Section 1

Q.1 Define the following terms (any five) [5 marks]

1. Pharmacodynamics

Pharmacodynamics is the branch of pharmacology that studies what a drug does to the body. It focuses on the mechanisms of action, biological effects, and the relationship between drug concentration and effect.

2. Drug

A drug is any chemical substance that, when administered to a living organism, produces a biological effect and is used for the prevention, diagnosis, treatment, or cure of diseases.It can modify physiological functions, either enhancing or inhibiting normal body processes, and is used in medical practice to restore health or relieve symptoms.

3. Toxicology

Toxicology is the branch of science that studies the harmful effects of substances on living organisms, including their detection, mechanism of action, symptoms, treatment, and prevention of poisoning.

4. Chemotherapy

Chemotherapy is the branch of pharmacology that involves the use of chemical substances (drugs) to kill or inhibit the growth of microorganisms, parasites, or cancer cells without causing excessive damage to the host. It is mainly used in the treatment of infections (antibacterial, antiviral, antifungal) and malignancies (anticancer drugs) by targeting the disease-causing cells or organisms, often affecting their reproduction or metabolism.

5. Adverse reaction

An adverse reaction refers to an unwanted or harmful effect experienced after the administration of a medication, vaccine, or treatment. These reactions can range from mild (e.g., rash, nausea) to severe (e.g., anaphylaxis, organ damage).

6. Mixed agonist and antagonist

A mixed agonist-antagonist is a drug that acts as an agonist (activator) at certain receptor subtypes while acting as an antagonist (blocker) at others. This dual action allows the drug to activate specific pathways while inhibiting others, often leading to a balanced or moderated physiological response

Q.2 Described the briefly drug used in tuberculosis (5)

Tuberculosis is primarily treated with a combination of anti-tubercular drugs to prevent resistance and ensure effective bacterial clearance. These drugs are classified as first-line and second-line anti-TB drugs.

First-Line Anti-Tubercular Drugs (Used in DOTS – Directly Observed Treatment Short Course)

Isoniazid (INH)

• It is a bactericidal drug that inhibits mycolic acid synthesis, which is essential for the integrity of the mycobacterial cell wall.
• It is used as a backbone drug in both active and latent TB infections and is given daily for at least 6–9 months.
• It may cause peripheral neuropathy, especially in malnourished or diabetic patients, so pyridoxine (vitamin B6) is co-administered to prevent this effect.
• It is metabolized in the liver, and hepatotoxicity is a major side effect requiring regular liver function monitoring.

Rifampicin (RIF)

• It is a bactericidal antibiotic that acts by inhibiting DNA-dependent RNA polymerase in Mycobacterium tuberculosis.
• It is responsible for rapidly reducing the bacterial load and is highly effective when used with INH and PZA.
• It can cause hepatotoxicity and hypersensitivity reactions, and also induces cytochrome P450 enzymes, leading to drug interactions with oral contraceptives, antiretrovirals, and warfarin.
• Patients should be educated that orange discoloration of urine, sweat, and tears is a normal side effect and not harmful.

Pyrazinamide (PZA)

• It is a bactericidal drug that acts effectively in the acidic environment of phagolysosomes where TB bacilli reside.
• It plays a crucial role in the initial 2-month intensive phase to shorten the total treatment duration.
• It may cause hepatotoxicity and hyperuricemia, which may lead to gout attacks or joint pains in some patients.
• It is not recommended in pregnant women and patients with severe liver disease due to its toxic profile.

Ethambutol (EMB)

• It is a bacteriostatic drug that inhibits arabinogalactan synthesis, a component of the bacterial cell wall.
• It is mainly used to prevent resistance to other drugs, especially in combination therapy.
• One of the major side effects is optic neuritis, which presents as loss of red-green color discrimination and blurred vision, so baseline and monthly eye exams are advised.
• It is relatively safe in renal impairment if dose adjustments are done appropriately.

Streptomycin (SM)

• It is an aminoglycoside antibiotic that inhibits protein synthesis by binding to the 30S ribosomal subunit.
• It is used as a second-line injectable drug due to its serious side effects and the emergence of resistance.
• It can cause ototoxicity (hearing loss, vertigo) and nephrotoxicity, especially in elderly or renal-impaired patients.
• It should be used cautiously in pregnant women, as it may cause fetal ototoxicity and congenital deafness.

Second-Line Anti-Tubercular Drugs (Used in MDR-TB and XDR-TB)

Kanamycin / Amikacin

• These are injectable aminoglycoside antibiotics that inhibit bacterial protein synthesis.
• They are mainly reserved for multidrug-resistant TB (MDR-TB) treatment regimens.
• They carry a high risk of hearing loss (ototoxicity) and kidney damage (nephrotoxicity), requiring frequent renal and audiometric monitoring.
• Dosage is calculated based on body weight, and administration is usually done via intramuscular injection.

Capreomycin

• It is a cyclic peptide antibiotic that inhibits protein synthesis and is active against drug-resistant TB strains.
• It is often used when aminoglycosides are not tolerated or resistance is present.
• Major side effects include nephrotoxicity, electrolyte imbalances, and local pain at injection site.
• Monitoring of hearing function, electrolytes, and renal function is essential during therapy.

Ethionamide

• It is a bactericidal agent similar in structure to INH and also inhibits mycolic acid synthesis.
• It is effective against MDR-TB, but is poorly tolerated due to GI side effects such as nausea, vomiting, and metallic taste.
• It can also cause hypothyroidism, especially when combined with PAS (para-aminosalicylic acid).
• It should be used cautiously in psychiatric patients, as it can aggravate depression and mental status changes.

Cycloserine

• It is a bacteriostatic antibiotic that works by inhibiting cell wall synthesis, particularly in resistant TB.
• It crosses the blood-brain barrier and is associated with CNS toxicity like headaches, tremors, irritability, and seizures.
• Pyridoxine (vitamin B6) supplementation is required to reduce neurotoxicity.
• It should be used cautiously in alcoholics and patients with seizure disorders.

Linezolid

• It is an oxazolidinone antibiotic that works by inhibiting bacterial protein synthesis at the 50S ribosomal unit.
• It is used in XDR-TB and resistant TB cases, often as a last-resort drug.
• Long-term use may cause bone marrow suppression, peripheral neuropathy, and lactic acidosis.
• CBC monitoring and eye exams are recommended during extended use.

Newer Reserved Anti-TB Drugs

Bedaquiline

• It is a novel anti-TB drug that inhibits the ATP synthase enzyme required for TB bacterial energy production.
• It is indicated for MDR-TB and XDR-TB cases under specialized programs.
• Side effects include QT interval prolongation, nausea, joint pain, and increased liver enzymes.
• It is not recommended in children or pregnant women, and ECG monitoring is essential.

Delamanid

• It is a nitroimidazole drug that inhibits mycolic acid synthesis, helping kill dormant TB bacilli.
• It is used in resistant TB strains and is often part of WHO-recommended regimens.
• Side effects include QT prolongation, GI upset, and dizziness.
• Its use is limited due to high cost and restricted availability in some countries.

Or

Q.2 Described drug used in malaria (5)

Malaria is a protozoal infection caused by different species of Plasmodium (e.g., P. falciparum, P. vivax, P. ovale, P. malariae).
Antimalarial drugs are used for treatment, prevention, and eradication of the parasite during its life cycle stages in humans.

Chloroquine

• It is a 4-aminoquinoline drug used as a blood schizonticide, effective mainly against P. vivax and P. ovale.

• It works by accumulating in parasite-infected red blood cells and inhibiting heme detoxification, leading to parasite death.
• It is given orally once a week for prophylaxis or daily for 3 days for treatment.
• It is not effective against chloroquine-resistant P. falciparum malaria.
• Common side effects include nausea, headache, blurred vision, pruritus, and QT interval prolongation.
• It should be used cautiously in patients with psoriasis and retinal disease.

Artemisinin and Derivatives (Artesunate, Artemether, Dihydroartemisinin)

• Artemisinins are rapid-acting blood schizonticides derived from the plant Artemisia annua.

• They act by producing free radicals inside the parasite, causing membrane and protein damage.
• They are the first-line treatment for falciparum malaria, especially in artemisinin-based combination therapy (ACT).
• Artesunate is usually given IV or IM in severe malaria, followed by oral ACT.
• Side effects include nausea, dizziness, transient heart rate changes, and mild liver enzyme elevation.
• They must always be used in combination to prevent resistance development.

Mefloquine

• It is a quinoline methanol derivative, used in chloroquine-resistant P. falciparum malaria.

• It kills intra-erythrocytic parasites and is given orally either for treatment or as prophylaxis.
• It has a long half-life which allows weekly dosing.
• Major adverse effects include neuropsychiatric symptoms like anxiety, depression, hallucinations, and GI disturbances.
• It is contraindicated in patients with epilepsy and psychiatric disorders.

Primaquine

• It is an 8-aminoquinoline drug that acts on the liver stage (hypnozoites) of P. vivax and P. ovale.

• It is the only drug that can eradicate hypnozoites and prevent relapses (radical cure).
• It is also gametocidal, meaning it prevents transmission of malaria.
• Side effects include abdominal cramps, methemoglobinemia, and hemolysis in G6PD-deficient patients.
• G6PD testing must be done before administration to avoid hemolytic anemia.

Quinine

• It is a natural alkaloid used mainly for severe falciparum malaria and drug-resistant strains.

• It interferes with heme polymerization, causing toxicity to the parasite.
• It is administered orally or intravenously, especially in life-threatening malaria.
• Common adverse effects include cinchonism (tinnitus, headache, nausea), hypoglycemia, and cardiotoxicity.
• It is often combined with doxycycline or clindamycin to shorten treatment duration and reduce resistance.

Atovaquone-Proguanil (Malarone)

• It is a fixed-dose combination used for both treatment and prophylaxis of P. falciparum malaria.

• Atovaquone inhibits mitochondrial electron transport, while proguanil inhibits dihydrofolate reductase, affecting nucleic acid synthesis.
• It is effective for uncomplicated malaria and is well-tolerated with fewer side effects.
• Common adverse effects are abdominal pain, mouth ulcers, headache, and diarrhea.
• It is used for short-term travelers to endemic areas.

Doxycycline

• It is a tetracycline antibiotic used as a suppressive prophylaxis and adjunct to quinine in malaria treatment.

• It acts by inhibiting protein synthesis in the apicoplast of the parasite.
• It is used for prophylaxis in travelers to drug-resistant areas, taken once daily starting 1–2 days before travel.
• Side effects include photosensitivity, GI upset, and esophageal ulceration if taken without water.
• It is contraindicated in children under 8 years and pregnant women.

Q.3 Classify NSAID and describe Aspirin in detail (8 mark)

Classification of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs)

NSAIDs are classified based on chemical structure, COX selectivity, and duration of action. Below are long, point-wise details for each type.

✅ A. Based on Chemical Structure

1️⃣ Salicylates

• It includes drugs that are chemically related to salicylic acid and exhibit anti-inflammatory, analgesic, and antipyretic properties.
• Examples: Aspirin, Sodium salicylate, Diflunisal.
• It is commonly used in cardiovascular prophylaxis due to its irreversible platelet inhibition.
• It can cause Reye’s syndrome in children when used during viral infections.
• Salicylates are also useful in treating mild musculoskeletal pain and fever.

