💊 ABCT 102 — Pharmacology & Toxicology Part 2 · L5–L9
How drugs work (pharmacodynamics) and how the body handles them (pharmacokinetics/ADME), then drug classes by organ system.
102 · L5 Respiratory System
Drug classes
- β2-agonists — SABA (salbutamol/albuterol, rescue) vs LABA (salmeterol, formoterol)
- Anticholinergic — ipratropium, tiotropium (COPD > asthma)
- Methylxanthines — theophylline (PDE inhibitor; narrow therapeutic window)
- Inhaled corticosteroids — beclomethasone, fluticasone (anti-inflammatory)
- Leukotriene modifiers — montelukast (receptor antag), zileuton (5-LOX inhibitor)
- Mast cell stabilizers (cromolyn, nedocromil) block calcium entry into mast cells, so the cells do not degranulate and histamine is never released. Because they act upstream, they work as prevention and are useless once an attack has started.
- Others: antihistamines, decongestants (α-agonist vasoconstriction), expectorants (guaifenesin), mucolytics (acetylcysteine), PDE4 inhibitor (roflumilast for severe COPD)
Respiratory anatomy, physiology & control of breathing
The respiratory system = lungs, airways (trachea, bronchi, bronchioles), diaphragm, voice box, throat, nose, mouth. Functions: breathe in O₂ / out CO₂; protect from particles & germs; allow smell & speech; purify, humidify and warm incoming air. Better peak lung capacity = more resilience against chronic respiratory disease later.
| Control type | Driver | Detail |
|---|---|---|
| Neural | Phrenic & intercostal nerves; medulla & pons | Eupnea = 12–15 breaths/min; Hyperpnea = forced (↑ volume) |
| Non-neural | Physical, volition, emotional, chemical (O₂/CO₂/pH) | Hyperventilation / hypoventilation |
Asthma & COPD — pathophysiology
Asthma: chronic (not curable, but controllable) inflammation of the bronchioles → airways become hypersensitive to allergens/irritants → narrowing, wheezing, cough, dyspnoea; smooth muscle tightens and mucus is overproduced → deaths possible if untreated.
COPD: chronic bronchitis (airway inflammation, "bronchi") + emphysema (damage to alveoli/small airways); caused by smoking, air pollution, fumes, dust; not curable.
Respiratory drug delivery & the inhalation advantage
Respiratory drugs come as oral tablets/liquids, injections or inhalations. Inhalation delivers medicine directly to the lungs, acting on lung tissue while minimising systemic side effects; many products combine agents (e.g. long-acting bronchodilator + glucocorticoid).
Anti-histamines & anti-asthmatic combinations
H₁ receptors sit in airways, blood vessels, stomach and oesophagus; allergens trigger histamine release → rash, sneezing, runny nose, bronchoconstriction. First-generation anti-histamines cross the BBB → sedation. Block H₁: Diphenhydramine, Promethazin, Chlorpheniramine, Loratadine (non-sedating).
Anti-asthmatic combinations pair agents that work differently: Albuterol (bronchodilator) + Budesonide (steroid); Dyphylline (bronchodilator) + Guaifenesin (expectorant).
Bronchodilators — adrenergic, anticholinergic & combinations
Adrenergic (β₂-agonists) dilate bronchi by direct action on bronchial β₂-receptors: Albuterol, Epinephrine (injection), Salmeterol, Levalbuterol (SABA), Indacaterol (LABA). Anti-cholinergic (muscarinic antagonists) occupy the M3 receptor on airway smooth muscle. Parasympathetic post-ganglionic fibres release acetylcholine, which normally binds M3 and signals through Gq → PLC → IP3 → Ca2+ to make the muscle contract — that contraction is what we call bronchospasm. With M3 occupied, acetylcholine has nowhere to bind, the contraction signal is never sent, and the muscle stays relaxed, so the airway widens: Ipratropium, Tiotropium (inhalation; COPD > asthma). Combinations: Formoterol (LABA) + Budesonide (steroid).
Methylxanthines (theophylline, from the purine xanthine): at low dose = immunomodulatory/anti-inflammatory/bronchoprotective; higher dose needed for bronchodilation but with toxicity — a narrow therapeutic window.
Anti-tussives, decongestants & expectorants
Anti-tussives (cough suppressants) inhibit the brainstem cough-coordinating region: Pholcodine, Codeine (drowsy/constipated/addictive), Dextromethorphan.
