BDS Dental Pharmacology Syllabus

Dental Pharmacology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Dental Pharmacology in BDS, not a summary of it.

1. 1

   General Principles of Pharmacology

   4 topics

   • Pharmacokinetics
     • Absorption
     • Distribution
     • Metabolism
     • Excretion
   • Pharmacodynamics
     • Drug-Receptor Interactions
     • Dose-Response Relationship
     • Therapeutic Index
   • Drug Interactions
     • Synergism and Antagonism
     • Pharmacokinetic Interactions
     • Pharmacodynamic Interactions
   • Adverse Drug Reactions
     • Types of Adverse Reactions
     • Management of Adverse Reactions
2. 2

   Local Anesthetics

   3 topics

   • Types of Local Anesthetics
     • Ester Local Anesthetics
     • Amide Local Anesthetics
   • Mechanism of Action
     • Nerve Membrane Stabilization
     • Sodium Channel Blockade
   • Clinical Use
     • Indications
     • Techniques of Administration
     • Complications and Management
3. 3

   Analgesics

   4 topics

   • Non-Opioid Analgesics
     • NSAIDs
     • Acetaminophen
   • Opioid Analgesics
     • Morphine
     • Codeine
     • Synthetic Opioids
   • Adjuvant Analgesics
     • Antidepressants
     • Anticonvulsants
   • Pain Management in Dentistry
     • Acute Pain Management
     • Chronic Pain Management
4. 4

   Antibiotics in Dentistry

   3 topics

   • Classification of Antibiotics
     • Beta-Lactams
     • Macrolides
     • Tetracyclines
     • Aminoglycosides
     • Quinolones
   • Mechanism of Action
     • Inhibition of Cell Wall Synthesis
     • Protein Synthesis Inhibition
     • Nucleic Acid Synthesis Inhibition
   • Clinical Use in Dentistry
     • Prophylactic Use
     • Therapeutic Use
     • Resistance and Stewardship
5. 5

   Antifungal and Antiviral Agents

   3 topics

   • Antifungal Agents
     • Azoles
     • Polyenes
     • Echinocandins
   • Antiviral Agents
     • Nucleoside Analogues
     • Protease Inhibitors
   • Clinical Use in Dentistry
     • Oral Candidiasis
     • Herpetic Infections
6. 6

   Sedatives and Hypnotics

   3 topics

   • Benzodiazepines
     • Mechanism of Action
     • Clinical Use
     • Side Effects
   • Non-Benzodiazepine Sedatives
     • Barbiturates
     • Z-Drugs
   • Sedation in Dentistry
     • Conscious Sedation
     • Deep Sedation
     • General Anesthesia
7. 7

   Emergency Drugs in Dental Practice

   3 topics

   • Cardiovascular Emergencies
     • Nitroglycerin
     • Aspirin
     • Epinephrine
   • Allergic Reactions
     • Antihistamines
     • Corticosteroids
     • Epinephrine
   • Respiratory Emergencies
     • Bronchodilators
     • Oxygen

Dental Pharmacology flashcards for BDS

20 of 51 cards from the Dental Pharmacology deck — real questions with worked answers.

1. Define pharmacokinetics and name its four main processes (the ADME scheme).

   Pharmacokinetics is the study of what the body does to a drug over time. Its four processes are Absorption, Distribution, Metabolism, and Excretion (ADME).

2. What is bioavailability (F), and what is its value for an intravenous drug?

   Bioavailability is the fraction of an administered dose that reaches the systemic circulation unchanged. For an IV drug $F = 1$ (100%), because it bypasses absorption and first-pass metabolism.

3. Write the equation relating volume of distribution to dose and plasma concentration.

   $$V_d = \frac{\text{Amount of drug in body}}{C_p}$$ where $C_p$ is the plasma drug concentration. A large $V_d$ implies extensive tissue distribution.

4. Define drug clearance (CL) and give its formula in terms of elimination rate.

   Clearance is the volume of plasma cleared of drug per unit time: $$CL = \frac{\text{Rate of elimination}}{C_p}$$ It can also be written $CL = k_e \cdot V_d$.

5. State the formula for elimination half-life in terms of $V_d$ and clearance.

   $$t_{1/2} = \frac{0.693 \cdot V_d}{CL}$$ where $0.693 = \ln 2$. Half-life is the time for plasma concentration to fall by 50%.

6. After how many half-lives is a drug considered effectively eliminated (or steady state reached)?

   About 4–5 half-lives. After 5 half-lives roughly 97% of the drug is eliminated, and steady state is reached during constant-rate dosing.

