HSBTE. Diploma Pharmacy, Pharmacology. May 2019 Question Paper Solution.

Pharmacology Feb 23

SECTION-A

Note: Multiple choice questions. All questions are compulsory (8x1=8)

• Q.1 LD 50 Means

• a) Lagging dose b) long dose c) Lethal dose d) None.

• Ans: c) Lethal dose

• Q.2 Placebo means

• a) Active Drug b) Inactive drug c) Metabolised drug d) Without drug.

• Ans: d) Without drugs.

• Q.3 Which is a Cardiotonic drug

• a) Aspirin b) Ibuprofen c) Digitalis d) Paracetamol.

• Ans: c) Digitalis

• Q.4 Ranitidine belongs to which category

• a) Anticancer b) Antipsychotic c) Antifungal d) Antacid.

• Ans: d) Antacid.

• Q.5 Cancer therapy causes the deficiency of

• a) Cyancobalamine b) Riboflavin c) Thiamine d) Blood Cells.

• Ans: d) Blood Cells

• Q.6 Trimethoprim is used in combination with

• a) Sulfamethoxazole b) Amoxycillin c) Rifampicin d) Gentamycin.

• Ans: a) Sulfamethoxazole

• Q.7 Which drug is not relevant in this group

• a) Pentoprazole b) Omeprazole c) Rabiprazole d) Albendazole.

• Ans: d) Albendazole.

• Q.8 Adrenergic receptor antagonist

• a) Biguanide b) Tolbutamide c) Ranitidine d) Atenolol.

• Ans: d) Atenolol.

SECTION-B

Note: Objective Completion type questions. All questions are compulsory. (8x1=8)

Q.9 Define Pharmacokinetics.

Ans: Pharmacokinetics is the branch of pharmacology that deals with the study of drug absorption, distribution, metabolism, and excretion by the body. It is referred to as ADME.

Q.10 Name topical routes of drug administration.

Ans: Dermal/Epidermal (Skin) Routes, Mucous Membrane Routes, Rectal Route.

Notes: Topical routes of drug administration involve the direct application of medications to the skin or mucous membranes. These routes are used for localized effects and are advantageous for treating conditions in specific areas without systemic absorption. The following are some common topical routes:

1. Dermal/Epidermal (Skin) Routes:

• Topical (or Cutaneous) Application: Application of drugs onto the skin surface. Examples include creams, ointments, gels, and patches.

• Transdermal Patches: Adhesive patches containing drug formulations that are applied to the skin, allowing controlled, continuous drug absorption.

2. Mucous Membrane Routes:

• Ophthalmic (Eye) Route: Application of medications to the eyes, including eye drops and ointments.

• Otic (Ear) Route: Application of medications to the ears, typically in the form of drops.

• Nasal Route: Administration of drugs through the nasal passages, including nasal sprays or drops.

• Buccal Route: Placement of drugs between the cheek and gum for absorption through the oral mucosa.

• Sublingual Route: Placement of drugs under the tongue for absorption through the sublingual mucosa.

3. Rectal Route:

Rectal Suppositories: Solid dosage forms inserted into the rectum, providing local or systemic effects.

Q.11 Give names of autonomic neurotransmitters.

Ans: Autonomic neurotransmitters are chemicals that transmit signals within the autonomic nervous system (ANS). This controls involuntary functions. There are two main types of autonomic neurotransmitters: Acetylcholine (Ach), and Norepinephrine (NE) and Epinephrine.

Note:

1. Acetylcholine (ACh): Acetylcholine is the neurotransmitter released by cholinergic neurons. It acts on both muscarinic and nicotinic receptors.

Muscarinic Receptors: Located on the effector cells of parasympathetic postganglionic neurons and some sympathetic postganglionic neurons. Examples include M1 to M5 receptors.

Nicotinic Receptors: Found on the cell membranes of autonomic ganglia (both sympathetic and parasympathetic) and at neuromuscular junctions. Examples include Nn (neuronal) and Nm (muscular) receptors.

2. Norepinephrine (NE) and Epinephrine:

Norepinephrine is the neurotransmitter released by adrenergic postganglionic sympathetic neurons.

Epinephrine (also known as adrenaline) is released by the adrenal medulla and acts as a hormone in the bloodstream and as a neurotransmitter in some sympathetic nerve terminals.

Q.12 What is angina pectoris?

Ans: Angina pectoris (angina) is a medical condition characterized by chest pain or discomfort that occurs when the heart muscle doesn't receive enough oxygen-rich blood. The term "pectoris" refers to the chest, and "angina" is derived from the Latin word for "strangling" or "choking.".

Note: The following are characteristics of angina pectoris

1. Chest Pain: Squeezing, pressure, heaviness, or tightness in the chest. It may also be felt in the arms, neck, jaw, shoulder, or back.