Decongestants activate α-adrenergic receptors (bind directly or stimulate noradrenaline) → vasoconstriction → shrink swollen nasal tissue. Examples: Pseudoephedrine, Phenylephrine, Oxymetazoline.
Expectorants raise airway-secretions water content → less sticky → easier to cough up (do not stop coughing): Guaifenesin (chesty/wet/productive coughs).
Leukotriene modifiers, lung surfactants & mucolytics
Leukotrienes (from mast cells, basophils, eosinophils) cause airway constriction, mucus production and swelling. Receptor antagonists: Montelukast, Zafirlukast. Synthesis inhibitor: Zileuton (blocks 5-lipoxygenase).
Lung surfactants are animal-lung extracts rich in phospholipids; made naturally by alveolar cells to stop alveoli collapsing and ease O₂ transfer. Examples: Beractant, Lucinactant, Calfactant; commonly Curosurf (porcine) and Survanta (bovine).
Mucolytics thin mucus: Acetylcysteine.
Inhaled anti-infectives, corticosteroids & PDE4 inhibitors
Inhaled anti-infectives act locally in the lungs: Zanamivir (anti-viral), Ribavirin (anti-viral), Tobramycin (antibiotic), Pentamidine (anti-fungal).
Inhaled corticosteroids (Beclomethasone, Fluticasone, Mometasone) inhibit arachidonic-acid release via phospholipase A₂ inhibition → direct airway anti-inflammation; much smaller dose than oral, fewer systemic side effects. They prevent attacks, not relieve acute bronchospasm.
Selective PDE4 inhibitors (Roflumilast) ↑ cAMP → broad anti-inflammatory effect in inflammatory cells; used in severe COPD to reduce exacerbations. Not a bronchodilator — not for acute bronchospasm.
Lifestyle & improving lung function
- Regular exercise reduces airway inflammation and strengthens breathing muscles.
- Lower dietary salt (excess worsens lung inflammation/fibrosis); eat more fish oils, antioxidants, vitamins C & E.
- Quit smoking and vaping to avoid inflammatory chemicals.
- Keep a healthy weight — abdominal fat impedes full lung inflation.
- Strengthen inspiratory muscles (singing, wind instruments) to slow age-related decline.
First-generation anti-histamines — extra uses (omitted)
The card lists first-generation anti-histamines only as sedating H₁ blockers, but the lecture adds a distinct clinical use: Diphenhydramine, Promethazine and others may be used for nausea or motion sickness — a use driven by their CNS penetration, the same property that causes sedation.
Mast cells — full scope of involvement (omitted)
The card mentions mast cells only in the context of degranulation and histamine release. The lecture explicitly lists the conditions mast cells are involved in: allergic rhinitis, allergic conjunctivitis, anaphylaxis, asthma, autoimmune diseases, eczema, itch, and reproductive disorders. Mast cells are a type of white blood cell and part of the immune response to antigens.
Respiratory inhalant delivery devices (omitted detail)
The card says inhalations deliver drug "directly to the lungs" but omits the device mechanics the lecture specifies: respiratory inhalant products are finely powdered or liquid drugs carried by special devices such as low-pressure aerosol containers. Inhaled anti-infectives are administered either as dry powder or as a solution via a nebulizer.
| Device / form | Used for |
|---|---|
| Low-pressure aerosol container (MDI) | General respiratory inhalants |
| Dry powder | Inhaled anti-infectives (e.g. tobramycin, zanamivir) |
| Nebulizer solution | Inhaled anti-infectives (e.g. ribavirin, pentamidine) |
H₁ receptor location — source wording (omitted nuance)
Beyond airways, the lecture places H₁ receptors in blood vessels, the stomach, the oesophagus (throat area), and the brain/spinal cord. The lecture's phrasing is that anti-histamines "block histamine release from histamine-1 (H₁) receptors" — note this is the lecture's simplification; the pharmacologically precise action is H₁-receptor blockade, not blocking histamine release. The card's "Block H₁" is the more accurate framing.
