Pharmacy viva questions and answers: 45 spoken answers for B.Pharm and D.Pharm lab and semester vivas

How do you tell an oil-in-water emulsion from a water-in-oil emulsion?

I use three bench tests. In the dilution test an o/w emulsion mixes freely with water while a w/o emulsion mixes with oil. In the dye test a water-soluble dye such as amaranth colours the continuous phase of an o/w emulsion uniformly under the microscope, and an oil-soluble dye such as Sudan III does the same for w/o. The conductivity test is the quickest: an o/w emulsion conducts electricity because water is the continuous phase.

Follow-up: 'which type is given orally?' Oil-in-water, because it is palatable and washes off the tongue.

What is HLB and how do you use it to pick an emulsifier?

HLB is the hydrophile-lipophile balance, a number from 0 to 20 on Griffin's scale that expresses how water-loving a surfactant is. Emulsifiers with an HLB of about 3 to 6 stabilise water-in-oil emulsions and those with 8 to 18 stabilise oil-in-water emulsions. In practice I calculate the required HLB of the oil phase from the published values of each oil, weighted by proportion, and blend two surfactants such as Span 80 and Tween 80 to match it.

If asked for the HLB of a wetting agent or a solubiliser: 7 to 9 for wetting, 13 to 15 for detergents, 15 to 18 for solubilisers.

Differentiate flocculated and deflocculated suspensions.

In a deflocculated suspension the particles exist as individual units, settle slowly, and form a dense, hard cake at the bottom that is difficult to redisperse, although the supernatant stays cloudy and the product looks elegant. In a flocculated suspension the particles form loose aggregates called flocs that settle quickly to a large, loosely packed sediment with a clear supernatant, but which redisperses easily on shaking. For a pharmaceutical suspension I want controlled flocculation, achieved with electrolytes, surfactants or polymers, so the dose stays uniform.

Sedimentation volume F equals Vu by Vo; F close to 1 means a well-flocculated system.

What are the common tablet defects and their causes?

Capping is the separation of the top or bottom crown of the tablet, and lamination is splitting into layers; both come from entrapped air, excess fines or too much pressure. Picking and sticking are material pulling onto the punch face, usually from excess moisture or too little lubricant. Mottling is uneven colour from a coloured drug or poorly mixed dye, and chipping is edge breakage from worn tooling. I would first check granule moisture, fines and lubricant level, then the machine.

The examiner wants cause and remedy together; 'capping, so I would reduce fines and increase binder' is a full answer.

What is the role of a disintegrant, a binder and a lubricant in a tablet?

A binder such as starch paste, PVP or HPMC holds the powder together into granules and gives the tablet mechanical strength. A disintegrant such as starch, sodium starch glycolate or croscarmellose swells or wicks water into the tablet so it breaks up in the stomach and releases the drug. A lubricant such as magnesium stearate reduces friction between the tablet and the die wall during ejection, while a glidant such as talc or colloidal silica improves powder flow into the die. Too much magnesium stearate slows dissolution, because it is hydrophobic.

That last sentence is the application the examiner is waiting for.

How is the friability test performed and what is the limit?

A sample of tablets, usually 10 or an amount close to 6.5 g for lighter tablets, is dedusted and weighed, placed in a Roche friabilator and rotated at 25 revolutions per minute for 4 minutes, which is 100 revolutions, dropping the tablets about 15 cm each turn. After dedusting again, the loss in weight should be not more than 1 per cent for conventional compressed tablets. Any cracked, cleaved or broken tablet means the batch fails regardless of the weight loss.

Hardness is tested separately with a Monsanto or Pfizer tester; a hard tablet can still be friable.

State the disintegration test conditions and the limit for uncoated tablets.

Six tablets are placed in the six tubes of the basket-rack assembly of the disintegration apparatus, which moves up and down through a distance of about 5 to 6 cm at 28 to 32 cycles per minute in water or the specified medium at 37 plus or minus 2 degrees. Uncoated tablets must disintegrate within 15 minutes according to the Indian Pharmacopoeia, with discs used if specified. Film-coated and enteric-coated tablets have longer limits and, for enteric tablets, a prior test in acid.

