# Pharmacology

Canonical URL: https://shipslides.com/d/health-pharmacology
Raw viewer URL: https://content.shipslides.com/d/health-pharmacology/raw
Category: Health
Slides: 15
Updated: 2026-05-17T20:47:46.074Z
Tags: health, pharmacology

## Summary

A clinician's spec sheet to drugs — pharmacokinetics, pharmacodynamics, and the major classes by mechanism, with named molecules. Key sections include: Pharmacology; What pharmacology is; ADME; Dose-response curves; Receptor families; Pain — the big four classes; Cardiovascular; Antibiotics by mechanism; Two molecules, drawn; The CYP450 system.

## Slide Outline

1. Pharmacology
2. What pharmacology is
3. ADME
4. Dose-response curves
5. Receptor families
6. Pain — the big four classes
7. Cardiovascular
8. Antibiotics by mechanism
9. Two molecules, drawn
10. The CYP450 system
11. Adverse drug reactions
12. From bench to bedside
13. The dispensary
14. Going deeper
15. Evidence quality

## Slide Transcript

### Slide 1: What pharmacology is

- Pharmacology is the science of how chemicals interact with living systems. Two halves: pharmacokinetics (what the body does to the drug) and pharmacodynamics (what the drug does to the body).
- Sub-disciplines
- Toxicology studies harm. Therapeutics studies use. Clinical pharmacology bridges molecule and patient. Pharmacogenomics personalizes choice and dose by genotype (e.g., CYP2D6, HLA-B*57:01).
- // Aphorism
- "All things are poisons; only the dose makes the poison." — Paracelsus, c. 1538.

### Slide 2: ADME

- Pharmacokinetics is captured in four letters:
- StepMeaningKey concepts
- A — AbsorptionDrug → bloodstreamBioavailability (F), first-pass effect
- D — DistributionBlood → tissueVolume of distribution (Vd), protein binding
- M — MetabolismBiotransformation (mostly liver)CYP450 enzymes (CYP3A4, CYP2D6)
- E — ExcretionDrug → outRenal (urine), biliary (feces)
- The half-life (t½) is the time for plasma concentration to fall by half. Steady state takes ~4–5 half-lives. Dosing frequency follows from t½.

### Slide 3: Dose-response curves

- The relationship between dose and effect is typically sigmoid on a log-dose scale. Two key parameters:
- EC₅₀ — dose producing 50% of maximum effect (potency)
- E_max — the ceiling of effect (efficacy)
- The therapeutic index = LD₅₀ / ED₅₀: the ratio of toxic to therapeutic dose. Drugs with narrow indices (warfarin, lithium, digoxin) require monitoring.
- // FIG_3.1 sigmoid log-dose response

### Slide 4: Receptor families

- FamilySpeedExamples
- Ion channelsmillisecondsNicotinic ACh, GABA-A, NMDA
- GPCRssecondsβ-adrenergic, opioid μ, muscarinic
- Kinase-linkedminutesInsulin, growth-factor receptors
- Nuclear (NHR)hoursEstrogen, glucocorticoid, thyroid
- Drugs may be agonists (activate), partial agonists (activate sub-maximally — e.g., buprenorphine), antagonists (block), or inverse agonists (suppress constitutive activity).

### Slide 5: Pain — the big four classes

- NSAIDs
- Inhibit cyclooxygenase (COX-1, COX-2), reducing prostaglandin synthesis. Anti-inflammatory, anti-pyretic, analgesic. Examples: ibuprofen, naproxen, aspirin, celecoxib. GI bleeding and renal effects are dose-dependent.
- Acetaminophen / Paracetamol
- Centrally acting analgesic and antipyretic. Mechanism still debated (likely COX-3 / endocannabinoid). Hepatotoxic above ~4 g/day in adults; the leading cause of acute liver failure in the US.
- Opioids
- Agonists at μ-opioid receptors. From weakest to strongest: codeine, tramadol, hydrocodone, oxycodone, morphine, fentanyl (~100× morphine). Constipation, respiratory depression, dependence.
- Adjuvants
- For neuropathic pain: gabapentin, pregabalin, tricyclics (amitriptyline), SNRIs (duloxetine).
- Black-box warning: opioids carry significant overdose and dependence risk. Naloxone reverses overdose and is available without prescription in many jurisdictions.