102 · L6 Central Nervous System
Key drug classes
| Class | Mechanism | Examples |
|---|---|---|
| Opioids (narcotic analgesic) | μ-receptor agonist | Morphine, Codeine, Fentanyl (100× morphine) |
| NSAIDs / COX-2 | Block COX → ↓ prostaglandins | Aspirin, Ibuprofen, Celecoxib |
| Acetaminophen | Weak PG synthesis inhibitor | Paracetamol |
| Anti-convulsants | Enhance GABA / block Na⁺, AMPA | Phenobarbital, Diazepam, Gabapentin, Perampanel |
| Anti-Parkinson | Restore dopamine (or block ACh) | Levodopa + Carbidopa, Bromocriptine, Selegiline |
| Anti-emetics | 5-HT₃ / NK1 / D2 / H1 / M | Ondansetron, Aprepitant |
| Anxiolytic/hypnotic | GABA-A potentiation | Benzodiazepines |
| Cholinesterase inhibitor | ↑ ACh | Donepezil (Alzheimer's) |
| General anaesthetic | CNS depression | Propofol, Ketamine, Sevoflurane |
CNS agents — scope & stimulant / depressant split
The CNS (brain + spinal cord) processes and controls most bodily functions. CNS agents include anesthetics, anti-convulsants, anti-emetics, anti-Parkinson agents, CNS stimulants, muscle relaxants, narcotic analgesics, non-narcotic analgesics (acetaminophen, NSAIDs) and sedatives. The lecture's top-level split is CNS Stimulants vs CNS Depressants.
| Category | Examples from the lecture list |
|---|---|
| Analgesics | Opioids, NSAIDs, salicylates, COX-2 inhibitors, acetaminophen |
| Anti-convulsants | Phenobarbital, Diazepam, Gabapentin, Perampanel |
| Anti-Parkinson | Levodopa/Carbidopa, Bromocriptine, Selegiline |
| Anti-emetic / anti-vertigo | Ondansetron, Aprepitant, Scopolamine |
| Anxiolytics / sedatives / hypnotics | Benzodiazepines |
| Cholinesterase inhibitors | Donepezil (Alzheimer's) |
| CNS stimulants | Amphetamine, Caffeine, Methamphetamine |
| ADHD / anorexiant / alcohol-dependence | Atomoxetine, Phentermine, Naltrexone, Disulfiram |
Blood–brain barrier — regulation & the lipophilicity trade-off
The BBB is a selective semi-permeable membrane between blood and brain interstitium that regulates molecule/ion movement and is the key element preserving CNS homeostasis — a natural protective barrier. It allows only passive diffusion of lipid-soluble drugs at MW < 400–600 Da.
Analgesics — classes beyond opioids & NSAIDs
Two common groups are NSAIDs and opioids, but the lecture enumerates the full analgesic menu:
| Subclass | Mechanism | Examples |
|---|---|---|
| Analgesic combinations | Analgesic + enhancer (e.g. caffeine) or sleep aid | Acetaminophen + Caffeine; Codeine + Acetaminophen; Ibuprofen + Diphenhydramine |
| Anti-migraine | Ergotamine = α-adrenergic vasoconstrictor (carotid bed); Sumatriptan narrows cranial vessels & blocks headache triggers | Ergotamine; Sumatriptan (injection) |
| COX-2 inhibitors | Block COX-2 → ↓ prostaglandins → ↓ pain/inflammation | Celecoxib |
| Salicylates | Derivative of salicylic acid (white willow bark / wintergreen); block COX-1 & COX-2 | Aspirin (acetylsalicylic acid) — analgesic, anti-inflammatory, antipyretic |
| Acetaminophen & misc. | Weak PG-synthesis inhibitor; Ziconotide blocks pain signals nerve → brain | Paracetamol; Ziconotide |
| Narcotic (opioid) | Bind μ-receptor (main; abundant in brain, spinal cord, stomach, lungs) | Morphine, Codeine, Fentanyl (100× morphine) |
Anorexiants & ADHD agents
Anorexiants suppress appetite via a stimulant effect on hypothalamic/limbic satiety centres; used in obesity — Phentermine, Methamphetamine, Phendimetrazine (sympathomimetic amine like amphetamine).
ADHD — adrenergic uptake inhibitors: prevent reuptake of norepinephrine → more norepinephrine at the synapse → improved focus/attention. Example: Atomoxetine, a selective norepinephrine reuptake inhibitor (SNRI).