2. Triggers: Angina pain is typically triggered by physical exertion, emotional stress, cold temperatures, heavy meals, or other situations that increase the heart's demand for oxygen.

3. Duration: The pain is usually temporary and relieved by rest or medications that improve blood flow to the heart.

There are different types of angina. These are stable angina, unstable angina, and variant (Prinzmetal's) angina. Stable angina is predictable and usually occurs with exertion, while unstable angina is more unpredictable and can occur at rest or with minimal exertion, posing a higher risk of a heart attack.

Angina is a warning sign that the heart may not be receiving sufficient blood supply. It requires medical attention to address the underlying causes and reduce the risk of complications, such as a heart attack. Treatment may include lifestyle modifications, medications, and, in some cases, medical procedures to improve blood flow to the heart.

Q.13 Comment on Bioassay of drugs.

Ans Bioassay of drugs involves using living organisms or biological systems to evaluate the pharmacological effects, potency, and efficacy of a substance. Purpose and Importance are Determination of Potency, Quality Control, and Comparative Studies:

Notes:

Types of Bioassays:

1. Quantal Bioassays: Evaluate the drug's effect on an "all-or-none" response, such as mortality or a specific physiological response.

2. Graded Bioassays: Measure the magnitude of a response on a continuous scale, providing a dose-response curve.

Q.14 Write two oral antidiabetic drugs.

Ans: Metformin and Sulfonylureas (e.g., Glimepiride, Glipizide, Gliclazide).

Note:

1. Metformin: Metformin is a first-line medication for the treatment of type 2 diabetes. It belongs to the biguanide class of drugs and works primarily by decreasing glucose production in the liver and improving insulin sensitivity in peripheral tissues. Metformin does not increase insulin secretion from the pancreas, so it doesn't cause hypoglycemia when used alone.

2. Sulfonylureas (e.g., Glimepiride, Glipizide, Gliclazide): Sulfonylureas are a class of drugs that stimulate insulin secretion from the beta cells of the pancreas. They are often used as second-line agents after metformin in the treatment of type 2 diabetes. Sulfonylureas work by closing ATP-sensitive potassium channels in the beta cells of the pancreas. This leads to depolarization of the cell membrane, calcium influx, and subsequent insulin release. Sulfonylureas can cause hypoglycemia (low blood sugar) and weight gain as side effects. They are typically taken before meals to stimulate insulin secretion in response to rising blood glucose levels.

Q.15 Tetracycline acts on which part of the cell.

Ans: Tetracycline is an antibiotic. It inhibits protein synthesis in bacteria by binding to the bacterial ribosome. It blocks the protein synthesis to disrupts bacterial growth and reproduction. This leads to bacteriostatic effects.

Q.16 Any two antimetabolite anticancer drugs.

Ans: Methotrexate and 5-Fluorouracil (5-FU)

Note:

1. Methotrexate: Methotrexate is a folate antagonist that inhibits the enzyme dihydrofolate reductase (DHFR). It is involved in the synthesis of tetrahydrofolate, a precursor for DNA synthesis. Methotrexate disrupts DNA synthesis by inhibiting DHFR. It is used in the treatment of various cancers, including leukemia, lymphoma, breast cancer, and lung cancer.

2. 5-Fluorouracil (5-FU): 5-Fluorouracil is a pyrimidine analog that interferes with DNA synthesis and RNA transcription by inhibiting the enzyme thymidylate synthase. Thymidylate synthase is essential for the synthesis of thymidine, a nucleotide required for DNA replication. By inhibiting thymidylate synthase, 5-FU disrupts DNA synthesis and leads to cell death. It is commonly used to treat cancers such as colorectal cancer, breast cancer, and gastric cancer.

SECTION-C

Note: Short answer type questions. Attempt any eight questions out of ten questions. (8x5=40)

Q.17 What is an Absorption drug?

Ans: Drug absorption is the irreversible process of moving a drug from its site of administration into the bloodstream. Drug Absorption determines the onset, intensity, and duration of drug action. The absorption of a drug depends on several factors, including:

• 1. Route of Administration: Drugs can be administered via various routes, including orally (by mouth), intramuscularly (into a muscle), subcutaneously (under the skin), topically (applied to the skin), rectally (into the rectum), and through inhalation (into the lungs), among others. The route of administration significantly influences the absorption characteristics of a drug.

• 2. Physicochemical Properties of the Drug: Factors such as molecular size, solubility, ionization state, and formulation affect the drug's ability to pass through biological membranes and be absorbed into the bloodstream.