Disintegration is not dissolution; the examiner's follow-up is why a tablet that disintegrates can still have poor bioavailability.

Name the USP dissolution apparatus types and when each is used.

Apparatus 1 is the rotating basket, used for capsules and for tablets that float or disintegrate slowly. Apparatus 2 is the rotating paddle, the commonest for ordinary tablets and capsules, usually at 50 or 75 rpm in 900 mL of medium at 37 degrees. Apparatus 3 is the reciprocating cylinder for extended-release products, and apparatus 4 is the flow-through cell for poorly soluble drugs and implants. The result is expressed as per cent drug released at a fixed time against the monograph's Q value.

Q is the amount of dissolved active ingredient specified in the monograph; the stage 1 test needs each unit at Q plus 5 per cent.

What does the angle of repose tell you and what are the limits?

The angle of repose is the maximum angle between the surface of a pile of powder and the horizontal plane, measured by the fixed-funnel method, and it reflects interparticle friction, so it predicts flow. An angle below 25 degrees means excellent flow, 25 to 30 is good, 30 to 40 is passable and may need a glidant, and above 40 means very poor flow. I confirm it with Carr's compressibility index and Hausner's ratio from the bulk and tapped densities.

Carr's index below 15 per cent is excellent flow; above 25 to 30 per cent is poor. Keep both scales ready.

Why is isotonicity important, and how do you adjust it?

An injection or eye drop should have the same osmotic pressure as body fluids, equivalent to about 0.9 per cent sodium chloride, because a hypotonic solution causes haemolysis and a hypertonic one causes crenation and pain. I calculate the adjustment by the sodium chloride equivalent method, where each ingredient's E value gives the amount of NaCl it is equivalent to, and add enough sodium chloride or dextrose to make up the deficit. The freezing point depression method is the alternative, using a target of minus 0.52 degrees.

Follow-up: name a product that is deliberately hypertonic. Mannitol 20 per cent for raised intracranial pressure.

State the conditions for moist heat and dry heat sterilisation.

Moist heat sterilisation in an autoclave uses saturated steam under pressure at 121 degrees and 15 pounds per square inch for 15 minutes, or 134 degrees for 3 minutes, and kills by coagulating proteins; it is used for aqueous injections, surgical dressings and culture media. Dry heat in a hot-air oven uses 160 degrees for 2 hours, or 170 degrees for 1 hour, kills by oxidation, and is used for glassware, oils, powders and ointments that steam cannot penetrate. Biological indicators are Geobacillus stearothermophilus for the autoclave and Bacillus atrophaeus for dry heat.

If asked about heat-sensitive products: filtration through a 0.22 micron membrane or gaseous sterilisation with ethylene oxide.

Classify ointment bases with an example of each.

Hydrocarbon or oleaginous bases such as white soft paraffin are occlusive and emollient but greasy and not water-washable. Absorption bases such as wool fat and hydrophilic petrolatum can take up water to form w/o emulsions. Water-removable bases such as hydrophilic ointment are o/w emulsions that wash off easily and are cosmetically acceptable. Water-soluble bases such as polyethylene glycol ointment contain no oil at all and are used when the drug must be released readily or the site is hairy.

If asked which base for a cream for a weeping lesion: a water-removable base, because an occlusive base traps exudate.

Differentiate first-order and zero-order kinetics with examples.

In first-order kinetics a constant fraction of the drug is eliminated per unit time, so the rate is proportional to concentration, the half-life is constant and a plot of log concentration against time is a straight line; most drugs follow this. In zero-order kinetics a constant amount is eliminated per unit time regardless of concentration because the enzymes are saturated, so a small dose increase produces a large rise in plasma level. Phenytoin at therapeutic doses, ethanol and high-dose aspirin are the standard examples.

The application: zero-order drugs need therapeutic drug monitoring because the dose-response is non-linear.

What is therapeutic index and why does it matter?