Anti-convulsants — mechanisms & subclasses
Anti-convulsants normalise nerve-impulse travel by acting on GABA, glutamate receptors (e.g. AMPA), or by changing neuronal Na⁺ / Ca²⁺ channels. The lecture lists many chemical subclasses:
| Subclass | Example(s) | Mechanism note |
|---|---|---|
| AMPA receptor antagonists | Perampanel | Non-competitive glutamate (AMPA) block — partial-onset seizures |
| Barbiturate | Phenobarbital, Primidone | Enhance GABA → Cl⁻ channel opening → membrane hyperpolarization |
| Benzodiazepine | Diazepam, Lorazepam, Midazolam, Clobazam, Clonazepam, Clorazepate | GABA-A potentiators; α1-subtype = sedation/amnesia/anticonvulsant, α2 = anxiety |
| GABA analogs | Acamprosate, Gabapentin, Pregabalin | Bind Ca²⁺ channels → boost GABA response / release |
| GABA reuptake inhibitors | Tiagabine, Stiripentol | Block GABA transporters → ↑ extracellular GABA |
| Neuronal K⁺ channel openers | Ezogabine | Activate Kv7 voltage-gated K⁺ channels → ↓ excitability |
Anti-Parkinson agents — cholinergic & dopaminergic arms
Parkinson's = dopamine deficiency in the basal ganglia; ACh and dopamine must be balanced for normal movement. Two arms:
- Anti-cholinergic (muscarinic antagonists) — suppress ACh to rebalance vs low dopamine: Benztropine, Trihexyphenidyl, Procyclidine (stiffness, tremor, spasms).
- Dopaminergic drugs either replace or mimic dopamine. Levodopa is given with carbidopa, a peripheral dopa-decarboxylase inhibitor, so that levodopa is not converted to dopamine before it reaches the brain; selegiline inhibits MAO-B, and bromocriptine acts directly as a dopamine receptor agonist.
Anti-emetics — vomiting pathways & four drug classes
Vomiting is coordinated by the vomiting centre in the medulla, triggered by four zones: chemoreceptor trigger zone (CTZ), vestibular nuclei, cerebral cortex, and GI tract. Receptors involved: 5-HT₃, muscarinic (M), H₁, dopamine (D₂).
| Class | Mechanism | Examples | Use |
|---|---|---|---|
| 5-HT₃ antagonists | Block serotonin on gut nerves → less signal to vomiting centre | Dolasetron, Granisetron, Ondansetron | Chemo / radiation / post-op nausea |
| Anti-cholinergic | Block M receptors, vestibular → vomiting centre | Scopolamine, Diphenhydramine | Motion sickness |
| NK1 antagonists | Block substance P at NK1 receptor | Aprepitant, Rolapitant, Fosaprepitant | Acute & delayed nausea (with 5-HT₃ + steroid) |
| Phenothiazine | Inhibit D₂, M, H₁ (vomiting centre + CTZ) | Prochlorperazine, Chlorpromazine, Perphenazine | Severe chemo / radiotherapy nausea |
Anxiolytics, sedatives & hypnotics
Benzodiazepines are the main class, enhancing inhibitory GABA. But the lecture notes SSRIs, SNRIs and tricyclic antidepressants are also used for anxiety — and are preferred over benzodiazepines because they rarely cause dependence, even though they act more slowly.
Cholinesterase inhibitors, CNS stimulants & alcohol-dependence drugs
Cholinesterase inhibitors block acetylcholinesterase → ↑ acetylcholine in the synaptic cleft; used in Alzheimer's (reduced brain ACh). Examples: Donepezil, Rivastigmine, Galantamine. ACh drives motor-neuron activation of muscle and arousal/attention/learning/memory/motivation.
CNS stimulants speed up mental/physical processes; ↑ dopamine, norepinephrine or serotonin; ↑ energy, BP, HR, respiratory rate; ↓ need for sleep/appetite. Examples: Amphetamine (ADHD), Methamphetamine, Caffeine, Phentermine.
Alcohol dependence: Naltrexone & Acamprosate reduce cravings; Disulfiram creates an incentive not to drink — alcohol + disulfiram → nausea & vomiting.
General anaesthetics — how synapses are silenced
General anaesthetics render a patient reversibly unconscious and unresponsive (IV or inhalation; anesthetist monitors vitals). Under GA the patient feels no pain and may wake with short-term amnesia. Examples: Ketamine, Propofol, Sevoflurane, Isoflurane.
