Pharmacology Past Paper PDF

PAPER 1 – PHARMA BBM Answer ALL 1. List 4 targets of drug action A. Receptor – drugs act on specific receptors on cell membrane or within cells to either activate(agonist) or block(antagonist) their function.E.g. Beta blockers on beta adrenergic receptors B. Ion...

PAPER 1 – PHARMA BBM Answer ALL 1. List 4 targets of drug action A. Receptor – drugs act on specific receptors on cell membrane or within cells to either activate(agonist) or block(antagonist) their function.E.g. Beta blockers on beta adrenergic receptors B. Ion channel – Drugs can modulate ion channels to flow across cell membrane , influencing cellular signalling and excitability. E.g.. Calcium channel blockers (Amlodipine ) inhibit voltage gated calcium channels C. Enzymes – Drugs can activate or inhibit enzymes that can control the biochemical pathway they regulate. E.g. ACE Inhibitors ( Enalapril) inhibit Angiotensin converting enzyme D. Transporter – Drugs can inhibit or facilitate the action of transporter proteins that move molecules across the membrane. E.g. Selective Serotonin Reuptake Inhibitor(SSRI’s ) (Fluoxetine) Inhibit serotonin reuptake transporter 2. List any TWO receptors which are located on the cell membrane; A. Ligand gated ion channel – Nicotinic acetylcholine receptor bind to acetylcholine B. G Protein coupled receptor – Beta adrenergic receptor bind to adrenaline List a drug with Cyclic GMP (cGMP) as a secondary messenger Nitroglycerin , Slidenafil(Viagra) Describe the relationship of pH of the medium and the ionisation of the drug molecules with an example List TWO drugs that can cause liver enzyme induction A. Antiepileptic drugs – Phenytoin , Phenobarbital , B. Anti Tubercular drugs – Rifampin , Rifabutin C. Antiretroviral drug – Efavirenz , Nevirapine List TWO clinical examples where this enzyme induction becomes relevant A. Reduced efficacy of oral contraceptives B. Subtherapeutic effect of Warfarin List TWO drugs that change kinetics from 1st order to 0 order at high doses and give a clinical setting where it becomes relevant A. Phenytoin B. Ethanol List TWO drugs which therapeutic monitoring is done. A. Warfarin B. Digoxin List TWO differences between dopamine and dobutamine List FOUR uses of adrenaline and list TWO sites where you would not mix a local anaesthetic with adrenaline A. Anaphylaxis B. Asthma C. Cardiac arrest D. Local anaesthesia 2 sites where you don’t mix local anaesthetic with adrenaline A. Fingers , nose , toes , eyes B. Penis List TWO use of noradrenaline. A. Hypotension and shock B. Cardiac arrest List TWO uses of prazosin (alpha blocker) A. Hypertension B. Benign prostatic hyperplasia C. PTSD D. CHD List TWO uses of labutalol? (alpha + beta blocker) A. Hypertension B. Hypertensive emergency C. Angina D. Heart failure Classify beta blockers and give importance to beta blockers with intrinsic sympathomimetic activity (not beta blockers in general Explain/discuss potency and efficacy of drugs. Define the terms ED 50, TD 50, LD 50. List atropine (Anticholinergic) substitutes used in ophthalmology. A. Tropicamide B. Cyclopentolate C. Homatropine List atropine substitutes used in respiratory conditions A. Ipratropium B. Tiotropium C. Oxitropium D. Glycopyrrolate List two uses of bethanecol(cholinergic agonist – muscarinic receptor agonist) USES A. Urinary retention B. Post operative ileus C. Neurogenic bladder ADVERSE EFFECTS A. CVS – Bradycardia , Hypotension B. GI – Abdominal cramps , Diarrhea List two differences between adverse effect of drug and side effects of drug Explain the terms addiction, physical dependence of drug, idiosyncrasy, loading dose of a drug, steady state concentration, plasma half life, orphan drugs Describe MOA of fluoroquinolones, macrolides Classify cephalosporins and penicillins Classify penicillins according to their duration of action List adverse effect of acyclovir A. GI disturbance – nausea , vomiting , diarrhoea , B. Headache C. Renal toxicity D. Neurotoxicity List TWO drugs used for Viral Hepatitis infection A. Hepatitis B: Tenofovir, Entecavir, Lamivudine, Adefovir, Pegylated interferon. B. Hepatitis C: Sofosbuvir, Ledipasvir, Daclatasvir, Ribavirin. C. Hepatitis D: Pegylated interferon. D. Hepatitis E: Ribavirin (in certain cases Classify antifungal drugs List FOUR uses of cephalosporins A. Respiratory tract infection B. UTI’s C. Skin and soft tissue infection D. Surgical Prophylaxis List names of drugs under 3rd Generation cephalosporins 1. Ceftriaxone 2. Cefotaxime  3. Ceftazidime 4. Cefdinir 5. Cefixime 6. Cefpodoxime 7. Cefoperazone 8. Ceftibuten MSK List TWO NSAIDs with high anti-inflammatory properties A. Indomethacin B. Diclofenac C. Piroxicam List TWO NSAIDs with high analgesic properties A. Morphine B. Ibuprofen C. Naproxen Explain the MOA of Aspirin on platelets at low doses MOA – Aspirin irreversible acetylates the COX 1 enzyme that is responsible for the production of Thromboxane A2 in platelets. Thromboxane A2 is a potent vasoconstrictor and it promote platelet aggregation (clumping). By reducing the production of Thromboxane A2 , aspirin leads to reduced platelet aggregation and prevent clot formation (thrombosis). The inhibition of COX 1 is irreversible and it lasts for around 7-10 days List TWO uses of selective COX-2 inhibitors A. Osteoarthritis B. Rheumatoid Arthritis List TWO uses of mefenamic