• 3. Gastrointestinal Factors (for oral drugs): pH of the stomach and intestine, gastric emptying rate, surface area available for absorption (affected by factors like the presence of food or certain diseases like Crohn's disease), and enzymatic activity in the gastrointestinal tract influence the absorption of orally administered drugs.

• 4. Drug Formulation: The formulation of a drug (e.g., immediate-release tablets, extended-release tablets, capsules, solutions) affects its dissolution and subsequent absorption in the gastrointestinal tract.

• 5. First-Pass Metabolism: Drugs absorbed from the gastrointestinal tract pass through the liver before reaching systemic circulation. Some drugs undergo significant metabolism (first-pass metabolism) in the liver before reaching systemic circulation, reducing their bioavailability.

• 6. Blood Flow to the Site of Administration: Blood flow to the site of administration affects the rate and extent of drug absorption. For example, intramuscular injections rely on blood flow to facilitate absorption into the bloodstream.

• 7. Drug-Drug Interactions: Interactions with other drugs or substances in the gastrointestinal tract can affect drug absorption. For instance, certain drugs may alter the pH of the gastrointestinal tract or compete for transport mechanisms, affecting the absorption of co-administered drugs.

Q.18 Differentiate antisecretory and antacids.

Ans: Antisecretory drugs and antacids are both used to treat gastrointestinal disorders related to the acidity of the stomach. They work through different mechanisms and have distinct roles in therapy. The following are the differences between them:

1. Antisecretory Drugs:

• a. Mechanism: Antisecretory drugs work by inhibiting the production of gastric acid in the stomach.

• b. Target: They target the cells in the stomach lining responsible for producing acid, such as parietal cells.

• c. Examples: Proton pump inhibitors (PPIs) such as omeprazole, esomeprazole, pantoprazole, and H2 receptor antagonists (H2 blockers) such as ranitidine, and famotidine.

• d. Effects: These drugs reduce the secretion of gastric acid, thereby decreasing the acidity of the stomach. They are often used to treat conditions such as gastroesophageal reflux disease (GERD), peptic ulcers, and Zollinger-Ellison syndrome.

• e. Onset of Action: Antisecretory drugs have a delayed onset of action but provide long-lasting suppression of acid secretion.

2. Antacids

• a. Mechanism: Antacids work by neutralizing existing gastric acid in the stomach.

• b. Targets: They directly interact with the acidic environment of the stomach.

• c. Examples: Aluminum hydroxide, magnesium hydroxide, calcium carbonate, sodium bicarbonate.

• d. Effects: Antacids rapidly raise the pH of the stomach by neutralizing acid. They provide quick relief from symptoms of heartburn, acid indigestion, and upset stomach.

• e. Duration of Action: Antacids provide short-term relief of symptoms but do not address the underlying cause of acid hypersecretion.

• f. Side Effects: Antacids may cause side effects such as constipation (with aluminum- or calcium-based antacids), diarrhea (with magnesium-based antacids), and acid-base imbalances (with sodium bicarbonate).

Q.19 Write pharmacological actions of procaine.

Ans: Procaine is a local anesthetic medication used for its numbing effect to block nerve impulses in specific areas of the body. The following are its pharmacological actions:

1. Local Anesthetics: procaine is not used topically due to poor absorption from mucous membranes. Lignocaine has completely replaced procaine as a local anesthetic. Procaine works by reversibly blocking nerve conduction. It acts by inhibiting the influx of sodium ions through voltage-gated sodium channels in the neuronal membrane. It prevents the generation and propagation of action potentials (impulses) along nerve fibers. This action results in temporary loss of sensation in the area where procaine is administered.

2. Antiarrhythmic: Procaine has weak antiarrhythmic properties and has been used in the treatment of certain cardiac arrhythmias like ventricular arrhythmias. It works by stabilizing the cardiac cell membrane and reducing excitability. This helps to suppress abnormal electrical activity in the heart.

Q.20 Classify antidiabetic drugs.

Ans: Antidiabetic drugs can be classified into several categories based on their mechanism of action and therapeutic targets.

Classification of antidiabetic drugs:

1. Insulin:

• a. Short-acting insulin: Regular insulin

• b. Rapid-acting insulin analogs: Insulin lispro, insulin aspart, insulin glulisine

• c. Intermediate-acting insulin: Neutral protamine Hagedorn (NPH) insulin

• d. Long-acting insulin analogs: Insulin glargine, insulin detemir, insulin degludec

2. Oral Antidiabetic Agents:

• a. Biguanides: Metformin

• b. Sulfonylureas: Glyburide (glibenclamide), glipizide, glimepiride

• c. Meglitinides (Glinides): Repaglinide, nateglinide

• d. Thiazolidinediones (TZDs): Pioglitazone, rosiglitazone

• e. Alpha-glucosidase inhibitors: Acarbose, miglitol

• f. Dipeptidyl peptidase-4 (DPP-4) inhibitors: Sitagliptin, saxagliptin, linagliptin

• g. Sodium-glucose cotransporter-2 (SGLT-2) inhibitors: Canagliflozin, dapagliflozin, empagliflozin

• h. Combination drugs: Various combinations of two or more classes of antidiabetic agents, such as metformin and sulfonylureas, metformin and DPP-4 inhibitors, etc.