2️⃣ Propionic Acid Derivatives

• These are widely used NSAIDs that provide effective relief from pain and inflammation.
• Examples: Ibuprofen, Naproxen, Ketoprofen, Flurbiprofen.
• These drugs are better tolerated in the gastrointestinal system compared to aspirin.
• Ibuprofen is also available in pediatric formulations and is safe in fever management in children.
• Naproxen has a longer duration of action and is preferred in chronic inflammatory diseases like arthritis.

3️⃣ Acetic Acid Derivatives

• These NSAIDs are structurally derived from acetic acid and have strong anti-inflammatory actions.
• Examples: Diclofenac, Indomethacin, Sulindac, Etodolac.
• Diclofenac is commonly used for postoperative pain, arthritis, and sports injuries.
• Indomethacin is particularly useful in gout and closure of patent ductus arteriosus in neonates.
• These drugs may cause significant GI and CNS side effects, including headache and dizziness.

4️⃣ Enolic Acid Derivatives (Oxicams)

• These NSAIDs belong to the oxicam family and are primarily used for long-term chronic pain management.
• Examples: Piroxicam, Meloxicam, Tenoxicam.
• These drugs have a very long half-life, allowing once-daily dosing for patient convenience.
• They are widely used in osteoarthritis and rheumatoid arthritis.
• These drugs carry a higher risk of gastric ulceration if not used with food or gastric protection.

5️⃣ Fenamates (Anthranilic acid derivatives)

• These drugs are effective for treating menstrual pain, muscle cramps, and mild-to-moderate pain.
• Examples: Mefenamic acid, Meclofenamate.
• Mefenamic acid is commonly prescribed in dysmenorrhea due to its strong analgesic effect on uterine contractions.
• It can cause diarrhea, GI upset, and nephrotoxicity in long-term use.
• This group is rarely used in chronic conditions due to safety concerns.

6️⃣ Pyrazolone Derivatives

• These are older NSAIDs with strong analgesic effects but are less commonly used now.
• Examples: Phenylbutazone, Oxyphenbutazone, Metamizole.
• Phenylbutazone is effective in acute gout but may cause bone marrow suppression.
• These drugs have high toxicity potential, including agranulocytosis and aplastic anemia.
• Due to their adverse effects, they are banned or restricted in many countries.

7️⃣ Selective COX-2 Inhibitors (Coxibs)

• These drugs selectively inhibit COX-2 enzyme and have minimal gastric irritation.
• Examples: Celecoxib, Etoricoxib, Valdecoxib, Parecoxib.
• They are especially useful in rheumatoid arthritis and osteoarthritis without GI bleeding risk.
• These drugs are not antiplatelet, so they do not interfere with bleeding time.
• However, they may increase cardiovascular risks, such as hypertension and thrombosis.

✅B. Based on COX Enzyme Selectivity

1️⃣ Non-Selective COX Inhibitors

• These inhibit both COX-1 and COX-2, leading to pain relief and inflammation control, but with gastric side effects.
• Examples: Aspirin, Ibuprofen, Diclofenac.
• They reduce prostaglandin synthesis in both stomach and inflamed tissues, hence effective but ulcerogenic.
• Long-term use may cause gastritis, peptic ulcer, or GI bleeding.
• They are contraindicated in patients with a history of gastric ulcer or bleeding disorders.

2️⃣ Preferential COX-2 Inhibitors

• These mainly inhibit COX-2, with lesser inhibition of COX-1, offering a balance between efficacy and safety.
• Examples: Nimesulide, Meloxicam, Etodolac.
• These are commonly used for musculoskeletal pain and post-operative pain.
• Nimesulide has hepatotoxic potential and should be avoided in liver disease patients.
• Etodolac offers fewer GI symptoms, especially when given short-term.

3️⃣ Selective COX-2 Inhibitors (Coxibs)

• These target only COX-2, thereby preserving gastric mucosa and platelet function.
• Examples: Celecoxib, Etoricoxib.
• Ideal in patients with GI risk or those requiring long-term NSAID use.
• They are not suitable for cardiac patients due to increased thrombotic events.
• Monitoring of blood pressure and renal function is necessary during long-term therapy.

✅ C. Based on Duration of Action

1️⃣ Short-Acting NSAIDs (Half-life <6 hrs)

• These are rapidly acting drugs with short duration, suitable for acute pain.
• Examples: Ibuprofen, Diclofenac, Indomethacin.
• They provide quick relief but require frequent dosing (2–3 times/day).
• Useful in acute dental pain, injury, or headache.
• Risk of rebound pain is higher if doses are skipped.

2️⃣ Long-Acting NSAIDs (Half-life >10 hrs)

• These are slow-releasing or long-duration NSAIDs ideal for chronic inflammatory conditions.
• Examples: Piroxicam, Meloxicam, Naproxen.
• Allow once or twice daily dosing, improving compliance in elderly or chronic patients.
• Effective in ankylosing spondylitis, osteoarthritis, and chronic back pain.
• Long-acting drugs may accumulate and cause renal toxicity in patients with impaired kidney function.

Aspirin

• It is classified as a Non-Steroidal Anti-Inflammatory Drug (NSAID).
• It belongs specifically to the Salicylate group of NSAIDs.
• It acts as both an analgesic, antipyretic, anti-inflammatory, and antiplatelet agent.

Mechanism of Action of Aspirin

• Aspirin irreversibly inhibits cyclooxygenase enzymes (COX-1 and COX-2), which are essential for the conversion of arachidonic acid into prostaglandins and thromboxane A2.
• By blocking COX-1, it reduces thromboxane A2 production, leading to inhibition of platelet aggregation, which helps in preventing clot formation.
• By blocking COX-2, it decreases prostaglandin synthesis, resulting in anti-inflammatory, analgesic (pain relief), and antipyretic (fever-reducing) effects.
• This effect on platelets is irreversible and lasts for the entire life of the platelet (7–10 days), making it effective as a long-acting antiplatelet agent.
• Aspirin is rapidly absorbed in the stomach and small intestine, metabolized in the liver, and excreted via the kidneys.

Indications of Aspirin

• Pain (mild to moderate), especially headache, toothache, and muscle pain
• Fever (antipyretic)
• Inflammation (e.g., arthritis, rheumatic fever)
• Acute coronary syndrome (e.g., myocardial infarction)
• Stroke and transient ischemic attack (TIA) prevention
• Deep vein thrombosis (DVT) and pulmonary embolism (PE) prevention
• Prophylaxis in patients with a history of ischemic heart disease
• Post-stent placement in combination with other antiplatelets

Adverse Effects of Aspirin

• Gastric irritation and peptic ulcer
• Heartburn, nausea, or vomiting
• Tinnitus (ringing in ears) at high doses
• Bleeding (GI bleeding, easy bruising)
• Allergic reactions (especially in asthmatics)
• Reye’s syndrome in children (especially with viral fever)
• Hepatotoxicity with prolonged use
• Renal impairment

Contraindications of Aspirin

• Hypersensitivity to aspirin or other NSAIDs
• History of peptic ulcer or GI bleeding
• Bleeding disorders (e.g., hemophilia)
• Children with viral infections (due to risk of Reye’s syndrome)
• Severe hepatic or renal impairment
• Asthma induced by NSAIDs
• Third trimester of pregnancy (risk of fetal complications)

Nursing responsibilities while Administering aspirin

1️⃣ Assessment & Monitoring

• The nurse must assess for history of GI disorders, bleeding tendencies, and allergies before administration.
• It is essential to monitor for signs of bleeding, such as petechiae, bruises, black tarry stools, or hematemesis.
• The nurse should check liver and kidney function tests during long-term use.

2️⃣ Patient Education

• The nurse must teach the patient to take aspirin with food or milk to reduce gastric irritation.
• It is necessary to instruct the patient to avoid alcohol while taking aspirin to reduce the risk of GI bleeding.
• The nurse must teach patients to report any signs of ringing in the ears, persistent stomach pain, or unusual bleeding.

3️⃣ Drug Interaction Precautions

• The nurse should monitor if the patient is taking other anticoagulants or antiplatelets (e.g., warfarin, clopidogrel), which can increase bleeding risk.
• NSAIDs like ibuprofen may interfere with the antiplatelet effect of aspirin if taken concurrently.

4️⃣ Dosage and Route

• The nurse should follow physician orders carefully, especially in cardiac cases where low-dose aspirin (75–150 mg/day) is used for antiplatelet action.
• Higher doses (300–600 mg) are used for pain and fever and must be given with caution.

5️⃣ Lab Monitoring and Follow-up

• Regular monitoring of CBC, PT/INR, and liver function tests may be necessary for long-term users.
• The nurse should ensure the patient attends follow-up appointments to review therapy efficacy and complications.

6️⃣ Prevention of Complications

• The nurse should monitor for signs of aspirin toxicity (salicylism), such as confusion, rapid breathing, sweating, or drowsiness, especially in elderly patients or those on high doses.
• It is important for the nurse to ensure the patient is well-hydrated, as dehydration can increase the risk of renal damage and salicylate accumulation.

7️⃣ Preoperative and Dental Procedure Caution

• The nurse must inform patients to notify healthcare providers before surgery or dental work, as aspirin may increase the risk of bleeding.
• Aspirin should be stopped 5–7 days before planned surgery under physician guidance, and the nurse must document and communicate accordingly.

Or

Q.3 Descibed various routes of drug administration (8 mark)

Drug administration routes refer to the path through which a drug is brought into contact with the body. These are mainly classified into enteral, parenteral, topical, and other specialized routes.

I. Enteral Route (Via Gastrointestinal Tract)

Oral Route (Per Os – PO)

• It is the most commonly used route where drugs are taken by mouth and absorbed through the gastrointestinal tract into the bloodstream.
• It is suitable for chronic therapy due to ease of administration and high patient compliance.
• It is unsuitable for patients with severe nausea, unconsciousness, or gastrointestinal obstructions.
• It may lead to reduced efficacy due to first-pass hepatic metabolism which breaks down the drug before it reaches systemic circulation.
• It requires proper patient education about drug timing, food interactions, and swallowing technique.

Sublingual Route

• It is the route where the drug is placed under the tongue and absorbed through the mucous membranes into the venous circulation.
• It provides rapid onset of action and is useful in emergency conditions like angina.
• It bypasses liver metabolism, leading to increased drug bioavailability.
• It is not suitable for drugs with bad taste or that irritate the oral mucosa.
• It is important to instruct the patient not to chew or swallow the tablet during administration.

Buccal Route

• It involves placement of the drug between the cheek and gums for slow, consistent absorption.
• It is useful in pediatric or elderly patients who cannot swallow oral tablets.
• It avoids enzymatic degradation in the gastrointestinal tract.
• It is ideal for sustained-release formulations and hormonal therapies.
• It may cause local irritation if prolonged contact is maintained with the mucosa.

Rectal Route

• It involves the insertion of suppositories or drug-filled enemas into the rectum where the drug is absorbed by rectal mucosa.
• It is beneficial for patients with vomiting, seizures, or post-operative status.
• It partially avoids first-pass metabolism, depending on the site of absorption.
• Absorption may be erratic due to the presence of fecal matter or rectal irritation.
• It is particularly useful in children and unconscious patients for fever or pain management.

