. Methocarbamol. Lexicomp Online. Hudson, Ohio. Wolters
Kluwer Clinical Drug Information, Inc.
• MIMS
• DRUGBANK