Para-Clinical Pharmacology Syllabus

Pharmacology syllabus — full chapter and topic list

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

1. 1

   General Pharmacology

   5 topics

   • Introduction to Pharmacology
     • Definition and Scope
     • Branches of Pharmacology
     • Sources of Drugs
   • Pharmacokinetics
     • Absorption
     • Distribution
     • Metabolism
     • Excretion
   • Pharmacodynamics
     • Mechanism of Drug Action
     • Dose-Response Relationship
     • Therapeutic Index
   • Drug Receptors
     • Types of Receptors
     • Receptor Theories
     • Receptor Regulation
   • Adverse Drug Reactions
     • Types of Adverse Reactions
     • Drug Toxicity
     • Management of Adverse Reactions
2. 2

   Autonomic Nervous System Pharmacology

   2 topics

   • Cholinergic Drugs
     • Cholinergic Agonists
     • Cholinesterase Inhibitors
     • Anticholinergic Drugs
   • Adrenergic Drugs
     • Adrenergic Agonists
     • Adrenergic Antagonists
     • Indirect-Acting Adrenergic Agents
3. 3

   Cardiovascular Pharmacology

   4 topics

   • Antihypertensive Drugs
     • Diuretics
     • Beta-Blockers
     • Calcium Channel Blockers
     • ACE Inhibitors
     • ARBs
   • Antianginal Drugs
     • Nitrates
     • Beta-Blockers
     • Calcium Channel Blockers
   • Antiarrhythmic Drugs
     • Classification of Antiarrhythmics
     • Mechanism of Action
     • Clinical Uses
   • Drugs for Heart Failure
     • Cardiac Glycosides
     • Diuretics
     • ACE Inhibitors
     • Beta-Blockers
4. 4

   Central Nervous System Pharmacology

   5 topics

   • Anxiolytics and Hypnotics
     • Benzodiazepines
     • Barbiturates
     • Non-Benzodiazepine Hypnotics
   • Antidepressants
     • SSRIs
     • SNRIs
     • Tricyclic Antidepressants
     • MAO Inhibitors
   • Antipsychotics
     • Typical Antipsychotics
     • Atypical Antipsychotics
   • Antiepileptic Drugs
     • Mechanism of Action
     • Classification of Antiepileptics
     • Clinical Uses
   • Analgesics
     • Opioid Analgesics
     • Non-Opioid Analgesics
     • Adjuvant Analgesics
5. 5

   Endocrine Pharmacology

   4 topics

   • Drugs for Diabetes Mellitus
     • Insulin
     • Oral Hypoglycemic Agents
     • Non-Insulin Injectable Agents
   • Thyroid and Antithyroid Drugs
     • Thyroid Hormones
     • Antithyroid Drugs
   • Corticosteroids
     • Glucocorticoids
     • Mineralocorticoids
     • Clinical Uses and Adverse Effects
   • Sex Hormones
     • Estrogens
     • Progestins
     • Androgens
6. 6

   Chemotherapy

   4 topics

   • Antibacterial Drugs
     • Penicillins
     • Cephalosporins
     • Macrolides
     • Quinolones
     • Aminoglycosides
   • Antiviral Drugs
     • Antiretrovirals
     • Antiviral Agents for Herpesviruses
     • Antiviral Agents for Influenza
   • Antifungal Drugs
     • Azoles
     • Echinocandins
     • Polyenes
   • Anticancer Drugs
     • Alkylating Agents
     • Antimetabolites
     • Natural Products
     • Targeted Therapies
7. 7

   Respiratory Pharmacology

   3 topics

   • Drugs for Asthma
     • Beta-Agonists
     • Corticosteroids
     • Leukotriene Modifiers
   • Drugs for COPD
     • Bronchodilators
     • Phosphodiesterase-4 Inhibitors
     • Combination Therapies
   • Antitussives and Expectorants
     • Opioid Antitussives
     • Non-Opioid Antitussives
     • Expectorants
8. 8

   Gastrointestinal Pharmacology

   3 topics

   • Drugs for Peptic Ulcer Disease
     • Proton Pump Inhibitors
     • H2 Receptor Antagonists
     • Antacids
   • Antiemetic Drugs
     • Serotonin Antagonists
     • Dopamine Antagonists
     • Antihistamines
   • Laxatives and Antidiarrheal Drugs
     • Bulk-Forming Laxatives
     • Stimulant Laxatives
     • Osmotic Laxatives
     • Antidiarrheal Agents

Pharmacology flashcards for Para-Clinical

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

1. Define pharmacology and distinguish its two main divisions, pharmacokinetics and pharmacodynamics.

   Pharmacology is the study of the interaction of drugs with living systems. Pharmacokinetics is what the body does to the drug (absorption, distribution, metabolism, excretion), whereas pharmacodynamics is what the drug does to the body (mechanism of action and effects).