Therapeutic index is the ratio of the median lethal dose to the median effective dose, LD50 over ED50, or in humans the ratio of the toxic dose to the effective dose in 50 per cent of patients. A high index, as with penicillin, means a wide safety margin; a low index, as with digoxin, lithium, warfarin, phenytoin and aminoglycosides, means plasma levels must be monitored and doses adjusted carefully. It is derived from quantal dose-response curves in animals during preclinical testing.

The examiner may ask for a better measure: the certain safety factor, LD1 over ED99, which accounts for overlap of the curves.

What is bioavailability and what is first-pass metabolism?

Bioavailability is the fraction of an administered dose that reaches the systemic circulation in unchanged form, and the rate at which it does so; intravenous bioavailability is 100 per cent by definition. First-pass metabolism is the loss of drug in the gut wall and liver before it reaches the systemic circulation after oral dosing, which is why drugs like glyceryl trinitrate, lignocaine and propranolol have low oral bioavailability. Sublingual, rectal and transdermal routes bypass the liver partly or fully.

Follow-up: bioequivalence. Two formulations are bioequivalent when their AUC and Cmax ratios fall within 80 to 125 per cent.

What is a prodrug? Give examples.

A prodrug is an inactive or less active compound that is converted in the body into the active drug, usually by enzymatic metabolism. It is designed to improve absorption, reduce toxicity, mask taste or target a tissue. Examples are enalapril, which is hydrolysed to enalaprilat; levodopa, which crosses the blood-brain barrier and is decarboxylated to dopamine; prednisone, which becomes prednisolone; and sulfasalazine, which is split by gut bacteria into 5-aminosalicylic acid at the site of action in the colon.

Give four examples in one breath; it signals preparation and ends the question.

Explain the mechanism of aspirin and why low-dose aspirin is antiplatelet.

Aspirin irreversibly acetylates cyclooxygenase, blocking the conversion of arachidonic acid to prostaglandins and thromboxane A2, which gives its analgesic, antipyretic and anti-inflammatory effects. Platelets have no nucleus and cannot resynthesise the enzyme, so a single low dose stops thromboxane production for the platelet's lifetime of about 7 to 10 days, whereas the vessel wall recovers its prostacyclin synthesis within hours. That is why 75 to 150 mg daily is used for cardiovascular prophylaxis.

Be ready for the contrast: ibuprofen inhibits COX reversibly, so its antiplatelet effect is short-lived.

What is the antidote for paracetamol poisoning and how does it work?

N-acetylcysteine is the antidote. In overdose, the glucuronide and sulphate pathways are saturated, so a larger share of paracetamol is oxidised by CYP2E1 to the toxic metabolite NAPQI, which depletes hepatic glutathione and binds liver cell proteins, causing centrilobular necrosis. N-acetylcysteine replenishes glutathione and acts as a substitute sulfhydryl donor, so it is most effective within 8 to 10 hours of ingestion but is still given later. Activated charcoal is used early if the patient presents within an hour or two.

Pair it with the other antidotes examiners ask together: naloxone for opioids, flumazenil for benzodiazepines, atropine and pralidoxime for organophosphates.

How are heparin and warfarin different in mechanism and monitoring?

Heparin acts immediately by potentiating antithrombin III, which inactivates thrombin and factor Xa, so it is given parenterally and monitored with the activated partial thromboplastin time; protamine sulphate is its antidote. Warfarin acts over 2 to 3 days by inhibiting vitamin K epoxide reductase, so the liver stops making active factors II, VII, IX and X; it is oral, monitored with the prothrombin time expressed as INR, and reversed with vitamin K or fresh frozen plasma. Warfarin is teratogenic, so heparin is used in pregnancy.

Low-molecular-weight heparins such as enoxaparin act mainly on Xa and do not need routine aPTT monitoring.

Why do ACE inhibitors cause a dry cough, and what is the alternative?

ACE, angiotensin-converting enzyme, is also kininase II, which degrades bradykinin. Inhibiting it raises bradykinin and prostaglandins in the bronchial mucosa, which sensitises cough receptors and causes a persistent dry cough in about 10 to 15 per cent of patients, more often in women and Asian populations. Angioedema is a rarer consequence of the same mechanism. The alternative is an angiotensin receptor blocker such as losartan or telmisartan, which blocks the AT1 receptor directly and leaves bradykinin unaffected.

