Pharmacology

Chemotherapy Of Malaria Important Notes

1. Chloroquine

• Antimalarial drug
• Causes chloroquine retinopathy characterized by
  • Visual disturbances
  • Blurred vision
  • Diplopia
  • Lenticular opacities

Chemotherapy Of Malaria Long Essays

Question 1. Classify the drugs used in malaria and briefly outline the mechanism of actions, uses, and toxicity of chloroquine.
Answer:

Malaria:

• Malaria is caused by 4 species of plasmodium.

Drugs used in malaria – antimalarial drugs:

• These drugs are used for prophylaxis, treatment, and prevention of relapse of malaria.

Antimalarial Drugs Classification:

1. 4-aminoquinolones – chloroquine, amodiaquine.
2. Quinoline – methanol – mefloquine.
3. Cinchona alkaloid – quinine, quinidine.
4. Biguanide – proguanil.
5. Diaminopyrimidine – pyrimethamine.
6. 8-aminoquinolones – primaquine.
7. Sulfonamides – sulfadoxine, dapsone.
8. Tetracyclines – tetracycline, doxycycline.
9. Sesquiterpine – lactones – artesunate, arthemether.
10. Aminoalcohols – halofantrine, lumefantrine.
11. Naphthoquinone – atovaquone.

Chloroquine:

• Chloroquine is a synthetic 4-aminoquinolone.

Chloroquine Mechanism of action:

• The mechanism of action of chloroquine is not clear.

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Chloroquine Uses:

1. Malaria.
   • Used for clinical cure and suppressive prophylaxis of all types of malaria.
2. Extraintestinal amoebiasis.
3. Rheumatoid arthritis.
4. Discoid lupus erythematosus.
5. Lepra reactions.
6. Photogenic reactions.

Chloroquine Adverse effects:

• GIT disturbances – nausea, vomiting, anorexia, epigastric pain.
• Pruritis, headache, visual disturbances, insomnia, skin rashes.
• Cardiomyopathy, peripheral neuropathy.
• Long-term therapy causes blurring of vision, loss of hearing, rashes, photoallergy mental disturbances, myopathy, and graying of hair.

Sulfonamides Cotrimoxazole And Quinolones Important Notes

1. Sulfonamides

• hey have a structural resemblance to PABA
• They compete with PABA for incorporation into folic acid
• They act by inhibiting the enzyme folic acid synthetase which is essential for bacterial growth

Sulfonamides, Cotrimoxazole And Quinolones Uses:

• Nocardial infection
• Leprosy
• Toxoplasmosis
• Ulcerative colitis

Sulfonamides, Cotrimoxazole And Quinolones Adverse Effects:

• Crystalluria
• Haematuria, anuria
• Kernicterus in newborns
• Fixed drug eruption by sulfadiazine
• Steven Johnson syndrome

2. Cotrimoxazole

• It is a combination of Sulfamethoxazole and trimethoprim
• It has a synergistic bacteriocidal effect
• Dose: trimethoprim 80 mg + Sulfamethoxazole 400 mg
• Uses:
• Uncomplicated UTI
  • Respiratory infections
  • Gonorrhoea
  • Otitis media

3. Fluoroquinolones

• Ciprofloxacin, ofloxacin, norfloxacin are fluoroquinolones
• They are contraindicated in children as they cause Arthropathy and damage to developing cartilage
• They are effective against facultative anaerobes
• They inhibit the bacterial enzyme DNA gyrase

Sulfonamides Cotrimoxazole And Quinolones Long Essays

Question 1. Classify sulphonamides. Discuss the mechanism of action, adverse effects, And uses of cotrimoxazole.
Answer:

Sulfonamides Classification:

1. Short-acting – sulfadiazine.
2. Intermediate-acting – sulfamethoxazole.
3. Long-acting – sulfadoxine.
4. Special purpose sulphonamide – Sulfasalazine, Silver sulfadiazine.

Cotrimoxazole:

• A combination of trimethoprim And sulfamethoxazole is called cotrimoxazole.

Cotrimoxazole Mechanism of action:

• Cotrimoxazole causes sequential blockage of folic acid synthesis.

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Cotrimoxazole Uses:

• Respiratory tract infections – tonsillitis, pharyngitis, sinusitis, bronchitis.
• Urinary tract infections – acute And chronic.
• Diarrhea And dysentery.
• Typhoid, chancroid, granuloma inguinale.
• Pneumocystis jiroveci pneumonia in AIDS patients.
• Orodental infections.

Cotrimoxazole Adverse effects:

• Nausea, vomiting, headache, stomatitis, rashes.
• Precipitate megaloblastic anemia.
• Blood disorders – anemia, granulocytopenia.
• Uremia in patients with renal diseases.
• Neonatal hemolysis And methemoglobinemia. When administered to pregnant women.

Question 2. Enumerate fluoroquinolones. Mention their antimicrobial spectrum, uses, And adverse effects.
Answer:

Fluoroquinolones:

• These are quinolones antimicrobials having one or more fluorine substitutes.

Fluoroquinolones Classification:

Antimicrobial spectrum:

1. Gram-positive organisms like

• Staphylococci, chlamydiae, mycoplasma, And mycobacterium.

2. Gram-negative organisms like

• Gonococci, meningococci, E-coli, salmonella, shigella, H. Pylori.

3. Some anaerobic organisms.

Antimicrobial spectrum Uses:

Antimicrobial spectrum Adverse effects:

• Nausea, vomiting, abdominal discomfort, diarrhea, rashes.
• Tendinitis.
• Damage to growing cartilage
• Headache, dizziness.
• Precipitate seizures in epileptic patients.

Question 3. Classify drugs used in the treatment of infections caused by gram-negative organisms. Mention the mechanism of action of fluoroquinolones.
Answer:

Fluoroquinolones Classification:

• Drugs used in the treatment of infections caused by gram-negative organisms are:

1. B-lactam antibiotics

• Penicillin, cephalosporin.

2. Tetracyclines – Doxycycline.

3. Aminoglycosides – Gentamicin, streptomycin.

4. Macrolides – erythromycin, Azithromycin.

5. Nitroimidazoles – Metronidazole.

6. Quinolones – Norfloxacin, Ciprofloxacin.

Fluorozuinolones (FQ):

Fluoroquinolones Mechanism of action:

• DNA gyrase enzyme is required for DNA replication.
• This enzyme has subunits A And B

2. At low doses.

Sulfonamides Cotrimoxazole And Quinolones Short Essays

Question 1. Write important side effects of sulphonamides.
Answer:

Sulphonamides:

• Sulfonamides were the first effective antibacterial agents to be used systemically in man.
• It contains a sulphonamide group.

Sulphonamides Adverse Effects:

1. GIT effects.

• Nausea, vomiting, anorexia, abdominal pain.

2. Renal effects.

• Renal irritation, hematuria, albuminuria. Crystalluria.
• It occurs due to the precipitation of the drug in acidic urine.
• Avoided by:
  • Intake of plenty of fluids.
  • Alkalinizing the urine with sodium bicarbonate.

3. Hypersensitivity reactions.

• Fever, rashes, anaphylaxis, urticaria, and photosensitivity – occur rarely.
• Stevens-Johnson syndrome And exfoliative dermatitis – occurs commonly.

4. Contact sensitization on topical application.

5. Hemolysis.

• Occurs in patients with G6PD deficiency.

6. Kernicterus.

• Occurs in newborns.
• Sulfonamides displace bilirubin from binding sites.
• This then crosses BBB And causes kernicterus.

Question 2. Sulfonamides are not very effective in the presence of pus. Explain.
Answer:

Some bacteria synthesize their own folic acid which consists of p-amino benzoic acid (PABA).

• Sulfonamide is structurally similar to PABA.
• Thus it competitively inhibits the formation of folic acid.
• Pus contains.
  • Purines And thymidine – which decreases the bacterial requirement for folic acid.
  • Antagonizes sulphonamide action.
  • It is rich in PABA.
  • Thus, sulphonamides are not very effective in the presence of pus.

Question 3. Explain the mechanism of action of co-trimoxazole.
Answer:

The combination of trimethoprim And sulfamethoxazole is cotrimoxazole.

Co-trimoxazole Mechanism of action:

• Individual drugs are bacteriostatic.
• While combination causes bacteriocidal action.
• Through their combined effect sequential blockade of folic acid synthesis occurs.

Sulfonamides Cotrimoxazole And Quinolones Short Question And Answers

Question 1. Long-acting sulphonamides.
Answer:

Long-acting sulphonamides are sulfadoxine And sul- famethopyrazine.

• The action lasts for more than 1 week because of
  • High plasma protein binding.
  • Slow renal excretion.
• They attain low plasma concentration so they are not suitable for the treatment of acute pyogenic infectious.

Long-acting sulphonamide Uses:

• In malaria in combination with pyrimethamine.
• Pneumocystis jiroveci pneumonia in AIDS patients.
• Toxoplasmosis.

Long-acting sulphonamide Adverse Reaction:

• Serious cutaneous reactions.

Question 2. The rationale of a combination of sulfamethoxazole with trimethoprim.
Answer:

Sulfamethoxazole And trimethoprim are individually bacteriostatic

• Sulfamethoxazole inhibits the conversion of PABA to dishy-dro folic acid while trimethoprim inhibits and prevents the reduction of dihydrofolate to tetrahydrofolate.
• Thus, combining sulfamethoxazole And trimethoprim causes sequential blockade of folic acid synthesis And has bacteriocidal action.

Question 3. Ciprofloxacin.
Answer:

Ciprofloxacin is first generation fluroquinolones.

• It has a wide spectrum of activity
• Has rapid bacteriocidal activity And high potency.
• It is less active at acidic pH
• It is rapidly absorbed orally.

Ciprofloxacin Uses:

• Systemic infections.
• Typhoid
• Gonorrhoea.
• Gastroenteritis.

Ciprofloxacin Adverse Reactions:

• GIT effects – nausea, vomiting, anorexia.
• CNS effects – Dizziness, headache, anxiety, insomnia, tremors.
• Hypersensitivity reactions – rash, pruritis, photosensitivity, urticaria.
• Tendonitis.

Question 4. Ciprofloxacin is contraindicated in children. Why?
Answer:

Ciprofloxacin is fluoroquinolone.

• It causes damage to the growing cartilage of weight-bearing joints.
• This results in arthropathy.
• Thus, it is contraindicated in children.