2. What is the difference between a drug's efficacy and its potency?

   Efficacy is the maximal effect a drug can produce ($E_{max}$), reflecting intrinsic activity. Potency is the amount of drug needed to produce a given effect, quantified by $EC_{50}$; a lower $EC_{50}$ means higher potency. A more potent drug is not necessarily more efficacious.

3. Define the therapeutic index and give its formula.

   The therapeutic index (TI) measures drug safety, defined as $$TI = \frac{TD_{50}}{ED_{50}}$$ (or $LD_{50}/ED_{50}$ in animals). A larger TI indicates a wider safety margin.

4. In pharmacokinetics, define bioavailability (F) and state its value for an intravenous drug.

   Bioavailability (F) is the fraction of an administered dose that reaches the systemic circulation unchanged. For an IV drug, $F = 1$ (100%) by definition; oral bioavailability is reduced by incomplete absorption and first-pass metabolism.

5. Give the formula for the volume of distribution ($V_d$) and explain what a large value implies.

   $$V_d = \frac{\text{Amount of drug in body}}{\text{Plasma drug concentration}}$$ A large $V_d$ implies extensive distribution into tissues (e.g., lipophilic or highly tissue-bound drugs), with relatively low plasma concentration.

6. What determines the rate of first-order elimination, and how does it differ from zero-order kinetics?

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

7. State the relationship between elimination half-life ($t_{1/2}$), volume of distribution, and clearance.

   $$t_{1/2} = \frac{0.693 \times V_d}{CL}$$ Half-life increases with larger $V_d$ and decreases with higher clearance (CL).

8. Write the formula for maintenance dosing rate at steady state.

   $$\text{Maintenance dose rate} = \frac{CL \times C_{ss}}{F}$$ where $CL$ is clearance, $C_{ss}$ is target steady-state concentration, and $F$ is bioavailability.

9. Write the loading dose formula and explain why a loading dose is used.

   $$\text{Loading dose} = \frac{V_d \times C_{target}}{F}$$ A loading dose rapidly achieves the target plasma concentration without waiting the ~4-5 half-lives needed to reach steady state by maintenance dosing alone.

10. Compare Phase I and Phase II drug metabolism reactions.

    Phase I reactions (oxidation, reduction, hydrolysis; mainly cytochrome P450) introduce or unmask a functional group, often yielding active/toxic metabolites. Phase II reactions are conjugations (glucuronidation, sulfation, acetylation, glutathione) that add polar groups to increase water solubility for excretion.

11. Distinguish an agonist, a competitive antagonist, and a non-competitive antagonist.

    An agonist binds a receptor and produces an effect (full or partial). A competitive antagonist binds reversibly at the same site, shifting the agonist dose-response curve right (surmountable, $E_{max}$ unchanged). A non-competitive antagonist binds irreversibly or allosterically, lowering $E_{max}$ (insurmountable).

12. What is a partial agonist, and how does it behave in the presence of a full agonist?

    A partial agonist binds the receptor but produces a submaximal response even at full occupancy (low intrinsic activity). In the presence of a full agonist it acts as a partial antagonist, reducing the full agonist's maximal effect.

13. Define an inverse agonist.

    An inverse agonist binds a receptor that has constitutive (basal) activity and produces the opposite effect, stabilizing the inactive state and reducing baseline activity below normal—distinct from a neutral antagonist, which merely blocks.

14. List the four major receptor superfamilies by signal transduction mechanism and their approximate response times.

    1) Ligand-gated ion channels (milliseconds, e.g., nicotinic ACh receptor); 2) G-protein-coupled receptors (seconds, e.g., adrenergic); 3) Enzyme-linked/kinase receptors (minutes, e.g., insulin receptor); 4) Intracellular nuclear receptors (hours, e.g., steroid receptors altering gene transcription).