Anti-convulsant chemical subclasses — the full lecture taxonomy
| Named subclass (source) | In card? | Detail given in source |
|---|---|---|
| AMPA receptor antagonists | Yes (Perampanel) | Mechanism + example |
| Barbiturate anti-convulsants | Yes | Mechanism + example |
| Benzodiazepine anti-convulsants | Yes | Mechanism + example |
| GABA analogs | Yes | Mechanism + example |
| GABA reuptake inhibitors | Yes | Mechanism + example |
| Neuronal potassium channel openers | Yes (Ezogabine) | Mechanism + example |
| Carbamate anti-convulsants | No | Named only |
| Carbonic anhydrase inhibitor anti-convulsants | No | Named only |
| Dibenzazepine anti-convulsants | No | Named only |
| Oxazolidinedione anti-convulsants | No | Named only |
| Succinimide anti-convulsants | No | Named only |
| Fatty acid derivative anti-convulsants | No | Named only |
| Pyrrolidine anti-convulsants | No | Named only |
| Triazine anti-convulsants | No | Named only |
Partial (focal) seizure — definition
102 · L7 Drug Safety & Side Effects
- ADR (adverse drug reaction) = leading cause of death; ~60% preventable
- Pharmacovigilance = post-market detection/assessment/prevention of adverse effects (signal-focused)
- GxP = "Good x Practice" quality frameworks
Drug-drug & food-drug interactions (by ADME stage)
| Stage | Example |
|---|---|
| Absorption | Colestipol ↓ absorption; tetracycline + milk (Ca²⁺ chelation) |
| Distribution | Aspirin displaces warfarin (97% protein-bound) → bleeding |
| Metabolism | Rifampicin (inducer) / erythromycin (inhibitor); grapefruit juice inhibits CYP3A4 → ↑ statins |
| Excretion | Aspirin + methotrexate compete for tubular secretion |
Drug development & the clinical-trial blind spot
A drug must pass animal testing and the phases of human clinical trials to establish safety and efficacy before marketing permission is granted. But clinical trials run in highly controlled conditions with serious limitations:
- Small patient populations (a few thousand at most)
- Exclusion of special populations — children, pregnant/lactating women, geriatric patients
- Stringent inclusion/exclusion criteria that do not reflect the general population who will use the drug
- Genetic factors, gender, environmental factors, and complete drug-drug interactions may not be studied
Drug landscape by the numbers (DrugBank & market)
| DrugBank Online metric (v5.1.12, 2024-03-14) | Count |
|---|---|
| Total Small Molecule Drugs | 12,718 |
| Total Biotech Drugs | 3,899 |
| Total Approved Drugs | 4,406 |
| Approved Small Molecule Drugs | 2,780 |
| Nutraceutical Drugs | 135 |
| Experimental Drugs | 6,723 |
| Illicit Drugs | 205 |
| Withdrawn Drugs | 318 |
| Total Drugs | 16,617 |
Why ADRs happen (preventable causes)
No medicine is risk-free, and as many as 60% of ADRs are preventable. The lecture lists the root causes:
- Incorrect diagnosis of the patient's medical condition
- Prescription of the inappropriate drug or incorrect dosage of the appropriate drug
- An undetected medical, genetic, or allergic condition causing a reaction
- Self-medication with prescription medicines
- Not following instructions for taking the medication
- Interactions with other drugs (including traditional medicines) and certain foods
- Use of sub-standard medication (composition/ingredients not meeting requirements) — ineffective and often hazardous
- Use of counterfeit medicines (no/inappropriate active ingredients) — dangerous or fatal
Classifying adverse effects — mild vs serious
| Mild adverse effects | More serious effects |
|---|---|
| Constipation | Suicidal thoughts |
| Skin rash or dermatitis | Abnormal heart rhythms |
| Diarrhoea | Internal bleeding |
| Dizziness | Cancer |
| Drowsiness | DEATH |
| Dry mouth | |
| Headache | |
| Insomnia | |
| Nausea |
Documented ADR examples (lecture table)
| Medicine | Adverse reaction |
|---|---|
| Amidopyrine (inflammation) | White blood cell disorder |
| Clioquinol (skin infections) | Visual impairment |
| Erythromycin estolate (antibacterial) | Hepatitis (liver disorder) |
| Oral contraceptives | Thromboembolism (blood clots) |
| Statins (cholesterol) | Muscle degeneration |
| Thalidomide (morning sickness) | Phocomelia (disfigured infants) |
Pregnant & lactating women — expanded detail
Each trimester (~9 months) is critical. A pregnant woman must consult a physician or pharmacist before any medication, as it may affect fetal formation (the thalidomide lesson). Critically, danger is not limited to pregnancy itself — deleterious effects can occur even if a medication is taken a short time before pregnancy (perhaps several weeks). Isotretinoin (Roaccutane, for acne) is among the most dangerous due to teratogenic effects.