Both classes are contraindicated in pregnancy and bilateral renal artery stenosis; say so before the examiner asks.

Why are non-selective beta blockers contraindicated in asthma?

Bronchial smooth muscle relaxes through beta-2 receptors stimulated by circulating adrenaline, and a non-selective blocker such as propranolol blocks them, causing bronchoconstriction that can be fatal in an asthmatic. Cardioselective beta-1 blockers such as atenolol, metoprolol and bisoprolol are safer but not completely safe, because selectivity is lost at higher doses. Beta blockers also mask the tachycardia of hypoglycaemia in diabetics, which is the other classic caution.

Answering with both the mechanism and the safer alternative covers the usual follow-up.

What is the mechanism of action of penicillins and why do they have selective toxicity?

Penicillins are beta-lactam antibiotics that bind penicillin-binding proteins, the transpeptidases that cross-link peptidoglycan chains in the bacterial cell wall, so the wall becomes weak and the bacterium lyses osmotically; they are bactericidal and act best on growing cells. They are selectively toxic because human cells have no cell wall and no peptidoglycan. Resistance comes mainly from beta-lactamase enzymes, which is why amoxicillin is combined with clavulanic acid, a beta-lactamase inhibitor.

If asked the commonest adverse effect: hypersensitivity, from mild rash to anaphylaxis, which is why a test dose or history is taken.

What are the main toxicities of aminoglycosides and how are they reduced?

Aminoglycosides such as gentamicin and amikacin cause ototoxicity, both cochlear and vestibular, which can be irreversible, and nephrotoxicity, which is usually reversible; they also cause neuromuscular blockade at high doses. Toxicity depends on trough levels, so I would use once-daily dosing, which gives a high peak for concentration-dependent killing and a long low trough for recovery, monitor serum levels and renal function, limit the course to about 7 days, and avoid combining them with loop diuretics or other nephrotoxic drugs.

The post-antibiotic effect is the pharmacological reason once-daily dosing works; name it.

What is the isolated rat ileum preparation used for, and what is Tyrode solution?

The isolated rat ileum is a classical organ-bath preparation for recording concentration-response curves to agonists such as acetylcholine or histamine and for studying competitive antagonism with atropine or an antihistamine, from which a pA2 value can be derived by a Schild plot. Tyrode solution is the physiological salt solution that keeps the tissue alive in the bath at 37 degrees, aerated with air or oxygen; it contains sodium chloride, potassium chloride, calcium chloride, magnesium chloride, sodium bicarbonate, sodium dihydrogen phosphate and glucose. Frog tissues use Frog Ringer, and the rat uterus uses De Jalon's solution.

Since CPCSEA restrictions, most colleges teach these with simulation software; be ready to say what the real experiment would show.

Name the apparatus used to screen analgesics, and anti-anxiety and CNS depressant drugs, in animals.

For analgesics, Eddy's hot plate measures the paw-licking or jump latency of a mouse at about 55 degrees, and the tail-flick analgesiometer measures withdrawal from radiant heat; both are for centrally acting analgesics, while the acetic acid writhing test picks up peripheral analgesics like NSAIDs. The actophotometer measures locomotor activity, which falls with CNS depressants, and the rota-rod measures motor coordination and grip, which muscle relaxants and sedatives impair. The elevated plus maze is the standard anxiety model.

Say the end-point for each apparatus; examiners accept the name alone only from D.Pharm students.

What is a primary standard and why is potassium hydrogen phthalate used?

A primary standard is a substance pure enough, stable enough and of high enough molecular weight to be weighed accurately and used to prepare a solution of exactly known concentration, from which a secondary standard such as sodium hydroxide is standardised. Potassium hydrogen phthalate meets all of these: it is available at better than 99.9 per cent purity, is not hygroscopic, does not decompose on drying and has a high equivalent weight, so weighing errors are small. Anhydrous sodium carbonate serves the same role for standardising acids.