15. Explain receptor up-regulation and down-regulation and give a clinical consequence of each.

    Down-regulation is a decrease in receptor number/sensitivity after chronic agonist exposure, causing tolerance/tachyphylaxis. Up-regulation is an increase after chronic antagonism or denervation, causing rebound/supersensitivity (e.g., beta-blocker withdrawal tachycardia).

16. Classify adverse drug reactions into Type A and Type B, giving features of each.

    Type A (Augmented) reactions are dose-dependent, predictable, related to the drug's pharmacology, common, and low mortality (e.g., bleeding from warfarin). Type B (Bizarre) reactions are dose-independent, unpredictable, not related to known pharmacology (immunologic/idiosyncratic), rare, but high mortality (e.g., anaphylaxis, Stevens-Johnson syndrome).

17. Name the four types of hypersensitivity reactions (Gell and Coombs) with a drug example of each.

    Type I: IgE-mediated immediate anaphylaxis (penicillin). Type II: antibody-mediated cytotoxic (methyldopa-induced hemolytic anemia). Type III: immune-complex (serum sickness). Type IV: T-cell-mediated delayed (contact dermatitis, some drug rashes).

18. Where are the main cholinergic receptor subtypes located, and what G-protein/channel do they use?

    Nicotinic receptors ($N_M$ at neuromuscular junction, $N_N$ at autonomic ganglia/CNS) are ligand-gated cation channels. Muscarinic receptors $M_1, M_3, M_5$ couple to $G_q$ (increase IP3/DAG), while $M_2, M_4$ couple to $G_i$ (decrease cAMP); $M_2$ predominates in the heart, $M_3$ in smooth muscle/glands.

19. Contrast the mechanisms of pilocarpine and neostigmine as cholinergic drugs.

    Pilocarpine is a direct-acting muscarinic agonist that stimulates receptors directly (used in glaucoma, xerostomia). Neostigmine is an indirect-acting reversible acetylcholinesterase inhibitor that raises endogenous ACh (used in myasthenia gravis, reversal of non-depolarizing blockade).

20. Describe the treatment of organophosphate (irreversible anticholinesterase) poisoning.

    Atropine blocks muscarinic effects (SLUDGE symptoms), and pralidoxime reactivates acetylcholinesterase if given before 'aging' of the enzyme. Supportive care and diazepam for seizures are also used. Atropine does not reverse nicotinic (muscle) effects.

21. For adrenergic receptors, summarize the main effects mediated by $\alpha_1$, $\alpha_2$, $\beta_1$, and $\beta_2$.

    $\alpha_1$: vasoconstriction, mydriasis, increased smooth muscle tone ($G_q$). $\alpha_2$: presynaptic inhibition of NE release, decreased sympathetic outflow ($G_i$). $\beta_1$: increased heart rate/contractility, renin release ($G_s$). $\beta_2$: bronchodilation, vasodilation, uterine relaxation ($G_s$).

22. How does the blood pressure response to epinephrine change after alpha-blockade (epinephrine reversal)?

    Normally epinephrine raises BP ($\alpha_1$ vasoconstriction dominates). After alpha-blockade, only $\beta_2$-mediated vasodilation remains, so epinephrine now lowers BP—this paradoxical fall is called epinephrine reversal.

23. Compare the receptor selectivity and clinical uses of phenylephrine, dobutamine, and isoproterenol.

    Phenylephrine is a selective $\alpha_1$ agonist (pressor, nasal decongestant, mydriatic). Dobutamine is a predominantly $\beta_1$ agonist (inotrope in acute heart failure). Isoproterenol is a non-selective $\beta$ agonist ($\beta_1 + \beta_2$), used rarely for bradycardia/heart block.

24. List the major classes of antihypertensive drugs with one example each.

    Diuretics (hydrochlorothiazide); ACE inhibitors (enalapril); ARBs (losartan); calcium channel blockers (amlodipine); beta-blockers (metoprolol); alpha-blockers (prazosin); central sympatholytics (clonidine, methyldopa); direct vasodilators (hydralazine); and direct renin inhibitors (aliskiren).

25. What is the mechanism of ACE inhibitors and their two characteristic adverse effects?

    ACE inhibitors block conversion of angiotensin I to angiotensin II and reduce bradykinin breakdown, causing vasodilation and reduced aldosterone. Characteristic adverse effects are a dry cough (bradykinin) and angioedema; they can also cause hyperkalemia and are contraindicated in pregnancy.

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