II. Parenteral Route (Bypassing the GIT – Injection)

Intravenous (IV)

• It involves direct administration of drugs into the venous blood, providing immediate effect.
• It is used for emergency situations, fluid replacement, or when high plasma concentrations are required.
• It allows controlled infusion over time, such as in drips and IV bolus.
• Risk of infection, thrombophlebitis, and overdose exists if not monitored.
• Nurses must perform strict aseptic techniques and monitor for infiltration or allergic reactions.

Intramuscular (IM)

• It involves injecting the drug deep into the muscle (e.g., deltoid, gluteal, or vastus lateralis muscles).
• It allows administration of oily or depot preparations for prolonged action.
• It provides faster absorption than subcutaneous but slower than intravenous route.
• Pain, swelling, and abscess formation may occur if not properly administered.
• Z-track technique may be used to prevent leakage of irritating drugs like iron preparations.

Subcutaneous (SC)

• It involves injecting drugs into the fatty tissue below the skin, usually at the upper arms, thighs, or abdomen.
• It allows slow, sustained absorption of medications like insulin and heparin.
• Rotation of injection site is essential to prevent lipodystrophy or skin hardening.
• It is not suitable for large volumes or drugs that irritate subcutaneous tissues.
• Nurses should use short, fine needles and monitor for bruising or bleeding.

Intradermal (ID)

• It involves injecting a small amount of drug just beneath the epidermis, commonly on the forearm.
• It is used primarily for diagnostic purposes such as Mantoux test or allergy testing.
• The drug remains localized and forms a small bleb at the injection site.
• The site should not be rubbed or pressed after injection.
• Proper needle angle (10–15 degrees) and volume control are essential for accurate results.

III. Topical (Local) Route

Transdermal Route

• It delivers drugs through skin using medicated patches for sustained release.
• It ensures continuous plasma drug level and avoids gastrointestinal side effects.
• Sites should be rotated to avoid skin irritation or sensitization.
• Used for hormone therapy, nicotine cessation, and chronic pain.
• It requires intact, clean, and dry skin surface for optimal absorption.

Cutaneous Route

• It includes creams, ointments, gels, or powders applied to the skin for local therapeutic effect.
• It is commonly used for dermatitis, fungal infections, and wound care.
• Drug absorption depends on skin thickness, hydration, and integrity.
• Gloves should be worn to prevent self-exposure during application.
• Repeated use may lead to local hypersensitivity or contact dermatitis.

Ophthalmic Route

• It involves the instillation of drops or ointments into the conjunctival sac.
• It is useful in treating eye infections, allergies, or glaucoma.
• The drug must be sterile and isotonic to prevent irritation.
• Eye should not be touched with dropper tip to avoid contamination.
• Apply pressure on the nasolacrimal duct to prevent systemic absorption.

Otic Route

• It includes drops placed into the external auditory canal for local action.
• It is used for ear infections, wax softening, or antifungal therapy.
• The solution should be at body temperature to prevent vertigo.
• In adults, pinna is pulled upward and backward; in children, downward and backward.
• Patient should remain in side-lying position for 5–10 minutes post administration.

Nasal Route

• Drugs are administered via nasal sprays or drops for local or systemic effects.
• It is useful in allergic rhinitis, hormonal therapy, and flu vaccines.
• Nasal mucosa provides rapid absorption due to rich blood supply.
• Nasal decongestants must not be overused to avoid rebound congestion.
• Patient should blow nose before application and avoid sneezing for a few minutes.

IV. Other Specialized Routes

Inhalation Route

• It involves inhalation of aerosolized drugs or gases directly into the lungs.
• It is ideal for treating respiratory diseases like asthma, COPD, and for anesthesia.
• It allows rapid action with minimal systemic side effects.
• Proper technique is crucial in using inhalers or nebulizers effectively.
• Patient should rinse mouth after using corticosteroid inhalers to prevent fungal infection.

Intrathecal Route

• It involves injecting drugs into the subarachnoid space of spinal cord using lumbar puncture.
• It bypasses the blood-brain barrier for direct action on CNS.
• It is used in spinal anesthesia, chemotherapy, or severe infections like meningitis.
• Strict asepsis is essential to prevent CNS infections.
• Risk of headache, nerve injury, or spinal block must be monitored.

Intra-articular Route

• It is the injection of drugs directly into the joint cavity under sterile conditions.
• It is commonly used for local steroid therapy in arthritis.
• It provides immediate pain relief and reduces inflammation.
• Limited to trained personnel due to complexity and infection risk.
• Joint should be rested post-injection to prevent trauma.

Vaginal Route

• Drugs are inserted into the vaginal canal as suppositories, creams, or tablets.
• It is useful for infections, contraception, or hormonal replacement therapy.
• Local action ensures minimal systemic side effects.
• Vaginal hygiene must be maintained during therapy.
• Instructions regarding bedtime application can improve absorption and reduce leakage.

Intraosseous Route

• It involves direct administration of drugs into the bone marrow cavity.
• It is used during emergency resuscitation when IV access is not possible.
• It allows rapid systemic absorption similar to IV route.
• Commonly used in pediatrics and critical care.
• Requires specialized equipment and strict aseptic technique.

Q.4 Wrie down the dose, action, indications, adverse effect & nursing responsibilies of the following drug (any four) [20 marks]

1. Atropine

Mechanism of Action of Atropine

• Atropine is a competitive antagonist of muscarinic acetylcholine receptors, mainly affecting the parasympathetic nervous system.
• It blocks the action of acetylcholine at muscarinic receptors in smooth muscles, exocrine glands, and the central nervous system, thereby inhibiting parasympathetic nerve impulses.
• In the heart, atropine blocks vagal stimulation of the SA node, resulting in increased heart rate (positive chronotropic effect) and improved AV conduction.
• In the respiratory tract, it reduces bronchial secretions and causes bronchodilation by relaxing smooth muscles of the airways.
• In the gastrointestinal and urinary systems, it reduces motility and secretions, causing smooth muscle relaxation.
• It also causes pupil dilation (mydriasis) and cycloplegia (loss of accommodation) by relaxing the sphincter muscle of the iris and the ciliary muscle.

Indications of Atropine

• Bradycardia (symptomatic)
• Pre-anesthetic medication (to reduce secretions)
• Organophosphate or nerve agent poisoning
• Pupil dilation during eye exams or surgery
• Reversal of muscarinic effects of anticholinesterases
• Irritable bowel syndrome or GI hypermotility (rare use)
• Asystole or pulseless electrical activity (as part of ACLS)

Adverse Effects of Atropine

• Dry mouth and dry eyes
• Tachycardia and palpitations
• Blurred vision and photophobia
• Urinary retention
• Constipation
• Confusion or hallucinations (especially in elderly)
• Hyperthermia (especially in children)
• Flushing and skin dryness

Contraindications of Atropine

• Glaucoma (especially narrow-angle)
• Prostatic hypertrophy causing urinary retention
• Myasthenia gravis
• Severe ulcerative colitis
• Paralytic ileus or bowel obstruction
• Hypersensitivity to atropine or belladonna alkaloids

Nursing Responsibilities While Administering Atropine

1️⃣ Assessment Before Administration

• The nurse must assess baseline vital signs, especially heart rate, respiratory status, and pupil size, before administering atropine to monitor for therapeutic and adverse effects.
• It is essential to review the patient’s history for glaucoma, urinary retention, or GI obstruction, as these are important contraindications to atropine use.

2️⃣ Correct Dose and Route Monitoring

• The nurse must ensure that atropine is administered through the correct route—IV for bradycardia, IM for pre-op, SC or IM for poisoning, and ophthalmic for eye exams—as per the condition being treated.
• IV doses should be given slowly over 1 minute, and the nurse should have resuscitation equipment ready in emergency use such as bradycardia or cardiac arrest.

3️⃣ Monitoring and Observation

• The nurse should closely monitor for improvement in heart rate (for bradycardia), pupil response (for ophthalmic use), and drying of secretions (for pre-operative use).
• It is important for the nurse to observe for signs of anticholinergic toxicity, such as confusion, hallucinations, dry skin, or rapid heart rate, and report them immediately.

4️⃣ Patient Education and Safety

• The nurse must instruct the patient that blurred vision and sensitivity to light may occur with eye use and to avoid driving or operating machinery until effects wear off.
• The nurse should teach the patient to increase fluid intake, chew sugarless gum, and use lubricating eye drops if dryness becomes uncomfortable during systemic therapy.

5️⃣ Special Precautions in Pediatrics and Elderly

• The nurse should use extreme caution when administering atropine to children, as they are more prone to hyperthermia and CNS excitation.
• Elderly patients should be monitored for confusion, agitation, or urinary retention, as these adverse effects are more common and more serious in this group.

6️⃣ Emergency Use and Antidote Support

• In organophosphate poisoning, the nurse must administer repeated doses of atropine until secretions dry up and be prepared to give pralidoxime (2-PAM) concurrently as a specific antidote.

7️⃣ Documentation and Communication

• The nurse must document dose, route, time, indication, response, and any adverse effects, and inform the healthcare team of any changes in vital signs or neurologic status.

2. Lasix

Mechanism of Action of Lasix (Furosemide)

• It is a potent loop diuretic that works primarily in the ascending limb of the loop of Henle in the nephron of the kidney.
• It inhibits the sodium-potassium-chloride (Na⁺/K⁺/2Cl⁻) co-transporter, which blocks the reabsorption of sodium and chloride ions.
• This action leads to increased excretion of sodium, chloride, potassium, calcium, and water, causing a powerful diuretic (urine-producing) effect.
• It results in a rapid decrease in blood volume and preload, which helps in reducing blood pressure and relieving pulmonary congestion or edema.
• It causes vasodilation of the blood vessels in the kidneys even before diuresis begins, helping to improve renal blood flow.

Indications of Lasix (Furosemide)

• Congestive Heart Failure (CHF) with pulmonary edema
• Acute and chronic renal failure
• Liver cirrhosis with ascites
• Hypertension (especially in patients with fluid overload)
• Hypercalcemia
• Pulmonary edema (emergency use)
• Nephrotic syndrome
• Cerebral edema (with other supportive care)

Adverse Effects of Lasix (Furosemide)

• Hypokalemia (low potassium levels)
• Hyponatremia (low sodium levels)
• Dehydration and hypotension
• Dizziness, headache
• Muscle cramps and weakness
• Ototoxicity (hearing loss at high doses or rapid IV push)
• Hyperuricemia and gout attacks
• Metabolic alkalosis

Contraindications of Lasix (Furosemide)

• Hypersensitivity to furosemide or sulfa drugs
• Anuria (absence of urine production)
• Severe electrolyte imbalance (especially low potassium/sodium)
• Hepatic coma or severe liver disease (relative contraindication)
• Pregnancy and lactation (use with caution)
• Dehydrated or hypotensive patients

Nursing Responsibilities While Administering Lasix (Furosemide)

1️⃣ Pre-administration Assessment

• The nurse must assess baseline blood pressure, pulse rate, respiratory status, and oxygen saturation before giving the drug.
• It is necessary to review serum electrolytes (Na⁺, K⁺, Cl⁻, Ca²⁺) and renal function tests (BUN, creatinine).