General Considerations Important Notes

1. Antibiotics

• Antibiotics are biological substances elaborated by micro-organisms that suppress the growth of other microorganisms or destroy them in high dilution

2. Classification of antibiotics

• Based on the mechanism of action

• Based on antibacterial activity

• Based on the spectrum of activity

3. Superinfection

• It refers to the appearance of a new infection as a result of antimicrobial therapy
• Drugs that cause superinfection are
  • Tetracyclines
  • Chloramphenicol
  • Ampicillin
  • Amoxycillin

4. Methods to prevent drug resistance

• Indiscriminate inadequate prolonged use of antibiotics should be avoided
• The drug should be given after a culture sensitivity test
• If antibiotics are to be given for a prolonged period, combination therapy should be instituted

5. Uses of a combination of drugs

• To achieve synergism
• To reduce the severity or incidence of adverse effects
• To prevent the emergence of resistance
• To broaden the spectrum of antimicrobial action

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6. Examples of combination of drugs

• Combination of two bacteriostatic drugs that are often additive and rarely synergetic
  • Tetracycline + chloramphenicol/ erythromycin
  • Sulfonamide + trimethoprim
  • Clavulanic acid + amoxicillin
• Combination of two bacteriocidal drugs that are frequently additive and sometimes synergetic
  • Penicillin/ ampicillin + streptomycin/ gentamycin
  • Carbenicillin + gentamycin
  • Ceftazidine + ciprofloxacin
  • Rifampicin + tuberculosis
• Combination of bacteriostatic and bacteriocidal drug
  • Penicillin + erythromycin
  • Penicillin + tetracycline/ chloramphenicol
  • Penicillin + sulfonamide
  • Streptomycin + tetracycline
  • Rifampicin + dapsone

General Considerations Long Essays

Question 1. Mention some examples of antibodies And describe the mechanism of action And side effects of two commonly used antibiotics.
Answer:

Antibiotics:

• Antibiotics are produced by microorganisms that selectively suppresses the growth or kill other microorganisms at very low concentration.

Antibiotics Classification:

1. Based on chemical structure.

• Sulfonamides – sulfones, dapsone.
• Diaminopyrimidies – trimethoprim.
• Quinolones – nalidixic acid, norfloxacin.
• p-lactam antibiotics – penicillin, cephalosporin.
• Tetracyclines – Oxytetracyclines.
• Aminoglycosides – streptomycin, gentamicin.
• Macrolide – erythromycin, Azithromycin.
• Polyene antibiotics – Nystatin.
• Azole derivatives – clotrimazole, ketoconazole.

2. Based on the mechanism of action.

• Inhibit cell wall synthesis.
  • Penicillin, cephalosporins.
• Cause leakage from the cell membrane.
  • Polypeptides – polymyxins, colistin.
• Inhibit protein synthesis.
  • Tetracyclines, chloramphenicol.
• Cause misreading of m-RNA
  • Aminoglycosides.
• Inhibit DNA gyrase – fluoroquinolones.
• Interfere with DNA function – Rifampicin.
• Interfere with DNA synthase – Acyclovir.
• Interfere with intermediary metabolism.
  • Sulfonamides, trimethoprim.

3. Based on the type of organisms against which it acts.

• Antibacterial – Penicillin, aminoglycosides.
• Antifungal – Griseofulvin, Amphotericin B.
• Antiviral – Acyclovir, Amantadine.
• Antiprotozoal – Cloroquine metronidazole, chloroquine .
• Anti helmintic – Mebendazole.

4. Based on the spectrum of activity.

• Narrow spectrum – Penicillin G, streptomycin.
• Broad spectrum – Tetracyclines.

5. Based on the type of action.

• Bacteriostatic – sulphonamides, tetracyclines.
• Bacteriocidal – Penicillins, Aminoglycosides.

Antibiotics Penicillins:

Penicillins Mechanism of action:

Penicillins Adverse effects:

1. Hypersensitivity reactions.

• Skin rashes, urticaria, fever, bronchospasm, serum sickness, anaphylaxis.

2. Paint the site of injection.

3. CNS effects.

• Confusion, muscle twitching, convulsions, coma.

4. Suprainfection.

5. Jarisch Herxheimer reaction.

• Occurs when penicillin is injected into the syphilitic patient
• It is characterized by the sudden destruction of spiro chapters And the release of its lytic products.

Antibiotics Sulfonamides:

Sulfonamides Mechanism of action:

• Many bacteria synthesize their own folic acid from p- amino benzoic acid (PABA) by enzyme folic acid synthetase.
• Sulfonamides is structurally similar to PABA.

• Thus sulphonamide is bacteriostatic in action.

Sulfonamides Adverse effects:

• Nausea, vomiting, epigastric pain.
• Renal Irritation, hematuria, albuminuria, And crystalluria.
• Hypersensitivity reactions.
• Kernicterus.
• Hemolysis in G-6 PD deficiency patients.
• Hepatitis.
• Stomatitis, conjunctivitis, And Arthritis

Question 2. Explain four advantages of the combined use of antimicrobials with examples.
Answer:

Advantages of a combination of antimicrobials:

1. To achieve synergism.

• The same drugs may be synergistic for one organism but antagonistic for another.

2. To reduce adverse effects.

• Combining two antimicrobials may reduce the dose of each agent.
• This may thereby reduce the toxicity of drugs.
• Example: Streptomycin + penicillin G for subacute bacterial endocarditis.

3. To prevent the emergence of resistance.

• It is used primarily for chronic infections needing prolonged therapy like tuberculosis, and leprosy.
• Rifampin + ciprofloxacin – prevents S.aureus resistance.

4. To broaden the spectrum of antimicrobial action.

General Considerations Short Essays

Question 1. What is superinfection? Give two examples.
Answer:

Superinfection:

• It refers to the appearance of a new infection as a result of antimicrobial therapy.

Superinfection Reason:

• Antimicrobial agents cause alteration in the normal flora of the intestine respiratory And genitor-urinary tracts.
• Normal microbial flora contributes to host defense.
• In it, the pathogen has to compete with the normal commensals for nutrition.
• But by the use of antimicrobial agents, there is a lack of competition.
• As a result, infection is caused easily.
• Broader the antimicrobial spectrum, the more the chances of superinfection.

Conditions Predisposing to Superinfection:

• Corticosteroid therapy.
• Leukemia.
• AIDS.
• Agranulocytosis.
• Diabetes.
• Disseminated lupus erythematous.

Superinfection Examples:

Androgens And Anabolic Steroids Short Essays

Question 1. Anabolic steroids.
Answer:

Anabolic steroids are synthetic androgen with higher anabolic and low androgenic activity.

• It enhances protein synthesis and increases muscle mass.

Anabolic steroids Uses:

• In catabolic states – to correct negative nitrogen balance.
• Senile osteoporosis – in elderly males.
• Growth stimulation in children – used for short periods.
• Chronic renal failure.
• In refractory anemia.
• Abuse in athletics

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Anabolic steroids Contraindications:

• Pregnancy.
• Carcinoma of the prostrate or breast in males.

Anabolic steroids Drugs used are:

• Nandrolone.
• Oxymetholone
• Stanozolol.
• Methandienone.

Anabolic steroids Adverse effects:

• Masculinization and acne in females.
• Hepatotoxicity.
• Increased libido.
• Precocious puberty.
• Salt and water retention.
• Suppression of spermatogenesis.

Antihypertensive Drugs Important Notes

1. Classification of antihypertensive drugs

• Drugs acting on the renin-angiotensin system
  • Angiotensin-converting enzyme inhibitors
  • Captopril
  • Enalapril
  • Lisinopril
  • Ramipril
• Angiotensin 2 receptor antagonists
  • Losartan
  • Candesartan
  • Olmesartan
  • Renin inhibitor
  • Aliskiren
• Sympatholytics
  • Centrally acting – Clonidine, Methyldopa
  • Ganglionic blockers – Trimethaphan
  • Adrenergic neuron blocker – Guanethidine, reserpine
  • Adrenergic receptor blocker
    • Alpha blocker – prazosin, doxazosin
    • Beta-blocker – propranolol, atenolol, esmolol
    • Alpha and beta-blocker – atenolol, carvedilol
• Diuretics
  • Thiazides – hydrochlorothiazides
  • Loop diuretics – frusemide, torsemide
  • Potassium-sparing diuretics – spironolactone, amiloride, triamterene
• Calcium channel blocker
  • Verapamil, niofedipine, nicardipine, nimodipine
• Vasodilators
  • Arteriolar dilators – hydralazine, minoxidil
  • Arteriolar and venular dilators – sodium nitroprusside

2. ACE inhibitors

• They are the first choice of drugs in all essential hypertension
• They are the most appropriate antihypertensives in patients with
  • Diabetes
  • Nephropathy
  • Left ventricular hypertrophy
  • Angina
  • Post MI

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• Advantage: lack of postural hypotension
• Most ACE inhibitors are prodrugs
• They need to be converted by hepatic osteolysis to active diacid metabolite
• ACE inhibitors that are prodrugs are
  • Fosinopril
  • Enalapril
  • Benazepril
  • Imidapril
  • Perindopril

3. Antihypertensives and pregnancy

Antihypertensive Drug Long Essays

Question 1. Classify drugs used in the treatment of hypertension or antihypertensive drugs. State mechanism of action, indications, and adverse effects of any three of them

Answer:

Antihypertensive drugs:

• These drugs are used to lower BP in hypertension.

Antihypertensive drugs Classification:

1. Diuretics:

• Thiazides – hydrochlorothiazide, indapamide.
• High ceiling – Furosemide.
• K+ sparing – Spironolactone, Amiloride.

2. ACE inhibitors.

• Captopril, enalapril, Lisinopril, perindopril.

3. Angiotensin Antagonists.

• Losartan, candesartan.

4. Calcium channel blockers.

• Verapamil, diltiazem, Nifedipine, Felodipine.

5. β Adrenergic blockers

• Propranolol, Atenolol, Metoprolol.

6. β and α drenergic blockers.

• Labetalol, carvedilol.

7. α Adrenergic blockers.

• Prazosin, Terazosin, Doxazosin, Phentolamine.

8. Central sympatholytics.

• Clonidine, methyldopa.

9. Vasodilators.

• Hydralazine, sodium nitroprusside.

Diuretics:

Diuretics Mechanism of action:

1. Enhances sodium and water excretion.
↓
Decreases plasma and ECF volume.
↓
Decreases cardiac output
↓
Decreases BP.
↓
2. Increased excretion of sodium and water
↓
Decreases body sodium
↓
Relaxation of vascular smooth muscle.
↓
Decreases peripheral vascular resistance.
↓
Reduces BP.

Diuretics Use:

• In uncomplicated mild to moderate hypertension.

Diuretics Adverse effects:

• Hypokalemia.
• Carbohydrate intolerance.
• Fatigue, loss of energy.
• Impotence.
• Hyperlipidaemia, hyperuricemia.
• Decreased libido.

Vasodilators – Hydralazine:

• Mechanism of action:

1. Arteriolar dilatation.
↓
Reduces vascular resistance
↓
Reduces BP.
↓
2. Compensatory mechanism.
Evoke tachycardia.
↓
Increases cardiac output and renin release.
↓
Increases aldosterone.
↓
Causes sodium and water retention.
↓
Decreases BP.

Vasodilators – Hydralazine Uses:

• Moderate to severe hypertension.
• Low doses are added to diuretics and β blockers.
• Only antihypertensive drugs are used in pregnancy.