Food–drug interactions — expanded
Beyond calcium + tetracyclines and grapefruit + statins (already noted), the lecture adds:
| Food / herb | Drug class | Effect |
|---|---|---|
| Tyramine-rich foods (cheese, red meat, excess chocolate) | MAO inhibitors (MAO-I, antidepressants) | Dangerous hypertensive crisis |
| St. John's wort (antidepressant herb) | Digoxin (and others) | Potent liver-enzyme inducer > lowers drug levels > reduced efficacy > worsening congestive heart failure |
| Grapefruit juice | Atorvastatin, lovastatin, simvastatin | Inhibits CYP450 > raises statin levels > toxicity |
Grading ADR frequency
| Term | Frequency (people affected per medicine) |
|---|---|
| Very common | ≥ 1 in 10 |
| Common | 1 in 10 to 1 in 100 |
| Uncommon | 1 in 100 to 1 in 1,000 |
| Rare | 1 in 1,000 to 1 in 10,000 |
| Very rare | < 1 in 10,000 |
Pharmacovigilance vs drug safety
| Dimension | Pharmacovigilance (PV) | Drug safety |
|---|---|---|
| Posture | Proactive — focused on signal interpretation | Reactive — focused on compliance reporting |
| Scope | Detection, assessment, understanding, prevention of ADRs / medicine problems | Frequency of treatment-emergent adverse effects (appear/worsen during treatment) |
| Lifecycle | Applied pre-market AND post-market | Ensures benefit-risk stays favorable across lifecycle |
Reducing the risk of ADRs — practical rules
- Always take medicines as advised by pharmacist/doctor (e.g. drowsiness-causing meds at night)
- For OTC medicines, follow the package directions exactly
- Never take medicines prescribed for other people or leftovers from prior visits
- Never take more than recommended
- Tell your doctor/pharmacist all medicines taken — prescription, pharmacy/supermarket, complementary, and food supplements
- Be careful mixing medicines with alcohol or certain foods
Sex/gender differences in drug response & research bias (omitted)
The card says responses vary by age and lists vulnerable populations, but the lecture adds two distinct points the card omits:
- Male vs female responses differ because of physiological differences between genders.
- In animal studies, most researchers "like" to use male animals (e.g. mice, rats) for experiments — a research-design bias that limits how well pre-clinical data generalise to females.
GxP — definition expansion (omitted)
The card mentions GxP only as "Good x Practice" quality frameworks. The lecture spells it out: GxP is the abbreviation of "Good x Practice", and the "x" stands for the field the guidelines and regulations apply to (e.g. GCP, GMP, GLP). It is the general term for the quality guidelines and regulations applied across the pharmaceutical industry.
Vulnerable populations — ethical framing (omitted nuance)
The card notes children, pregnant/lactating women and the elderly are excluded from trials, but the lecture adds the explicit ethical label: these groups are vulnerable populations; "UN-ETHICAL to run clinical trials" on them. That is why safety data for paediatric and geriatric use is so often missing — not just practical exclusion but an ethical barrier.
Doctor–patient relationship as a safety determinant (omitted)
The card's practical-rules section covers patient education, but the lecture states the broader principle explicitly: a good relationship between the medical team and the patient is one of the most important determinants for drug safety. Risk is minimised through patient education about drug safety and openness that lets the patient ask questions about their disease or medicines.
102 · L8 Chemotherapy & Biologics
Chemotherapy classes
| Class | Mechanism | Examples |
|---|---|---|
| Alkylating agents | Damage DNA (crosslink) | Cisplatin, Cyclophosphamide, Temozolomide (nitrosoureas cross BBB) |
| Antimetabolites | Block DNA/RNA building blocks | 5-FU, Methotrexate, Gemcitabine |
| Topoisomerase inhibitors | Block DNA uncoiling | Etoposide, Irinotecan, Topotecan |
| Mitotic inhibitors | Block microtubules (mitosis) | Paclitaxel, Vincristine, Docetaxel |
| Antitumor antibiotics | Intercalate/damage DNA | Doxorubicin, Bleomycin, Epirubicin |
Biologics in cancer & autoimmunity
- TNF inhibitors — Adalimumab, Infliximab, Etanercept (RA, psoriasis, IBD)
- Anti-CD20 — Rituximab, Ocrelizumab (B-cell lymphoma, MS)
- Anti-VEGF — Ranibizumab (wet AMD, intravitreal)
- IL-6 / IL-1 — Tocilizumab, Anakinra
The cell cycle & why chemotherapy works
Both cancer and healthy cells reproduce during the cell cycle — a cell copies its DNA and divides to form new cells. Healthy cells die when no longer useful (apoptosis), but cancer cells become virtually immortal: they multiply out of control and form tumors that damage healthy tissue. Chemotherapy drugs interfere with the cell cycle to kill cancer cells.