Q.21 Elaborate on the mechanism of action of Sulphamethoxazole.

Ans: Mechanism of action: Sulphamethoxazole acts as an antibacterial agent by inhibiting folate synthesis. Bacterial cell membranes are impermeable to folic acid. Bacterial cells synthesize their own folic acid from PABA, by using the enzyme dihydropteroate synthetase. This folic acid is required to synthesize purine and pyrimidine. Purine and pyrimidine are precursors of Nucleic acids RNA and DNA synthesis

Sulfonamides are synthetic analogs of PABA and have structural similarities with PABA. Sulfonamides and PABA have similar pharmacokinetics. Thus, sulfonamides competitively block the enzyme dihydropteroate synthetase to inhibit folic acid synthesis from PABA. Folic acid synthesis inhibition leads to blocking nucleic acids RNA and DNA synthesis, bacterial cell growth, and their multiplication. Thus sulfonamides act as bacteriostatic.

Q.22 Explain the life cycle of a malarial parasite and the drugs used in its treatment.

Ans:

The life cycle of malarial parasites

The life cycle of the malarial parasite involves several stages that occur both within the human host and the female Anopheles mosquito vector.

Human Host Stage (Asexual Phase):

1. Infection: Malaria begins when an infected female Anopheles mosquito bites a human and injects sporozoites (the infective stage) into the bloodstream.

2. Liver Stage (Exoerythrocytic Stage): Sporozoites infect the liver and multiply asexually to form merozoites. It is asymptomatic and lasts from several days to weeks.

3. Erythrocytic Stage: Merozoites enter the bloodstream from the liver and invade red blood cells (RBCs). Merozoites multiply asexually inside RBCs. This leads to rupture-infected RBCs and the release of more merozoites. This leads to fever. Merozoites infect other healthy RBCs. Merozoites develop gametocytes (sexual stage)during this invasion and rapture of RBCs.

4. Mosquito Vector Stage:

• a. Transmission: An uninfected female Anopheles mosquito feeds on an infected human host. They ingest gametocytes (sexual stage) of the parasite along with the blood meal.

• b. Mosquito Midgut Stage: Gametocytes develop into male and female gametes (microgametocytes and macrogametocytes) in the mosquito midgut.

• c. Fertilization occurs, forming zygotes, which develop into ookinetes and then oocysts.

5. Mosquito Salivary Gland Stage: Oocysts rupture, releasing sporozoites, which migrate to the mosquito's salivary glands, ready to infect another human host during a subsequent blood meal.

Q.23 Describe MOA, Uses, and adverse effects of Paracetamol.

Ans: Paracetamol (acetaminophen) is a widely used over-the-counter medication known for its antipyretic (fever-reducing) and analgesic (pain-relieving) properties.

1. Mechanism of Action (MOA): It inhibits the enzyme cyclooxygenase (COX), primarily in the central nervous system (CNS). Paracetamol reduces the production of prostaglandins in the brain by inhibiting COX-2. This involves pain perception and fever regulation.

2. Uses:

Fever Reduction: It is used to reduce fever (Antipyretic).

Pain Relief: It is commonly used to relieve mild to moderate pain. (Mild Analgesic).

Combination Therapies: It is used in combination medications to enhance pain relief and fever reduction, such as in cold and flu remedies or prescription pain medications.

Adverse Effects:

1. Liver Toxicity: One of the most serious adverse effects of paracetamol is hepatotoxicity (liver toxicity). The toxic metabolite of paracetamol, N-acetyl-p-benzoquinone imine (NAPQI), accumulates in the liver and causes hepatocellular necrosis. This leads to acute liver failure and fatal outcomes.

2. Renal Toxicity: Prolonged use of high doses of paracetamol causes kidney damage, although this is less common than liver toxicity.

3. Gastrointestinal Effects: Paracetamol is generally well-tolerated at recommended doses, but it can occasionally cause gastrointestinal upset, including nausea, vomiting, and abdominal pain.

4. Blood Disorders: In rare cases, paracetamol has been associated with blood disorders such as thrombocytopenia (low platelet count) and leukopenia (low white blood cell count).

5. Overdose: Accidental or intentional overdose of paracetamol can result in severe hepatotoxicity and liver failure, which can be life-threatening if not promptly treated.