Vasodilators – Hydralazine Adverse effects:

• Flushing, headache, dizziness, palpitation.
• Precipitate angina.
• Paraesthesia, tremor, muscle cramps.
• Rheumatoid arthritis.

ACE – Inhibitors:

• Mechanism of action:

Prevent formation of angiotension 2 and aldosterone.
↓
Causes vasodilation.
↓
Peripheral vascular resistance disease.
↓
BP decreases.

ACE – Inhibitors Uses:

• Hypertension.
• Myocardial infarction.
• Coronary artery disease.
• Chronic renal failure.
• Scleroderma renal crisis.

ACE – Inhibitors Adverse effects:

• Persistent dry cough.
• Angioneurotic edema.
• Hypotension.
• Hyperkalemia.
• Skin rashes
• Teratogenicity
• Others – headache, nausea, abdominal pain, proteinuria, neutropenia.

Question 2. Discuss the pharmacological actions, uses, and adverse effects of angiotensin-converting enzyme inhibitors – ACE inhibitors.

Answer:

ACE-Inhibitors:

ACE-Inhibitors Actions:

1. On Renin-Angiotensin system.

• Angiotensin 1 is converted into angiotensin 2 by angiotensin converting enzyme.
• Thus, if this enzyme is inhibited by ACE inhibitors, it prevents the formation of angiotensin 2.
• This further prevents the formation of aldosterone.
• This leads to vasodilation and a decrease in peripheral vascular resistance.

2. On Bradykinin level.

• ACE inhibitors raise bradykinin levels, which is a potent vasodilator.
• This causes a fall in B.P.

3. On vital organs.

• By selective vasodilation, ACE inhibitors increase blood flow to vital organs.

ACE-Inhibitors Uses:

1. Hypertension

• ACE inhibitors are first-line drugs for hypertension.
• Used in all grades of hypertension.
• Combining it with diuretics increases its efficacy.
• It can be used in hypertensive patients along with the following diseases.
  • Left ventricular failure
  • Diabetics
  • Renal diseases.
  • Co-existing ischaemic heart disease.

2. Congestive cardiac failure (CCF)

• ACE inhibitors cause arteriolar and vasodilatation in it
• This reduces preload and afterload.

3. Myocardial infarction.

• ACE inhibitors reduce early as well as long-term mortality.

4. Prophylaxis in high cardiovascular-risk patient

• Protects myocardium and vasculature.

5. Diabetic nephropathy.

• Prolonged use of ACE-inhibitor prevents or delays end-stage renal disease.

6. Scleroderma crisis.

• The life-saving drug in it

Question 3. Classify antihypertensive agents. Discuss the pharmacological actions, uses, and adverse effects of calcium channel blockers.

Answer:

Classification of Antihypertensive Drugs:

• Drugs acting on the renin-angiotensin system
  • Angiotensin-converting enzyme inhibitors
    • Captopril
    • Enalapril
    • Lisinopril
    • Ramipril
  • Angiotensin 2 receptor antagonists
    • Losartan
    • Candesartan
    • Olmesartan
  • Renin inhibitor
    • Aliskiren
• Sympatholytics
  • Centrally acting – Clonidine, Methyldopa
  • Ganglionic blockers – Trimethaphan
  • Adrenergic neuron blocker – Guanethidine, reserpine
  • Adrenergic receptor blocker
    • Alpha blocker – prazosin, doxazosin
    • Beta-blocker – propranolol, atenolol, esmolol
    • Alpha and beta-blocker – labetalol, carvedilol
• Diuretics
  • Thiazides – hydrochlorothiazides
  • Loop diuretics – frusemide, torsemide
  • Potassium-sparing diuretics – spironolactone, amiloride, triamterene
• Calcium channel blocker
  • Verapamil, niofedipine, nicardipine, nimodipine
• Vasodilators
  • Arteriolar dilators – hydralazine, minoxidil
  • Arteriolar and venular dilators – sodium nitroprus- side

Calcium Channel Blockers (CCB) Actions:

1. Action on smooth muscle

• Vascular smooth muscle
  • Relaxation of arteriolar smooth muscle reduced peripheral vascular resistance → reduction in blood pressure
• Other smooth muscle
  • Relaxation of GIT and bronchial smooth muscles
  • Relaxes the uterus which is useful in preterm labor

2. Action on heart

• Depresses myocardial contractibility
• Reduces heart rate
• Reduces cardiac work

3. Action on coronary circulation

• Dilates coronary vessels
• Increases coronary blood flow

Calcium Channel Blockers (CCB)  Uses:

• Angina pectoris
  • CCB reduces the frequency and severity of angina
• Hypertension
• Arrhythmias
  • Verapamil controls ventricular rate in atrial flatter or fibrillation
• Peripheral vascular disease
  • Used in Raynaud’s disease for its vasodilator effects

Calcium Channel Blockers (CCB)  Adverse Effects:

Antihypertensive Drugs Short Essays

Question 1. Captopril.

Answer:

Captopril is an orally active dipeptide ACE inhibitor.

• It is a sulfhydryl-containing dipeptide.

Captopril Mechanism of Action:

• Prevents the formation of Angiotensin 2 and aldosterone.
• Increases bradykinin levels.
• Causes vasodilation and fall of BP.
• Both systolic and diastolic BP decreases.
• It has no action on cardiac output.

Captopril Pharmacokinetics:

• Orally administered.
• About 70% of the drug is absorbed.
• The plasma half-life is approx. 2 hours.
• Duration of action – 6 -12 hours.

Captopril Adverse effects:

• Hypotension.
• Hyperkalemia.
• Cough.
• Rashes, urticaria.
• Angioedema.
• Loss of alteration in taste sensation.
• Fetal growth retardation.
• Headache, dizziness, nausea.
• Acute renal failure.
• Granulocytopenia.

Question 2. Calcium channel blockers are used in the treatment of hypertension.

Answer:

Calcium channel blockers used in the treatment of hypertension include.

1. Phenylalkylamines – Verapamil.

2. Benzothiazepines – Diltiazem.

3. Dihydropyridines – Nifedipine, felodipine, Amlodipine, Lacidipine, Nimodipine.

• These drugs are well-tolerated and effective.
• They dilate arterioles resulting in reduced peripheral vascular resistance.
• Effective in elderly patients.
• Can be used alone or in combination with other an¬tihypertensive drugs.
• Nifedipine produces some reflex tachycardia.
• Fluid retention is negligible.
• Short-acting drugs are associated with increased mortality and risk of sudden death.
• They are used in patients with angina.
• Not preferred in patients who also have left ventricu¬lar hypertrophy and previous myocardial infarction.
• They are used for short periods for smoother control of BP.
• Nifedipine is administered sublingually and is used for hypertensive emergencies.
• It effectively lowers BP in 10 min.

Question 3. Mention two centrally acting antihypertensive drugs and mention their adverse effects.

Answer:

Question 4. The rationale of using clonidine in hypertension.

Answer:

Clonidine is an imidazoline derivative.

it is a partial agonist with high affinity and high intrinsic activity at α2 receptors.

Clonidine in Hypertension Action:

1. Stimulation of α2 receptors in the medulla.
↓
Decreases central sympathetic outflow.
↓
Blocks the release of noradrenaline from the nerve terminal.
↓
Results in fall in BP and bradycardia.

2. Clonidine active specific imidazoline receptors in the brain.

• This causes a fall in BP.

Pharmacokinetics:

• Effective orally.
• Plasma half-life – 8 -12 hours.
• The effect lasts for 6 – 24 hours.

Question 5. The rationale of using p-blockers in hypertension.

Answer:

Beta-blockers used in hypertension are propranolol, atenolol, esmolol, and metoprolol.

• They are effective and well-tolerated.
• They are mild antihypertensive.
• They reduce cardiac output and lowers plasma renin activity.
• This reduces BP.
• They can be used alone or in combination with other antihypertensive.
• Beta-blockers should always be tapered while with-drawing.
• They can be used in patients with angina and cardiac arrhythmia.
• Esmolol is used in intraoperative and postoperative hypertension and in hypertensive emergencies.
• It is used better than other antihypertensive drugs because of.

1. Absence of postural hypotension.

2. Absence of bowel alteration.

3. Absence of salt and water retention.

4. Less side effects.

5. Low cost

Antihypertensive Drugs Short Answers

Question 1. Clonidine.

Answer:

Clonidine is an imidazoline derivative.

• It is a selective α2 -agonist

Clonidine Mechanism:

Stimulation of α2 receptors.
↓
Decreases central sympathetic outflow.
↓
Blocks release of noradrenaline.
↓
Resulting in a fall in BP.

Clonidine Uses:

• Hypertension.
• Opioid withdrawal syndrome.
• Postoperative epidural analgesia.
• Menopausal syndrome.

Question 2. Reserpine.

Answer:

Reserpine is an alkaloid obtained from Rauwolfia serpentina.

Reserpine Mechanism:

Destruction of vesicles in the adrenergic neurons.
↓
Depletion of monoamines like noradrenaline, dopamine, and 5-HT.
↓
Reduces BP.

Reserpine Uses:

• Hypertension.
• Psychosis.

Question 3. Mention two uses and two adverse effects of thiazide.

Answer:

Thiazide Uses:

• Mild hypertension.
• Congestive heart failure.
• Hepatic or renal edema.
• Renal stones
• Diabetes insipidus.

Thiazide Adverse effects:

• Hypokalemia.
• Hyperglycaemia.
• Hyperuricaemia.
• Hyperlipidaemia.
• Impotence.
• Decreased libid

Question 4. Enaiapril.

Answer:

Enalapril is an angiotensin-converting enzyme inhibitor.

• It is a prodrug, thus it has to be converted in the body to the active form.
• Hence it acts slowly.

Enaiapril Uses:

• Hypertension
• Congestive cardiac failure.
• Myocardial infarction.

Enaiapril Adverse effects:

• Persistent dry cough.
• Hyperkalaemia.
• Taste alteration.

Question 5. Chlorothiazide diuretics used in hypertension.

Answer:

Chlorothiazide is a thiazide diuretic that is used in the treatment of mild hypertension.

Mechanism:

Decreases plasma volume
↓
Decreases cardiac output.
↓
Decreases sodium
↓
Decreases peripheral vascular resistance (PVR)
↓
Increases sodium and water excretion
↓
Reduces BP.

• Thiazides cause hypokalaemia and hence they are used with potassium-sparing diuretics.

Question 6. Advantages of ACE inhibitors over other anti-hypertensive drugs.

Answer:

ACE inhibitors have the following advantages.

• Lack of postural hypotension, electrolyte disturbances, feeling of weakness, and CNS effects.
• Safer in asthmatics, diabetics, and peripheral vascular disease patients.
• Reverse left ventricular hypertrophy.
• No hyperuricemia, no harmful effect on plasma lipid profile.
• No rebound hypertension on withdrawal.
• Minimum worsening of quality of life.

Question 7. Compare chlorothiazide and propanoiol.