2️⃣ During Administration

• The nurse must administer IV doses slowly (e.g., 20 mg/min) to avoid ototoxicity.
• Oral Lasix should be given in the morning to prevent nocturia (urination at night).
• The nurse should ensure that the patient has easy access to a bathroom due to increased urine output.

3️⃣ Monitoring

• It is important to monitor daily weight, intake/output, and signs of fluid volume deficit.
• The nurse should watch for symptoms of hypokalemia such as muscle weakness, fatigue, or ECG changes.
• Vital signs must be monitored for signs of orthostatic hypotension or sudden drop in BP.

4️⃣ Patient Education

• The nurse must teach the patient to take the drug in the morning and avoid taking it late in the day.
• The nurse should advise the patient to report signs of dizziness, irregular heartbeat, muscle cramps, or tinnitus.
• It is important to advise potassium-rich diet or supplements (e.g., banana, orange juice), unless contraindicated.

5️⃣ Lab Follow-up

• The nurse must follow-up with regular blood tests to monitor electrolytes and kidney function.
• Urinalysis and blood pressure readings should be documented and evaluated regularly.

3. Morphine

Mechanism of Action of Morphine

• Morphine is a potent opioid agonist that binds specifically to mu-opioid receptors in the central nervous system (CNS) and gastrointestinal tract.
• Upon binding, it inhibits the release of pain neurotransmitters like substance P, and reduces neural excitability, resulting in altered pain perception and emotional response to pain.
• Morphine also activates the descending inhibitory pain pathway, which suppresses transmission of pain signals from the spinal cord to the brain.
• It produces analgesia, sedation, euphoria, and respiratory depression depending on the dose and route of administration.
• Morphine delays gastric emptying, reduces peristalsis, and increases smooth muscle tone, leading to constipation as a common side effect.
• It has no ceiling effect, meaning increasing the dose enhances pain relief—but also increases the risk of toxicity and respiratory depression.

Indications of Morphine

• Severe acute and chronic pain (e.g., post-operative, cancer)
• Myocardial infarction (for chest pain and anxiety relief)
• Pulmonary edema (to relieve dyspnea)
• Palliative and end-of-life care
• Trauma or burn-related pain
• Pain unresponsive to non-opioid analgesics
• Pre-anesthetic medication (occasionally used)

Adverse Effects of Morphine

• Respiratory depression
• Sedation and dizziness
• Nausea and vomiting
• Constipation and dry mouth
• Urinary retention
• Hypotension and bradycardia
• Miosis (pupil constriction)
• Tolerance, dependence, and addiction (with long-term use)

Contraindications of Morphine

• Respiratory depression or severe asthma
• Head injury or increased intracranial pressure
• Hypersensitivity to morphine or opioids
• Severe hepatic or renal impairment
• Paralytic ileus or bowel obstruction
• Pregnancy and breastfeeding (use with caution)
• Alcohol intoxication or CNS depressant overdose

Nursing Responsibilities While Administering Morphine

1️⃣ Pre-Administration Assessment

• The nurse must assess the patient’s pain intensity, respiratory rate, level of consciousness, and vital signs before administering morphine to prevent respiratory or CNS depression.
• It is essential for the nurse to review the patient’s medical history, including any previous opioid use, allergies, and history of substance abuse.

2️⃣ Safe Administration Guidelines

• The nurse must administer morphine through the correct route (IV, IM, SC, oral, or epidural) as prescribed, and use slow IV push (over 4–5 minutes) to prevent rapid onset of hypotension or respiratory depression.
• The nurse should ensure that naloxone (opioid antidote) and resuscitation equipment are available in case of overdose or respiratory arrest.

3️⃣ Monitoring During Therapy

• The nurse must continuously monitor respiratory rate, oxygen saturation, and sedation level, especially in opioid-naïve patients or the elderly.
• The nurse should also observe for early signs of toxicity, including confusion, pinpoint pupils, decreased responsiveness, or shallow breathing.

4️⃣ Gastrointestinal and Urinary Monitoring

• The nurse must assess bowel function regularly, encourage fluids, fiber, and administer stool softeners or laxatives to prevent opioid-induced constipation.
• It is necessary to monitor for urinary retention, especially in elderly male patients or those with prostate issues, and report bladder distension.

5️⃣ Patient Education and Safety

• The nurse must educate the patient to avoid alcohol, driving, or operating machinery during morphine therapy due to risk of sedation and impaired coordination.
• It is important to inform the patient about risk of dependence with long-term use, and to take the drug exactly as prescribed.

6️⃣ Double-Check Protocol and Documentation

• Morphine is a high-alert and controlled drug, so the nurse must double-check the dose and patient ID with another licensed nurse before administration.
• The nurse should accurately document the time, dose, route, pain score before and after administration, and the patient’s response.

7️⃣ Follow-Up and Evaluation

• The nurse must evaluate effectiveness of pain relief, monitor for sedation level using sedation scale, and adjust the next dose timing accordingly in coordination with the physician.

4. Insulin

Mechanism of Action of Insulin

• Insulin is a naturally occurring hormone produced by the beta cells of the pancreas (Islets of Langerhans), essential for glucose metabolism and energy utilization.
• It acts by binding to insulin receptors on the surface of target cells (like muscle, fat, and liver), which triggers cellular uptake of glucose from the bloodstream.
• In the liver, insulin promotes glycogen synthesis and inhibits gluconeogenesis, helping to store excess glucose and reduce blood sugar levels.

• In muscle and adipose tissue, it enhances glucose uptake, protein synthesis, and fat storage, helping maintain energy balance.
• Insulin also prevents the breakdown of fats and proteins by inhibiting lipolysis and proteolysis, preserving body tissues.
• Exogenous (injected) insulin mimics natural insulin and is used to control hyperglycemia in diabetes mellitus, especially in Type 1 and insulin-dependent Type 2 diabetes.

Indications of Insulin

• Type 1 Diabetes Mellitus
• Type 2 Diabetes Mellitus (when oral hypoglycemics are ineffective)
• Diabetic ketoacidosis (DKA)
• Hyperosmolar hyperglycemic state (HHS)
• Gestational diabetes
• Hyperkalemia (short-term emergency use)
• Perioperative or critical care glycemic control

Adverse Effects of Insulin

• Hypoglycemia (most common; signs include sweating, shakiness, confusion)
• Weight gain
• Lipodystrophy at injection site (lipoatrophy or lipohypertrophy)
• Allergic reaction (rare)
• Hypokalemia (due to shift of potassium into cells)
• Injection site pain or redness
• Insulin resistance (long-term use)

Contraindications of Insulin

• Hypoglycemia (do not administer if blood sugar is already low)
• Hypersensitivity to insulin or formulation components
• Caution in renal or hepatic impairment
• Avoid abrupt discontinuation (risk of DKA)
• Use with caution in patients with adrenal or pituitary disorders

Nursing Responsibilities While Administering Insulin

1️⃣ Assessment Before Administration

• The nurse must check the patient’s blood glucose level using a glucometer before administering insulin, and ensure it is within the appropriate range for injection.
• It is essential to verify the correct type, dosage, and timing of insulin as prescribed, because using the wrong type can cause serious hypo- or hyperglycemia.

2️⃣ Proper Preparation and Technique

• The nurse should ensure insulin is drawn into the syringe correctly, avoiding air bubbles, and if mixing insulins, clear insulin (short-acting) should be drawn before cloudy (intermediate-acting) to avoid contamination.
• It is important to rotate injection sites (abdomen, thighs, arms) to prevent lipodystrophy and ensure proper absorption.

3️⃣ Monitoring and Hypoglycemia Management

• The nurse must closely monitor for signs and symptoms of hypoglycemia (e.g., sweating, confusion, irritability, tremors), especially in patients who are NPO or after exercise.
• In case of hypoglycemia, the nurse should immediately administer fast-acting carbohydrates orally, or IV glucose/glucagon if the patient is unconscious.

4️⃣ Patient Education

• The nurse must teach the patient to self-monitor blood glucose regularly, recognize signs of hypoglycemia and hyperglycemia, and manage them appropriately.
• It is important to instruct the patient on correct storage of insulin, which should be refrigerated when unopened and used within a specified period once opened (usually 28 days at room temp).

5️⃣ Diet and Timing Coordination

• The nurse must ensure that meals are available shortly after administering rapid-acting insulin, as skipping meals can result in hypoglycemia.
• The nurse should also educate the patient to maintain a consistent diet and physical activity routine, and report any illness that could affect glucose control.

6️⃣ Double-checking and Documentation

• It is mandatory for the nurse to double-check insulin doses with another licensed nurse, especially for pediatric or critical care patients, and to document the dose, time, site, and blood glucose levels accurately.

7️⃣ Lab Monitoring and Long-term Care

• The nurse should coordinate with the physician for monitoring HbA1c levels, serum potassium, and renal function, especially in long-term insulin users.

5. Salbutamol

Mechanism of Action of Salbutamol

• Salbutamol is a selective beta-2 adrenergic receptor agonist that primarily acts on the smooth muscle of the bronchi in the respiratory tract.
• It stimulates beta-2 receptors, causing activation of adenylyl cyclase, which increases cyclic AMP (cAMP) levels inside the bronchial smooth muscle cells.
• Elevated cAMP levels cause relaxation of bronchial smooth muscle, leading to bronchodilation, and therefore relief from bronchospasm.
• It also helps to improve mucociliary clearance, inhibit mast cell mediator release, and reduce airway resistance, improving oxygen exchange.
• Though selective to beta-2 receptors, in high doses, it can stimulate beta-1 receptors in the heart, leading to side effects like tachycardia.
• The onset of action is within 5 minutes (inhaled route), and it lasts for 4 to 6 hours, making it ideal for acute symptom relief in asthma or COPD.

Indications of Salbutamol

• Acute bronchial asthma
• Chronic obstructive pulmonary disease (COPD)
• Exercise-induced bronchospasm
• Wheezing and reversible airway obstruction
• Acute exacerbation of bronchitis
• Hyperkalemia (IV route in emergency settings)

Adverse Effects of Salbutamol

• Tremors or shakiness
• Tachycardia or palpitations
• Nervousness or anxiety
• Headache or dizziness
• Nausea or dry mouth
• Muscle cramps
• Hypokalemia (in IV/high-dose use)
• Paradoxical bronchospasm (rare)

Contraindications of Salbutamol

• Hypersensitivity to salbutamol or components of inhaler
• Severe cardiac disease (e.g., arrhythmia, ischemic heart disease)
• Uncontrolled hyperthyroidism
• Use with caution in pregnancy and lactation
• Concomitant use with beta-blockers (e.g., propranolol)

Nursing Responsibilities While Administering Salbutamol

1️⃣ Pre-administration Assessment

• The nurse must assess respiratory rate, breath sounds, oxygen saturation, and peak expiratory flow rate (PEFR) before and after salbutamol administration to evaluate effectiveness.
• It is essential for the nurse to assess for history of cardiac conditions, diabetes, or hyperthyroidism, as salbutamol can exacerbate these disorders.