Q.24 Classify antihypertensive agents and add a note on each category.

Ans: Antihypertensive agents are used to treat high blood pressure (hypertension). They are classified into several categories based on their mechanism of action.

1. Diuretics: Thiazides, Frusemide, etc

Note: Diuretics increase the excretion of sodium and water from the body. This leads to a decrease in blood volume and a subsequent reduction in blood pressure. They are often used as first-line agents in the treatment of hypertension.

2. β ADRENERGIC RECEPTOR BLOCKERS: Propranolol, Atenolol and metoprolol.

Note: Beta-blockers inhibit the action of adrenaline (epinephrine) and other stress hormones on the heart and blood vessels. This results in decreased heart rate and cardiac output. They are effective in reducing blood pressure. However, they are not preferred in patients with asthma or diabetes.

3. VASODILATORS: Minoxidil, Hydralazine, and Sodium nitroprusside.

Note: Direct-acting vasodilators produce blood vessels and smooth muscle relaxation. That reduces peripheral blood vessel resistance in blood flow. This leads to a decrease in blood pressure. Usually, vasodilators are not preferred to treat hypertension due to their side effects reflex tachycardia,

4. Calcium Channel Blockers (CCBs): Diphenyl alkylamines: Verapamil

• a. Benzothiazine derivatives: Diltiazem

• b. Dihydropyridine: Nifedipine

Note: Calcium channel blockers block the entry of calcium ions into smooth muscle cells of the heart and blood vessels. This leads to relaxation of the muscles and vasodilation. They are effective in lowering blood pressure.

There are two main classes of CCBs: dihydropyridine CCBs (e.g., amlodipine, nifedipine) and non-dihydropyridine CCBs (e.g., verapamil, diltiazem).

5. Angiotensin-Converting Enzyme (ACE) Inhibitors: Benazepril, Captopril, Enalapril, Fosinopril.

Note: ACE inhibitors block the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. It reduces blood pressure and decreases peripheral resistance. They are commonly used in patients with hypertension, heart failure, or chronic kidney disease. ACE inhibitors may cause a persistent dry cough in some patients and can lead to hyperkalemia (high potassium levels).

6. ANGIOTENSIN ANTAGONIST: Losartan

Note: Angiotensin antagonists such as losartan act by blocking angiotensin II receptors without affecting the formation of angiotensin II. Its pharmacological effects are similar to ACE inhibitors or just opposite to the angiotensin II effect such as relaxation of smooth muscles in a renal artery leading to vasodilation, blocking the secretion of aldosterone leading to excretion of water and sodium, and decreasing ventricular hypertrophy.

8. α ADRENERGIC RECEPTOR BLOCKERS: Prazosin

Note: α1 adrenergic receptors are located in smooth muscles of blood vessels. α1 adrenergic receptors stimulate and produce contraction in smooth muscles of blood vessels. This leads to vasoconstriction, an increase in peripheral vascular resistance to blood flow, and an increase in blood pressure. α1 adrenergic receptor blockers competitively block α1 adrenergic receptors present on smooth muscles of blood vessels. This leads to the relaxation of these smooth muscles to produce both arteriolar dilation and venous dilation.

9. CENTRAL SYMPATHETIC DRUGS: Clonidine: Clonidine is an imidazoline derivative that has a high affinity for α2 adrenergic receptors in CNS. It stimulates α2 adrenergic receptors in the CNS to decrease sympathetic activity.

Q.25 What is the biotransformation of drugs?

Ans: Biotransformation of drugs, (drug metabolism) is the chemical alterations in a drug molecule within the body. These transformations involve enzymatic reactions that convert the drug into metabolites.

There are two main phases of drug metabolism:

1. Phase I Metabolism: In Phase I metabolism, the drug molecule undergoes chemical reactions such as oxidation, reduction, or hydrolysis. Cytochrome P450 (CYP) enzymes catalyze the metabolic reactions. These reactions produce polar metabolites. Phase I metabolism can either activate or inactivate a drug. It depends on the nature of the metabolites produced.

2. Phase II Metabolism: Phase II metabolism involves the conjugation of the drug or its Phase I metabolites with endogenous compounds such as glucuronic acid, sulfate, glycine, or glutathione. This conjugation reaction increases the water solubility of the drug or its metabolites. This facilitates their excretion from the body via urine or bile. Common Phase II reactions include glucuronidation, sulfation, acetylation, methylation, and conjugation with glutathione.

Metabolism results in the formation of inactive, less active metabolites or more active compounds.

Q.26 Write the symptoms & treatment of amoebiosis.

Ans: Amoebiasis (amoebic dysentery) is a parasitic infection caused by the protozoan parasite Entamoeba histolytica. It commonly affects the intestine but can also spread to other organs, such as the liver, causing serious complications if left untreated.