Answer:

Question 8. Mention two ACE inhibitors and two calcium channel blockers.

Answer:

• ACE inhibitors: Captopril, Enalapril, Lisinopril
• Calcium channel blockers: Verapamil, Diltiazem, Nifedipine.

Question 9. Enlist two Angiotensin receptor blockers and write the mechanism of action.

Answer:

Mechanism of Action:

• Blocks angiotensin 1 receptor
• Relaxes vascular smooth muscles
• Promotes salt and water excretion
• Reduces plasma volume

Examples:

• Losartan, candesartan, irbesartan

Antihypertensive Drugs Viva Voce:

1. Sodium nitroprusside is arteriolar and venous dilator
2. Hydralazine is arteriolar dilator

Drugs Used In Angina Pectoris and Myocardial Infarction Important Notes

1. Classification of nitrates

• Short-acting
  • Glyceryl trinitrate
  • Nitroglycerine
• Long-acting
  • Isosorbide dinitrate
  • Isosorbidemononitrate

2. Isosorbidemononitrate

• Long-acting
• Undergoes little first-pass metabolism
• Bioavailability is high

3. Nitrates

• Its most prominent action is exerted on vascular smooth muscle
• It dilates veins more than arteries
• Causes peripheral pooling of blood
• This decreases venous return
• Decrease load on the heart

4. Nitroglycerine

• Used by sublingual route
• Acts within 1-2 min as it is directly absorbed into the systemic circulation

Drugs Used In Angina Pectoris and Myocardial Infarction Long Essays

Question 1. Classify vasodilators. Describe the pharmacol¬ogical actions of nitrates, their clinical uses, and side effects.

Answer:

Classification of Vasodilators:

1. Arteriolar dilators – decreases afterload.

• Hydralazine, Nifedipine, Nicorandil.

2. Venodilators – Decreases preload.

• Nitrates – Glyceiyl trinitrate, isosorbide dinitrate.

3. Mixed dilators – Decreases both pre and after-load.

• ACE inhibitors, prazosin, sodium nitroprusside.

Read And Learn More: Pharmacology Question and Answers

Nitrates:

• Nitrates are prodrugs.

Actions:

1. Preload reduction.

Nitrates dilates veins
↓
Causes peripheral pooling of blood
↓
Decreases venous return
↓
Reduces preload.

2. Afterload reduction.

Nitrates dilate arteries.
↓
Decreases vascular resistance
↓
Decreases afterload.

• Decreases in preload afterload result in a decrease in cardiac workload.

3. Redistribution of coronary flow.

• Nitrates relax bigger conducting coronary arteries.
• Causes redistribution of blood flow to ischaemic areas in angina pectoris.

4. Other vasculature.

• Dilates cutaneous vessels → causes flushing.
• Dilates meningeal vessels → causes headache.

Question 2. Enumerate four antianginal drugs that belong to different groups. Write the mechanism of action.

Answer:

Anti-anginal drugs Classification:

1. Nitrates.

• Short-acting – Glyceryl trinitrate, Nitroglycerine.
• Long-acting – Isosorbide dinitrate, Isosorbide mononitrate.

2. Beta blockers.

• Propranolol, Metoprolol, Atenol.

3. Calcium channel blockers.

• Verapamil, Diltiazem, Nifedipine.

4. Potassium channel opener- Nicorandil.

5. Others

• Dipyridamole, Trimetazidine.

Short-Acting Drugs – Nitrates:

• Short-acting drugs are among nitrates.

Mechanism of Action:

Denitration of organic nitrates in the smooth muscle cells.
↓
Releases reactive free radical nitric oxide.
↓
Causes activation of cytosolic guanylyl cyclase.
↓
Increases cGMP
↓
Causes dephosphorylation of myosin light chain kinase
(MLCK)
↓
This interferes with the activation of myosin.
↓
Myosin fails to interact with actin.
↓
No contraction occurs, thus it causes relaxation.

Drugs Used In Angina Pectoris and Myocardial Infarction Short Essays

Question 1. List one cardioselective and one nonselective beta-blocker. Mention two therapeutic uses of them.

Answer:

1. Cardioselective beta blocker:

• They selectively block the bl receptor and weakly the b2 receptor.
• Their inhibition of glycogenolysis is low.
• Impairs exercise performance to a lesser degree.

Cardioselective Beta Blocker Uses:

• Safer is diabetics
• Cardiac arrhythmia.
• Angina pectoris.
• Hypertension.

Cardioselective Beta Blocker Examples:

• Atenolo, metoprolol and esmolo.

2. Non-selective beta blockers.

Non-Selective Beta Blockers Uses:

• Glaucoma.
• Anxiety
• Pheochromocytoma.
• Thyrotoxicosis.
• Prophylaxis of migraine.

Non-Selective Beta Blockers Examples:

• Timolol, propranolol, nadolol, sotalol.

Drugs Used In Angina Pectoris and Myocardial Infarction Short Answers

Question 1. Nitroglycerine.

Answer:

Nitroglycerine is a short-acting antianginal drug.

Nitroglycerine Mechanism:

Conversion of nitroglycerine to nitric oxide.
↓
Causes relaxation of vascular smooth muscles
↓
Leads to vasodilation.
↓
Reduces venous return and preload on the heart

Nitroglycerine Pharmacokinetics:

• Effective sublingually.
• Well absorbed from buccal mucosa.

Nitroglycerine Uses:

• Angina
• Cardiac failure
• Myocardial infarction.
• Cyanide poisoning.

Question 2. Name drugs causing gingival hyperplasia.

Answer:

Drugs causing gingival hyperplasia:

1. Anticonvulsants.

• Phenytoin sodium – phenobarbitone, carbamazepine.

2. Antihypertensive-nifedipine, amlodipine, nimodipine.

3. Immunosuppressants – cyclosporine.

Question 3. Name organic nitrates used in the treatment of angina pectoris.

Answer:

Organic nitrates used in the treatment of angina pectoris are.

1. Short acting-Glyceryl trinitrate Nitroglycerine.

2. Long-acting – Isosorbide dinitrates, isosorbide mononitrate.

Question 3. Angina pectoris

Answer:

Angina pectoris is a pain syndrome due to the induction of an adverse oxygen supply-demand situation in a portion of a myocardium.

Angina pectoris Forms:

1. Classical/Stable angina.

• The attack is provoked by exercise, emotion, and eating.
• In it, blood flow fails to increase during increased demand despite dilatation of resistance vessels and pain occurs.

2. Variant angina.

• Attacks occur at rest or during sleep.
• Occurs due to recurrent localized coronary vaso-spasm in the presence of atherosclerotic coronary artery disease.

Drugs Used In Angina Pectoris and Myocardial Infarction Viva Voce:

1. Nitroglycerine is used by the sublingual route

Cardiac Glycosides And Drugs For Cardiac Failure Important Notes

1. Digitalis

• Digitalis Used in the treatment of congestive cardiac failure
• Digitalis To control arrhythmias
• Digitalis increases
  • Force of contraction
  • Decreases heart rate
  • Raises oxygen consumption
  • Depresses conduction system
• Enhances potassium uptake and sodium excretion

Cardiac Glycosides And Drugs For Cardiac Failure Short Essays

Question 1. Therapeutic uses and adverse effects of digoxin.

Answer:

Digoxin is cardio glycoside obtained from seeds of strophanthus gratus.

Digoxin Uses:

1. Congestive cardiac failure (CCF)

• Digoxin induces an increase in contractility which increases ventricular ejection

2. Cardiac arrhythmias.

• Digoxin is used for controlling atrial fibrillation associated with CCF.
• A parenteral administration may terminate arrhythmia by increasing vagal tone.

3. Used for initiation and maintenance.

• Used in patients with severe left ventricular systolic dysfunction after initiation of ACE inhibitor and diuretic therapy.

Digoxin Adverse effects:

1. Cardiac effects.

• Arrhythmias like extrasystoles, bradycardia, pulse bigeminy, and terminal ventricular fibrillation AV block.

2. GIT effects:

• Nausea, vomiting, anorexia, abdominal pain.

3. CNS effects.

• Headache, confusion, irritation, hallucinations, blurred vision, gynaecomastia, psychosis, disorientation, CTZ stimulation.

4. Other.

• Mesenteric vasoconstriction, weakness, skin rashes hyperpnoea.

Read And Learn More: Pharmacology Question and Answers

Question 2. Side effects of digoxin and treatment.

Answer:

Digoxin Adverse Effects:

• GIT effects
  • Nausea, vomiting, anorexia, abdominal pain
• CNS effects
  • Headache, confusion, irritation, hallucination, blurred vision, Gynaecomastia, psychosis, disorientation, CTZ stimulation
• Mesenteric contraction
• Skin rashes
• Hyperapnoea
• Cardiac effects
• Arrhythmias like extrasystoles, bradycardia, pulse bigeminy, terminally ventricular fibrillation AV block

Digoxin Treatment:

• Stop administration of digoxin
• Oral or parenteral administration of potassium supplements is given
• Ventricular arrhythmias are treated with lidocaine
• Atrial arrhythmias are treated by propranolol
• Severe bradycardia/ AV block is treated with atropine

Cardiac Glycosides And Drugs For Cardiac Failure Short Answers

Question 1. Digitoxin.

Answer:

Digitoxin is obtained from leaves of digitalis purpurea.

Pharmacokinetics:

• Given orally.
• 90 – 100% is observed
• The onset of action – 30 – 120 min.
• Plasma half-life – 5 – 7 days.

Digitoxin Uses:

• Cardiac arrhythmia.
• Congestive cardiac failure.

Question 2. The rationale of using digoxin in atrial fibrillation.

Answer:

Digoxin decreases the number of impulses passing down the AV node and bundle of his.

• Results in ventricular rate
• Increases effective refractory period of AV node by direct vagomimetic and antiadrenergic action.
• Thus, digoxin is used in atrial fibrillation.

Question 3. Cardiac toxicity of digoxin.

Answer:

Digoxin has a low safety threshold and a high incidence of adverse effects.

• It produces cardiac toxicity characterized by arrhythmias, like extrasystoles, bradycardia, pulse bigeminy, and AV blocks.
• It enhances hypokalemia.

Cardiac Toxicity of Digoxin Treatment:

• Stop administration of digoxin.
• Oral or parenteral administration of potassium supplements is given.
• Ventricular arrhythmia – treated by lidocaine.
• Atrial arrhythmias – treated with propranolol.
• Severe bradycardia/A-V block – treated with atropine.

