ANTICAN: Cytotoxic dG : Alkylating agnt: Nitrogen mustards: Mechlorethamine, Cyclophosphamide,
Ifosphamide, Chlorambucil, Bendamustine, Melphalan. Ethylenimine: Thiotepa, Altretamine. Nitrosoureas:
Carmustine, Lomustine. Alkylsulfonate: Busulfan. Triazine: Dacarbazine ,Temozolomide . Methyl hydrazine:
Procarbazine. Antimetabolites: Folate antago: Methotrexate, Pemetrexed. Purine antago:
6,Mercaptopurine,6,Thioguanine, Azathioprine, Fludarabine. Pyrimidine antago: 5,Fluorouracil,
Capecitabine ,Doxyfluridine, Cytarabine, Gemcitabine. Microtubule damaging agts: Vinca alkaloids:
Vincristin ,Vinblastine, Vinorelbine. Taxanes: Paclitaxel , Docetaxel.Topoisomerase,2 inhb: Etoposide.
Topoisomerase,1 inhibitor: Topotecan, Irinotecan. Antibio: Actinomycin D Doxorubicin, Idarubicin,
Epirubicin, Aclarubicin, Bleomycins, Mitomycin C. Misc: Hydroxyurea,L,Asparaginase, Arsenic trioxide.
Targeted drug : BCR,ABL tyrosine Kinase inhb :Imatinib, Dasatinib Nilotinib. EGF(HER) Recp inhibitor:
Gefitinib, Erlotinib, Cetuximab,Trastuzumab,Lapatinib.. Angiogenesis Inhibitors: Bevacizumab Sunitinib,
Sorafenib. Proteasome Inhibitor : Bortezomib. CD20 inhibitor: Rituximab.
Hormonal dG: Glucocorti..: Prednisolone. SERMS:Tamoxifen Toremifene. Aromatase inhb: Letrozole,
Exernestane, Anastrozole. 5§ reductase inhibitor : Finasteride Dutasteride. Progestins :
hydroxy progesterone. Estrogens: Ethinyl estradiol Fosfestrol. SER down: Regulator ,Fulvestrant.
Antiandrogens : Flutamide, Bicalutamide. GnRH analog: Nafarelin, Leuprorelin Triptorelin.
AntiAsthama : Leukotriene Antagonists::: Montelukast, Zafirlukast. Mast Cell Stabilizers::: Sod.
Cromoglycate, Ketotifen. Bronchodilators:: β,Sympathomimetics::: Salbutamol, Terbutaline, Bambuterol,
Salmeterol, Formoterol. Methylxanthines:* Theophylline, Aminophylline, Choline Theophyllinate,
Hydroxyethyl Theophyllin, Doxophylline. Anticholinergics::: Ipratropium Bromide, Tiotropium Bromide.
Corticosteroids::: Systemic:*Hydrocortisone, Prednisolone Inhal::: Flunisolide, Beclomethasone, Budesonide,
Fluticasone Propionate, Ciclesonide. Anti IgE Antibody:::Omalizumab
Anti Tb Drug: 1 Line:::, Isoniazid, Rifampin, Pyrazinamide, Ethambutol, Streptomycin.
2 line ::: Oral Drugs:, Ethionamide, Prothionamide, Terizidone, Para-aminosalicylic acid, Rifabutin,
Thiacetazone. Injectable Drugs:, Amikacin, Kanamycin, Capreomycin. Fluoroquinolones:,
Levofloxacin, Moxifloxacin, Ciprofloxacin, ofloxacin.
Drug for cough: Pharyngeal Demulcents::: Glycerine, Liquorice. Expectorant: Secretion Enhancers:::
Potassium Citrate,Potassium Iodide, Tolu Balsam, Vasaka, Ammonium Chloride. Mucolytics: Bromhexin,
Ambroxol, Acetyl Cysteine, Carbocisteine
Adjuvant Antitussives::: Bronchodilators:Salbutamol, Terbutaline. Antitussives (Cough Centre
Suppressants): Opioids: Codeine, Ethylmorphine, Pholcodine. Nonopioids: Noscapine, Chlophedianol,
Dextromethorphan, , Antihistamines: Chlorpheniramine, Diphenhydramine, Promethazine.
Anti peptic Ulcer: Gastric Acid Secretion Inhibitors:: H2 Antagonists:: Cimetidine, Ranitidine,
Famotidine, Roxatidine. Proton Pump Inhibitors:: Omeprazole, Esomeprazole, Rabeprazole, Dexrabeprazole.
Anticholinergics::: Pirenzepine, Propantheline, Oxyphenonium. Prostaglandin Analogue::: MisoprostolGastric
Acid Neutralizers (Antacids):::Systemic:: Sodium Bicarbonate, Sodium Citrate. Nonsystemic:: Magnesium
Hydroxide, Magnesium Trisilicate, Aluminum HydroxideMagaldrate, Calcium Carbonate. Anti H. pylori
Drugs::: Amoxicillin, Clarithromycin, Metronidazole, Tinidazole, Tetracycline. Ulcer Protectives:::
Sucralfate, Colloidal Bismuth Subcitrate (CBS)
drugs for diarrhea classification: .Antimicrobial Drugs:: Norfloxacin, Ciprofloxacin, Rifaximin,
Cotrimoxazole, Ampicillin, Tetracycline, Erythromycin, Metronidazole. Probiotics:Lactobacillus
sp. ,Bifidobacterium, Bifulum, Strep, faecalis, Enterococcus sp, Bacillus clausii, Saccharomyces, Boulardii.
Drug for inflammatory bowel disease : 5,ASA Compounds: Sulfasalazine, Mesalazine, Balsalazide,
Olsalazine. Glucocorticoids: Prednisolone, Hydrocortisone (enema), Sulfasalazine, Olsalazine.
Immunosuppressant’s:, Azathioprine, Methotrexate, Cyclosporine, Infliximab.
Nonspecific Antidiarrheal Drugs: Adsorbents:::, Ispaghula, Methylcellulose, Kaolin, Pectin. Antisecretory
Drugs:::, Rasecadotril, Bismuth Subsalicylate. Antimotility Drugs:::, Codeine, Diphenoxylate, Loperamid.
antiemetics classification: Anticholinergics::: Hyoscine, Dicyclomine. Neuroleptics (D2 Blockers):::
Chlorpromazine, Triflupromazine, Prochlorperazine. H1 Antihistamines::: Promethazine,
Diphenhydramine, Dimenhydrinate, Doxylamine, Meclozine (Meclizine). Prokinetic Drugs:::
Metoclopramide, Domperidone, Cisapride, Mosapride, Itopride. NK1 Receptor Antagonists::: Aprepitant,
Fosaprepitant. 5-HT3 Antagonists::: Ondansetron, Granisetron, Palonosetron, Ramosetron . Adjuvant
Antiemetics::: Dexamethasone, Benzodiazepines, Dronabinol, Nabilone.
laxatives (purgatives, cathartics) : Stool Softener: Docusates , Liquid paraffin. Bulk Forming Agents:
Dietary fiber , Psyllium(Plantago) , Ispaghula , Methyl cellulose. Osmotic Purgatives:, Magnesium Sulfate,
Magnesium Hydroxide, Sodium Sulfate, Sodium Phosphate, Sodium Potassium Tartrate, Lactulose. Stimulant
Purgatives: Diphenylmethanes: , Phenolphthalein , Bisacodyl, Sodium Picosulfate. Anthraquinones
(Emodins): Senna, Cascara Sagrada.
5HT₄ Agonist: Prucalopride. Fixed Oil: Castor Oil.
Penicillins ::: Natural Pen:::, Benzyl penicillin (Pen G). Semisyn Pen:::, Acid Resistant Alternative to
Pen G::: Phenoxymethyl penicillin (Pen V). Pen..ase Resistant Pen:, Methicillin, Cloxacillin, Dicloxacillin.