Symptoms:

1. Diarrhea: Often severe, with loose stools that may contain blood or mucus.

2. Abdominal pain: Cramping and tenderness in the abdominal region, localized in the lower abdomen.

3. Fatigue: General tiredness and weakness, which may accompany dehydration from diarrhea.

4. Weight loss: Due to decreased appetite, nausea, and diarrhea.

5. Fever: Low-grade fever may be present, especially if the infection has spread beyond the intestines.

6. Rectal pain: Pain during bowel movements or when passing stools, especially if there are ulcers present in the rectum.

7. Complications: If left untreated, amoebiasis can lead to severe complications such as liver abscess, perforation of the intestines, and systemic infection.

Treatment:

1. Antimicrobial agents: They are used to kill the parasite. Commonly prescribed antimicrobial agents are metronidazole, tinidazole, or nitazoxanide. These medications are typically taken for 5 to 10 days.

2. Antiparasitic drugs: Antiparasitic drugs such as paromomycin may be prescribed to eliminate the amoebas from the intestine and prevent recurrence.

3. Hydration: It's essential to maintain hydration by drinking plenty of fluids, especially if diarrhea is severe. Oral rehydration solutions (ORS) containing electrolytes can help replace lost fluids and minerals.

4. Pain relief: Over-the-counter (OTC) pain relievers such as acetaminophen or ibuprofen can help alleviate abdominal pain and fever. However, avoid using aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) if there is evidence of bleeding.

SECTION-D

Note: Long answer type questions. Attempt any three questions out of four questions. (3x8=24)

Q.27 Classify and explain the advantages and disadvantages of various routes of drug administration.

Ans: Routes of drug administration have their own advantages and disadvantages. It affects the rate of drug absorption, onset of action, patient compliance, and adverse effects.

1. Oral Administration:

Advantages:

• · Convenient and non-invasive: Oral drugs are easy to administer and do not require specialized equipment.

• · Patient compliance: Patients usually find oral medications more acceptable and are more likely to adhere to prescribed regimens.

• · Economical: Oral drugs are typically cost-effective compared to other routes.

Disadvantages:

• · Variable absorption: Food, pH levels, and gastrointestinal motility affect drug absorption.

• · First-pass metabolism: Drugs absorbed through the gastrointestinal tract undergo metabolism in the liver before reaching systemic circulation. This reduces bioavailability.

• · Potential for gastrointestinal irritation: Some drugs may cause irritation or damage to the gastrointestinal mucosa.

2. Injectable Administration:

Advantages:

• · Rapid onset of action: Injectable drugs bypass the digestive system, leading to faster onset of action.

• · Precise dosage: Injectable formulations allow for accurate dosing.

• · Higher bioavailability: Absorption is predictable and complete compared to oral administration.

Disadvantages:

• · Invasiveness: Injection requires piercing the skin, which can be painful and may increase the risk of infection.

• · Need for healthcare professional: Injectable drugs require a trained healthcare provider for drug administration.

• · Risk of tissue damage: Improper injection technique or use of irritating drugs can cause tissue damage or necrosis.

4. Topical Administration:

Advantages:

• · Targeted delivery: Topical drugs are applied directly to the site of action, minimizing systemic side effects.

• · Non-invasive: Topical formulations are easy to apply and do not require needles or invasive procedures.

• · Reduced systemic exposure: Topical administration limits systemic absorption. This reduces the risk of systemic adverse effects.

Disadvantages:

• · Limited penetration: Some drugs may have poor penetration through the skin or other barriers, limiting their efficacy.

• · Skin irritation: Topical drugs may cause skin irritation or allergic reactions in some individuals.

• · Compliance issues: Patients may forget to apply topical medications regularly or may find the application process cumbersome.

5. Inhalation Administration:

Advantages:

• · Rapid onset of action: Inhaled drugs reach the bloodstream quickly through the lungs, leading to rapid onset of action.

• · Targeted delivery: Inhalation allows drugs to be delivered directly to the respiratory tract, making it effective for treating respiratory conditions.

• · Reduced systemic side effects: Inhalation minimizes systemic exposure, reducing the risk of systemic side effects.

Disadvantages:

• · Device dependency: Inhalation requires specialized devices such as inhalers or nebulizers. These require training to administer drugs correctly.

• · Risk of local irritation: Some inhaled drugs may irritate the respiratory tract, leading to coughing or bronchospasm.

• · Limited applicability: Inhalation is primarily used for treating respiratory conditions and may not be suitable for all drugs or patients.

7. Transdermal Administration:

Advantages:

• · Prolonged drug release: Transdermal patches provide continuous drug delivery over an extended period, maintaining steady plasma levels of drug.