Sodium hydroxide can never be a primary standard because it absorbs water and carbon dioxide from air.

Explain the assay of aspirin tablets by back titration.

Aspirin is an ester that is difficult to titrate directly, so a weighed sample is heated with a known excess of standard sodium hydroxide, which hydrolyses it to sodium salicylate and sodium acetate, consuming two equivalents of base per mole. The unreacted sodium hydroxide is then back-titrated with standard sulphuric acid using phenol red or phenolphthalein. The difference between the base added and the base left over gives the amount of aspirin, and the percentage is calculated from the equivalent factor in the Indian Pharmacopoeia monograph.

If asked why heating is needed: the ester hydrolysis is slow at room temperature; boiling under reflux completes it.

What is non-aqueous titration and when is it used?

Non-aqueous titration is an acid-base titration carried out in a solvent other than water, used for substances that are too weakly acidic or basic to give a sharp end-point in water, or that are insoluble in it. Weak bases such as many alkaloid drugs, antihistamines and sulphonamide salts are titrated with perchloric acid in glacial acetic acid, using crystal violet as indicator, because acetic acid enhances the basicity of the sample. Weak acids are titrated with sodium methoxide or tetrabutylammonium hydroxide in dimethylformamide.

Mercuric acetate is added when titrating hydrochloride salts to remove the interfering halide ion; examiners love that detail.

What is the principle of complexometric titration and what indicator is used for calcium?

Complexometric titration estimates metal ions by forming a stable, water-soluble 1:1 complex with disodium EDTA, a hexadentate ligand. For calcium or magnesium the solution is buffered at pH 10 with ammonia-ammonium chloride and Eriochrome Black T is the indicator, changing from wine red, when bound to the metal, to blue at the end-point when EDTA has taken all the metal. Mordant black and calcon are alternatives, and murexide is used for calcium in the presence of magnesium.

Application: the assay of calcium gluconate tablets and the determination of water hardness.

Describe the limit test for chlorides.

A limit test is a semi-quantitative test that checks that an impurity does not exceed a specified limit. For chlorides, the sample is dissolved in water, acidified with dilute nitric acid to prevent interference from carbonates and phosphates, and silver nitrate solution is added; chloride gives a white opalescence of silver chloride. The turbidity is compared in Nessler cylinders against a standard prepared from a known amount of sodium chloride, and the sample passes if its opalescence is not greater than the standard.

Sulphate uses barium chloride in HCl; iron uses thioglycollic acid giving a pink to purple colour; heavy metals use hydrogen sulphide or sodium sulphide.

Define acid value, saponification value and iodine value.

Acid value is the number of milligrams of potassium hydroxide required to neutralise the free fatty acids in one gram of fat or oil, so it indicates rancidity. Saponification value is the milligrams of potassium hydroxide needed to saponify one gram of fat completely, which is inversely related to the average molecular weight of the fatty acids. Iodine value is the grams of iodine absorbed by 100 grams of fat, a measure of unsaturation. Together they identify an oil and detect adulteration; castor oil, for instance, has a characteristic low iodine value.

Ester value is saponification value minus acid value. It is the next question.

What is the Karl Fischer method used for and what is its principle?

The Karl Fischer titration is the pharmacopoeial method for determining water content in drugs and excipients, especially where loss on drying would be wrong because the substance also loses volatile matter or decomposes. The reagent, iodine, sulphur dioxide, a base and methanol, reacts stoichiometrically with water, iodine being reduced by sulphur dioxide only in the presence of water. The end-point is detected visually by the persistence of the iodine colour or, in practice, electrometrically, and the reagent is standardised against sodium tartrate dihydrate or a known amount of water.

If asked why it is run in a closed system: atmospheric moisture would consume reagent and overestimate water.

State Beer-Lambert's law and its limitations.

Beer-Lambert's law states that the absorbance of a solution is directly proportional to the concentration of the absorbing species and to the path length, A equals epsilon c l, where epsilon is the molar absorptivity. It holds only for dilute solutions of monochromatic light, so deviations occur at high concentration where molecules interact, with polychromatic light, when the analyte dissociates, associates or reacts with the solvent, and when there is scattering or stray light. In the lab I check it by plotting a calibration curve and using only its linear range.