Cardiac Glycosides And Drugs For Cardiac Failure Viva Voce

• Digitoxin is a cardiac glycoside
• It is used in congestive cardiac failure
• Calcium augments the ionotropic effect of digitalis

Insulin And Oral Hypoglycaemics Important Notes

1. Insulin And Oral Hypoglycaemics Classification of Insulins

• Conventional
  • Short-acting – regular insulin, prompt insulin zinc suspension
  • Intermediate-acting – insulin zinc suspension, neutral protamine (Isophane)
  • Long-acting – extended insulin zinc suspension, protamine zinc suspension
• A highly purified insulin preparation
  • Single peak insulin
  • Monocomponent insulin

2. Insulin And Oral Hypoglycaemics Oral hypoglycaemic drugs

• Sulphonylureas
  • First generation – tolbutamide, chlorpropamide
  • Second generation – glibenclamide, glopizide
• Biguanides
  • Metformin, phenformin
• Meglitinides
  • Repaglinide
• Alpha glycosidase inhibitor – acarbose

3. Insulin And Oral Hypoglycaemics Sulphonylureas

• Stimulators of beta cells
• Reduces blood glucose in normal subjects and type 2 diabetes
• Mode of action
  • Brings the release of insulin by activating receptors on beta cells of the pancreas
  • Reduces glucagon secretion
  • Increases insulin receptors on target cells
  • Inhibits gluconeogenesis in the liver

4. Insulin And Oral Hypoglycaemics Metformin

• It is a biguanide, an oral hypoglycaemic drug
• Contraindications
  • Hypotension
  • CVS diseases
  • Respiratory diseases
  • Hepatic and renal diseases
  • Alcoholics
• Action
  • Suppresses hepatic gluconeogenesis and glucose output from the liver
  • Interferes with mitochondrial respiratory chain
• Not metabolized at all
• Excreted unchanged in the urine

5. Insulin And Oral Hypoglycaemics Chlorpropamide

• Long-acting hypoglycaemic
• Reduces urine volume in diabetes insipidus
• Sensitizes kidney to ADH action

Read And Learn More: Pharmacology Question and Answers

Insulin And Oral Hypoglycaemics Long Essays

Question 1. Classify antidiabetic drugs and write about oral antidiabetic drugs.
Answer:

Anti-diabetic drugs:

• These drugs used lower blood glucose levels.

Anti-diabetic drugs Classification:

1. Insulin.

• Ultra short-acting or rapid-acting.
  • Insulin lispro, insulin aspart, insulin glulisine.
• Short-acting.
  • Regular insulin.
• Intermediate acting.
  • Insulin zinc suspension, neutral protamine hagedorn.
• Long-acting.
  • Protamine zinc insulin, insulin glargine.

2. Oral hypoglycaemics.

• Sulfonylureas.
  • First generation – tolbutamide, chlorpropamide.
  • Second generation – Glibenclamide, Glipizide.
• Biguanide – metformin.
• Meglitinide or phenylalanine analogues.
  • Repaglinide, Nateglinide.
• Thiazolidin editions.
  • Rosiglitazone, pioglitazone.
• Alpha-glucosidase inhibitors.
  • Acarbose, miglitol.
• Dipeptidyl peptidase – 4 inhibitor.
  • Sitagliptin, vildagliptin.

1. Anti-diabetic drugs Sulfonylureas:

• They were the first oral hypoglycaemic drugs.

Sulfonylureas Mechanism of action:

Sulfonylureas Uses:

• Used in patients with type II diabetes mellitus

Sulfonylureas Adverse effects:

• Hypoglycaemia.
• Nausea, vomiting, diarrhoea, headache, weight gain, paraesthesia, weight gain.
• Hypersensitivity reactions.

2. Anti-diabetic drugs Biguanides:

Biguanides Actions:

• Inhibit hepatic gluconeogenesis.
• Enhances insulin-mediated glucose disposal in muscle and fat
• Retards intestinal absorption of glucose.
• Promotes peripheral utilization of glucose

BiguanidesUse:

• Used in obese patients with type II diabetes mellitus.

3. Anti-diabetic drugs Meglitinide Analogues:

Meglitinide Analogues Mechanism:

Meglitinide Analogues Uses:

• Used in type 2 DM either alone or with metformin.

4. Anti-diabetic drugs Thiazolidinediones:

• They are selective agonists for the receptor nuclear peroxisome proliferator-activated receptor gamma.

Thiazolidinediones Uses:

• Type; 2 diabetes mellitus.
• Used to supplement sulfonylureas or metformin and in case of insulin resistance.

5. Anti-diabetic drugs Alpha-glucosidase inhibitors:

• Acarbose is one of the alpha-glucosidase inhibitors.
• It slows down digestion and absorption of polysaccharides and glucose.
• As an adjuvant to diet in obese diabetics.

Question 2. Describe the different preparations of insulin. Add a note on their merits and demerits.
Answer:

Insulin preparations:

• Insulin preparations differ in their source and duration of action.

1. Insulin preparations Conventional insulins:

• Rapid-acting.
  • Insulin lispro, insulin aspart, insulin glulisine.
• Short during.
  • Regular insulin.
• Intermediate acting.
  • Insulin zinc preparation, neutral protamins hatedom.
• Long-acting.
  • Protamine zinc insulin.

Conventional insulins Advantages/Mertis:

• Rapid onset
• Longer duration of action.

Conventional insulins Disadvantages/Demerits:

• Allergic.
• Not very stable
• Degraded in GIT, so not given orally.
• Antigenic.

2. Insulin preparations Highly purified insulins:

• Single peak insulin – regular, lente.
• Monocomponent insulin – regular, lente.

Highly purified insulins Advantages:

• Purified, thus contamination is negligible.
• Less antigenic.
• More stable.
• Lesser chances of resistance.
• Lesser chances of lipodystrophy.

Highly purified insulins Disadvantages:

• Expensive.

3. Insulin preparations Human insulin:

• Produced by recombinant DNA technology
• They are regular, lente, and isophane.

Human insulin Advantages:

• Less antigenic.
• So less allergic reactions.
• Less injection site lipodystrophy.

Human insulin Disadvantages:

• Expensive

4. Insulin preparations Insulin analogues:

• Synthesized by genetic engineering.
• They include insulin lispro, insulin aspart, insulin glargine, insulin glulisine, and insulin detemir.

Insulin analogues Advantages:

• Rapid absorption.
• Can be given 10 minutes before food.
• Less hypoglycaemia.
• Favourable pharmacokinetics.
• Better blood glucose control.
• Greater stability

Insulin analogues Disadvantages:

• Expensive preparation.

Question 3. Discuss Insulin pharmacological actions and adverse effects.
Answer:

Insulin Pharmacological Actions:

1. Carbohydrate metabolism.

• Insulin decreases blood glucose levels by
  • Increasing glucose uptake and glycogen synthesis.
  • Inhibits glycogenolysis and glucose output
  • Inhibits gluconeogenesis.
  • Facilitates glucose transport across the cell membrane
  • Alters activity of enzymes involved in metabolism.

2. Protein metabolism.

• Facilitates protein synthesis.
• Inhibits protein breakdown.
• Thus, has an anabolic effect

3. Lipid metabolism.

• Promotes synthesis of triglycerides.
• Inhibits lipolysis.

4. Insulin increases potassium entry into cells and decreases urea output from the liver.

Insulin Adverse effects:

1. Hypoglycaemia.

• Most common side effect.
• Occurs due to large doses, improper time of administration, missing a meal, and vigorous exercise.
• Prolonged hypoglycaemia may cause permanent brain damage.

2. Local reactions.

• Swelling, erythema and stinging at the site of injection.
• Localized lipodystrophy.

3. Allergy.

• Occurs due to contaminating proteins.
• Utricaria, angioedema and anaphylaxis occur.

4. Insulin resistance.

• Develops when insulin requirement is increased.

Question 4. Write the mechanism of action and therapeutic uses of insulin.
Answer:

Insulin:

Insulin is a hormone that is synthesized in the beta cells of pancreatic islets.

Insulin Mechanism of action:

Insulin Uses:

• In juvenile diabetes.
• When diabetes is not controlled by diet or exercise.
• Underweight patients.
• Failure of oral hypoglycaemic drugs.
• The stress of surgery, infections, trauma, pregnancy and labour.
• Complications of diabetes – diabetic coma, ketoacidosis, gangrene of extremities.

Question 5. Write the mechanism of action, uses and adverse effects of sulfonylureas.
Answer:

Sulfonylureas:

• They were the first oral hypoglycaemic drug to be introduced.

Sulfonylureas Mechanism of action:

Sulfonylureas Uses:

• Maturity onset diabetes
• Insulin resistant diabetes
• Diabetes insipidus.

Sulfonylureas Adverse effects:

• Hypoglycaemia.
• Nausea, vomiting, diarrhoea, constipation.
• Headache, paresthesia.
• Weight gain.
• Hypersensitivity – rashes, photosensitivity, purpura.
• Agranulocytosis, transient leukopenia.

Question 6. Mention the hormones secreted by the pancreas. What is diabetic coma? What are the principles of treatment?
Answer:

Hormones secreted by the pancreas are:

1. Hormones secreted by the pancreas Insulin.

• It is a hypoglycaemic hormone.
• Synthesized by p cells of pancreatic islets.
• It is two chain polypeptide having 51 amino acids.
• It facilitates glucose transport and inhibits glycol- analysis, and gluconeogenesis.
• Thus lowering blood glucose levels.

2. Hormones secreted by the pancreas Glucagon.

• It is a hyperglycaemic hormone.
• Secreted by cells of pancreatic islets.
• It enhances glycogenolysis and gluconeogenesis.
• Thus increasing blood glucose levels.

Glucagon Diabetic coma:

• Severe hyperglycaemia and glycosuria result in severe dehydration and increased plasma osmolarity leading to coma.
• Seen in insulin-dependent diabetes mellitus.

Glucagon Symptoms:

• Hyperglycaemia.
• Acidosis
• Hyperventilation
• Dehydration
• Hypotension
• Shock
• Impaired consciousness.

Glucagon Management:

1. Correction of hyperglycaemia.

• Intravenous regular insulin 0.1 U/kG bolus followed by 0.1 U/kg/hour by continuous IV infusion till patient recovers.

2. Correction of dehydration.

• IV fluids – normal saline IV1 litre/hour.

3. Correction of acidosis,

• Use of sodium bicarbonate.

4. Correction of hypokalemia.

• By IV KC1 infusion.

5. Supportive treatment – done by use of antibiotics.

Insulin And Oral Hypoglycaemics Short Essays

Question 1. Sulfonylurea.
Answer:

Sulfonylurea was the first oral hypoglycaemic drug to be introduced.

Sulfonylurea Classification:

1. First generation – Tolbutamide, chlorpropamide

2. Second generation – Glibenclamide, glipizide, Gli- clazide, Glimepride.

Question 2. Oral antidiabetic drugs.
Answer:

Oral antidiabetic drugs are drugs that lower blood glucose levels and are effective orally.

Oral antidiabetic drugs Classification:

1. Sulfonylureas.

• First generation – Tolbutamide, chlorpropamide.
• Second generation – Glibenclamide, glipizide.

2. Biguanide – metformin.

3. Meglitinide, phenylalanine analgues.

• Repaglinide, nateglinide.

4. Thiazolidinediones.

• Rosiglitazone, pioglitazone.

5. Alpha-glucosidase inhibitors.

• Acarbose, miglitol.