• · Non-invasive: Transdermal administration does not involve needles or invasive procedures. This enhances patient acceptance.

• · Avoids first-pass metabolism: Drugs absorbed through the skin bypass the liver. This avoids first-pass metabolism and improves bioavailability.

8. Disadvantages:

• · Limited drug absorption: Some drugs have poor skin permeability, limiting their effectiveness when administered transdermally.

• · Skin irritation: Transdermal patches may cause skin irritation or allergic reactions in some individuals.

• · Size limitations: Transdermal patches have size limitations, restricting the amount of drug that can be delivered. 

Q.28 What are NSAIDs? Write detailed notes on each category.

Ans: Classification

Conventional NSAIDs: They are nonselective COX inhibitors

• 1. Salicylates: Aspirin, Diffunisol

• 2. Arylacetic acid derivatives: Diclofenac

• 3. Indole and Indene acetic acid: Indomethacin, sulindac, etodoloc, fenamate

• 4. Arylpropionic acid derivatives: Fenoprofen, Flurbiprofen, Ibuprofen, Ketoprofen, naproxen, oxaprozin

• 5. Pyrazolone derivatives: Phenylbutazone, oxyphenbutazone, Azapropazon ecarprofen, metamizole

• 6. Anthraquinone acid derivatives: Mefenamic acid

• 7. Oxicam derivatives : piroxicam, tenoxicam

• 8. Pyrollo Pyrrole derivatives: ketorolac

• 9. Preferential COX-2 inhibitors: Nomsulide, meloxicam, nabumetone

Selective COX-2 Inhibitors: celecoxib, rafecoxib, valdecoxib

OR

NSAIDs, or Nonsteroidal Anti-Inflammatory Drugs, are a class of medications commonly used to relieve pain, reduce inflammation, and lower fever. They work by inhibiting the enzyme cyclooxygenase (COX). There are several categories of NSAIDs, each with its characteristics and properties:

1. Traditional NSAIDs: Traditional NSAIDs, also known as non-selective NSAIDs. They inhibit both COX-1 and COX-2 enzymes. Examples are ibuprofen, naproxen, diclofenac, indomethacin, aspirin, etc.

These drugs provide pain relief, reduce inflammation and lower fever. However, they may also increase the risk of gastrointestinal ulcers and bleeding due to inhibition of the protective prostaglandins in the stomach lining.

Aspirin, in addition to its anti-inflammatory and analgesic properties, is also used for its antiplatelet effects. This is beneficial for preventing blood clots and reducing the risk of heart attack and stroke.

2. COX-2 Inhibitors: COX-2 inhibitors selectively target the COX-2 enzyme. COX-2 is involved in inflammation and pain. COX-2 inhibitors spare COX-1. COX 1 plays a role in protecting the stomach lining. Examples of COX-2 inhibitors are celecoxib (Celebrex), etoricoxib, and rofecoxib (no longer available due to safety concerns).

COX-2 inhibitors are associated with a lower risk of gastrointestinal side effects. However, they may increase the risk of cardiovascular events, such as heart attack and stroke, particularly with long-term use or at high doses. These drugs are typically prescribed for conditions such as osteoarthritis, rheumatoid arthritis, and acute pain.

Selective COX-1 Inhibitors: Selective COX-1 inhibitors target the COX-1 enzyme. COX-1 is involved in maintaining normal physiological functions. They protect the stomach lining and support kidney function. Thus Selective COX-1 inhibitors produce gastrointestinal side effects like ulcers and bleeding. Thus these drugs are less commonly used compared to traditional NSAIDs and COX-2 inhibitors.

3. Topical NSAIDs: Topical NSAIDs are formulations applied directly to the skin at the site of pain or inflammation. Examples include diclofenac gel, ibuprofen cream, and ketoprofen patches. Topical NSAIDs produce localized pain relief with minimal systemic absorption. This reduces the risk of systemic side effects compared to oral NSAIDs. They are commonly used for conditions such as osteoarthritis, tendonitis, and muscle strains.

4. Combination NSAIDs: Combination NSAIDs contain more than one active ingredient. They contain an NSAID with another pain reliever. Examples are ibuprofen and paracetamol combinations or NSAIDs combined with stomach protectants. These combinations aim to provide enhanced pain relief and symptom management while minimizing potential side effects. 

Q.29 Describe Penicillin antibiotics.

Ans: Penicillin antibiotics are a group of antibiotics derived from the fungus Penicillium. They were the first antibiotics to be discovered and are still widely used today to treat a variety of bacterial infections.