2️⃣ Correct Dose and Route Preparation

• The nurse should ensure that salbutamol is administered via the appropriate route—inhalation (MDI or nebulizer), oral tablet, or IV—as prescribed.
• When using an MDI (Metered Dose Inhaler), the nurse must teach the patient to shake the inhaler, use a spacer if required, and breathe in slowly and deeply during administration.

3️⃣ Monitoring and Observation

• The nurse must observe for clinical improvement in breathlessness, wheezing, and air entry, as well as adverse effects such as tremors, tachycardia, or restlessness.
• For patients on repeated doses or high-dose nebulization, the nurse must monitor serum potassium levels, as hypokalemia can occur.

4️⃣ Patient Education

• The nurse should educate the patient to use salbutamol only as a “rescue medication” for acute symptoms, and not as a substitute for daily long-term controller therapy (e.g., corticosteroids).
• The nurse must teach proper inhaler technique, timing between puffs (1 minute), and to rinse the mouth after nebulization to reduce throat irritation.

5️⃣ Storage and Drug Interaction Precautions

• The nurse must ensure proper storage of inhalers (away from heat or moisture) and check for the expiration date before each use.
• It is important for the nurse to monitor for drug interactions, especially with beta-blockers, diuretics, or MAO inhibitors, which can alter salbutamol effects.

6️⃣ Documentation and Follow-up

• The nurse must document the dose, time, route, respiratory assessment findings, and patient’s response to salbutamol therapy, especially during an acute episode.

7️⃣ Emergency Readiness

• The nurse should ensure oxygen therapy and resuscitation equipment are available in case of severe asthma attack or paradoxical bronchospasm during or after administration.

6. Amikacin

Mechanism of Action of Amikacin

• Amikacin is a bactericidal antibiotic that works by inhibiting bacterial protein synthesis, especially in aerobic gram-negative bacteria.
• It binds irreversibly to the 30S ribosomal subunit of bacterial cells, leading to misreading of mRNA, production of faulty proteins, and ultimately bacterial cell death.
• Amikacin also interferes with the initiation complex of translation, preventing the proper formation of peptides.
• It is resistant to many aminoglycoside-inactivating enzymes, making it more effective in treating resistant bacterial strains compared to other aminoglycosides.
• It shows concentration-dependent killing, meaning the higher the plasma level, the more effective it is at killing bacteria.
• It is effective against Pseudomonas aeruginosa, E. coli, Klebsiella, Proteus, and Enterobacter species and is often used in nosocomial infections.

Indications of Amikacin

• Severe gram-negative bacterial infections
• Urinary tract infections (UTIs)
• Respiratory tract infections (e.g., hospital-acquired pneumonia)
• Bone and joint infections
• Intra-abdominal infections (in combination therapy)
• Sepsis or bacteremia
• Tuberculosis (as second-line drug)
• Skin and soft tissue infections

Adverse Effects of Amikacin

• Nephrotoxicity (kidney damage)
• Ototoxicity (hearing loss, tinnitus, vertigo)
• Neuromuscular blockade (rare)
• Headache and dizziness
• Injection site pain or irritation
• Rash or allergic reaction
• Electrolyte imbalance (hypomagnesemia, hypocalcemia)

Contraindications of Amikacin

• Hypersensitivity to amikacin or other aminoglycosides
• Pre-existing hearing impairment
• Severe renal impairment
• Neuromuscular disorders (e.g., myasthenia gravis)
• Pregnancy (Category D – may cause fetal harm)
• Caution in elderly and neonates

Nursing Responsibilities While Administering Amikacin

1️⃣ Pre-administration Assessment

• The nurse must assess baseline renal function (BUN, serum creatinine) and hearing ability (audiometry if available) before starting amikacin therapy.
• It is essential to assess for allergy to aminoglycosides, and review patient history for neuromuscular disorders or concurrent nephrotoxic drugs.

2️⃣ Correct Dosage and Administration Technique

• The nurse must ensure that amikacin is administered via IM or IV route as prescribed, and IV doses should be infused over 30–60 minutes to avoid toxicity.
• It is important to calculate dose accurately based on body weight, especially in pediatric and renal-impaired patients to prevent overdose.

3️⃣ Monitoring and Toxicity Prevention

• The nurse should closely monitor serum drug levels (peak and trough) if ordered, especially in prolonged therapy or renal-compromised patients.
• The nurse must observe for early signs of nephrotoxicity (decreased urine output, increased creatinine) and ototoxicity (tinnitus, hearing changes, balance issues).

4️⃣ Patient Education and Safety

• The nurse must teach the patient to report any hearing loss, dizziness, or ringing in the ears, as these may indicate early signs of ototoxicity.
• It is necessary to advise the patient to stay well hydrated during therapy, unless contraindicated, to reduce kidney stress.

5️⃣ Preventing Complications and Interaction Caution

• The nurse should avoid concurrent use with other nephrotoxic or ototoxic agents (e.g., vancomycin, loop diuretics) unless specifically ordered and monitored.
• The nurse must assess for signs of neuromuscular blockade, especially if the patient has a history of muscle weakness or is receiving neuromuscular blockers

6️⃣ Documentation and Drug Accountability

• The nurse must document dose, time, route, injection site (if IM), and patient’s response, and ensure proper inventory and safe handling of this restricted antibiotic.

7️⃣ Follow-up and Lab Coordination

• The nurse must coordinate repeated renal function tests, audiometric evaluations if indicated, and culture sensitivity tests to assess effectiveness and adjust therapy.

7. Heparin

Mechanism of Action of Heparin

• Heparin is an indirect anticoagulant that works by activating antithrombin III, a natural inhibitor of several clotting factors.
• Once activated, antithrombin III inactivates thrombin (factor IIa) and factor Xa, thereby inhibiting the conversion of fibrinogen to fibrin, which is essential for clot formation.
• By preventing the formation of fibrin, heparin halts the progression of existing clots and prevents the formation of new thrombi but does not dissolve existing clots.
• Unfractionated Heparin (UFH) acts on both factor IIa and Xa, whereas LMWH acts more selectively on factor Xa.
• Heparin works rapidly when given intravenously, and its action is reversed with protamine sulfate, a heparin antidote.

Indications of Heparin

• Deep Vein Thrombosis (DVT) prevention and treatment
• Pulmonary Embolism (PE)
• Acute Coronary Syndrome (e.g., myocardial infarction)
• Atrial fibrillation with embolism risk
• During dialysis and open-heart surgery (to prevent clotting)
• Prevention of clotting in central venous lines
• Disseminated Intravascular Coagulation (DIC) (with caution)

Adverse Effects of Heparin

• Bleeding (internal or external)
• Heparin-Induced Thrombocytopenia (HIT)
• Osteoporosis (with long-term use)
• Skin rashes or injection site irritation
• Hyperkalemia (due to aldosterone suppression)
• Hypersensitivity reactions
• Bruising or hematoma at injection site

Contraindications of Heparin

• Active bleeding or hemorrhagic disorders
• Recent surgery or trauma (e.g., CNS, eye, spinal)
• Severe hypertension (uncontrolled)
• Heparin-induced thrombocytopenia (HIT) history
• Liver or kidney dysfunction (use with caution)
• Alcoholism or peptic ulcer disease
• Known hypersensitivity to heparin

Nursing Responsibilities While Administering Heparin

1️⃣ Assessment Before Administration

• The nurse must assess the patient’s baseline coagulation profile, including aPTT (activated partial thromboplastin time) for UFH and platelet count to detect risk of bleeding or thrombocytopenia.
• It is essential for the nurse to check for any history of bleeding disorders, recent surgery, or peptic ulcers, which increase bleeding risk.

2️⃣ Correct Dose and Route Handling

• The nurse should confirm the correct form, dose, and route (IV or SC) as ordered, because heparin is never given IM due to risk of hematoma.
• It is important to rotate subcutaneous injection sites (e.g., abdomen) and avoid rubbing the area post-injection to prevent bruising.

3️⃣ Monitoring During Therapy

• The nurse must monitor aPTT levels regularly (for UFH) and adjust the dosage according to protocol to maintain therapeutic range (typically 1.5 to 2.5 times control).
• The nurse should observe closely for any signs of bleeding, such as hematuria, melena, bleeding gums, or bruising, and report them promptly.

4️⃣ Antidote and Emergency Readiness

• The nurse should ensure protamine sulfate is readily available in case of heparin overdose or uncontrolled bleeding.
• It is important to have emergency equipment ready if the patient is receiving IV heparin during invasive procedures or high-risk situations.

5️⃣ Patient Education and Safety

• The nurse must educate the patient to report any signs of bleeding, avoid activities that may cause injury, and not take aspirin or NSAIDs unless prescribed.
• It is necessary to advise the patient not to massage injection sites, and to inform all healthcare providers of ongoing heparin therapy.

6️⃣ Documentation and Double-Check Protocol

• The nurse must double-check heparin doses and pump settings with another nurse, especially in IV continuous infusion, as errors can cause fatal bleeding.
• Accurate documentation of dose, time, site of administration, lab results, and patient response is essential for legal and safety reasons.

7️⃣ Lab Coordination and Communication

• The nurse should coordinate frequent lab tests (aPTT, platelet count) with the laboratory and communicate critical values to the physician promptly.
• In case of low platelet counts or abnormal aPTT values, the nurse must withhold the next dose and notify the doctor to avoid complications.

Section 2

Q.5 Define the following terms (any five) [5 mark]

1. Hypertrophy

• Hypertrophy is a condition characterized by the increase in the size of cells in a tissue or organ, leading to an overall enlargement of the affected organ without an increase in the number of cells.
• It commonly occurs in response to increased workload or stimulation, such as skeletal muscle hypertrophy due to exercise or left ventricular hypertrophy due to hypertension.

2. Transduate

• Transudate is a type of fluid that accumulates in body cavities (such as pleural, peritoneal, or pericardial spaces) due to imbalance in hydrostatic and oncotic pressure, without inflammation.
• It is typically clear, watery, low in protein content, and low in cellular elements, and is commonly seen in conditions like congestive heart failure, nephrotic syndrome, or liver cirrhosis.

3. Gangrene

• Gangrene is a serious medical condition characterized by the death and decay of body tissues, usually as a result of loss of blood supply, infection, or trauma.
• It often affects the extremities such as toes, fingers, and limbs, but can also involve internal organs. Gangrene may be classified as dry, wet, or gas gangrene, and requires urgent medical or surgical treatment to prevent further spread and complications.

4. Infarction

• Infarction is the process of tissue death (necrosis) that occurs due to a sudden and complete obstruction of the blood supply to a specific part of the body, usually caused by a thrombus, embolus, or severe vasospasm.
• It most commonly affects organs like the heart (myocardial infarction), brain (cerebral infarction), or lungs, and results in irreversible damage to the affected tissue if not treated promptly.

5. Anurysm

• Aneurysm is a localized, abnormal dilation or ballooning of the wall of a blood vessel, usually an artery, due to weakening of the vessel wall.

• It most commonly occurs in arteries such as the aorta, brain (cerebral aneurysm), or abdominal aorta, and may remain asymptomatic until rupture, which can lead to life-threatening internal bleeding, stroke, or shock.