6. Dipeptidyl peptidase – 4 inhibitor.

• Sitaglipitin, vildagliptin.

Oral antidiabetic drugs uses:

Question 3. Insulin and sulphonylureas.
Answer:

Question 4. Advantages of newer insulin.
Answer:

Newer insulins are derived from the human pancreas.

• Hence, the risk of antigen-antibody reactions is avoided.
• They are highly purified preparations.
• Can be used in insulin resistance diabetes
• Can be used during pregnancy without teratogenicity.
• Can be used in case of injection site lipodystrophy caused by conventional preparation.

Question 5. Give reasons – glibenclamide is not useful in treating childhood diabetes mellitus.
Answer:

Glibenclamide is a second-generation sulphonylurea.

• Sulphonylurea causes the release of insulin from the pancreas.
• They act on receptors present on the pancreatic beta cell membrane.
• Causes depolarization by reducing the conductance of ATP-sensitive K+ channels.
• This enhances Ca²⁺ influx degeneration and insulin resistance.
• They cannot cause hypoglycaemia in pancreatic-atomized animals or in type I diabetes mellitus.
• Since type I diabetes occurs in children glibenclamide cannot be used to treat it.

Question 6. Compare and contrast conventional insulin with newer insulin.
Answer:

Question 7. Compare and contrast sulphonylurea and biguanides
Answer:

Question 8. Biguanides.
Answer:

• It is an oral hypoglycaemic drug
• It is not metabolized at all
• Excreted unchanged in the urine

Biguanides Actions:

• Inhibits hepatic gluconeogenesis
• Enhances insulin-mediated glucose disposal in muscle and fat
• Retards intestinal absorption of glucose
• Promotes peripheral utilization of glucose

Biguanides Use:

• Used in obese patients with type II diabetes

Biguanides Contra-Indications:

• Hypotension
• CVS diseases
• Respiratory diseases
• Hepatic and renal diseases
• Alcoholics

Insulin And Oral Hypoglycaemics Short Question And Answers

Question 1. Advantages of newer insulins.
Answer:

Derived from the human pancreas.

• So, lesser risks of antigen-antibody reactions.
• They are highly purified.
• Can be used in insulin resistance diabetes
• Can be used during pregnancy.
• Can be used in case of injection site lipodystrophy.

Question 2. Sulphonylurea.
Answer:

Sulphonylurea was the first oral hypoglycaemic drug introduced.

Sulphonylurea Classification:

1. First generation – tolbutamide and chlorpropamide.

2. Second generation – Glibenclamide, glipizide.

Sulphonylurea Uses:

• Maturity onset diabetes.
• Insulin resistant diabetes
• Diabetes insipidus.

Question 3. Tolbutamide.
Answer:

Tolbutamide is an oral hypoglycaemic drug.

• It is first generation sulphonylurea.

Tolbutamide Features:

• Weaker
• Short-acting.
• Flexible dosage.
• Safer for those prone to hypoglycaemia.
• Daily dose – 0.4 – 3 g.
• Half-life – 6 – 8 hours.
• Duration of action – 6 – 8 hours.

Tolbutamide Use:

• Type II diabetes mellitus.

Question 4. Glibenclamide.
Answer:

Glibenclamide is an oral hypoglycaemic drug.

• It is second generation sulphonylurea.

Glibenclamide Features:

• Potent
• Slow acting.
• Marked insulinemic action.
• Effective in a single dose.
• Higher incidence of hypoglycaemia.
• Plasma t ½ – 4 – 6 hours.
• Duration of action – 18 – 24 hours.
• Daily dose 5-15 mg.

Glibenclamide Use:

Type II diabetes mellitus.

Question 5. Insulin preparations.
Answer:

Based on onset and duration of action, insulin preparations are:

1. Rapid acting.

• Insulin lispro, insulin aspart, insulin glulisine.

2. Short-acting – regular insulin.

3. Intermediate-acting – insulin zinc suspension iso-phane insulin.

4. Long-acting – protamine zinc insulin, insulin glargine.

Question 6. Uses of insulin.
Answer:

Uses are diabetes is not controlled by diet and exercise.

• Primary or secondary failure of oral hypoglycaemic drugs.
• In underweight patients.
• Temporary to overcome infections, trauma, and surgery.
• In complications of diabetes like ketoacidosis, gangrene of extremities.

Question 7. Drug treatment of juvenile diabetes.
Answer:

Juvenile diabetes is insulin-dependent diabetes mellitus.

• It is immune-mediated.

juvenile diabetes Treatment:

• Insulin therapy along with diet
• Started with regular insulin parenterally before each major meal.
• Condition is assessed by regular testing of urine or
• blood glucose level.

Question 8. Adverse effects of insulin.
Answer:

• Hypoglycaemia.
• Local reactions – swelling, erythema and stinging.
• Localized lipodystrophy.
• Allergy – urticaria, angioedema and anaphylaxis.

Question 9. Oral hypoglycaemic drugs.
Answer:

1. Sulphonylurea.

• First generation – Tolbutamide, chlorpropamide.
• Second generation – Glibenclamide, glipizide.

2. Biguanide – metformin.

3. Meglitinide analogues – repaglinide, nateglinide.

4. Thiazolidinediones – rosiglitazone, pioglitazone.

5. Alpha glucosidase inhibitors.

• Acarbose, miglitol.

6. Dipeptidyl peptidase – 4 inhibitor.

• Sitagliptin, vildagliptin.

Question 10. Protamine zinc insulin.
Answer:

It is a long-acting oral hypoglycaemic drug.

• The onset of action – 4 – 6 hours.
• Duration of action – 24 – 36 hours.
• It can be mixed with regular insulin.
• Produces relatively low, smooth and peakless blood Insulin levels.
• Once daily administration produces constant Insulin action.

Question 11. Glimepiride.
Answer:

• It is second generation sulphonylurea
• Has stronger extrapancreatic action
• Has less hyperinsulinaemia
• Daily dose – 1-6 mg
• Plasma half-life – 5-7 hours
• The duration of action is 24 hours

Thyroid Hormones And Anti Thyroid Drugs Important Notes

1. Thyroid Hormones And Anti Thyroid Drugs Thyroid storm

• It means thyrotoxicosis
• Treatment is to reduce the production and conversion of thyroid hormones
• Drugs used for it are
  • Inhibiting thyroid hormone synthesis.
    • Propylthiouracil
    • Methimazole
    • Carbimazole
  • Inhibiting hormone release
    • Iodine
    • Iodide
  • Destroying thyroid tissue
    • Radioactive iodine
  • To counteract adrenal insufficiency
    • Corticosteroids
  • To control sympathetic symptoms
    • Propanolol

2. Thyroid Hormones And Anti-thyroid drugs

• Propylthiouracil, carbimazole, and radioactive iodine are anti-thyroid drugs
• Used in the treatment of
  • Hyperthyroidism
  • Preparation of patients for thyroid surgery

Thyroid Hormones And Anti Thyroid Drugs Long Essays

Question 1. Enumerate antithyroid drugs. Explain the action of the thioamides giving the indications, advantages, and adverse effects of each.
Answer:

Antithyroid drugs:

• These drugs inhibit hormone synthesis.
• They are thioureylenes or thionamides which includes.
  • Propylthiouracil.
  • Methimazole.
  • Carbimazole.

Antithyroid drugs Actions:

Antithyroid drugs Indications/uses:

1. Graves disease or diffuse toxic goiter.

• Needs long-term treatment with antithyroid drugs.

2. Toxic nodular goiter.

• Used when surgery is not indicated like in elderly patients.

3. Preoperatively in hyperthyroid patients.

• Used along with radioactive iodine to hasten recovery in thyrotoxicosis.

4. Rarely used in hyperthyroidism in pregnancy.

5. Thyroid storm or thyrotoxic crisis.

• It is a sudden, severe, exacerbation of thyrotoxicosis.
• Propylthiouracil is used IV.

Read And Learn More: Pharmacology Question and Answers

Antithyroid drugs Advantages:

• No surgery is required.
• No injury to parathyroid or recurrent laryngeal nerve.
• Hypothyroidism, if occurs, is reversible.
• Can be used in children and young adults also.

Antithyroid drugs Disadvantages:

• Long-term treatment is required.
• Poor patient compliance.
• Drug toxicity.

Antithyroid drugs Adverse effects:

• Allergic reactions – skin rashes.
• Jaundice
• Headache.
• Hypothyroidism.
• Agranulocytosis.
• GIT disturbances.
• Joint pain.
• Nephritis, hepatitis
• Loss of hair, loss of taste.

Thyroid Hormones And Anti Thyroid Drugs Short Essays

Question 1. Radioactive iodine.
Answer:

Radioactive iodine is a thyroid tissue-destroying agent

• When given orally, it is rapidly absorbed and is concentrated by the thyroid in the follicles.
• It emits X-rays as well as β particles.
• It is used as a sodium salt of ³¹I dissolved in water.

Radioactive iodine Uses:

1. Small doses – 25 -100 m curie.

• Used for diagnosis in thyroid function tests.

2. Large doses – 3 – 6 cm curie.

• Used for treatment of hyperthyroidism.
• β particles emitted destroy thyroid cells.
• Thus, it is used in carcinoma of the thyroid.

Radioactive iodine Advantages:

• Simple and convenient
• Inexpensive.
• No surgical risks.
• Hyperthyroidism is permanently cured.

Radioactive iodine Disadvantages:

• Slow-acting.
• The long latent period of response.
• Hypothyroidism develops.
• Not suitable for pregnant women, children, and young adults.

Thyroid Hormones And Anti Thyroid Drugs Short Question And Answers

Question 1. Lugol’s iodine.
Answer:

Lugol’s iodine is a solution of 5% iodine in 10% potassium iodide solution.

• A daily dose of 5 -15 drops can be used.

Lugol’s iodine Uses:

• As expectorant
• In preoperative preparation for thyroidectomy.
• Thyroid storm.
• Prophylactic in endemic goiter.
• As antiseptic.

Question 2. Iodine.
Answer:

Iodine inhibits the release of thyroid hormone

• In thyrotoxic patients, symptoms subside in 1 – 2 days.
• The gland becomes firm and shrinks in size in 10 -14 days.
• Effects decrease after 15 days.

Iodine Uses:

• Preoperatively in thyroidectomy.
• In thyroid storm.
• Prophylactically in endemic goiter.
• As antiseptic
• As expectorant.

Iodine Adverse effects:

• Allergic reactions – skin rashes, conjunctivitis.
• Swelling of lips and salivary glands.
• Fever
• Lymphadenopathy.

Question 3. Carbimazole.
Answer:

Carbimazole is a thioamide.

• Act as thyroid hormone synthesis inhibitor.
• It is more potent and long-acting.
• It crosses the placental barrier.

Carbimazole Uses:

• long-term therapy of thyrotoxicosis.
• To hasten recovery in thyrotoxicosis.
• Used in thyrotoxic crisis.