### Slide 6: Cardiovascular

- ClassMechanismExample
- StatinsHMG-CoA reductase inhibitorsatorvastatin, rosuvastatin
- ACE inhibitors↓ angiotensin IIlisinopril, ramipril
- ARBsAT1 receptor blocklosartan, valsartan
- β-blockersβ-adrenergic antagonistmetoprolol, carvedilol
- Ca²⁺ blockersL-type Ca channelamlodipine, diltiazem
- Diuretics↑ Na/water excretionhydrochlorothiazide, furosemide
- Anticoagulants↓ clotting factorswarfarin, apixaban, heparin
- AntiplateletsBlock platelet activationaspirin, clopidogrel

### Slide 7: Antibiotics by mechanism

- Cell wall
- β-lactams: penicillin, amoxicillin, cephalexin, ceftriaxone, meropenem. Glycopeptides: vancomycin.
- Protein synthesis
- 30S inhibitors: tetracyclines, aminoglycosides (gentamicin). 50S: macrolides (azithromycin), clindamycin, linezolid.
- DNA / folate
- Fluoroquinolones (ciprofloxacin) inhibit DNA gyrase. Sulfonamides + trimethoprim (Bactrim) block folate synthesis.
- Resistance
- Selection pressure favors resistant strains. WHO lists antibiotic resistance as a top global threat — MRSA, ESBL E. coli, CRE, MDR-TB.

### Slide 8: Two molecules, drawn

- // FIG_8.1 paracetamol
- // FIG_8.2 atorvastatin

### Slide 9: The CYP450 system

- Cytochrome P450 enzymes in the liver (and gut) metabolize ~75% of clinically used drugs. The dominant isoforms:
- Isoform% of drugsNotable substrates
- CYP3A4~50%statins, midazolam, many oncology drugs
- CYP2D6~25%codeine → morphine, many antidepressants
- CYP2C9~10%warfarin, NSAIDs
- CYP1A2~5%caffeine, theophylline
- Inducers (rifampin, St. John's Wort) accelerate metabolism and lower drug levels. Inhibitors (clarithromycin, grapefruit juice for CYP3A4) raise them. Drug-drug interactions are frequently mediated through CYP enzymes.

### Slide 10: Adverse drug reactions

- ADRs are classified by Rawlins-Thompson:
- Type A — Augmented — predictable, dose-related (NSAID GI bleed, opioid sedation). ~80%.
- Type B — Bizarre — idiosyncratic, often immunologic (penicillin anaphylaxis, SJS).
- Type C — Chronic — long-term (steroid osteoporosis).
- Type D — Delayed — teratogenicity, carcinogenicity.
- Type E — End-of-treatment — withdrawal (benzodiazepines, β-blockers).

### Slide 11: From bench to bedside

- PhaseSubjectsQuestion
- Pre-clinicalCells, animalsSafe enough?
- Phase I20–80 healthySafety, PK
- Phase II100–300 patientsEfficacy signal, dose-finding
- Phase III1,000–5,000Efficacy vs. comparator, safety at scale
- Phase IVPost-marketingRare ADRs, real-world effectiveness
- Most candidates fail. From IND to FDA approval, ~10% of drugs entering Phase I succeed. Average development cost: $1–2 billion.

### Slide 12: The dispensary

- A modern pharmacy stocks ~3,000 drug products. Worldwide, the WHO Model List of Essential Medicines names roughly 480 — the medicines a basic functioning health system requires.

### Slide 13: Going deeper

- // MedCram — Pharmacology series
- Roger Seheult, MD walks through clinical pharmacology in concise lectures suitable for first-year medical students and the curious public.
- Watch on YouTube →

### Slide 14: Evidence quality

- Approved drugs are among the most rigorously tested chemicals in human history. Yet effect sizes vary widely between individuals (pharmacogenomics) and between populations (under-representation in trials). Real-world effectiveness is often smaller than RCT efficacy. The WHO Model List, FDA Orange Book, and BNF (British National Formulary) are authoritative starting references.
- Drug names appear here for educational reference. Do not start, stop, or adjust prescriptions without a clinician. Counterfeit medications are a global threat — buy only from licensed pharmacies.


## Related Decks

- [Pharmacology / How drugs find their targets](https://shipslides.com/d/catalog-health-pharmacology)
- [The Science of Sleep](https://shipslides.com/d/health-sleep-science)
- [Dental Health](https://shipslides.com/d/health-dental-health)
- [Epidemiology](https://shipslides.com/d/health-epidemiology)