Study of Chemotherapeutic drugs

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RAMDAS BHAT
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CHEMOTHERAPY
INTRODUCTION
Prepared by,
RAMDAS BHAT
Assistant Professor
Srinivas college of Pharmacy,
Mangalore
7795772463
Ramdas21@gmail.com

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Introduction
• The word chemotherapy can be defined as the treatment of any disease by
synthetically and microbiologically derived substances (drugs) by killing or inhibiting the
growth of microorganisms and fast-growing cells in the body.
• Generally, it is used for treating cancer as cancer cells grow and multiply much more
rapidly than other cells of the body.
• Chemotherapy (sometimes cancer chemotherapy) can broadly be considered as the
treatment of cancer with an antineoplastic drug or with a combination of such drugs into
a standardized treatment regimen.
• Chemotherapeutic agents or Anti-Microbial Agents (AMAs) can be described as synthetic
or microbiologic substances used to suppress growth or kill microorganisms.
Chemotherapeutic drugs can be used either alone or in combination to treat a wide
variety of cancers.
• Although it is an effective way to treat many types of cancer, the treatment also carries a
risk of side effects.
GENERAL PRINCIPLES OF CHEMOTHERAPY
1. Selectivity:
• All the antimicrobial agents effective clinically show selective toxicity for the bacterium
rather than the host.
• This distinguishes antibiotics from disinfectants as they do not harm normal cells, while
disinfectants do.
• Antibiotics show elective toxic effects on the bacterium.
• It remains non-toxic over the human cells, i.e., when selectivity is high the antibiotics are
normally not toxic but can still cause severe side effects.
2. Therapeutic Index:
• The therapeutic index can be defined as the ratio of the toxic dose to the effective
therapeutic dose. Higher the therapeutic index, the better the antibiotic effect.
3. Categories of Antibiotics:
• Antibiotics are categorized as per their action of producing a cidal or static effect.
• They act as bactericides if they kill the susceptible bacteria and as bacteriostatic if they
reversibly inhibit the growth of bacteria.
4. Antibiotic Susceptibility Testing:
• The basic quantitative measures of the in vitro antibiotic activity are as follows:
a) Minimum Bactericidal Concentration (MBC):
• Minimum concentration that kills 99.9% of the original inoculum.
b) Minimum Inhibitory Concentration (MIC):
• Minimum concentration that inhibits of visible growth of bacteria.

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5. Combination Therapy: Two or more antibiotics when combined (combination therapy)
can be used in special cases:
a) Emergency cases when an etiological diagnosis is still in progress.
b) Emergence of resistant strains.
6. Antibiotic Synergism: It occurs when the effects of a combination of antibiotics are
greater than the sum of the effects of the individual antibiotics.
Classification of antimicrobials
A. Chemical structure
B. Mechanism of action
C. Range of activity.
D. Type of action (bacteriostatic and bactericidal)
E. Source of antibiotics
F. Organisms Against which Primarily Active
• Chemotherapeutic agents are chemicals used to treat cancer. It is usually used to refer to
antineoplastic drugs.
• They can be classified on the following basis:
A. Classification of Chemotherapeutic Agents According to the Chemical Structure:
i. Antibiotics
a) ß-Lactam Antibiotics: Penicillins, Cephalosporins, Monobactams, Carbapenems, etc.
b) Aminoglycosides: Streptomycin, Gentamycin, Framycetin, Neomycin, etc.
c) Macrolide Antibiotics: Roxithromycin, Erythromycin, Clarithromycin, Azithromycin, etc.
d) Tetracyclines: Oxytetracycline, Doxycycline, Minocycline, etc.
e) Nitrobenzene Derivatives: Chloramphenicol, etc.
f) Polypeptide Antibiotics: Polymyxin-B, Colistin, Bacitracin, Tyrothricin, etc.
g) Polyene Antibiotics: Nystatin, Hamycin, Amphotericin-B, etc.
h) Miscellaneous Agents: Rifampicin, Lincomycin, Vancomycin, Fusidic acid, Cycloserine,
Viomycin, Griseofulvin, etc.
ii. Chemotherapeutic Agents Other than Antibiotics
a) Sulphonamides and Related Agents: Sulfadiazine, Sulfamethoxazole, Sulfones (Dapsone),
Para-aminobenzoic acid (PAS), etc.
b) Diaminopyrimidines: Pyrimethamine.
c) Quinolones and Fluoroquinolones: Nalidixic acid, Norfloxacin, Ciprofloxacin, ofloxacin,
etc.
d) Nitrofuran Derivatives: Nitrofurantoin, Furazolidone, etc.
e) Nitroimidazoles: Metronidazole, Tinidazole etc.
f) Imidazole Derivatives: Miconazole, Clotrimazole, Ketoconazole, Fluconazole, etc.
g) Nicotinic Acid Derivatives: Isoniazid, Pyrazinamide, Ethionamide, etc.
h) Miscellaneous Agents: Ethambutol, Thioacetazone, Clofazimine, etc.
B. Classification of Chemotherapeutic Agents According to the Mechanism of action:
i. Agents that Inhibit Cell Wall Synthesis:
• These agents Inhibit cell wall synthesis of bacteria, thereby resulting in osmosis and
rupture of a bacterial cell.