A 1 per cent, 1 cm value is the absorbance of a 1 per cent w/v solution in a 1 cm cell; it is how the IP expresses it.

How is paracetamol synthesised in the lab, and how is aspirin?

Paracetamol is made by acetylating p-aminophenol with acetic anhydride in water, with a little acetic acid, which converts the amino group into an acetamido group; the product is recrystallised from hot water. Aspirin is made by acetylating the phenolic hydroxyl of salicylic acid with acetic anhydride using a few drops of concentrated sulphuric acid as catalyst, giving acetylsalicylic acid, which is recrystallised from ethanol-water. Both are tested by melting point, about 169 to 170 degrees for paracetamol and about 135 to 136 degrees for aspirin, and aspirin should give no violet colour with ferric chloride if free of salicylic acid.

The ferric chloride test for unreacted phenol is the applied point; it checks purity, not identity.

Why does pKa matter for drug absorption?

Most drugs are weak acids or bases, and only the unionised form crosses lipid membranes readily, so the fraction absorbed depends on the drug's pKa and the pH of the site, by the Henderson-Hasselbalch equation. A weak acid like aspirin, pKa about 3.5, is mostly unionised in the acidic stomach and is absorbed there, while a weak base like morphine is better absorbed in the alkaline small intestine. The same principle explains ion trapping: alkalinising urine with sodium bicarbonate increases excretion of acidic drugs such as salicylates and phenobarbitone in overdose.

Ion trapping is the application that turns a chemistry answer into a pharmacology one; examiners like the bridge.

What are the methods of evaluation of a crude drug?

A crude drug is evaluated organoleptically by colour, odour, taste, size and shape; microscopically by its cell types, stomata, trichomes, starch grains and calcium oxalate crystals; physically by ash values, extractive values, moisture content, volatile oil content and refractive index; chemically by identity and assay tests for its active constituents; and biologically by its effect in a bioassay, as for digitalis. The Indian Pharmacopoeia monograph for each drug prescribes which tests apply and their limits.

Follow-up: 'why ash value?' Total ash detects inorganic adulterants like sand; acid-insoluble ash separates silica from the plant's own salts.

Name the tests for alkaloids and the colour of each result.

Mayer's reagent, potassium mercuric iodide, gives a cream or white precipitate; Dragendorff's reagent, potassium bismuth iodide, gives an orange-red precipitate; Wagner's reagent, iodine in potassium iodide, gives a reddish-brown precipitate; and Hager's reagent, saturated picric acid, gives a yellow precipitate. I run them on an acidic aqueous extract because alkaloids are basic and form soluble salts in acid. Specific tests include the Vitali-Morin test for tropane alkaloids and the thalleioquin test for quinine.

Caffeine and some purine bases do not precipitate with Mayer's reagent; that is the standard exception.

What are the tests for cardiac and anthraquinone glycosides?

Cardiac glycosides are identified by the Keller-Killiani test, where the extract in glacial acetic acid with a trace of ferric chloride forms a reddish-brown ring at the junction with concentrated sulphuric acid that turns bluish green, specific for the deoxy sugar, and by the Legal and Baljet tests for the unsaturated lactone ring. Anthraquinone glycosides in senna, aloe and rhubarb give the Borntrager test: after hydrolysis and extraction into benzene or ether, shaking with dilute ammonia turns the ammoniacal layer pink to red. For bound C-glycosides as in aloe, the modified Borntrager test with ferric chloride is used.

Senna's active constituents are sennosides A and B; they act as stimulant laxatives after conversion by colonic bacteria.

Give the biological source and chief constituent of Digitalis, Cinchona, Rauwolfia and Vinca.