7. Distinguish first-order from zero-order elimination kinetics.

   In first-order kinetics a constant fraction of drug is eliminated per unit time (rate proportional to concentration). In zero-order kinetics a constant amount is eliminated per unit time (rate is constant, saturable), e.g., ethanol, phenytoin, aspirin at high doses.

8. What is the first-pass effect and which routes avoid it?

   First-pass effect is metabolism of an orally absorbed drug in the gut wall and liver before reaching systemic circulation, reducing bioavailability. Sublingual, rectal (partially), IV, IM, and transdermal routes largely bypass it.

9. Contrast Phase I and Phase II biotransformation reactions.

   Phase I reactions (oxidation, reduction, hydrolysis; often via cytochrome P450) introduce or expose a functional group. Phase II reactions are conjugations (glucuronidation, sulfation, acetylation) that add an endogenous molecule to increase water solubility for excretion.

10. Define pharmacodynamics.

    Pharmacodynamics is the study of what the drug does to the body — the biochemical and physiological effects of drugs and their mechanisms of action, including receptor binding and dose–response relationships.

11. Differentiate an agonist, a competitive antagonist, and an inverse agonist.

    An agonist binds a receptor and produces the maximal response (full efficacy). A competitive antagonist binds reversibly with no intrinsic activity, blocking the agonist (surmountable). An inverse agonist binds and produces the opposite effect to the agonist, reducing constitutive activity.

12. Define potency and efficacy, and state which is described by $EC_{50}$.

    Potency is the amount of drug needed to produce a given effect; efficacy is the maximal effect a drug can produce. $EC_{50}$ (the concentration giving 50% of maximal effect) describes potency — a lower $EC_{50}$ means higher potency.

13. What is the therapeutic index (TI) and how is it calculated?

    The therapeutic index is a measure of drug safety: $$TI = \frac{TD_{50}}{ED_{50}}$$ (or $LD_{50}/ED_{50}$ in animals). A larger TI indicates a wider safety margin.

14. Define partial agonist and explain its dual behaviour.

    A partial agonist binds a receptor but produces a submaximal response even at full occupancy (lower efficacy than a full agonist). In the presence of a full agonist it can act as an antagonist by competing for the receptor.

15. Classify the four main types of drug interaction by mechanism.

    Pharmaceutical (physicochemical incompatibility before administration), pharmacokinetic (altered absorption, distribution, metabolism, or excretion), and pharmacodynamic (additive, synergistic, or antagonistic effects at the site of action).

16. How does enzyme induction versus inhibition affect a co-administered drug's plasma level?

    Enzyme inducers (e.g., rifampicin, carbamazepine, phenytoin) increase metabolism and lower plasma levels of affected drugs. Enzyme inhibitors (e.g., erythromycin, ketoconazole, cimetidine) decrease metabolism and raise plasma levels, risking toxicity.

17. Why should adrenaline-containing local anesthetics be used cautiously with non-selective beta-blockers or tricyclic antidepressants?

    Non-selective beta-blockers can cause unopposed alpha stimulation leading to hypertension and reflex bradycardia; tricyclic antidepressants potentiate adrenaline's pressor effect by blocking noradrenaline reuptake — both can produce a hypertensive response.

18. Define an adverse drug reaction (ADR) and distinguish Type A from Type B reactions.

    An ADR is any noxious, unintended response to a drug at normal therapeutic doses. Type A (Augmented) reactions are dose-dependent, predictable extensions of pharmacology (e.g., bleeding with warfarin). Type B (Bizarre) reactions are dose-independent, unpredictable, often immunological (e.g., penicillin anaphylaxis).

19. Name the four Gell and Coombs hypersensitivity types with a drug example each.

    Type I: immediate/IgE-mediated (penicillin anaphylaxis). Type II: cytotoxic/antibody-mediated (drug-induced hemolytic anemia). Type III: immune complex (serum sickness). Type IV: delayed cell-mediated (contact dermatitis to topical agents).

20. What oral adverse effect is characteristic of long-term phenytoin, and of chronic tetracycline use in children?

    Phenytoin causes gingival hyperplasia (overgrowth). Tetracyclines taken during tooth development cause intrinsic tooth discoloration and enamel hypoplasia, so they are avoided in children under 8 and in pregnancy.

See more Dental Pharmacology flashcards →

Planning Dental Pharmacology for BDS

Dental Pharmacology (BDS) FAQ