Carbimazole Adverse effects:

• Allergic reactions
• Hypothyroidism.
• GI intolerance
• Hepatitis, nephritis.
• Joints pain.
• Agranulocytosis.

Question 4. Alendronate.
Answer:

• It is second generation bisphosphonate
• Mainly used in osteoporosis
• Advice to be given on an empty stomach in the morning with plenty of water
• Avoid lying or having food for at least 30 minutes to avoid oesophagitis
• Calcium and iron preparation and NSAIDs should not give along with it

Non Steroidal Anti Inflammatory Drugs Important Notes

1. Non-Steroidal Anti-Inflammatory Drugs Classification 

2. Non-Steroidal Anti-Inflammatory Drugs Aspirin

• Non-Steroidal Anti-Inflammatory Drugs Aspirin Actions
  • Inhibits prostaglandin synthesis with resultant analgesic and antipyretic action
  • Reduces fever by promoting heat loss
  • At high doses, it has anti-inflammatory action
  • Stimulates respiration
  • Causes dyspepsia, peptic ulceration with GIT hemorrhage
• Non-Steroidal Anti-Inflammatory Drugs Aspirin Adverse effects
  • Mucosal damage and peptic ulceration
  • Induces asthma by inhibition of prostaglandin synthesis
  • Prevent platelet aggregation
  • In children causes Reye’s syndrome
  • Prolonged intake causes salicylism characterized by
    • Tinnitus
    • Vertigo
    • Drowsiness
    • Impairment of vision and hearing
• Non-Steroidal Anti-Inflammatory Drugs Aspirin Contraindications
  • Diabetics
  • Heart failure patients
  • Peptic ulcers
  • Pregnant
  • Patients receiving oral anticoagulants
  • Should be stooped 1 week before elective surgery
• Non-Steroidal Anti-Inflammatory Drugs Aspirin Uses:
  • As analgesic, antipyretic, and anti-inflammatory
  • The first drug of choice in acute rheumatic fever and rheumatoid arthritis
  • In post-myocardial infarction and post-stroke patients
  • For local application as keratolytic, fungistatic, and antiseptic

Read And Learn More: Pharmacology Question and Answers

3. Non-Steroidal Anti-Inflammatory Drugs Paracetamol

• Exerts analgesic, antipyretic action
• Has negligible anti-inflammatory action
• Has a high therapeutic index
• Acute Paracetamol poisoning causes
  • Skin reactions
  • Liver tenderness
  • Hepatotoxicity
  • Centrilobular hepatic necrosis, renal tubular necrosis, and hypoglycemia
  • Haemolysis
  • Methemoglobinemia

4. Non-Steroidal Anti-Inflammatory Drugs Phenylbutazone

• Causes
  • Bone marrow depression
  • Agranulocytosis
  • Sodium and water retention
  • Precipitates congestive cardiac failure

5. Non-Steroidal Anti-Inflammatory Drugs Diclofenac

• Analgesic, antipyretic, and anti-inflammatory drug
• Accumulates in synovial fluid
• Has a longer duration of action
• Uses:
  • Rheumatoid arthritis
  • Osteoarthritis
  • Renal colic

6. Non-Steroidal Anti-Inflammatory Drugs Mefenamic acid

• Has weaker analgesic action
• Useful in
  • Chronic and dull aching pain
  • Dysmenorrhea

7. Non-Steroidal Anti-Inflammatory Drugs Ibuprofen

• Has the analgesic and mild anti-inflammatory effect
• Produces less gastric irritation
• Inhibits platelet aggregation
• Prolongs bleeding time
• Contraindicated in
  • Pregnant
  • Peptic ulcer patients

8. Non-Steroidal Anti-Inflammatory Drugs Uses of selective COX-2 inhibitors

• Osteoarthritis
• Rheumatoid arthritis
• Dental and post-operative pain

Non Steroidal Anti Inflammatory Drugs Long Essays

Question 1. Classify nonsteroidal anti-inflammatory drugs. Explain the mechanism of action and uses of ibuprofen.
Answer:

Non-steroidal Anti-inflammatory drugs:

• These are non-opioid analgesics.
• They have anti-inflammatory, antipyretic, and uricosuric properties.

Non-steroidal Anti-inflammatory drugs Classification:

1. Non-selective COX inhibitors.

• Salicylates – aspirin.
• Propionic acid derivatives.
  • Ibuprofen, naproxen, ketoprofen.
• Anthranilic acid derivative – mefenamic acid.
• Aryl-acetic acid derivatives – diclofenac, ace- clofenac.
• Oxicam derivatives – perioxicam, tenoxicam.
• Pyrrolo – pyrrole derivative – ketorolac.
• Indole derivative – indomethacin.
• Pyrazolone derivatives – phenylbutazone.

2. Preferential COX-2 inhibitors.

• Nimesulide, meloxicam, nabumetone.

3. Selctive COX-2 inhibotors.

• Celecoxib, etoricoxib, parecoxib.

4. Analgesic – antipyretics with poor anti-inflammatory action.

• Para-aminophenol derivative – paracetamol.
• Pyrazolone derivative – metamizol.
• Benzoxazocine derivative – nefopam.

Ibuprofen:

• Ibuprofen is propionic acid derivative.

Ibuprofen Mechanism of action:

Inflammation
↓
Liberation of arachidonic acid from phospholipids
↓
Cyclo-oxygenase enzyme
↓
Prostaglandin.
↓
Ibuprofen inhibits cyclo-oxygenase enzyme.
↓
Inhibits prostaglandin synthesis.

Ibuprofen Uses:

• As analgesic – in a painful condition.
• As antipyretic – in fever.
• Used when pain is more prominent than inflammation in rheumatoid arthritis, osteoarthritis, and musculoskeletal disorders.
• Soft tissue injuries, fractures.
• Following tooth extraction.
• To relieve postoperative pain.
• Dysmenorrhea.
• Osteoarthritis.
• Gout
• Surgical removal of impacted teeth. It is combined with muscle relaxant

Question 2. Mention therapeutic uses and adverse effects of aspirin.
(or)
Describe pharmacological actions and therapeutic uses of salicylates.
Answer:

Salicylates/Aspirin:

• Aspirin is acetylsalicylic acid.

Salicylates Actions:

1. Analgesia.

• Aspirin inhibits prostaglandin synthesis and acts as an analgesic.
• It is a weak analgesic.

2. Antipyretic.

• Reduces fever by promoting heat loss.
• It resets the thermostat at a normal level.

3. Anti-inflammatory reaction.

• Aspirin act as an anti-inflammatory at high doses.
• It interferes with the formation of chemical mediators in the kallikrein system.

4. Respiratory.

• Increases consumption of oxygen increases CO₂ production.
• This stimulates the respiratory center.
• As a result, the rate, and depth of respiration increase.

5. Acid-base and electrolyte balance.

• At anti-inflammatory doses, salicylates increase CO₂ production.
• This results in respiratory alkalosis and pH becomes alkaline.

6. CVS action.

• High doses increase cardiac output

7. GIT action.

• Aspirin is a gastric irritant.
• It causes epigastric distress, nausea, and vomiting.
• At high doses, it stimulates CTZ.

8. Metabolism.

• Aspirin enhances cellular metabolism.

9. Blood.

• It inhibits thromboxane A₂ synthesis by platelets.
• Interferes with platelet aggregation.

Salicylates Uses:

1. As analgesic.

• For headache, toothache, backache, joint pain, myalgia, neuralgia, and dysmenorrhoea.

2. As antipyretic.

• Effective in any type of fever.

3. Acute rheumatic fever.

• Aspirin 4 – 6 g/day in 4 – 6 divided doses is given.
• It results in dramatic relief of signs and symptoms in 24 – 48 hours.

4. Rheumatoid arthritis.

• Dose – 3 – 5 g/day.
• Relieves pain, and reduces swelling and redness of joints.

5. Osteoarthritis.

• Provide symptomatic relief.

6. Postmyocardial infarction.

• Aspirin inhibits platelet aggregation and lowers the incidence of reinfarction.

7. Rarely used for.

• Pregnancy-induced hypertension.
• Patent ductus arteriosus in the newborn.
• Familial colonic polyposis.
• Prevention of colon cancer.
• Prevent flushing attending nicotinic acid ingestion.

Salicylates Adverse effects:

• GIT effects – nausea, vomiting, epigastric distress increased occult blood loss in stools.
• Hypersensitivity reactions – rashes, urticaria, rhino-rhea, angioedema, anaphylactoid reaction.
• CNS – headache, dizziness, confusion
• Respiratory system – precipitates asthma.
• Hemolysis – In GPD deficiency patients.
• Hepatotoxicity.
• Nephrotoxicity.
• Reye’s syndrome – a form of hepatic encephalopathy.
• Pregnancy – delays onset of labor.

Salicylates Acute Salicylate Poisoning:

• More common in children.
• Fatal dose -15 – 30 g in adults.
• Symptoms are:
  • Vomiting, dehydration, electrolyte imbalance, hyperpyrexia, GI irritation, restlessness, delirium, hallucinations, convulsions, tremors, and death.
• Treatment – symptomatic:
  • Gastric lavage.
  • Correction of acid-base balance and dehydration by IV fluids.
  • Control of temperature by external cooling.
  • Blood transfusion and vit K. Administration.
  • Use of Vv fluids with Na⁺, K⁺, HCo₃^–, and glucose.

Question 3. Describe pharmacological actions, uses, and adverse effects of propionic acid derivatives.
Answer:

Proprionic Acid Derivatives:

• Proprionic acid derivatives – ibuprofen, naproxen, ke- toprofen, flurbiprofen.
• Proprionic Acid Derivatives Actions:
  • Analgesia.
  • Anti-pyretic.
  • Anti-inflammatory.
• Proprionic Acid Derivatives Uses:
  • As analgesic in painful conditions.
  • Fever.
  • Soft tissue injuries, fractures.
  • Following tooth extraction.
  • Gout
  • Used when pain is more prominent than inflammation in rheumatoid arthritis, osteoarthritis, and musculoskeletal disorders.
  • To relieve postoperative pain.
  • Dysmenorrhoea.
  • Surgical removal of impacted teeth – combined with a muscle relaxant.

Proprionic Acid Derivatives Adverse effects:

• GIT effects – Nausea, vomiting, gastric discomfort
• CNS effects – headache, dizziness, blurring of vision, tinnitus, depression.
• Hypersensitivity reactions – rashes, itching.
• Fluid retention.

Question 4. Compare morphine and aspirin. Write contraindications of morphine.
Answer:

Morphine and aspirin:

Contra-indication of morphine:

• In extremes of age.
• In patients with respiratory insufficiency.
• In bronchial asthma.
• Elderly males.
• Head injury.
• Hypovolemic shock.
• Undiagnosed acute abdominal pain.
• Unstable personalities.
• Hypothyroidism, renal and liver diseases?