Digitalis is the dried leaf of Digitalis purpurea or Digitalis lanata, family Scrophulariaceae, containing cardiac glycosides, with digoxin obtained from Digitalis lanata. Cinchona is the dried bark of Cinchona species, family Rubiaceae, containing quinine and quinidine. Rauwolfia is the dried root of Rauwolfia serpentina, family Apocynaceae, containing reserpine, used as an antihypertensive. Vinca or Catharanthus roseus, also Apocynaceae, gives the anticancer alkaloids vincristine and vinblastine from its leaves.

Add the use for each as you name it; it pre-empts the follow-up and shows you link the drug to the clinic.

What is the lignin test and what is the starch test under the microscope?

For lignin, a section or powder is treated with phloroglucinol followed by concentrated hydrochloric acid; lignified tissues such as fibres, vessels and sclereids turn pink to red, which helps distinguish, for example, the fibrous bark of cinchona from adulterants. For starch, a drop of dilute iodine solution stains starch grains blue to blue-black; the size, shape and hilum of the grains are characteristic, as in the oval eccentric-hilum grains of potato versus the small polygonal grains of maize. Ruthenium red stains mucilage and Sudan III stains fixed oils and cuticle.

Calcium oxalate crystals are identified as raphides in squill, rosettes in senna and prisms in cascara; they dissolve in HCl without effervescence.

What are stomatal index and palisade ratio, and why are they used?

Stomatal index is the percentage of stomata among the total epidermal cells, stomata plus epidermal cells, in a given area of leaf surface, and it is nearly constant for a species regardless of the leaf's age or size. Palisade ratio is the average number of palisade cells beneath one upper epidermal cell. Along with vein-islet number and stomatal number, these leaf constants identify powdered leaf drugs such as senna, digitalis and belladonna and detect adulteration, where the whole leaf is not available for comparison.

Senna leaflets have paracytic stomata; Datura has anisocytic; the type is also a leaf constant.

How is volatile oil content determined, and what is the chief constituent of clove oil?

Volatile oil content is determined by hydrodistillation in the Clevenger apparatus, where the weighed crude drug is boiled with water, the steam and oil condense, and the oil separates in a graduated tube so its volume per 100 grams of drug can be read directly; xylene is added for oils heavier than water. Clove, the dried flower buds of Syzygium aromaticum, family Myrtaceae, yields about 15 to 20 per cent oil, of which eugenol is the chief constituent, giving the dental analgesic and antiseptic use. Clove sinks in water because of the high oil content, which is a quick purity check.

Eugenol is phenolic, so it dissolves in strong potassium hydroxide; exhausted cloves float. These are the classic adulteration spotters.

Name the tests for tannins and saponins.

Tannins give a bluish-black colour with ferric chloride for hydrolysable tannins and a greenish-black colour for condensed tannins, a precipitate with gelatin solution, and the goldbeater's skin test, where treated skin turns brown or black with ferrous sulphate. Saponins are detected by the foam test, where shaking an aqueous extract gives a persistent honeycomb froth for at least 15 minutes, and by their haemolytic action on red blood cells on a slide. Examples are catechu and myrobalan for tannins, and liquorice, quillaia and ginseng for saponins.

If asked for a glycyrrhizin use: liquorice is an expectorant and sweetener, and glycyrrhetinic acid is anti-inflammatory.

What are the parts of a prescription?

A prescription has the date and the prescriber's details, the patient's name, age, sex and address, the superscription, which is the symbol Rx meaning 'take thou', the inscription naming the drugs with strength and quantity, the subscription giving directions to the pharmacist on compounding and the number to dispense, the signa or directions to the patient, and the prescriber's signature and registration number. As a pharmacist I check it for completeness, dose, interactions and legibility before dispensing, and I never guess an illegible drug name.

Under the Drugs and Cosmetics Rules, Schedule H and H1 drugs can be dispensed only against a prescription by a registered practitioner.

Differentiate Schedule H, H1 and X drugs.

Schedule H drugs are prescription-only medicines that must be sold against a prescription and carry the Rx symbol with the warning on the label; most antibiotics and antihypertensives are here. Schedule H1, added in 2013, covers drugs prone to misuse such as third- and fourth-generation cephalosporins, carbapenems, anti-tubercular drugs and some sedatives: the label carries a red box warning and the pharmacist must keep a separate register of sales with the prescriber's and patient's details for three years. Schedule X covers narcotic and psychotropic substances with stricter licensing, record keeping and storage under lock and key.