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ii. Agents that Cause Leakage from Cell Membranes:
Polypeptides Polymyxins, Colistin, Bacitracin, Polyenes — Amphotericin B, Nystatin,
Hamycin.
iii. Agents that Cause Misreading of m-RNA Code and Affect Permeability:
Aminoglycosides — Streptomycin, Gentamicin, etc.
iv. Agents that Inhibit DNA Gyrase: Fluoroquinolones — Ciprofloxacin, etc.
v. Agents that Interfere with DNA Function: Rifampin and Metronidazole.
vi. Agents that Interfere with DNA Synthesis: Acyclovir and Zidovudine.
vii. Agents that Interfere with Intermediary Metabolism: Sulphonamides, Sulphones, PAS,
Trimethoprim, Pyrimethamine, and Ethambutol.
viii. Antimetabolites: These are agents that inhibit biochemical pathways of bacterial
metabolism. For example, sulphonamides, sulfones, p-amino salicylic acid (PAS), isoniazid,
ethambutol, trimethoprim, and anticancer agents inhibit the conversion of p-amino
benzoic acid (PABA) to folic acid and folinic acid.
ix. Agents that Damage Cytoplasmic Membrane: These agents disrupt cell membranes and
thereby kill the bacteria, e.g., polymyxin, colistin, polyene antibiotics, and amphotericin-
B.
x. Agents that Inhibit Protein Synthesis: The bacterial ribosome is made up of a 50S sub-
unit and a 30S sub-unit whereas the mammalian ribosome is made of 60S and 40S sub-
unit. Paromomycin, streptomycin, tetracyclines, gentamycin, kanamycin, and
spectinomycin bind to 30S ribosomes to inhibit protein synthesis. Erythromycin,
chloramphenicol,
lincomycin, and oleandomycin bind to 50S ribosome to inhibit protein synthesis.
C. Classification of Chemotherapeutic Agents According to their Range of Action:
i. Broad Spectrum: These are effective against gram +ve, gram- ve, rickettsia and chlamydia,
e.g., Tetracycline and Chloramphenicol.
ii. Narrow Spectrum Antibiotics:
a) These are effective only against gram +ve bacteria, e.g., Penicillin, Erythromycin group,
and Vancomycin.
b) These are effective only against gram —ve bacteria, e.g., Streptomycin and other
aminoglycoside antibiotics, Colistin, and Polymyxin-B.
c) Antifungal Antibiotics: Hamycin, Nystatin, and Griseofulvin. and
d) Anticancer Antibiotics: Actinomycin, Bicomycin, Mitomycin, Mithramycin.
iii. Relative Broad-Spectrum Antibiotics: These are effective against gram +ve and gram -ve
bacteria, e.g., Ampicillin group, Cephalosporins, and Rifamycin.