acid A. Pain relief B. Anti Inflammatory List THREE side effects of NSAIDs A. GI irritation – stomach ulcer , acid reflux , nausea B. Renal Impairment - C. CVS risk – Heart attack , stroke List TWO contraindications for use of NSAIDs A. Active peptic ulcer disease B. Renal impairment List uses of aspirin as per dose A. Low dose (75-100mg/day) – CVS protection ( heart attack. TIA , stroke), Antiplatelet effect B. Moderate dose (300-600mg/day) – Pain relief (menstrual cramps , headache , toothache , fever C. High dose (1-3g/day) – Anti inflammatory ( Rheumatoid arthritis , Osteoarthritis) , Severe pain relief (GOUT) Describe MOA of methotrexate MOA – Methotrexate is a folate antagonist that inhibit dihydroflorate reductase (DHFR) ‘ an enzyme that is involved in the conversion of dihydrofolate to tetrahydrofolate which is necessary in the synthesis of purines and pyrimidines , which are essential components of DNA , RNA , protein synthesis. Thus inhibiting it can limit the synthesis of the nucleotides thus imparing the DNA and RNA synthesis important for rapidly dividing cells USE – Leukemia , Breast cancer List TWO adverse effects of methotrexate A. Bone Marrow suppression B. Hepatotoxicity C. Mouth Ulcer D. GI Distress Describe MOA of allopurinol MOA – Xanthine Oxidase Inhibitor which inhibits the enzyme Xanthine Oxidase which catalyses the conversion of hypoxanthine to xanthine , xanthine to uric acid. By preventing the conversion , allopurinol prevent the formation of uric acid , reduces the level of uric acid in blood and urine USE A. GOUT B. Hyperuricaemia ADVERSE EFFECTS A. Nausea , Vomiting B. Skin rash C. Severe hypersensitivity reaction List TWO uses of infliximab USE A. Rheumatoid arthritis B. Chron’s Disease C. Ulcerative Colitis ADVERSE EFFECTS A. Fever , Chills , Rash B. Dyspnoea , Hypotension C. Reactivation of latent tuberculosis List FOUR monoclonal antibodies used in treatment of Rheumatoid Arthritis with their targets of action Describe MOA of hydroxychloroquine in terms of a patient with rheumatoid arthritis List two adverse effects of Hydroxychloroquine in patients of rheumatoid arthritis A. Retinopathy B. Nausea , Vomiting Classify neuromuscular blockers These drugs block cholinergic transmission between motor nerve endings and the nicotinic receptors on the skeletal muscle They possess some chemical similarities to ACh, and they act either as antagonists (nondepolarizing type) or as agonists (depolarizing type) at the receptors on the endplate of the NMJ. Non-Depolarizing Neuromuscular Blockers (Competitive blockers) These drugs act by competitively inhibiting the action of acetylcholine at the nicotinic receptors on the motor endplate. They prevent depolarization of the muscle and thus cause muscle relaxation. Examples: Pancuronium Vecuronium Rocuronium Atracurium Depolarizing Neuromuscular Blockers (Depolarizing agents) These drugs mimic acetylcholine and bind to the nicotinic receptors, causing an initial depolarization (muscle twitching or fasciculation) followed by persistent depolarization, which makes the muscle unresponsive to further nerve impulses, resulting in muscle paralysis. Example: Succinylcholine Explain relationship of succinylcholine action with the genetic makeup of a person The action of succinylcholine, a depolarizing neuromuscular blocker, is influenced by the genetic makeup of an individual, particularly regarding the activity of pseudocholinesterase Succinylcholine is normally broken down by pseudocholinesterase, an enzyme found in the liver and plasma. However, some individuals have a genetic variation that leads to a deficiency or abnormality of pseudocholinesterase, which results in a prolonged action of succinylcholine. In individuals with normal pseudocholinesterase activity, succinylcholine is rapidly metabolized after administration, leading to a short duration of paralysis (usually 5-10 minutes). In people with genetic polymorphism leading to pseudocholinesterase deficiency or abnormal pseudocholinesterase activity, succinylcholine is broken down more slowly. As a result, the neuromuscular blockade lasts much longer, and the individual may experience prolonged paralysis, sometimes lasting hours. This is because the drug remains at the neuromuscular junction for a longer period of time, continuing to cause depolarization and preventing repolarization. List two non-depolarising neuromuscular blockers and explain their interactions with use of aminoglycosides A. Rocuronium B. Vecuronium Aminoglycosides (e.g., gentamicin, tobramycin, amikacin) are a class of antibiotics that can enhance the effects of non-depolarizing neuromuscular blockers Mechanism of Interaction: Aminoglycosides act by binding to bacterial ribosomes and inhibiting protein synthesis. However, they also have a secondary effect on the neuromuscular junction. They can decrease the release of acetylcholine from the presynaptic nerve endings by inhibiting calcium influx, leading to reduced neuromuscular transmission. Non-depolarizing neuromuscular blockers (such as rocuronium and vecuronium) compete with acetylcholinefor binding to nicotinic receptors on the muscle cell membrane, leading to muscle paralysis. The inhibition of acetylcholine release by aminoglycosides exacerbates the action of these blockers, resulting in a more profound or prolonged muscle paralysis