Combination chemotherapy & drug resistance
A patient may receive one drug or a combination chemotherapy regimen. Using more than one drug type increases treatment effectiveness (different drug types target cancer cells differently) and reduces the likelihood of resistance. Once drug resistance develops, the "same" drug may no longer work as a cancer treatment.
Complete chemotherapy formulary (per class)
The card lists representative examples; the lecture enumerates the full formulary. Reproduced below for completeness:
| Class | Full drug list (as named in the lecture) |
|---|---|
| Alkylating agents | Altretamine, Ifosfamide, Bendamustine, Mechlorethamine, Busulfan, Melphalan, Carboplatin, Oxaliplatin, Chlorambucil, Procarbazine, Cisplatin, Temozolomide, Cyclophosphamide, Thiotepa, Dacarbazine, Trabectedin |
| Nitrosoureas (subclass of alkylating agents) | Carmustine, Lomustine, Streptozocin — uniquely cross the BBB to treat brain tumors |
| Antimetabolites | 5-Fluorouracil (5-FU), 6-Mercaptopurine, Azacitidine, Capecitabine, Cladribine, Clofarabine, Cytarabine, Decitabine, Floxuridine, Fludarabine, Gemcitabine, Hydroxyurea, Methotrexate (MTX), Nelarabine, Pemetrexed, Pentostatin, Pralatrexate, Thioguanine, Trifluridine / tipiracil |
| Topoisomerase inhibitors | Etoposide, Irinotecan, Irinotecan liposomal, Mitoxantrone*, Teniposide, Topotecan (*also classified as an antitumor antibiotic) |
| Mitotic inhibitors (plant alkaloids) | Cabazitaxel, Docetaxel, Nab-paclitaxel, Paclitaxel, Vinblastine, Vincristine, Vincristine liposomal, Vinorelbine |
| Antitumor antibiotics (incl. Anthracyclines) | Anthracyclines: Daunorubicin, Doxorubicin, Doxorubicin liposomal, Epirubicin, Idarubicin, Mitoxantrone, Valrubicin — others: Bleomycin, Dactinomycin, Mitomycin-C |
Chemotherapy side-effect profile
Because chemo targets all rapidly dividing cells, it damages skin, hair follicles, mouth and digestive tract, and blood-forming bone-marrow cells. The lecture's explicit side-effect list:
| Common chemotherapy side effects |
|---|
| Fatigue |
| Diarrhoea |
| Constipation |
| Hair loss |
| Mouth sores |
| Loss of appetite |
| Nausea and vomiting |
| Lower blood cell count > at risk for anemia and neutropenia (harder for the immune system to fight infections) |
What exactly is a biologic?
A biologic is created from, or is similar to, substances produced by living cells (as opposed to chemically synthesized chemo), usually via recombinant DNA technology. Vaccines and biosynthetic human insulin are examples. Biologic therapies use the body's own immune system to remove cancer or lessen side effects, and are turned to when other treatments do not work.
Types of biologics
| Biologic category | Lecture examples |
|---|---|
| Proteins | Insulin, Growth Hormone |
| Antibodies (monoclonal) | Infliximab, Rituximab, Adalimumab |
| Vaccines | HPV, Flu, Shingle |
| Stem Cell Therapies | (cell-based regenerative products) |
| Viral Vectors | (gene-delivery vectors) |
| Gene Therapies | Alipogene tiparvovec (LPL gene) |
| Antibody-Drug Conjugates | (antibody linked to cytotoxic payload) |
| Biosimilars | 38 FDA-approved (May 2025) |
| Nucleic acids | (RNA / DNA therapeutics) |
Biologics vs conventional pharmaceutical drugs
| Feature | Biologics | Pharmaceutical (small molecule) |
|---|---|---|
| Manufacturing | In a living system (microorganism, animal or plant cell) | Chemical process — mixing specific ingredients in order |
| Complexity | Large, complex molecules; hard to characterize | Small, well-defined molecules |
| Sensitivity | Heat-sensitive & susceptible to microbial contamination | Not heat- / microbial-sensitive |
| Typical route | Recombinant-DNA; injection / infusion | Oral tablets / capsules common |
Biologic targets & matched products
| Type | Name(s) | Target |
|---|---|---|
| TNF inhibitor | Golimumab, Certolizumab, Etanercept, Adalimumab, Infliximab | Tumour Necrosis Factor (TNF) |