Question 5. Mention two contraindications to morphine.
Answer:

Contraindications of aspirin:

1. Aspirin is contraindicated in patients who are sensitive to aspirin.

2. In peptic ulcers – because.

• It irritates gastric mucosa.
• Stimulates CTZ.
• Inhibits PG synthesis, delays, healing reduces platelet aggregations.
• Decreases gastric acid secretion
• Promotes bleeding in ulcer

3. In children suffering from chickenpox or influenza.

• Develops Reye’s syndrome.

4. In chronic liver disease.

• Causes hepatic necrosis.

5. In bronchial asthma – precipitates attacks.

6. In diabetes.

• Aspirin causes hyperglycemia due to central sympathetic stimulation.

7. Pregnancy

• Delays onset of labor
• Leads to premature closure of ductus arteriosus.
• Increase postpartum bleeding.

8. In Lactating mothers.

9. In G₆PD deficiency patients.

• Leads to hemolysis.

Question 6. Define analgesics. List four non-steroidal antiinflammatory drugs belonging to four different chemical groups. Mention therapeutic uses of aspirin. Explain the pharmacological basis of anyone.
Answer:

• Analgesic:
  • Analgesic is a drug that selectively relieves pain by acting in the CNS or on peripheral pain mechanisms without significantly altering consciousness.

Non-steroidal anti-inflammatory drugs:

• Salicylates – aspirin.
• Proprionic acid derivatives – Ibuprofen.
• Anthranilic acid derivative – mefenamic acid.
• Aryl acetic acid derivative – diclofenac, aceclofenac.
• Oxicam derivative – piroxicam, tenoxicam,

Uses of Aspirin:

1. As analgesia.

Aspirin act on peripheral pain receptors.
↓
Prevent prostaglandin-mediated
sensitization of nerve endings.
↓
Inhibit prostaglandin synthesis.
↓
Causes analgesia.

2. As antipyretic.

Resets hypothalamic thermostat
↓
Promotes heat loss
↓
Reduces fever.

3. Anti-inflammatory.

Inhibits prostaglandin synthesis
↓
Interferes with the formation of chemical mediators.
↓
Decreases adherence of granulocyte.
↓
Decreases migration of macrophages at the site of inflammation.

4. Acute rheumatic fever.

5. Rheumatoid arthritis.

6. Osteoarthritis.

7. Post myocardial infarction.

Non Steroidal Anti Inflammatory Drugs Short Essays

Question 1. Mention an antidote for paracetamol poisoning. How does it act?
Answer:

Paracetamol Poisoning:

• When a large dose of paracetamol is taken serious toxicity can occur.

Manifestations:

• Early manifestations – Nausea, vomiting, abdominal pain, liver tenderness.
• After 12 – 18 hours – Centrilobular hepatic necrosis, renal tubular necrosis, hypoglycemia, coma.
• After 2 days – jaundice.
• Later – Fulminating hepatic failure and death

Mechanism:

1. At normal doses.

Paracetamol.
↓
M etabolite N -acteyl-p-benzoquinoneimine.
↓
Gets detoxified by glutathione.

2. At high doses.

High doses of paracetamol
↓
Increases production of metabolite
↓
Glutathione is depleted
↓
Thus, metabolite covalently binds to
proteins in liver cells.
↓
Causes necrosis.

Antidote:

• N-acetylcysteine is infused by IV or given orally.
• It replenishes hepatic glutathione.
• Prevents binding of metabolite to another cellular constituent

Question 2. Compare paracetamol and aspirin.
Answer:

Question 3. Selective COX-2 inhibitors.
Answer:

Selective COX-2 inhibitors are coxibs-celecoxib, rofecoxib, parecoxib, etoricoxib and valdecoxib.

Selective COX-2 inhibitors Advantages:

• Less gastric irritation.
• Less occurrence of peptic ulcers.
• Do not depress thromboxane A₂ production by platelets.
• Do not inhibit platelet aggregation.

Selective COX-2 inhibitors Disadvantages:

• Increases risk of
• Cardiovascular events
• Cerebrovascular thrombotic events.
• Myocardial infarction.

Selective COX-2 inhibitors Indications:

• Patients who cannot tolerate NSAIDs
• Patients with a high risk of developing.
  • Peptic ulcers.

Selective COX-2 inhibitors Contraindications:

• It is avoided in patients with.
  • Ischaemic heart disease.
  • Hypertension
  • Cardiac failure.
  • Cerebrovascular disease.

Question 4. Write a brief account of drugs in dental pain.
Answer:

The selection of drugs depends on.

1. Nature of pain – acute or chronic.
2. Type of pain-mild, moderate, severe
3. Cause of pain.
4. Risk factors
5. Individual preference.
6. Presence or absence of inflammation.

Question 5. Explain why nimesulide is preferred over aspirin as an anti-inflammatory agent.
Answer:

Nimesulide:

• It exhibits relative COX-2 selectivity.
• It is completely absorbed orally.
• 99% plasma bounded.
• Exerts reduce the generation of superoxide by neutrophils.
• Acts as a free radical scavenger.
• Inhibits metalloproteinase activity in cartilage.
• Aspirin:
• Produces salicylism.
• In children – may cause liver damage.
• In adults – causes hepatic injury.
• Contraindicated in patients with.
  • Peptic ulcer
  • Children suffering from influenza
  • Chronic liver diseases.
  • Diabetes.
  • Lactating mothers.
• Thus, nimesulide is superior to aspirin.

Question 6. Aspirin.
Answer:

• It is acetyl-salicylic acid

Aspirin Actions:

• Analgesia – inhibits prostaglandin synthesis
• Antipyretic – promotes heat loss
• Anti-inflammatory – interferes with the formation of chemical mediators of the Kallikeren system
• Respiratory
  • Increases consumption of oxygen
  • Increases production of carbon dioxide
  • Stimulates respiratory center
  • Increases rate and depth of respiration
• Acid-base and electrolyte balance
  • Causes an increase in the production of carbon dioxide leading to respiratory alkalosis
• CVS action – increases cardiac output
• GIT action
  • Stimulates CTZ
  • Causes epigastric distress, nausea, vomiting
• Metabolism – enhances cellular metabolism
• Blood
  • Inhibits thromboxane A2 synthesis
  • Interferes with platelet aggregation

Aspirin Uses:

• As an analgesic for headaches, dental pain, back pain, and joint pain, myalgia
• As antipyretic
• Acute rheumatic fever – dose – 4-6 g/day in 4-6 divided dose
• Rheumatoid arthritis – dose – 3-5 g/day
• Osteoarthritis
• Postmyocardial infarction – inhibits platelet aggregation
• Rarely used in
  • Pregnancy induces hypertension
  • Patent ductusarteriosus in newborn
  • Familial colonic polyposis
  • Prevention of colon cancer

Aspirin Adverse Effects:

• GIT effects – nausea, vomiting, epigastric distress, increased occult blood loss in stool
• Hypersensitivity reactions – rashes, urticaria, rhinos-rhea, angioedema, anaphylactic reaction
• CNS – headache, dizziness, confusion
• Respiratory system – precipitates asthma
• Hemolysis
• Hepatotoxicity
• Nephrotoxicity
• Reye’s syndrome
• In pregnancy – delays the onset of labor

Non Steroidal Anti Inflammatory Drugs Short Question And Answers

Question 1. Paracetamol.
Answer:

Paracetamol is active metabolite of phenacetin.

Paracetamol Actions:

• Central analgesic action.
• Good antipyretic
• Weak anti-inflammatory.
• Active on cyclo-oxygenase in the brain.

Paracetamol Uses:

• As analgesic – toothache, headache, myalgia.
• As antipyretic – to reduce fever.
• In dentistry – in chronic pulpitis, periodontal abscess, post-extraction – used with ibuprofen.

Paracetamol Adverse effects:

• Nausea.
• Rashes
• Rarely leukopenia.

Question 2. A low dose of aspirin is administered prophylactically.
Answer:

• Aspirin in low doses irreversibly inhibits thromboxane A2 synthesis.
• It produces an antiplatelet effect
• Thus, it is used in the prophylactic treatment of various thromboembolism like myocardial infarction.
  • To reduce the incidence of recurrent infarction.
  • To decrease mortality in post-MI patients.

Question 3. Uses of aspirin.
Answer:

• As analgesic
• As antipyretic.
• Acute rheumatic fever
• Rheumatoid arthritis.
• Osteoarthritis.
• Postmyocardial infarction.
• Rarely in
  • Pregnancy-induced hypertension.
  • Patent ductus, arteriosus in newborns.
  • Familial colonic polyposis.
  • Prevention of colon cancer.
  • To prevent flushing attending nicotinic acid ingestion.

Question 4. Contraindications of aspirin.
Answer:

• In patients sensitive to aspirin.
• In peptic ulcers.
• In children suffering from chickenpox or influenza.
• In chronic liver disease
• In bronchial asthma.
• In diabetics
• Pregnancy.
• Lactating mothers.
• In G₆PD deficiency patients.

Question 5. Nimesulide.
Answer:

Nimesulide is a sulphonamide compound.

• It is a weak inhibitor of PG synthesis.

Nimesulide Actions:

• Inhibits leukocyte function.
• Prevents release of mediators.
• Has antihistaminic and antiallergic properties.
• Has analgesics, antipyretic and anti-inflammatory actions.

Nimesulide Uses:

• Used primarily for short-lasting painful inflammatory conditions like sports injuries, sinusitis, ENT disorders, dental surgery, bursitis, and dysmenorrhoea.

Adverse Effects:

• GIT effects – heart bum, nausea, loss of stools
• Skin effects – rashes, pruritis.
• Nephrotoxicity.
• Prolonged use causes hepatotoxicity.

Question 6. Phenylbutazone.
Answer:

Phenyl butanone is a pyrazolone derivative.

• It is good anti-inflammatory action.
• But poor analgesic and antipyretic action.

Phenylbutazone Uses:

• Rheumatoid arthritis.
• Ankylosing spondylitis.
• Osteoarthritis.
• Gout
• Musculoskeletal disorders.

Phenylbutazone Adverse Effects:

• GIT effects – dyspepsia, epigastric distress, nausea, vomiting.
• Precipitate CCF, edema.
• CNS effects – insomnia, vertigo, optic neuritis, convulsions.
• Inhibit iodine uptake.
• Hypersensitivity reactions – rashes, serum sickness, stomatitis, dermatitis.
• Hematological complications – bone marrow depression, aplastic anemia, agranulocytosis, thrombocytopenia.

Question 7. The rationale of using aspirin in post-myocardial infarction.
Answer:

Aspirin irreversibly inhibits platelet cyclo-oxygenase
↓
Inhibits thromboxane A2 synthesis by platelets
↓
Interferes with platelet aggregation
↓
Lower incidence of reinfarction.
↓
Decreases incidence of transient ischaemic attacks and stroke.

• Thus, aspirin is used in postmyocardial infarction.

Question 8. Enumerate COX-2 inhibitors. Describe their mode of action.
Answer:

COX-2 inhibitors are: