Chemistry in Everyday LifeNEET Chemistry · Class 12 · NCERT Chapter 12

Drugs and Medicines

A drug is a chemical substance that, when taken into the body, interacts with a target molecule and produces a biological effect. In medicine, drugs are used to diagnose, prevent, cure, or treat disease.

A medicine is a drug formulated for therapeutic use in humans or animals. Not all chemical substances with biological effects are medicines: some chemicals are toxic at all doses (poisons), while others are useful only at specific concentrations.

Classification by Pharmacological Effect

One way to classify drugs is by the body system or disease they affect:

Classification by Target or Chemical Structure

Drugs can also be grouped by how they interact with the body at a molecular level: enzyme inhibitors, receptor modulators (agonists or antagonists), and drugs that interact with nucleic acids or cell membranes. You will study these in the next section.

Important Drug Terms

Narcotic: a drug that induces sleep, relieves severe pain, and can cause dependence (addiction) with repeated use. Narcotic analgesics are mostly opioids (morphine, codeine).

Non-narcotic: analgesics that relieve mild to moderate pain without causing dependence. Examples: aspirin, paracetamol, ibuprofen.

Broad-spectrum antibiotic: effective against both gram-positive and gram-negative bacteria. Examples: tetracycline, chloramphenicol, streptomycin.

Narrow-spectrum antibiotic: effective against only a limited group of bacteria. Example: penicillin G (mainly gram-positive organisms).

Drug-Target Interaction

For a drug to have a therapeutic effect, it must interact with a specific target molecule in the body. The main targets are: enzymes, receptors, nucleic acids (DNA/RNA), and structural proteins. The selectivity of a drug for its target determines both its effectiveness and its side effects.

Enzymes as Drug Targets

Many drugs work by inhibiting an enzyme. Enzymes have an active site where the substrate binds and is converted to a product.

Competitive inhibition: the drug molecule is structurally similar to the substrate (it is an analogue). It competes with the substrate for the active site. When the drug occupies the active site, no reaction takes place. The drug does not undergo the enzymatic reaction itself; it just blocks the substrate from binding.

Example: sulfonamide drugs are structural analogues of PABA (para-aminobenzoic acid). Bacteria need to bind PABA to the enzyme dihydropteroate synthase to make folic acid. Sulfonamide competes with PABA for the enzyme's active site, blocking folic acid synthesis, and the bacteria cannot grow.

Non-competitive inhibition: the inhibitor binds to a site other than the active site (an allosteric site). This changes the shape of the enzyme, reducing its activity. Some drugs like heavy metals work this way.

Receptors as Drug Targets

Receptors are protein molecules (usually on the cell surface or inside the cell) that receive chemical signals. When a natural molecule (like a hormone or neurotransmitter) binds a receptor, it triggers a biological response.

Agonist: a drug that binds to a receptor and mimics the natural chemical signal, triggering the same biological response. The drug "activates" the receptor. Example: morphine acts on opioid receptors like the natural endorphins, producing pain relief.

Antagonist: a drug that binds to a receptor but does NOT trigger the biological response. Instead, it blocks the natural ligand from binding. Example: antihistamines (H1 blockers) bind histamine receptors but do not activate them. They simply prevent histamine from binding, reducing allergy symptoms. Ranitidine is an antagonist at H2 receptors.

Drugs Interacting with DNA

Some anticancer drugs and antibiotics interact with DNA directly, preventing replication or transcription. For example, fluoroquinolone antibiotics (like ofloxacin) inhibit bacterial DNA gyrase (a type II topoisomerase), an enzyme needed to unwind supercoiled DNA during replication. Without gyrase activity, bacterial DNA cannot replicate and the bacteria die. Some anticancer drugs intercalate between DNA base pairs, blocking transcription.

Summary: How Drug Target Affects Drug Use

Analgesics and Antipyretics

Analgesics relieve pain. Antipyretics reduce fever. Many drugs have both effects. The two major groups are non-narcotic and narcotic analgesics.

Non-narcotic (Non-opioid) Analgesics

These relieve mild to moderate pain and are safe for regular use at recommended doses. They do not cause dependence.

Aspirin (Acetylsalicylic acid)

Aspirin is both an analgesic and an antipyretic. It also has anti-inflammatory effects. Its mechanism: aspirin irreversibly acetylates the serine residue in the active site of COX-1 and COX-2 (cyclooxygenase enzymes). These enzymes are needed for the first step in prostaglandin synthesis from arachidonic acid. Prostaglandins sensitise pain receptors and raise body temperature. By blocking COX enzymes, aspirin reduces prostaglandin levels, relieving pain and fever.

Additional effects of aspirin:

• Inhibits platelet aggregation (antiplatelet effect) used in low doses to prevent heart attacks and strokes
• Can cause gastric irritation and ulcers with long-term use (COX-1 also protects the stomach lining)
• NOT given to children with viral infections: can cause Reye's syndrome (rare but serious liver and brain condition)

Paracetamol (Acetaminophen)

Paracetamol is an analgesic and antipyretic but has very little anti-inflammatory effect. It works primarily in the CNS by inhibiting prostaglandin synthesis in the brain and spinal cord. It is the preferred drug for fever in children. At recommended doses it is safe; overdose causes severe liver damage (hepatotoxicity).

Ibuprofen

Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) that reversibly inhibits both COX-1 and COX-2. It is analgesic, antipyretic, and anti-inflammatory. It is used for headache, dental pain, menstrual pain, and arthritis.

Comparison of Non-narcotic Analgesics

Narcotic (Opioid) Analgesics

Narcotic analgesics relieve severe pain by acting on the central nervous system. They bind to opioid receptors (mu, kappa, and delta receptors) in the brain and spinal cord, mimicking the natural painkillers called endorphins.

They cause pain relief, euphoria, sedation, and suppression of cough. With prolonged use they cause tolerance (need higher doses for the same effect) and physical dependence (addiction). They are controlled substances.

Morphine

Morphine is the primary alkaloid from the opium poppy (Papaver somniferum). It is the strongest natural opioid and is used for severe pain (post-surgical, cancer pain). It acts on all three opioid receptor subtypes. Side effects: respiratory depression (dangerous in overdose), constipation, nausea.

Codeine

Codeine is a weaker opioid also found in opium. It is metabolised in the liver to morphine. Used for mild to moderate pain and as a cough suppressant (antitussive). Less addictive potential than morphine.

NEET Key Points: Analgesics

• Non-narcotic analgesics: aspirin, paracetamol, ibuprofen mechanism: COX inhibition
• Narcotic analgesics: morphine, codeine mechanism: opioid receptor agonism in CNS
• Aspirin inhibits COX irreversibly; ibuprofen inhibits reversibly
• Paracetamol is the safe antipyretic for children (not aspirin)
• Morphine is narcotic, can cause dependence, used only for severe pain

Antibiotics

Antibiotics are chemical substances produced by microorganisms (bacteria, fungi) that kill or inhibit the growth of other microorganisms, especially bacteria. In practice the term now includes synthetic compounds with similar antibacterial activity.

The first antibiotic discovered was penicillin, by Alexander Fleming in 1928, from the fungus Penicillium notatum. This discovery transformed medicine.

Bactericidal vs Bacteriostatic

This is the most important classification for NEET:

Penicillin

Penicillin is bactericidal. It inhibits the transpeptidase enzyme (also called penicillin-binding protein) that cross-links peptidoglycan strands in the bacterial cell wall. Without cross-linking, the cell wall is weak and cannot withstand the osmotic pressure difference between the inside of the bacterium and its surroundings. The bacterium bursts (lysis).

Penicillin is mostly effective against gram-positive bacteria (narrow spectrum for original penicillin G). Semi-synthetic penicillins (ampicillin, amoxicillin) have a broader spectrum.

Important: some bacteria produce beta-lactamase (penicillinase), an enzyme that hydrolyses the beta-lactam ring of penicillin, making the bacteria resistant. Methicillin-resistant Staphylococcus aureus (MRSA) is a well-known example.

Streptomycin

Streptomycin is bactericidal and broad-spectrum. It is an aminoglycoside antibiotic isolated from Streptomyces griseus. It irreversibly binds to the 16S rRNA of the 30S ribosomal subunit. This binding causes misreading of mRNA codons, leading to incorporation of wrong amino acids into proteins. The resulting abnormal proteins kill the bacteria.

Streptomycin was the first antibiotic effective against tuberculosis (Mycobacterium tuberculosis). It is now used mainly as part of multi-drug regimens for TB.

Ofloxacin

Ofloxacin is a fluoroquinolone antibiotic. It is bactericidal, broad-spectrum. It inhibits bacterial DNA gyrase (topoisomerase II), an enzyme needed to relieve supercoiling tension in DNA during replication. Without functioning gyrase, DNA replication stops and bacteria die.

Tetracycline

Tetracycline is bacteriostatic and broad-spectrum. It reversibly binds the 30S ribosomal subunit and blocks binding of aminoacyl-tRNA to the A site of the ribosome. Without aminoacyl-tRNA binding, peptide chain elongation stops and protein synthesis halts. Because binding is reversible, bacteria can resume growth when tetracycline is removed.

Erythromycin

Erythromycin is bacteriostatic. It binds the 50S ribosomal subunit and blocks translocation: the movement of the ribosome along the mRNA from the A site to the P site after each amino acid is added. This halts protein synthesis. Erythromycin is often used as an alternative for patients who are allergic to penicillin.

Chloramphenicol

Chloramphenicol is bacteriostatic and broad-spectrum. It binds the 50S ribosomal subunit and inhibits the peptidyl transferase reaction (the formation of the peptide bond). It was widely used but is now reserved for serious infections due to rare but serious side effects (aplastic anaemia in susceptible individuals). NEET often asks about chloramphenicol as it is broad-spectrum and bacteriostatic.

Sulfonamides (Sulpha Drugs)

Sulfonamides are synthetic (not natural) antibiotics. They were the first class of antibiotics developed, before penicillin was widely available.

Mechanism: sulfonamides are structural analogues of para-aminobenzoic acid (PABA). Bacteria must synthesise their own folic acid from PABA using the enzyme dihydropteroate synthase. Sulfonamides compete with PABA for the enzyme's active site (competitive inhibition). When sulfonamide is bound, PABA cannot bind, folic acid synthesis stops, and the bacteria cannot make purines or certain amino acids. This stops bacterial growth (bacteriostatic effect).

Why humans are unaffected: human cells cannot synthesise folic acid. We obtain folic acid from our diet and do not have the enzyme dihydropteroate synthase. So sulfonamides selectively affect only bacterial cells.

Example: sulphamethoxazole, often combined with trimethoprim (which blocks the next step in the folic acid pathway) as co-trimoxazole.

NEET Quick Reference: Antibiotics

Antacids and Antihistamines

Antacids

Antacids are drugs used to treat hyperacidity (excess stomach acid) and conditions like gastritis, heartburn, and peptic ulcers. The stomach normally secretes hydrochloric acid (HCl) for digestion. When too much acid is produced or the stomach's protective mucus lining is damaged, it causes pain and ulcers.

Simple Chemical Antacids (Neutralise Acid)

These react with HCl to neutralise it:

• Sodium bicarbonate (NaHCO3, baking soda): reacts quickly with HCl to form NaCl + H2O + CO2. The CO2 causes belching. Sodium bicarbonate is absorbed into the blood and can cause alkalosis with overuse. Not ideal for frequent use.
• Magnesium hydroxide, Mg(OH)2 (milk of magnesia): reacts with HCl: Mg(OH)2 + 2 HCl → MgCl2 + 2 H2O. No CO2 produced. Acts slowly and has a mild laxative effect. Poorly absorbed.
• Aluminium hydroxide, Al(OH)3: Al(OH)3 + 3 HCl → AlCl3 + 3 H2O. Can cause constipation. Often combined with Mg(OH)2 to balance the GI effects.

H2 Receptor Blockers (Reduce Acid Secretion)

Parietal cells in the stomach secrete HCl when stimulated by histamine binding to H2 receptors. H2 blockers competitively antagonise H2 receptors on parietal cells, reducing acid secretion.

• Ranitidine (Zantac): the most widely used H2 blocker. It is a competitive antagonist at H2 receptors, significantly reducing the volume and acidity of gastric juice. Used for peptic ulcers and gastro-oesophageal reflux disease (GERD).
• Cimetidine: an older H2 blocker with more drug interactions.

Proton Pump Inhibitors (Most Potent)

Proton pump inhibitors (PPIs) block the H+/K+ ATPase pump (the proton pump) in the parietal cell membrane. This is the final step in acid secretion. PPIs are the most effective drugs for reducing stomach acid.

• Omeprazole (Prilosec): the first PPI developed. It is a prodrug activated in the acidic environment of the stomach. The activated form covalently inhibits the H+/K+ ATPase pump, blocking acid secretion from all stimuli (histamine, gastrin, acetylcholine). Used for peptic ulcers, GERD, and Helicobacter pylori eradication.

Summary: Types of Antacids

Antihistamines

Histamine is a biogenic amine released by mast cells and basophils during an allergic reaction or tissue injury. It binds to specific receptors:

• H1 receptors: on blood vessels (causing dilation and increased permeability), mucous membranes (causing itching, runny nose), bronchial smooth muscle (causing bronchoconstriction). H1 activation produces the classic allergy symptoms: sneezing, itching, watery eyes, hives (urticaria), and in severe cases anaphylaxis.
• H2 receptors: on parietal cells in the stomach lining (causing HCl secretion). H2 activation leads to excess acid production.

H1 Antihistamines (Allergy Drugs)

H1 antihistamines competitively block H1 receptors, preventing histamine from binding. They do not inhibit histamine synthesis or release they simply prevent histamine from acting on the H1 receptor.

First-generation H1 antihistamines (sedating): diphenhydramine (Benadryl), chlorpheniramine. These cross the blood-brain barrier and cause drowsiness by blocking H1 receptors in the brain. Used for allergies and also as sleep aids.

Second-generation H1 antihistamines (non-sedating): terfenadine, cetirizine, loratadine. These do not cross the BBB as readily. Used for daytime allergy management.

H2 Antihistamines (Already covered as antacids above)

Ranitidine and cimetidine are technically H2 antihistamines used as antacids. Remembering both categories helps you understand NEET questions asking about "antihistamine" vs "antacid."

Antiseptics and Disinfectants

Both antiseptics and disinfectants kill or inhibit microorganisms but differ in where and how they are used.

Phenol

Phenol is the classic example showing the concentration-dependent classification:

• 0.2% phenol solution: safe for use on skin and mucous membranes. Used as an antiseptic in some throat lozenges and skin preparations.
• 1% phenol solution (carbolic acid): too strong for skin application. Used as a disinfectant on floors, toilets, and medical equipment. Joseph Lister first used phenol as a surgical antiseptic/disinfectant in the 1860s.

Phenol works by denaturing proteins and disrupting bacterial cell membranes.

Chlorine

Chlorine (as Cl2 gas or as hypochlorous acid HOCl formed when dissolved in water) is a powerful disinfectant. It is used in water treatment plants to kill bacteria and viruses in drinking water and swimming pools at 0.2 to 0.4 ppm (parts per million). It is not used on living tissue due to its toxicity at effective concentrations.

Ozone

Ozone (O3) is a powerful oxidising agent used as a disinfectant for water purification. It kills bacteria, viruses, and other pathogens. Like chlorine, it is not applied to living tissue. It leaves no harmful residues in water.

Iodoform (Triiodomethane, CHI3)

Iodoform is an antiseptic used on wounds. It releases iodine slowly, which kills bacteria. It is applied to cuts and minor wounds. It has a distinctive strong smell. Note: iodoform itself is an antiseptic; it is used on living tissue.

Dettol

Dettol is a commercial antiseptic. Its active ingredient is chloroxylenol (a chlorinated derivative of xylenol/phenol) dissolved in terpineol (a terpene alcohol). The combination kills bacteria and fungi on skin. Used to clean wounds, as a general skin antiseptic, and added to bathing water.

NEET facts about Dettol: it contains chloroxylenol + terpineol; it is an antiseptic (used on skin); it turns milky when mixed with water (because terpineol is not water-soluble and forms an emulsion).

Bithional

Bithional (2,2'-thiobis(4,6-dichlorophenol)) is a halogenated bisphenol antiseptic added to soaps. It inhibits bacteria on the skin surface, preventing body odour by stopping the bacterial breakdown of sweat compounds into odorous molecules. NEET frequently asks: "Bithional is added to soaps to prevent body odour."

Hydrogen Peroxide (H2O2)

Dilute hydrogen peroxide (3%) is an antiseptic used for cleaning wounds and gargling. It releases oxygen on contact with tissues and bacteria, and the oxidative power kills bacteria. Concentrated H2O2 is a disinfectant and bleach.

Summary Table: Antiseptics and Disinfectants

Soaps and Detergents

Soaps

Soaps are sodium or potassium salts of higher fatty acids (long-chain carboxylic acids, typically C12 to C18). They are made by saponification: heating a fat or oil (a triglyceride) with a concentrated solution of NaOH (for hard soaps) or KOH (for soft/liquid soaps).

General saponification reaction: Triglyceride + 3 NaOH → 3 R-COONa (soap) + glycerol

Examples of soaps: sodium stearate (C17H35COONa), sodium palmitate (C15H31COONa), sodium oleate (C17H33COONa).

Structure of a Soap Molecule

Each soap molecule has two distinct parts:

• Hydrophilic (water-loving) head: the ionic carboxylate group (-COO- Na+). It dissolves in water.
• Hydrophobic (water-fearing) tail: the long non-polar hydrocarbon chain (typically 12–18 carbons). It is insoluble in water but dissolves in oils and grease.

Cleansing Action of Soap (Micelle Formation)

When soap is dissolved in water, above a certain concentration (the critical micelle concentration, CMC), soap molecules spontaneously organise into spherical structures called micelles.

When you wash a greasy surface:

1. Soap molecules approach the oil/grease particle.
2. Hydrophobic tails insert themselves into the greasy droplet (like dissolves like).
3. Hydrophilic heads remain pointing outward into the water, forming the outer shell of the micelle.
4. The negative charges on the outer shell repel other micelles, keeping them dispersed in water.
5. The micelles (with trapped grease) are suspended in the water and washed away.

This process of suspending oil in water using soap is called emulsification. The resulting mixture is an emulsion.

Why Soap Does Not Work in Hard Water

Hard water contains dissolved calcium (Ca2+) and magnesium (Mg2+) ions.

When soap is added to hard water, these ions react with the carboxylate head of the soap:

2 R-COONa + CaCl2 → (R-COO)2Ca (insoluble) + 2 NaCl

Calcium and magnesium soaps are insoluble in water. They precipitate as a grey scum. This scum:

• Wastes soap (you need more to get a lather)
• Leaves grey deposits on clothes and skin
• Clogs pores in fabric, making clothes look dull

Detergents solve this problem because their head groups form soluble salts with Ca2+ and Mg2+.

Detergents

Detergents are synthetic cleaning agents with a structure similar to soaps but with a sulfonate (-SO3-) or sulfate (-OSO3-) head group instead of a carboxylate head. They are made from petroleum-derived raw materials.

The most common type is linear alkylbenzene sulfonate (LAS): a benzene ring with a linear alkyl chain attached, plus a sulfonate group.

Why Detergents Work in Hard Water

Calcium sulfonates and calcium alkyl sulfates are soluble in water (unlike calcium soaps which are insoluble). So even in hard water with plenty of Ca2+ and Mg2+ ions, detergent molecules do not precipitate. They continue to form micelles normally and clean effectively.

Biodegradability Issue

Early synthetic detergents had branched alkyl chains (branched-chain alkylbenzene sulfonates). Bacteria could not break down the branched chains easily. These detergents were non-biodegradable: they accumulated in rivers and lakes, causing foam and environmental damage.

Modern detergents use linear alkyl chains (LAS). Bacteria can break down linear chains efficiently. These are biodegradable.

NEET key distinction: branched chain = non-biodegradable; linear chain = biodegradable.

Types of Detergents

• Anionic detergents: the hydrophilic head is negatively charged (e.g. sodium lauryl sulfate). Most common type. Used in dishwashing liquids, shampoos.
• Cationic detergents: the head group is a quaternary ammonium salt (positively charged). Have antiseptic properties. Used in fabric softeners and disinfectants.
• Non-ionic detergents: no charge in the head group. Used in liquid detergents for delicate fabrics. Less irritating to skin.