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D. Type of activity: It includes the drugs that kill or inhibit microbe growth.
E. Classification of Chemotherapeutic Agents According to the Source of Antibiotic:
i. Fungi: Penicillin, Griseofulvin, and Cephalosporin.
ii. Bacteria: Polymyxin B, Tyrothricin, Colistin, Aztreonam, and Bacitracin.
iii. Actinomycetes: Aminoglycosides, Macrolides, Tetracyclines, Polyenes, Chloramphenicol.
F. Classification of Chemotherapeutic Agents According to the Types of Organisms Against
which Primarily Active:
i. Antibacterial: Penicillins, Aminoglycosides, Erythromycin, etc.
ii. Antifungal: Griseofulvin, Amphotericin B, Ketoconazole, etc.
iii. Antiviral: Acyclovir, Amantadine, Zidovudine, etc.
iv. Antiprotozoal: Chloroquine, Pyrimethamine, Metronidazole, Diloxanide, etc.
v. Anthelmintic: Mebendazole, Pyrantel, Niclosamide, Diethylcarbamazine, etc.
BACTERIOSTATIC BACTERIOCIDALS
Sulfonamides Penicillins
Tetracyclines Aminoglycosides
Chloramphenicol Polypeptides
Erythromycin Rifampicin
Ethambutol Isoniazid
Clindamycin Pyrazinamide
Linezolid Vancomycin
Cephalosporins
Cotrimoxazole
Nalidixic acid

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Choice of an antimicrobial agent:
1. Patient-related factors:
• Patient age (chloramphenicol produce gray baby syndrome in newborn; Tetracyclines
deposition in teeth and bone below the age of 6 years)
• Renal and hepatic function (aminoglycoside, vancomycin-renal failure; erythromycin,
tetracycline- liver failure)
• Drug allergy (History of known AMAs allergy should be obtained).
➢ Syphilis patient allergic to penicillin – drug of choice is a tetracycline
➢ Fluoroquinolones cause erythema multiforme
➢ Impaired host Defence.
Drug factor:
• Pregnancy: All AMAs should be avoided in pregnancy many cephalosporins and
erythromycin are safe, while safety data on most others is not available.
• Genetic factors: Primaquine, sulfonamide, and fluoroquinolones are likely to produce
hemolysis in G-6-PD deficient patients).
2. Organism-related considerations:
• A clinical diagnosis should first be made, and the choice of the AMAs selected
• Clinical diagnosis itself directs the choice of the AMA
• Choice to be based on bacteriological examination (Bacteriological sensitivity testing).
Drug factor:
• Spectrum of activity (Narrow/ broad spectrum)
• Type of activity
• Sensitivity of the organism (MIC)
• Relative toxicity
• Pharmacokinetic profile
• Route of administration
• Cost
PROBLEMS WITH AMA’S:
1. Toxicity
2. Hypersensitivity
3. Drug resistance
4. Drug tolerance
5. Superinfection.

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1. TOXICITY:
Local irritancy:
• exerted site of administration. E.g.: Gastric irritation, pain, and abscess formation at the
site of i.m. injection, thrombophlebitis of injected vein.
Systemic toxicity:
Dose-related organ damage.
• High therapeutic index agents may not damage host cells, e.g.: penicillin, or erythromycin.
• The agent which has a low therapeutic index exhibits more toxicity. E.g.: aminoglycosides
(renal and CNS toxicity), tetracycline (liver and renal toxicity), and, chloramphenicol (bone
marrow depression).
• Very low therapeutic index drug is used when no suitable alternative AMAs are available,
E.g.:
a. Vancomycin (hearing loss, kidney damage, “red man’ syndrome)
b. polymyxin B (neurological and renal toxicity)
2. HYPERSENSITIVITY REACTION
• All AMAs are capable of causing hypersensitive reactions, and these reactions are
unpredictable and unrelated to dose. E.g.: Penicillin-induced anaphylactic shock (prick
skin testing)

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3. RESISTANCE
• Unresponsiveness of a microorganism to an AMA, and is similar to the phenomenon of
drug tolerance.
a) Natural resistance
b) Acquired resistance
a) Natural resistance: Some microbes have resistant to certain AMAs. E.g.: Gram-negative
bacilli not affected by penicillin G; M. tuberculosis insensitive to tetracyclines.
b) Acquired resistance: Development of resistance by an organism (which was sensitive
before) due to the use of AMA over a period of time. E.g.: Staphylococci and tubercle
bacilli develop resistance to penicillin (widespread use for>50 yr.). Gonococci quickly
developed resistance to sulfonamides in 30 yr.
Development of resistance
• Resistance mainly developed by mutation or gene transfer.
• Mutation: Resistance developed by mutation is a stable and heritable genetic change that
occurs spontaneously and randomly among microorganisms (usually on plasmids).
• Mutation resistance may be single-step or multistep.
a. Single gene mutation may confer a high degree of resistance. E.g.: enterococci to
streptomycin
b. Multistep mutation may modify the greater number of genes that will decrease the
sensitivity of AMAs to pathogens.
MECHANISM OF AMA’S Resistance:
1. GENETIC METHODS OF AMA RESISTANCE:
• They are classified into 2 types i.e., a) Chromosomal and b) Extrachromosomal.
1. Chromosomal method:
• Mutation refers to a change in the DNA structure of a gene.
• The spontaneous mutation in bacterial cells occurs at a frequency of about one per million
cells.
• During the therapy of antibiotics, sensitive bacteria may die but the resistant ones
continue to grow resulting in a “selection of mutants”.
• Such mutants confer resistance to the antibiotic. Such mutants Create a big clinical
problem, especially in mycobacteria (tuberculosis and leprosy) and in Staphylococcus
aureus by forming methicillin-resistant organisms (MRSA).
2. Extra-chromosomal mechanisms:
• Plasmids are extra-chromosomal genetic materials that can replicate independently and
freely in the cytoplasm.
• Plasmids that carry genes resistant to antibiotics (r-genes) are called R-plasmids.
• These r-genes can be readily transferred from one R-plasmid to another plasmid or a
chromosome.
• Much of the drug resistance encountered in clinical practice is plasmid-mediated.
• It is exerted by two mechanisms: from one bacterium to another or between plasmids of
the same bacteria.

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Gene transfer (Infectious resistance):
From one organism to another organism.
1. Conjugation
2. Transduction
3. Transformation
1. Conjugation:
• Cell-to-cell contact; transfer of chromosomal or
extrachromosomal DNA from one bacterium to another
through sex pili.
• The gene carrying the resistance or ‘R’ factor is transferred
only if another “resistance transfer factor” (RTF) is present.
• This will frequently occur in gram-negative bacilli.
• The nonpathogenic organisms may transfer the ‘R’ factor to
pathogenic organisms, which may become widespread by
contamination of food and water.
• The multidrug resistance has occurred by conjugation.
Eg:
a) Chloramphenicol resistance to typhoid bacilli
b) Penicillin resistance to Hemophilus, gonococci
c) Streptomycin resistance to E. coli.
2. Transduction:
• Transfer resistance gene through bacteriophage (bacterial
virus) to other bacteria of the same species.
• E.g.: Transmission of resistance gene between strains of
staphylococci and between strains of streptococci.
3. Transformation:
• It will occur in natural conditions.
• Bacteria take up naked DNA from their
environment and incorporate it into their
genome through the normal crossover
mechanism.

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STEPS TO PREVENT DRUG RESISTANCE:
• Although resistance is not a new phenomenon, the incidence has increased dramatically
over the past 2 decades. The development of new drugs has slowed considerably and may
be unable to keep pace with the continuing growth of pathogen resistance.
• Therefore, effective strategies are needed to prevent the continuing emergence of
antimicrobial resistance. These include the avoidance of unnecessary antibiotic
administration and increasing the effectiveness of prescribed antibiotics, as well as
implementing improvements in infection control and optimizing medical practice.
Patients to prevent antibiotic resistance:
• Tell your healthcare professional you are concerned about antibiotic resistance.
• Ask your healthcare professional if there are steps you can take to feel better and get
symptomatic relief without using antibiotics.
• Take the prescribed antibiotic exactly as your healthcare professional tells you.
• Discard any leftover medication.
• Ask your healthcare professional about vaccines recommended for you and your family
to prevent infections that may require an antibiotic.
• Never skip doses.
• Never take an antibiotic for a viral infection like a cold or the flu.
• Never pressure your healthcare professional to prescribe an antibiotic. Never save
antibiotics for the next time have you got sick.
• Never take antibiotics prescribed for someone else.
Healthcare professionals can prevent the spread of antibiotic resistance by
• Prescribing an antibiotic only when it is likely to benefit the patient.
• Prescribing an antibiotic that targets the bacteria that is most likely causing their patient’s
illness when an antibiotic is likely to provide benefit.
• Encouraging patients to use the antibiotic as instructed.
• Collaborating, with office staff, and patients to promote appropriate antibiotic use.
• Continue reviewing and following the latest clinical practice guidelines for common
infections, such as CDC’s Adult and Pediatric Academic Detailing Sheets.
• If the antibiotic shows resistance, Use of combinational therapy can be done to treat the
condition.
4. Drug Tolerant
• Loss of affinity of target
biomolecule of the
microorganism with
particular AMAs, e.g.:
Penicillin resistance to
Pneumococcal strain
(alteration of penicillin-
binding proteins).

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5. Superinfection (Suprainfection)
• A new infection occurring in a patient having a preexisting infection. Superinfections are
the most difficult to treat.
• Development of superinfection associated with the use of broad/ extended-spectrum of
antibiotics, such as tetracyclines, chloramphenicol, ampicillin, and newer
cephalosporins.
• Superinfections are more common when host Defence is compromised.
• Superinfections are generally the most difficult to treat.
– bacterial superinfection in viral respiratory disease
– infection of a chronic hepatitis B carrier with hepatitis D virus
– Piperacillin-tazobactam may cause superinfection with candida
Treatment for superinfection
• Candida albicans: Monilial diarrhea, Candida vulvovaginitis or vaginal thrush (an
infection of the vagina's mucous membranes) treat with nystatin or clotrimazole
• Resistant Staphylococci: treat with cloxacillin or its congeners
• Pseudomonas: Urinary tract infection, treat with carbenicillin, piperacillin, or gentamicin.
Superinfections minimized by
• Using specific (narrow-spectrum) AMA (whenever possible)
• Avoid using (do not use) antimicrobials to treat self-limiting or untreatable (viral)
infection
• Avoid prolonged antimicrobial therapy.
CHEMOPRPHYLAXIS:
• Chemoprophylaxis refers to the use of medications or chemical agents to prevent the
development or spread of a disease.
• It involves the administration of specific drugs to individuals who are at risk of contracting
a particular infection or disease, in order to reduce the chances of infection or minimize
the severity of the disease if contracted.
Different types of Chemoprophylaxis with examples:
1. Antimalarial Chemoprophylaxis: Examples: Chloroquine, Mefloquine, Atovaquone-
proguanil, Doxycycline
2. Antibacterial Chemoprophylaxis: Examples: Fluoroquinolones (e.g., Ciprofloxacin,
Levofloxacin) for anthrax exposure, Rifampin for close contacts of meningococcal

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meningitis, Trimethoprim-sulfamethoxazole for Pneumocystis jiroveci pneumonia (PCP)
prevention in immunocompromised individuals.
3. Antiviral Chemoprophylaxis: Examples: Oseltamivir or Zanamivir for influenza
prophylaxis, Valacyclovir or Acyclovir for herpes simplex virus prophylaxis.
4. Antiretroviral Chemoprophylaxis: Examples: Truvada (a combination of tenofovir
disoproxil fumarate and emtricitabine) for pre-exposure prophylaxis (PrEP) against HIV.
5. Antifungal Chemoprophylaxis: Examples: Fluconazole or Itraconazole for fungal
infections in immunocompromised patients, such as those with HIV/AIDS or undergoing
chemotherapy.
6. Antiparasitic Chemoprophylaxis: Examples: Ivermectin for prevention of certain parasitic
infections like onchocerciasis (river blindness) and lymphatic filariasis.
7. Chemoprophylaxis for Travel Medicine: Examples: Mefloquine, Doxycycline,
Atovaquone-proguanil for malaria prevention in travelers.
8. Chemoprophylaxis for Occupational Exposure: Examples: Hepatitis B vaccine and/or
antiviral drugs for healthcare workers, post-exposure prophylaxis (PEP) with antiretroviral
medications for occupational HIV exposure.
RATIONAL BEHIND COMBINED USE OF ANTIMICROBIALS (COMBINATIONAL THERAPY)
1. Increased efficacy: Combination therapy enhances the overall effectiveness of treatment
by targeting multiple aspects of microbial survival. Example: Rifampin and isoniazid for
tuberculosis.
2. Synergistic effects: Combined action of drugs is greater than their individual effects,
resulting in improved microbial killing. Example: Sulfamethoxazole and trimethoprim (co-
trimoxazole) for certain bacterial infections.
3. Broad spectrum coverage: Combination therapy provides coverage against a wide range
of pathogens. Example: Amoxicillin and clavulanic acid (Augmentin) for bacterial
infections.
4. Prevention of resistance: Using drugs with different mechanisms of action makes it
harder for microorganisms to develop resistance. Example: Azithromycin and ethambutol
for Mycobacterium avium complex (MAC) infections.
5. Treatment of polymicrobial infections: Combination therapy targets and eliminates
different types of pathogens in infections caused by multiple microorganisms. Example:
Ceftriaxone, metronidazole, and vancomycin for intra-abdominal infections.

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6. Reduction of treatment duration: Combination therapy may allow for a shorter
treatment duration compared to single-drug therapy. Example: Amphotericin B and
flucytosine for invasive fungal infections.
10 MARKS
1. Write the mechanism of action and uses of sulfonamides.
2. Write the mechanism of action and uses of penicillins.
3. Classify cephalosporins with examples and mention the therapeutic uses.
4. What are urinary antiseptics? Explain the mechanism of action and side effects of nitrofurantoin
5. What are polyene antibiotics? Write the pharmacology of bacitricin ?
6. Explain life cycle of malarial parasite.
7. Write the pharmacology of drugs used in the treatment of giardiasis.
8. Name any two helminthial infestations. Classify anthelmintics with examples. Write the
pharmacology of albendazole.
9. Classify the anticancer agents with examples.
10. Write about MOPP regimen.
11. Write the pharmacology of taxol.
12. Write the pharmacology of vincristin.
13. Write the pharmacology of methotrexate
14. Write the pharmacology of 5-fluorourocil.
15. Write the pharmacology of mercaptopurine
16. Write the pharmacology nitrogen mustards.
17. Role of steroids in the treatment of cancer.
18. Explain different mechanism of antibiotics.
5 MARKS
1. Write about mode of antimicrobial resistance in microbes.
2. Suggest measures to prevent superinfection and microbial resistance.
3. Write the antimicrobial spectrum and mechanism of action of a true broad-spectrum antibiotic.
4. Write the mechanism of action and uses of ampicillin.
5. Explain rationale behind co-trimaxazole combination. Write its advantages and uses.
6. Classify cephalosporins with examples and mention the therapeutic uses.
7. Write antimicrobial spectrum, mechanism of action and adverse effects of fluoroquinolines.
8. Name four triazole anti-fungal agents? Write their merits and mechanism of
9. effects and uses of albendazole.
10. Differentiate between paucibacillary and multibacillary leprosy. Add a note on their treatment.
11. Classify the anticancer agents with examples. action.
12. Write the pharmacology of drugs used in the treatment of giardiasis.
13. Classify helminthes and anthelmintics with examples.
14. Write the mechanism of action, adverse

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15. Give cell cycle-based classification of anticancer drugs.
16. Write the pharmacology of taxols.
17. Write the mechanism of action, adverse effects and uses of vincristine.
18. Write the mechanism of action, adverse effects and uses of methotrexate.
19. Write the mechanism of action, adverse effects and uses of 5-fluorourocil.
20. Write the mechanism of action, adverse effects and uses of mercaptopurine.
21. Outline life cycle of plasmodium three species.
22. Write briefly on therapeutic classification of antimalarial agents.
23. Classify anti-retroviral agents with examples? Mention their important adverse effects.
24. Enlist aminoglycoside antibiotics and write their adverse effects.
25. Write about common features of aminoglycosides and write therapeutic uses of gentamicin.
26. Classify fluoroquinolones with examples and write their therapeutic uses.
27. Describe the adverse effects of anti-neoplastic agents.
2 MARKS:
1. What is superinfection?
2. What is multidrug therapy? Give example.
3. What is grey baby syndrome?
4. Enlist the drugs causing ototoxicity?
5. Enlist the drugs causing nephrotoxicity?
6. What is anaphylaxis?
7. What are the drugs used in treatment of tapeworm infection?
8. What are the drugs used in treatment of round worm infection?
9. What are the drugs used in filariasis?
10. Which are the causative organisms of filariasis?
11. What is amoebiasis? Name two drugs used in the treatment of amebiasis?
12. Enlist the four uses of tetracyclines/doxycycline/oxytetracyclin
13. Enlist the four toxic effects of chlormphenicol.
14. Name the causative organisms of malaria.
15. Name the opportunistic infections in HIV.
16. What is multidrug regimen for the treatment of TB and name the drugs.
17. What is DOTS therapy?
18. Mention β-lactamase inhibitors. Mention their use.
19. Mention any four blood schizonticides.

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20. What is chemoprophylaxis? Give examples.
21. Write uses of griseofulvin.
22. Mention DHFR inhibitors. Write their uses.
23. What are probiotics? Give examples.
24. What is crystaluria? How can it be prevented?
25. Mention four adverse effects of anti-cancer drugs.