Schedule G drugs are to be taken under medical supervision; Schedule K lists exemptions such as household remedies.

What is the Pharmacy and Therapeutics Committee and what is a hospital formulary?

The Pharmacy and Therapeutics Committee is a hospital committee of physicians, pharmacists, nurses and administrators that decides which drugs the hospital will stock, reviews adverse drug reactions and medication errors, sets prescribing policies and educates staff. Its main output is the hospital formulary, a continually revised list of the drugs approved for use in that hospital with information on dose, strength and cost, which promotes rational, economical prescribing. The chief pharmacist is usually its secretary.

If asked the advantages of a formulary: fewer duplicate brands, lower inventory, better evidence-based use, and easier procurement.

How is an adverse drug reaction reported in India?

An adverse drug reaction is any noxious, unintended response to a drug at normal doses, and in India it is reported under the Pharmacovigilance Programme of India, run by the Indian Pharmacopoeia Commission as the national coordination centre under the CDSCO. A pharmacist, doctor, nurse or patient fills the suspected ADR reporting form, available online or through the ADR monitoring centres in medical colleges, giving patient details, the suspected drug, the reaction, the outcome and causality. The reports go to the WHO Uppsala Monitoring Centre's VigiBase.

Causality assessment uses the WHO-UMC scale or the Naranjo algorithm; name one of them.

What is ABC and VED analysis in hospital drug inventory?

ABC analysis classifies inventory items by annual consumption value: A items are the 10 to 20 per cent of items that account for about 70 per cent of expenditure and need tight control, B items are the middle group, and C items are the many cheap items with loose control. VED analysis classifies by criticality: vital drugs without which patients may die, essential drugs that are important, and desirable drugs that are low priority. Combining the two in an ABC-VED matrix tells the pharmacy which items to order frequently and never allow to stock out.

Economic order quantity and lead time are the two terms that usually follow.

Why is therapeutic drug monitoring done and for which drugs?

Therapeutic drug monitoring is the measurement of plasma drug concentration to adjust the dose for an individual patient. It is justified for drugs with a narrow therapeutic index, a poor relationship between dose and plasma level, serious toxicity, or no easy clinical end-point. The standard list is digoxin, lithium, phenytoin, carbamazepine, valproate, theophylline, aminoglycosides, vancomycin, cyclosporine and tacrolimus. Samples are usually taken at trough, just before the next dose, after steady state is reached at about four to five half-lives.

The steady-state sentence is what tells the examiner you understand kinetics, not just the list.

What are the phases of a clinical trial?

Phase 1 tests safety, tolerability and pharmacokinetics in 20 to 80 healthy volunteers, or patients for cytotoxic drugs. Phase 2 tests efficacy and dose in a few hundred patients with the disease. Phase 3 is the large randomised controlled trial in thousands of patients that compares the drug with standard treatment or placebo and supports marketing approval. Phase 4 is post-marketing surveillance that detects rare adverse effects after the drug is in general use. In India, trials are regulated under the New Drugs and Clinical Trials Rules 2019 with CDSCO approval and ethics committee oversight.

If asked what Schedule Y is: the earlier schedule of the Drugs and Cosmetics Rules that governed clinical trials before the 2019 rules.

What should a pharmacist cover when counselling a patient on a new inhaler?

I would first ask what the patient already knows, then explain the purpose of the inhaler and whether it is a reliever or a preventer, demonstrate the technique with a placebo device, shake the metered-dose inhaler, exhale fully, seal the lips, press and inhale slowly and deeply, hold the breath for about ten seconds, and have the patient repeat it back to me. I would mention rinsing the mouth after a steroid inhaler to prevent oral thrush, how to count doses, when to seek help, and I would recommend a spacer for children and the elderly. Counselling ends with an open question to confirm understanding.

Teach-back is the phrase examiners want: 'show me how you will use it'.