Soap vs Detergent: Key Comparison for NEET

Food Chemistry

Chemistry plays a key role in the food we eat every day. Food additives are substances added to food to preserve it, improve its taste, or enhance its appearance. The main categories tested in NEET are: artificial sweeteners, food preservatives, and antioxidants.

Artificial Sweeteners

Artificial sweeteners provide sweetness without significant calories. They are used by diabetics and people managing weight.

Food Preservatives

Preservatives prevent microbial growth and slow down the chemical deterioration of food, extending its shelf life.

• Sodium benzoate (C6H5COONa): the most widely used food preservative. It is the sodium salt of benzoic acid. In acidic conditions (jams, juices, carbonated drinks), it is converted to benzoic acid, which inhibits mold and yeast growth. Approved as safe at low concentrations. E211 in food labelling.
• Salt (NaCl): high concentrations of salt draw water out of microbial cells by osmosis, killing them (this is why salted meat and pickles last longer).
• Sugar: high sugar concentration similarly creates an osmotic environment unfavourable for microbes. Used in jams and preserves.
• Vinegar (dilute acetic acid): the acidic pH inhibits the growth of most bacteria. Used in pickling.

Antioxidants in Food

Fats and oils can undergo oxidation (rancidity) when exposed to air, light, or heat. The products of oxidation have unpleasant taste and smell. Antioxidants prevent this oxidation, extending shelf life.

• BHA (butylated hydroxyanisole) and BHT (butylated hydroxytoluene): synthetic phenolic antioxidants added to oils, snack foods, and cereals. They scavenge free radicals and prevent chain-reaction oxidation of fats.
• Vitamin E (tocopherol): a natural antioxidant found in vegetable oils. It protects polyunsaturated fatty acids from oxidation both in food and in the body.
• Vitamin C (ascorbic acid): added to fruit juices and preserved foods. Prevents enzymatic browning and acts as an antioxidant.
• Propyl gallate: added to fats and oils as an antioxidant.

Worked NEET Problems

Summary Cheat Sheet

Drug Classification Quick Reference

Soaps and Detergents at a Glance

• Soap: sodium or potassium salt of fatty acid; carboxylate head; fails in hard water (insoluble Ca/Mg scum)
• Detergent: sodium salt of sulfonic acid; sulfonate head; works in hard water (soluble Ca/Mg salts)
• Micelle: soap or detergent molecules cluster with hydrophobic tails inward (oil), hydrophilic heads outward (water)
• Branched-chain detergent: non-biodegradable; linear-chain detergent: biodegradable
• Saponification: fat + NaOH → soap + glycerol

Antiseptics vs Disinfectants at a Glance

• Same chemical, different concentration: 0.2% phenol = antiseptic; 1% phenol = disinfectant
• Dettol = chloroxylenol + terpineol (antiseptic, turns milky in water)
• Bithional = added to soaps, prevents body odour
• Iodoform (CHI3) = antiseptic for wounds
• Chlorine 0.2-0.4 ppm = disinfects drinking water
• Ozone = water disinfectant, no harmful residue

Food Chemistry at a Glance

• Saccharin: 300-500x sweeter; not metabolised; no calories; suitable for diabetics
• Aspartame: 100-160x sweeter; NOT for phenylketonuria patients (contains phenylalanine); unstable to heat
• Alitame: 2000x sweeter; very potent
• Sucralose: 600x sweeter; chlorinated sucrose; heat-stable; not metabolised
• Sodium benzoate: food preservative in acidic foods (jams, juices)
• BHA and BHT: synthetic antioxidants in fats/oils; scavenge free radicals

High-Frequency NEET Questions from This Chapter

• Bactericidal vs bacteriostatic: memorise which list belongs to which
• Sulfonamides: structural analogue of PABA, competitive inhibition of dihydropteroate synthase
• Aspirin: irreversible COX inhibitor; ibuprofen: reversible COX inhibitor
• Ranitidine = H2 blocker; omeprazole = PPI; both reduce stomach acid but by different mechanisms
• Dettol = antiseptic (chloroxylenol + terpineol), turns milky in water
• Soap fails in hard water; detergent does not due to solubility of Ca/Mg salts
• Aspartame is not for phenylketonuria patients