6. Carcinoma in situ

• Carcinoma in situ is a pre-invasive stage of cancer in which abnormal malignant cells are present only in the epithelial layer of a tissue and have not yet invaded the basement membrane or surrounding tissues.
• It is considered an early form of cancer and is often highly curable if detected and treated promptly, commonly seen in areas such as the cervix (CIN), breast (DCIS), skin, or colon.

Q.6 Write down the etiopathogenesis in detail (any four) (20)

1. Acute inflammation

Etiology of Acute Inflammation

1. Infectious Agents

It may be caused by bacteria, viruses, fungi, or parasites that invade tissues and trigger an immune-inflammatory response.

2. Physical Agents

It can result from trauma, cuts, abrasions, burns, radiation, or extreme temperatures (heat or cold).

3. Chemical Agents

Exposure to toxins, acids, alkalis, or irritants like chemical burns and foreign bodies can initiate inflammation.

4. Immunological Reactions

It may arise from hypersensitivity reactions (e.g., allergies) or autoimmune diseases where the body attacks its own tissues.

5. Tissue Necrosis / Ischemia

It can be triggered by cell death due to lack of blood supply (e.g., in myocardial infarction, stroke) causing release of inflammatory signals.

6. Foreign Bodies

Entry of splinters, sutures, or dust particles may induce a localized acute inflammatory reaction.

Pathogenesis of Acute Inflammation

1. Tissue Injury or Insult

• The process of acute inflammation begins with an injury to body tissues due to infectious agents (bacteria, viruses, fungi), physical trauma, chemical irritants, thermal injury (burns/frostbite), or ischemia (lack of oxygen supply).
• This injury causes cell membrane disruption, leading to the release of intracellular contents, triggering the inflammatory response.

2. Release of Inflammatory Chemical Mediators

• Damaged tissues and activated immune cells such as mast cells, macrophages, and endothelial cells release inflammatory mediators, including:
• Histamine from mast cells
• Bradykinin from plasma proteins
• Prostaglandins from arachidonic acid metabolism
• Leukotrienes from leukocytes
• Cytokines like Interleukin-1 (IL-1) and Tumor Necrosis Factor-alpha (TNF-α)
  → These mediators initiate and regulate the vascular and cellular responses during inflammation.

3. Vasodilation (Increased Blood Flow)

• Histamine and prostaglandins induce arteriolar vasodilation, which increases blood flow to the affected site.
• This results in erythema (redness) and localized heat, classic signs of inflammation (rubor and calor).

4. Increased Vascular Permeability

• Chemical mediators cause endothelial cell retraction, forming intercellular gaps in the capillary walls.
• This allows plasma proteins, antibodies, and leukocytes to leak into the interstitial space, forming protein-rich exudate.
• The accumulation of fluid in tissue causes edema (tumor) and contributes to pain (dolor) due to pressure on nerve endings.

5. Leukocyte Recruitment (WBC Migration)

• Chemotactic substances (e.g., IL-8, C5a, leukotriene B4) attract neutrophils to the inflammation site.
• The leukocyte recruitment involves:
• Margination – WBCs move to the edge of blood vessels
• Rolling and Adhesion – Temporary then firm attachment to endothelium via selectins and integrins
• Diapedesis (Transmigration) – Neutrophils migrate through endothelial gaps into the tissue

6. Phagocytosis and Microbial Killing

• At the site, neutrophils and macrophages engulf pathogens and debris through phagocytosis.
• Inside the phagocyte, lysosomal enzymes, reactive oxygen species (ROS), and nitric oxide (NO) are released to kill and digest the microbes.
• This step is essential for clearing the cause of inflammation and initiating tissue repair.

7. Resolution or Chronic Progression

• If the injurious agent is neutralized, anti-inflammatory mediators like IL-10 and transforming growth factor-beta (TGF-β) promote healing and resolution.
• If the insult persists or damage is extensive, the process may transition into chronic inflammation, abscess formation, or fibrosis (scar tissue).

2. Megaloblastic anemia

Etiology of Megaloblastic Anemia

1. Vitamin B12 Deficiency (Cobalamin Deficiency)

It is one of the most common causes and occurs due to inadequate dietary intake (seen in strict vegetarians), malabsorption syndromes, or lack of intrinsic factor (as in pernicious anemia).

2. Folic Acid (Vitamin B9) Deficiency

It may result from poor dietary intake, alcoholism, malabsorption, or increased demand during pregnancy, lactation, or hemolytic anemia.

3. Malabsorption Disorders

Conditions such as celiac disease, tropical sprue, or Crohn’s disease interfere with the intestinal absorption of folate and vitamin B12.

4. Increased Requirement of Vitamins

Seen in pregnancy, lactation, infancy, and rapid cell turnover states, where folic acid and B12 demand is high.

5. Chronic Alcoholism

It causes poor nutritional intake, impaired absorption, and interference with folate metabolism, leading to megaloblastic anemia.

6. Drug-Induced Causes

Certain drugs like methotrexate, phenytoin, trimethoprim, sulfasalazine, and oral contraceptives may interfere with DNA synthesis or folate metabolism.

7. Congenital Enzyme Defects

Rare inherited defects in DNA synthesis pathways (e.g., orotic aciduria) can cause megaloblastic anemia in infants and children.

8. Gastric Surgery or Ileal Resection

Surgeries like gastrectomy or ileal resection may cause loss of intrinsic factor or impaired absorption of vitamin B12, resulting in anemia.

9. Chronic Infections or Inflammatory Diseases

Long-standing infections or autoimmune diseases may interfere with vitamin absorption or utilization, contributing to deficiency.

Pathogenesis of Megaloblastic Anemia

1. Deficiency of Vitamin B12 or Folic Acid

• Megaloblastic anemia develops primarily due to deficiency of vitamin B12 (cobalamin) and/or folic acid (vitamin B9), both of which are essential for DNA synthesis in rapidly dividing cells.
• These vitamins act as coenzymes in the conversion of uridine to thymidine, a critical step in DNA production.

2. Impaired DNA Synthesis

• In the absence of adequate vitamin B12 or folate, there is disruption in thymidine nucleotide production, leading to defective DNA replication in hematopoietic cells.
• This affects the bone marrow, where blood cell precursors (especially red blood cells) are rapidly dividing and require constant DNA synthesis.

3. Nuclear-Cytoplasmic Asynchrony

• Due to impaired DNA synthesis, the nucleus of developing red cells matures slowly, whereas the cytoplasm matures normally.
• This creates an abnormal cell morphology called nuclear-cytoplasmic asynchrony, resulting in large, immature red cells with open chromatin—called megaloblasts.

4. Ineffective Erythropoiesis in Bone Marrow

• The megaloblasts are often destroyed within the bone marrow before they mature and enter circulation.
• This leads to ineffective erythropoiesis, meaning there is a high rate of precursor cell destruction, contributing to anemia despite an active bone marrow.

5. Peripheral Blood Abnormalities

• Few abnormal cells that escape into the peripheral blood are macrocytic (large-sized) and oval-shaped (macro-ovalocytes).
• There is also anisocytosis (variation in size) and poikilocytosis (variation in shape) of RBCs.
• Hypersegmented neutrophils are another classic finding in the peripheral blood smear.

6. Additional Clinical Implications

• In vitamin B12 deficiency, neurological symptoms such as peripheral neuropathy, memory loss, and ataxia occur due to defective myelin synthesis.
• In folate deficiency, there are no neurological symptoms, but it is particularly dangerous in pregnancy, as it may lead to neural tube defects in the fetus.

3. COPD

Etiology of Chronic Obstructive Pulmonary Disease (COPD)

1. Cigarette Smoking (Most Common Cause)

It is the leading cause of COPD due to chronic irritation and inflammation of the airways and alveoli from smoke.

2. Environmental and Occupational Exposure

Long-term exposure to air pollution, dust, chemical fumes, and biomass fuel smoke (e.g., firewood, cow dung) can lead to COPD.

3. Genetic Factors

Alpha-1 antitrypsin deficiency, a hereditary condition, can cause early-onset emphysema even in non-smokers.

4. Recurrent Respiratory Infections

Repeated lung infections, especially during childhood, can cause chronic airway inflammation and contribute to COPD.

5. Aging and Lung Function Decline

Natural age-related decline in lung elasticity and strength makes the lungs more vulnerable to COPD.

6. Poor Socioeconomic Conditions

Associated with poor ventilation, overcrowding, malnutrition, and limited healthcare access, which increase COPD risk.

7. Passive Smoking (Second-Hand Smoke)

Long-term exposure to inhaled smoke from others can also lead to chronic airway inflammation and obstruction.

8. Asthma-COPD Overlap

Chronic asthma may gradually lead to irreversible airway obstruction, contributing to COPD-like symptoms.

Pathogenesis of COPD

1. Chronic Exposure to Noxious Stimuli

• The pathogenesis of COPD begins with long-term inhalation of irritants, most commonly cigarette smoke, but also biomass fuel smoke, air pollution, and occupational dust or chemicals.
• These irritants continuously damage the airways, alveoli, and pulmonary vasculature.

2. Inflammatory Response Activation

• These irritants stimulate the innate and adaptive immune system, leading to recruitment of neutrophils, macrophages, and CD8+ T lymphocytes in the airways.
• These immune cells release inflammatory mediators like TNF-α, IL-8, and leukotrienes, which sustain and amplify lung inflammation.

3. Oxidative Stress and Enzyme Imbalance

• Smoking and inflammation increase oxidative stress, leading to cellular injury and inactivation of protective enzymes like alpha-1 antitrypsin.
• This creates an imbalance between proteases (elastase) and antiproteases, allowing elastase to degrade elastin in the alveolar walls.

4. Structural Changes in Airways and Alveoli

• In chronic bronchitis, the bronchi undergo mucus gland hypertrophy and hypersecretion, leading to airway obstruction by mucus plugs.
• In emphysema, alveolar walls are destroyed, causing permanent enlargement of air spaces, loss of surface area, and loss of lung elasticity.
• These changes result in air trapping and hyperinflation of the lungs.

5. Airflow Limitation and Gas Exchange Abnormalities

• Due to airway narrowing, inflammation, and alveolar destruction, there is persistent airflow limitation, especially during expiration.
• Ventilation-perfusion mismatch develops, leading to hypoxemia (low oxygen) and in later stages hypercapnia (high CO₂).

6. Pulmonary Vascular Changes

• Chronic hypoxia causes pulmonary vasoconstriction, leading to pulmonary hypertension.
• Over time, this increases the workload on the right side of the heart, possibly leading to cor pulmonale (right heart failure secondary to lung disease).

7. Progressive Functional Decline

• As COPD progresses, patients experience dyspnea, chronic cough, and reduced exercise tolerance due to increased work of breathing and impaired gas exchange.
• The disease becomes progressively disabling and may result in acute exacerbations, further declining lung function.

4. RHD

Etiology of Rheumatic Heart Disease (RHD)

1. Group A Beta-Hemolytic Streptococcal (GABHS) Infection

It is the primary cause of rheumatic heart disease, occurring after untreated or inadequately treated streptococcal throat infection.

2. Autoimmune Response

The body’s immune system mistakenly attacks its own heart tissues due to molecular mimicry between streptococcal antigens and cardiac tissue.