| IL-6 inhibitor | Tocilizumab | Interleukin-6 (IL-6) |
| IL-1 inhibitor | Anakinra | Interleukin-1 (IL-1) |
| Anti-B-lymphocyte | Rituximab | B cells (a type of white blood cell) |
| Anti-T-lymphocyte | Abatacept | T cells (a type of white blood cell) |
Immuno-modulating, hormonal & other biologics
Beyond the target table, the lecture catalogues broad biologic families:
- Immuno-modulating: MAb (Infliximab), fusion protein (Etanercept)
- Hormones: Insulin, Growth Hormone
- Vaccines: HPV, Flu
- Growth Factors: Erythropoietin, Thrombopoietin
- Enzymes for hereditary disease
- Homeostasis / clotting: Factors VII, VIII, XI and other clotting factors / fibrinolysis activators
- Gene Therapy: Alipogene tiparvovec — delivers the LPL gene; LPL (lipoprotein lipase) is the enzyme that degrades circulating triglycerides in the bloodstream
Autoimmune & other indications treated
| Indication | Biologics (lecture-named) |
|---|---|
| Rheumatic diseases | Abatacept, Tocilizumab, Anti-TNF: Adalimumab, Golimumab |
| Psoriasis | Etanercept, Infliximab, Ustekinumab |
| Inflammatory Bowel Disease (IBD) | Infliximab (ulcerative colitis, fistulating Crohn's); Adalimumab (serious Crohn's) |
| Asthma bronchiale | Keliximab, Pitrakinra, Daclizumab |
| Multiple Sclerosis (MS) | Anti-CD20 MAb: Rituximab, Ocrelizumab, Ofatumumab, Alemtuzumab; Anti-CD25 MAb: Daclizumab |
| Ophthalmology | Ranibizumab (anti-VEGF-A MAb; AMD & CNV; intravitreal) |
Named biological products & biologic side effects
Approved-use examples from the lecture:
- Botox — dermatological and neurological uses
- Herceptin — a certain type of breast cancer
- Vaccines — Shingle vaccine, flu vaccine
- Enbrel — rheumatoid arthritis, psoriasis
Biologic side effects are mostly injection-site reactions: redness, itching, swelling, and pain. Biologics are well-researched, well-tested, and generally well-tolerated — serious symptoms are rare.
HK cancer incidence — full 2021 statistics (omitted)
The card gives the top-5 cancers and "1 in 4 before 75", but the lecture carries the complete incidence picture. Reproduced from the source:
| Metric (HK, 2021) | Value |
|---|---|
| Total new cancer cases | 38,462 (▲ 4,283 / +12.5% vs 2020) |
| New cases per day (average) | 105 |
| New cases — males | 18,943 (▲ 2,240 / +13.4% vs 2020) |
| New cases — females | 19,519 (▲ 2,043 / +11.7% vs 2020) |
| Crude incidence / 100,000 — men | 560 |
| Crude incidence / 100,000 — women | 484 |
| Female : male ratio | 103 : 100 (women > men, 2 consecutive years) |
| Top-5 share of all new cases | 57.9% |
HK cancer deaths — leading causes (omitted)
The card only notes "lung = top killer (26.7% of deaths)". The lecture's full death table:
| Cancer (leading deaths, 2021) | Cases | % of total deaths |
|---|---|---|
| Lung | 4,037 | 26.7% |
| Colorectum | 2,298 | 15.2% |
| Liver | 1,447 | 9.6% |
| Pancreas | 889 | 5.9% |
| Breast | 795 | 5.3% |
Chemotherapy in context & scale (omitted)
- Chemotherapy, surgery and radiation are the three most common cancer treatments (lecture framing the card does not state).
- Per the CDC (USA), about 650,000 people with cancer receive chemotherapy in an outpatient setting each year.
- Topoisomerase I is a vital enzyme controlling DNA topology during replication, transcription and recombination; elevated levels are found in many carcinomas, making it an attractive anticancer target (mechanism context the card omits).
Biologics — parental/IVF hormone detail (omitted nuance)
The card lists recombinant hormones (Insulin, Glucagon, GH, IGF, Parathyroid hormone, Calcitonin, FSH, LH, hCG) but omits the lecture's stated functions: FSH drives sexual development and reproduction in both sexes; LH and hCG support follicular maturation and ovulation. These gonadotropins are used in IVF — a recurring high-value commercial market the card names but does not explain.