Pharma-Physio Solved Question Paper (2021)

1. Attempt any two of the following:

(a) Write a detailed note on models of drug administration.

1. Oral Route:

   • Common and non-invasive.
   • Includes tablets, capsules, and syrups.
   • Advantages: Easy to use, economical, safe.
   • Disadvantages: First-pass metabolism, delayed onset.

2. Parenteral Route:

   • Includes intravenous, intramuscular, and subcutaneous injections.
   • Advantages: Bypasses first-pass effect, rapid action.
   • Disadvantages: Invasive, requires sterile conditions.

3. Topical Route:

   • Applied directly to skin or mucous membranes.
   • Advantages: Localized effect, minimal side effects.
   • Disadvantages: Limited systemic absorption.

4. Inhalation Route:

   • Drugs delivered via respiratory tract.
   • Advantages: Rapid absorption, useful for respiratory diseases.
   • Disadvantages: Requires proper technique.

5. Sublingual and Buccal Routes:

   • Placed under the tongue or in the cheek.
   • Advantages: Avoids first-pass metabolism, rapid onset.
   • Disadvantages: Limited to specific drugs.

(b) Discuss various factors affecting drug metabolism.

1. Genetic Factors:

   • Genetic polymorphism affects enzyme activity (e.g., CYP450 variations).

2. Age:

   • Neonates and elderly have reduced enzymatic activity.

3. Sex:

   • Hormonal differences may influence metabolism.

4. Pathological Conditions:

   • Liver diseases impair drug metabolism.

5. Drug Interactions:

   • Enzyme inhibitors (e.g., cimetidine) or inducers (e.g., rifampin).

6. Diet and Lifestyle:

   • Grapefruit juice inhibits certain enzymes; smoking induces others.

7. Route of Administration:

   • Influences first-pass metabolism.

(c) Describe the process of drug absorption.

1. Definition:

   • Movement of a drug from the site of administration to the bloodstream.

2. Mechanisms:

   • Passive Diffusion: Driven by concentration gradient.
   • Facilitated Diffusion: Involves carrier proteins.
   • Active Transport: Requires energy (e.g., P-glycoprotein).
   • Endocytosis: For large molecules (e.g., insulin).

3. Factors Influencing Absorption:

   • Physicochemical Properties: Solubility, molecular size.
   • Formulation: Coatings, excipients.
   • Physiological Factors: Gastric pH, motility, blood flow.

2. Attempt any two of the following:

(a) Differentiate between drug toxicity and drug allergy.

Parameter	Drug Toxicity	Drug Allergy
Cause	Excessive dose or prolonged use.	Immune system hypersensitivity.
Mechanism	Direct damage to tissues/organs.	Mediated by antibodies or T-cells.
Predictability	Predictable, dose-dependent.	Unpredictable, dose-independent.
Examples	Liver damage from paracetamol overdose.	Anaphylaxis from penicillin.

(b) What are the factors affecting drug action?

1. Physiological Factors:

   • Age, sex, body weight.

2. Pathological Factors:

   • Diseases affecting absorption, distribution, metabolism, excretion.

3. Pharmacokinetic Factors:

   • Bioavailability, half-life, plasma protein binding.

4. Drug-Drug Interactions:

   • Additive or antagonistic effects.

5. Tolerance and Sensitivity:

   • Tolerance reduces efficacy over time.

6. Genetic Factors:

   • Polymorphisms in drug-metabolizing enzymes.

(c) Differentiate between drug potency and efficacy.

Parameter	Potency	Efficacy
Definition	Amount of drug needed to produce an effect.	Maximum effect a drug can achieve.
Measurement	EC50 (Effective Concentration for 50%).	Plateau of the dose-response curve.
Significance	Determines dosage.	Determines therapeutic outcome.

3. Write brief notes on any two of the following:

(a) Anxiolytics

1. Definition:

   • Drugs that reduce anxiety and promote calmness without causing sedation.

2. Mechanism of Action:

   • Most act on GABA-A receptors, enhancing the inhibitory effects of gamma-aminobutyric acid.

3. Examples:

   • Benzodiazepines: Diazepam, Alprazolam.
   • Non-Benzodiazepines: Buspirone.

4. Uses:

   • Generalized Anxiety Disorder, Panic Disorder, Phobias.

5. Adverse Effects:

   • Drowsiness, dependence, withdrawal symptoms.

(b) Sedatives

1. Definition:

   • Drugs that induce a calming effect and reduce irritability.

2. Mechanism of Action:

   • Depress central nervous system activity, often acting on GABA-A receptors.

3. Examples:

   • Barbiturates: Phenobarbital.
   • Benzodiazepines: Lorazepam.

4. Uses:

   • Insomnia, pre-anesthesia sedation, anxiety.

5. Adverse Effects:

   • Respiratory depression, tolerance, addiction.

(c) Muscle Relaxants

1. Definition:

   • Drugs that reduce skeletal muscle tone to alleviate spasms.

2. Types:

   • Centrally Acting: Baclofen, Diazepam.
   • Peripherally Acting: Dantrolene, Botulinum toxin.

3. Mechanism of Action:

   • Inhibit signals at the neuromuscular junction or suppress CNS activity.

4. Uses:

   • Spasticity (e.g., in cerebral palsy, multiple sclerosis), muscle injuries.

5. Adverse Effects:

   • Weakness, dizziness, sedation.

4. What is the difference between general and local anesthetics? Write classification of general and local anesthetics.

(a) Differences Between General and Local Anesthetics

Parameter	General Anesthetics	Local Anesthetics
Definition	Induce loss of consciousness and sensation.	Block nerve conduction in a specific area.
Mechanism	Act on the central nervous system.	Act locally at the site of administration.
Administration	Intravenous or inhalational.	Topical, infiltration, spinal, or epidural.
Uses	Major surgeries.	Minor surgeries, dental procedures.

(b) Classification

1. General Anesthetics:

   • Inhalational:
     • Volatile liquids: Halothane, Isoflurane.
     • Gases: Nitrous oxide.
   • Intravenous:
     • Barbiturates: Thiopental.
     • Non-barbiturates: Propofol, Ketamine.

2. Local Anesthetics:

   • Esters:
     • Procaine, Benzocaine.
   • Amides:
     • Lidocaine, Bupivacaine.

5. Answer any two of the following:

(a) Define drug antagonism.

1. Definition:

   • Drug antagonism occurs when one drug reduces or blocks the effect of another.

2. Types:

   • Competitive Antagonism:
     • Antagonist competes with the agonist for the same receptor (e.g., Naloxone blocks opioids).
   • Non-Competitive Antagonism:
     • Antagonist binds to a different site, altering receptor function (e.g., Ketamine on NMDA receptors).
   • Functional Antagonism:
     • Two drugs produce opposite physiological effects (e.g., adrenaline vs histamine).

3. Clinical Importance:

   • Used in treating overdoses, such as Naloxone for opioid toxicity.

(b) Classification of antihistaminic agents.

1. Definition:

   • Drugs that block histamine receptors.

2. Classification:

   • H1 Receptor Antagonists:
     • First Generation: Diphenhydramine, Chlorpheniramine (cause sedation).
     • Second Generation: Loratadine, Cetirizine (non-sedative).
   • H2 Receptor Antagonists:
     • Ranitidine, Famotidine (reduce gastric acid secretion).
   • H3 and H4 Receptor Antagonists (under research).

3. Uses:

   • H1: Allergies, motion sickness.
   • H2: Peptic ulcers, GERD.

(c) What is drug resistance?

1. Definition:

   • The reduced effectiveness of a drug in treating a disease.

2. Types:

   • Natural Resistance:
     • Inherent insensitivity (e.g., Gram-negative bacteria to penicillin G).
   • Acquired Resistance:
     • Develops over time due to mutations or selection pressure (e.g., multidrug-resistant tuberculosis).

3. Mechanisms:

   • Enzyme production (e.g., beta-lactamases destroy antibiotics).
   • Altered drug target (e.g., mutated receptors).
   • Decreased drug uptake or increased efflux.

4. Prevention:

   • Rational drug use, combination therapy, patient compliance.