3. Genetic Susceptibility

Individuals with certain genetic markers (e.g., HLA-DR, HLA-DQ) are more prone to developing autoimmune reactions leading to RHD.

4. Socio economic status

It is more common in low-income settings due to :

• Overcrowding
• Poor sanitation
• Limited access to antibiotics or medical care

5. Recurrent Streptococcal Infections

Repeated episodes of streptococcal pharyngitis increase the risk of progressive valve damage and chronic rheumatic heart disease.

6. Age and Gender

It is more commonly seen in children aged 5–15 years, and females are slightly more affected than males.

Pathogenesis of Rheumatic Heart Disease

1. Initiation by Group A Streptococcal Infection

• The pathogenesis of RHD begins after a person experiences an untreated or inadequately treated pharyngeal infection caused by group A beta-hemolytic Streptococcus (GAS).
• The streptococcal antigens trigger an abnormal immune response in genetically susceptible individuals.

2. Molecular Mimicry and Cross-reactivity

• The streptococcal M protein shares antigenic similarity with proteins in human cardiac tissue, particularly myosin and tropomyosin.
• The immune system mistakenly produces antibodies and activated T cells that cross-react with the heart tissue, a phenomenon called molecular mimicry.

3. Autoimmune Inflammatory Reaction

• The immune cells (especially CD4+ T lymphocytes) and antibodies target cardiac muscle, valves, and connective tissue, leading to pancarditis—inflammation of all layers of the heart.
• The heart valves, particularly the mitral valve, are most commonly affected due to repeated immune attacks.

4. Valvular Inflammation and Lesion Formation

• During the acute phase, Aschoff bodies (granulomatous lesions with necrosis and inflammatory cells) form within the myocardium.
• The valves develop edema, fibrinoid necrosis, and tiny vegetations along the edges (especially at the mitral valve leaflet), leading to deformities.

5. Healing by Fibrosis and Valvular Deformity

• With time and repeated episodes, the inflammatory lesions heal through fibrosis, resulting in thickening, calcification, and fusion of valve leaflets and chordae tendineae.
• These fibrotic changes cause valvular stenosis (narrowing) or regurgitation (leakage)—most commonly affecting the mitral valve, followed by the aortic valve.

6. Chronic Hemodynamic Consequences

• Damaged valves disrupt normal blood flow, causing increased pressure and volume overload in cardiac chambers.
• This leads to chamber hypertrophy and dilation, eventually resulting in heart failure, arrhythmias, and pulmonary hypertension.

5. Hepatitis

Etiology of Hepatitis (Cause of Hepatitis)

1. Viral Infections

It is most commonly caused by hepatotropic viruses, such as:

• Hepatitis A Virus (HAV)
• Hepatitis B Virus (HBV)
• Hepatitis C Virus (HCV)
• Hepatitis D Virus (HDV)
• Hepatitis E Virus (HEV)

2. Alcoholic Hepatitis

It is caused by chronic alcohol intake, which leads to inflammation and damage to liver cells.

3. Autoimmune Hepatitis

It is caused by autoimmune reaction, where the immune system mistakenly attacks liver tissues.

4. Drug-induced Hepatitis

It may be caused by toxicity or hypersensitivity reactions to drugs such as:

• Paracetamol (overdose)
• Isoniazid
• Methyldopa
• Rifampicin
• NSAIDs

5. Toxin Exposure

It is caused by industrial chemicals or poisons like carbon tetrachloride, aflatoxins, etc.

6. Metabolic Disorders

Conditions like Wilson’s disease, Hemochromatosis, or Alpha-1 antitrypsin deficiency can lead to hepatitis.

7. Non-Alcoholic Steatohepatitis (NASH)

It occurs due to obesity, diabetes, and hyperlipidemia causing fat buildup and inflammation in the liver.

8. Ischemic Hepatitis

It is caused by reduced blood flow to the liver, often due to shock, heart failure, or severe hypotension.

Pathogenesis of Hepatitis

1. Entry of Hepatitis Virus or Other Causative Agents

• The pathogenesis begins when a hepatitis virus (A, B, C, D, or E) or other agent like toxins, alcohol, or autoimmune processes enters the body.
• The mode of transmission depends on the type :

1. Fecal-oral route – Hepatitis A and E
2. Blood-borne or parenteral route – Hepatitis B, C, and D

• After entry, the virus travels through the bloodstream and targets liver tissue, specifically hepatocytes (functional liver cells).

2. Viral Replication Inside Hepatocytes

• Once inside the liver, the hepatitis virus enters the hepatocytes and begins to replicate using the host’s cellular machinery.
• The infected hepatocytes express viral antigens on their surface, which are recognized by the immune system as foreign.

3. Immune System Activation

• The host’s immune system responds by activating cytotoxic T lymphocytes (CD8+ cells), natural killer (NK) cells, and macrophages.
• These immune cells attack infected hepatocytes in an attempt to destroy the virus, causing collateral damage to liver tissue.
• Inflammatory mediators are also released, contributing to liver inflammation.

4. Hepatocellular Injury and Inflammation

• The immune-mediated destruction causes :

1. Degeneration and necrosis of hepatocytes
2. Release of liver enzymes (ALT, AST) into the bloodstream
3. Edema and infiltration of inflammatory cells (especially lymphocytes) in the portal tracts
   The liver becomes swollen, tender, and functionally impaired due to this injury.

5. Clinical and Biochemical Changes

• The liver’s ability to process bilirubin is impaired, leading to jaundice (yellowing of skin and eyes).
• Other symptoms include fatigue, nausea, vomiting, abdominal discomfort, and dark urine.
• Laboratory tests show elevated transaminases, high bilirubin, and positive viral markers (e.g., HBsAg for Hepatitis B).

6. Resolution or Chronic Progression

• If the immune system successfully clears the virus (as in Hepatitis A and E), the liver regenerates and returns to normal.
• If the virus persists (as in Hepatitis B and C), chronic infection may develop, leading to :

1. Chronic hepatitis
2. Progressive liver fibrosis and scarring
3. Cirrhosis of the liver
4. Hepatocellular carcinoma (HCC) in long-standing cases

Q.7 Write down the short notes (any one) (5)

1. Semen analysis

Definition of Semen Analysis

• It is defined as a laboratory test that assesses the quantity and quality of a man’s semen and sperm, which is essential for evaluating male fertility.
• It is also known as sperm count test or seminogram.
• It helps in identifying causes of male infertility, post-vasectomy success, or infections in the reproductive tract.
• It includes analysis of sperm concentration, motility, morphology, volume, pH, liquefaction time, and presence of abnormal cells.

Indications of Semen Analysis

• It is done in cases of male infertility evaluation.
• It is indicated to assess sperm quality before assisted reproductive procedures like IVF.
• It is performed after vasectomy to confirm absence of sperm in semen.
• It is used to detect infection or inflammation in the male reproductive system.
• It helps in determining hormonal imbalances or testicular dysfunctions.

Procedure for Semen Collection

• The patient is instructed to maintain 3–5 days of sexual abstinence before collecting the sample.
• The sample is collected through masturbation directly into a sterile container.
• Collection should occur in a private room at the laboratory or within 1 hour at home, maintaining body temperature.
• The semen should not be collected using condoms or withdrawal method, as they may contain spermicidal agents.
• The sample is labeled and immediately sent to the lab for microscopic and chemical evaluation.

Parameters Assessed in Semen Analysis

The World Health Organization (WHO) provides normal reference values

Volume

• It is considered normal if it is 1.5 mL or more.
• Lower volumes may suggest ejaculatory duct obstruction or hypogonadism.

pH Level

• Normal pH range is 7.2 to 8.0.
• Low pH suggests seminal vesicle blockage; high pH suggests infection.

Liquefaction Time

• Semen normally liquefies within 15–30 minutes after ejaculation.
• Delayed liquefaction may interfere with sperm motility.

Sperm Concentration (Count)

• Normal sperm concentration is 15 million/mL or more.
• Less than this is called oligospermia; absence is called azoospermia.

Motility

• At least 40% of sperm should be motile.
• Motility is divided into progressive, non-progressive, and immotile types.

Morphology

• 4% or more normal forms (as per Kruger strict criteria) is considered acceptable.
• Abnormal morphology may result in failed fertilization.

Vitality

• This measures live vs. dead sperm.
• Normally, 58% or more sperm should be alive.

White Blood Cells (WBCs)

• Presence of more than 1 million WBCs/mL suggests infection or inflammation.

Agglutination

• Sperm clumping may indicate presence of antisperm antibodies.

Nursing Responsibilities During Semen Analysis

• It is the nurse’s duty to educate the patient about proper collection technique and abstinence period.
• The nurse should ensure the collection container is sterile, non-toxic, and properly labeled with patient ID and time.
• The nurse should assist in maintaining privacy and dignity of the patient during the collection process.
• The nurse must ensure that the sample is transported to the lab within 1 hour at body temperature (around 37°C).
• The nurse should document the collection time, patient complaints, and any medications being used that may affect results.
• In case of abnormal findings, the nurse may coordinate with physicians for further diagnostic tests or counseling.
• Nurses should provide psychological support to couples undergoing fertility evaluation or treatment.

Clinical Significance of Semen Analysis

• It helps in diagnosing male factor infertility.
• It is essential in planning for assisted reproductive techniques (ART).
• It detects genitourinary tract infections and inflammation.
• It serves as a follow-up post-vasectomy to ensure effectiveness.
• It helps in identifying congenital, hormonal, or obstructive causes of infertility.

2. Gestational trophoblastic disease

Definition

Gestational Trophoblastic Disease (GTD) refers to a group of rare tumors that arise from the abnormal proliferation of trophoblastic tissue in the uterus after conception.
It includes both benign (hydatidiform mole) and malignant forms (invasive mole, choriocarcinoma, and placental site trophoblastic tumor).
GTD can be life-threatening if untreated, but is often curable with early diagnosis and follow-up.

Etiology

• Abnormal fertilization of ovum
• Age extremes (<20 years or >40 years)
• Previous molar pregnancy
• Nutritional deficiencies (vitamin A, folic acid)
• Genetic abnormalities (empty ovum, triploidy)

Pathophysiology

• Abnormal fertilization causes overgrowth of the trophoblastic layer of the placenta.
• In complete mole, the ovum has no maternal DNA and is fertilized by one or two sperm — no embryo forms.
• In partial mole, there is a triploid set of chromosomes — abnormal fetus and placenta may develop.
• Trophoblasts produce excessive beta-hCG, causing symptoms like severe nausea, uterine enlargement, and ovarian cysts.
• These trophoblastic tissues invade the uterine wall, and in some cases can metastasize (e.g., choriocarcinoma) to lungs, liver, brain.
• If untreated, GTD may cause hemorrhage, infection, and progression to malignancy.