Mechanism of Action: Penicillin antibiotics inhibit the synthesis of bacterial cell walls by binding to and inhibiting the enzyme transpeptidase (also known as penicillin-binding proteins or PBPs). Transpeptidase is responsible for cross-linking the peptidoglycan strands in the bacterial cell wall. This is essential for maintaining cell wall integrity and rigidity. By inhibiting transpeptidase, penicillin antibiotics weaken cell walls and cause cell lysis, ultimately bacterial death.

Types of Penicillin Antibiotics:

• 1. Natural Penicillins: These include penicillin G (benzylpenicillin) and penicillin V (phenoxymethylpenicillin). They are effective against a narrow range of gram-positive bacteria. It includes Streptococcus and some Staphylococcus species.

• 2. Penicillinase-Resistant Penicillins: These include methicillin, oxacillin, and dicloxacillin. They resist inactivation by bacterial enzymes penicillinases (beta-lactamases). They are produced by some bacteria to degrade penicillin.

• 3. Aminopenicillins: This group includes amoxicillin and ampicillin. They have an extended spectrum (broad spectrum) of activity. They are effective against both gram-positive and gram-negative bacteria.

• 4. Extended-Spectrum Penicillins: These include piperacillin and ticarcillin, which have an even broader spectrum of activity. They include many gram-negative bacteria and are often used in combination with beta-lactamase inhibitors to enhance efficacy.

Clinical Uses: Penicillin antibiotics are used to treat a wide range of bacterial infections, including streptococcal infections (such as strep throat and scarlet fever), staphylococcal infections (such as skin infections and cellulitis), pneumococcal infections, meningococcal infections, and syphilis.

Adverse Effects: Penicillin antibiotics are generally well-tolerated, but allergic reactions can occur, ranging from mild rash and itching to severe anaphylaxis. Common side effects include gastrointestinal disturbances such as nausea, vomiting, and diarrhea.

Resistance:

1. Bacterial resistance to penicillin antibiotics has emerged due to the production of beta-lactamase enzymes, which hydrolyze the beta-lactam ring of penicillin, rendering it inactive.

2. Resistance mechanisms also include alterations in penicillin-binding proteins (PBPs) or efflux pumps that remove antibiotics from bacterial cells.

Q.30 Define, Classify, and Write notes on each category of Antiarrhythmic drugs.

Ans: Antiarrhythmic drugs are used to prevent or treat abnormal heart rhythms (arrhythmias). Arrhythmias can occur when the electrical signals to coordinate heartbeats are disrupted. This leads to irregular heart rhythms that can be too fast (tachyarrhythmias) or too slow (bradyarrhythmias). Antiarrhythmic drugs work by either stabilizing the heart's electrical activity or modifying the heart's response to electrical signals. Antiarrhythmic drugs are classified into four main classes based on their mechanism of action.

1. Class I Antiarrhythmics - Sodium Channel Blockers: Class I drugs inhibit the influx of sodium ions into sodium channels in cardiac cell membranes during phase 0 of the cardiac action potential. This action slows the rate of depolarization and conduction velocity. This stabilizes the heart's electrical activity. Class I drugs are further subdivided into three subclasses based on their effects on cardiac tissue:

• · Class IA: Moderate sodium channel blockade with additional effects on potassium channels. Examples include procainamide, quinidine, and disopyramide.

• · Class IB: Weak sodium channel blockade with fast dissociation from sodium channels. Examples include lidocaine, mexiletine, and phenytoin.

• · Class IC: Potent sodium channel blockade with slow dissociation from sodium channels. This leads to a significant slowing of conduction. Examples include flecainide and propafenone.

2. Class II Antiarrhythmics - Beta-Adrenergic Blockers: Class II drugs exert their antiarrhythmic effects by blocking beta-adrenergic receptors in the heart. They reduce the effects of sympathetic stimulation on the heart.

They decrease sympathetic activity that slows the heart rate, reduces myocardial contractility, and prolongs the refractory period, leading to the suppression of arrhythmias. Examples include propranolol, metoprolol, and esmolol.

3. Class III Antiarrhythmics - Potassium Channel Blockers: Class III drugs target potassium channels in cardiac cell membranes, prolonging the action potential duration and refractory period. They stabilize the heart's electrical activity. Prolongation of the action potential duration helps prevent reentrant arrhythmias by prolonging the refractory period and reducing premature depolarizations. Examples include amiodarone, sotalol, dofetilide, and dronedarone.

4. Class IV Antiarrhythmics - Calcium Channel Blockers: Class IV drugs inhibit calcium channels in cardiac cells, reducing the influx of calcium ions during phase 2 of the cardiac action potential. These drugs slow conduction through the AV node, prolonging AV nodal refractoriness and reducing heart rate by inhibiting calcium influx. Examples include verapamil and diltiazem.