Clinical Manifestations

• Dark vaginal bleeding (prune juice discharge)
• Enlarged uterus for gestational age
• Severe nausea and vomiting
• Absence of fetal heart sounds
• Passage of grape-like vesicles
• High beta-hCG levels
• Early-onset preeclampsia

Diagnostic Evaluation

• Serum β-hCG level (markedly elevated)
• Transvaginal ultrasound (“snowstorm” pattern)
• CBC, liver and renal function tests
• Chest X-ray (for metastasis)
• Histopathology (post-evacuation confirmation)

Medical & Surgical Management

• Suction evacuation (D&C) is the preferred method to remove molar tissue from the uterus.
• Oxytocin or misoprostol may be administered post-evacuation to contract the uterus and control bleeding.
• Methotrexate or actinomycin-D is used as chemotherapy in cases of persistent trophoblastic disease or choriocarcinoma.
• Serial beta-hCG monitoring is done weekly until three consecutive negatives, followed by monthly monitoring for 6–12 months.
• Pregnancy must be avoided for at least one year after treatment to monitor for recurrence.
• In cases unresponsive to chemotherapy or if childbearing is complete, hysterectomy may be indicated.

Nursing Management of GTD

1. Monitoring and Diagnostic Support

• Monitor vaginal bleeding, uterine size, and vital signs to detect complications such as hemorrhage.
• Assist with ultrasound, beta-hCG testing, and preoperative investigations for evacuation.
• Observe for signs of uterine perforation, infection, or retained products after D&C.
• Maintain accurate intake/output and daily weight records for fluid balance assessment.

2. Medication and Post-Evacuation Care

• Administer oxytocics, analgesics, and antibiotics as prescribed to control bleeding and prevent infection.
• Monitor for side effects of chemotherapy, such as mouth ulcers, GI upset, and neutropenia.
• Ensure the patient understands the importance of completing the full course of chemotherapy if initiated.
• Provide antiemetics for nausea due to high hCG or chemotherapy.

3. Health Education and Discharge Planning

• Educate the patient about the importance of avoiding pregnancy for 1 year and using effective contraception.
• Teach the schedule and importance of serial β-hCG monitoring for recurrence detection.
• Instruct the patient to report any abnormal bleeding, pelvic pain, or respiratory symptoms immediately.
• Provide written materials or charts to help the patient follow medication and appointment schedules.

4. Emotional and Psychosocial Support

• Offer grief counseling for pregnancy loss and provide time for emotional expression.
• Support the patient in coping with fears about cancer, infertility, or treatment side effects.
• Involve the partner or family to ensure practical and emotional support at home.
• Refer to a psychologist or support group if the patient exhibits signs of prolonged depression or anxiety.

Complications

• Hemorrhage
• Uterine perforation
• Choriocarcinoma
• Metastasis to lungs, liver, brain
• Infertility (rare)
• Emotional trauma or depression

Q.8 Write down the short notes (any one) (6)

1. Genetic counseling

Definition of Genetic Counseling

• Genetic counseling is the process by which individuals or families affected by or at risk of a genetic disorder are advised about the nature of the disorder, its inheritance pattern, its possible outcomes, and the options available for management and prevention.
• It is a communication-based, educational, and supportive interaction between the healthcare professional (often a genetic counselor or doctor) and the patient or family, especially in the context of reproductive planning, hereditary disease, or abnormal test results.

Aims and Objectives of Genetic Counseling

• It is to help the individual or couple to understand the medical facts, including diagnosis, progression, and possible treatments of a genetic condition.
• It is to make the person aware of how heredity contributes to the development and recurrence of the disease.
• It is to help individuals understand their risk of transmitting or inheriting genetic conditions.
• It is to assist in making informed decisions about reproduction, prenatal diagnosis, or treatment options.
• It is to provide psychological support and education, reducing anxiety, and helping families cope with the condition.
• It also supports early detection and possible prevention of hereditary diseases.

Indications for Genetic Counseling

Genetic counseling is suggested in the following clinical scenarios :

• If there is a family history of genetic or inherited disorders, such as thalassemia, hemophilia, or cystic fibrosis.
• When a previous child is born with a birth defect or developmental delay.
• In case of recurrent spontaneous abortions or stillbirths, especially if unexplained.
• When there is a consanguineous marriage (marriage between close relatives).
• If the mother’s age is above 35 years, due to increased risk of chromosomal abnormalities like Down syndrome.
• When abnormal results are found in prenatal screening tests like ultrasound or amniocentesis.
• When one or both partners are known carriers of a genetic disease, identified via blood testing.
• If the couple is planning to use assisted reproductive techniques (IVF, ICSI).
• When an individual has a known chromosomal condition like Turner syndrome or Klinefelter syndrome.

Types of Genetic Counseling

Prospective (Preconceptional) Counseling:

• It is done before conception to identify couples at risk and to guide them in reproductive decision-making.
• It is helpful in preventing genetic disorders through carrier screening and prenatal planning.

Retrospective Counseling:

• It is given after the birth of a child with a genetic disorder to assess recurrence risk in future pregnancies.

Prenatal Counseling:

• It is provided during pregnancy if screening indicates fetal anomalies or chromosomal abnormalities.

Postnatal Counseling:

• It is done after birth if the infant shows physical, developmental, or neurological problems.

Directive Counseling:

• In this approach, the counselor provides advice or recommendations about specific options, such as avoiding pregnancy or undergoing IVF with donor eggs.

Nondirective Counseling:

• Here, the counselor provides complete information but allows the individual or family to make their own decisions without influence.

Carrier Counseling:

• It is provided to people who are carriers of genetic mutations but do not have symptoms of the disease.

Predictive or Presymptomatic Counseling:

• It is provided for late-onset disorders like Huntington’s disease, especially if there is a family history.

Steps in the Genetic Counseling Process

Initial Evaluation:

It involves detailed collection of family history (pedigree chart), medical history, and previous investigations.

Risk Assessment:

The counselor calculates the probability of disease recurrence or occurrence using genetic principles.

Diagnostic Testing:

The client is advised on appropriate tests such as karyotyping, molecular DNA testing, amniocentesis, or chorionic villus sampling.

Communication of Results:

The counselor explains results in understandable terms, including disease severity, inheritance pattern, and management options.

Decision Making:

The family is helped to choose options such as continuing or terminating pregnancy, IVF, donor programs, adoption, or preparation for special care.

Emotional Support and Follow-up:

The process involves psychosocial counseling to handle fear, guilt, or stress and planning for long-term follow-up

Role of Nurse in Genetic Counseling

• It is the nurse’s role to collect family history and construct a pedigree chart, helping in the early detection of inherited disorders.
• The nurse must assist in educating patients about genetic conditions, inheritance risks, and available testing or treatments.
• It is the responsibility of the nurse to support the emotional and psychological needs of families dealing with genetic risks.
• The nurse should collaborate with genetic counselors, doctors, and laboratory services to ensure accurate testing and follow-up.
• It is essential for the nurse to maintain confidentiality, respect cultural beliefs, and provide non-judgmental counseling support.
• The nurse may participate in community-based genetic awareness programs, promoting early screening and preventive health.

2. Discuss sex linked inheritance in detail

Definition of Sex-Linked Inheritance

• Sex-linked inheritance is defined as the type of inheritance in which genes are located on the sex chromosomes (X or Y chromosomes), and the transmission and expression of these genes depend upon the biological sex (male or female) of the individual.
• It is important to note that X-linked inheritance is more common than Y-linked, because the X chromosome is larger and carries many more genes than the Y chromosome.
• In this pattern of inheritance, males (XY) are more likely to be affected by X-linked recessive disorders, as they have only one X chromosome and no second copy to compensate for a defective gene.

2. Types of Sex-Linked Inheritance

A. X-Linked Inheritance

This refers to traits or disorders that are caused by genes located on the X chromosome. It can be further divided into two main types:

i. X-Linked Recessive Inheritance

• This occurs when the defective gene is present on the X chromosome and is recessive in nature.
• It affects mostly males, because males have only one X chromosome, and a single defective gene is enough to express the disorder.
• Females are usually carriers if only one of their X chromosomes carries the mutation, and they rarely express the disease unless both X chromosomes are affected.
• An affected male can pass the gene to all daughters (who become carriers) but none of his sons, as sons inherit the Y chromosome from the father.
• Carrier females have a 50% chance of passing the defective gene to sons (affected) and a 50% chance to daughters (carriers).
• Examples of X-linked recessive disorders include:
• Hemophilia A and B
• Duchenne muscular dystrophy
• Red-Green color blindness
• G6PD deficiency

ii. X-Linked Dominant Inheritance

• This occurs when a dominant gene on the X chromosome causes the disorder, even if only one copy is present.
• Both males and females can be affected, but the condition tends to be more severe in males, who only have one X chromosome.
• Affected males pass the disorder to all daughters but never to their sons.
• Affected females have a 50% chance of passing the condition to both sons and daughters.
• This type of inheritance is less common than X-linked recessive.
• Examples of X-linked dominant disorders include:
• Fragile X syndrome
• Rett syndrome
• Vitamin D-resistant rickets

B. Y-Linked Inheritance (Holandric Inheritance)

• This type of inheritance involves genes located only on the Y chromosome, which is present only in males.
• Therefore, only males are affected, and the trait is passed directly from father to son.
• Since the Y chromosome has fewer genes, Y-linked disorders are rare.
• All sons of an affected male will inherit the disorder, and daughters are never affected.
• Examples of Y-linked traits include:
• Hairy ears
• Y-chromosome infertility
• SRY gene (Sex-determining Region Y) – essential for male development

3. Pedigree Patterns in Sex-Linked Inheritance

• In X-linked recessive inheritance, the trait often skips generations through carrier females.
• In X-linked dominant inheritance, the trait is seen in every generation and affects both sexes.
• In Y-linked inheritance, only males are affected, and the trait is seen in each generation of males in the family.
• Pedigree charts help identify the pattern and assist in risk prediction and genetic counseling.

4. Clinical Significance of Sex-Linked Inheritance

• Sex-linked disorders can cause severe, lifelong disabilities, especially in males with X-linked recessive diseases.
• It is important in prenatal diagnosis, genetic counseling, and family planning.
• Carrier detection and pedigree analysis are essential to prevent transmission in future generations.
• Early identification can help in appropriate treatment, rehabilitation, or gene therapy.
• It highlights the importance of nursing roles in early screening, patient education, and emotional support.

5. Role of Nurse in Sex-Linked Genetic Disorders

• The nurse should take a complete family history and identify potential carriers or affected individuals.
• It is the nurse’s responsibility to assist in pedigree charting and risk assessment during genetic counseling.
• The nurse should educate patients and families about the mode of inheritance, recurrence risk, and testing options.
• The nurse should help in coordinating genetic testing, counseling sessions, and follow-up services.
• It is essential to provide emotional support, maintain confidentiality, and respect cultural beliefs during the entire process.

Q.9 Define the following terms (any one)(1)

1. Locus

• Locus refers to the specific, fixed position on a chromosome where a particular gene or genetic marker is located.
• Example : The gene for eye color may be found at a specific locus on chromosome 15.

2. Ring chromosome

• A ring chromosome is a structurally abnormal chromosome in which the ends of a chromosome have fused together, forming a circular structure, usually due to the loss of terminal segments.
• Example : Ring chromosome 14 is associated with growth retardation, seizures, and developmental delay.

3. Allele

• An allele is an alternative form of a gene found at the same locus on a pair of homologous chromosomes, which governs variations in a specific trait.
• Example : The gene for flower color may have two alleles—one for red and another for white color.