Amino pen :, Ampicillin, Bacampicillin, Amoxicillin, Ureido pen : Piperacillin, Mezlocillin. Carboxy pen :
Carbenicillin. Β,lactamase Inhibitors:, Clavulanic acid, Sulbactam, Tazobactam.
Cepholosporins: 1GEN: Cephapirin, Cefazolin Cephalexin Cefadroxil. 2 G: Cefoxitin Cefaclor Cefprozil,
Cefuroxime Cefotetan. 3 G: Cefotaxime Ceftizoaxime Cefoperazone Cefixime Cefodoxime Cefdinir. 4 G:
Cefepime. 5 G: Ceptaroline Ceftobiprole.
Aminoglycosides: Streptomycin, Neomycin, Kanamycin.
Tetracyclines: S Act (HF 6-8hr): Tetracycline, Chlortetra..., Oxytetra...
Interm.Act (HF ~12 hr): Demeclocycline, Methacycline.
L Act (16hr +): Doxycycline, Minocycline, Meclocycline.
Macrolide: 14-mem ring:Erythromycin Roxithr..., Clarythr....
15-mem ring: Azithr..... 16-mem ring: Spiramycin, Rokitamycin.
Misc: Chloramphenicol, Clindamycin.
::Sulfonamides::
ShortActing:::, Sulfadiazine. Intermediate Acting:::, Sulfamethoxazole. Long Acting:::, Sulfadoxine. Special
Purpose:::, Sulfamethopyrazine, Sulfacetamide sod., Sulfasalazine, Silver sulfadiazine, Mafenide
Quinolone Antimicrobials:::Nonfluorinated Quinolone:::, Nalidixic acid.
Fluoroquinolones:::.First Generation:::, Norfloxacin. Second Generation:::, Ciprofloxacin, Ofloxacin,
Pefloxacin. Third Generation:::, Levofloxacin, Moxifloxacin, Gemifloxacin, Prulifloxacin. Fourth
Generation:::, Lomefloxacin, Sparfloxacin.
ANTIVIRAL DRUGS (Non,retroviral):: Anti,herpes virus drug: Idoxuridine, Trifluridine, Acyclovir,
Valacyclovir, Famciclovir, Ganciclovir, Valganciclovir, Cidofovir, Foscarnet, Fomivirsen.
Anti,influenza virus drugs:- Amantadine, Rimantadine, Oseltamivir, Zanamivir.
Anti,hepatitis virus/ Nonselective antiviral drug: For hepatitis B: Lamivudine, Adefovir dipivoxil,
Tenofovir. For hepatitis C:Ribavirin, Interferon A
Antiretroviral drugs classification: Nucleoside Reverse Transcriptase Inhibitors (NRTIs): Zidovudine.
Nevirapine. Didanosine. Efavirenz. Stavudine, Delavirdine, Lamivudine. Abacavir. Emtricitabine. Tenofovir.
Non Nucleoside Reverse Transcriptase Inhibitors (NNRTIs):, Efavirenz, Delavirdine. Protease Inhibitors :
Ritonavir. Atazanavir, Indinavir, Nelfinavir, Saquinavir. Amprenavir, Lopinavir. CCR-5 Receptor Inhibitor:
Maraviroc. Integrase Inhibitor: Raltegravir. Entry Inhibitor:- Enfuvirtide.
Antiamoebic drugs classification: Tissue Amoebicides: (for intestinal and extraintestinal
amoebiasis): Nitroimidazoles: Metronidazole , Tinidazole , Secnidazole , Ornidazole , Satranidazole.
Alkaloid:: Emetine, Dehydroemetine
(for extraintestinal amoebiasis only):Chloroquine. Luminal Amoebicides: Amides:, Diloxanide
furoate , Nitazoxanide Antibiotics:, Tetracycline, Paromomycin. 8,Hydroxyquinolines:,
Quiniodochlor (Iodochlorohydroxyquin), Diiodohydroxyquin (Iodoquinol).
Anthelmintic drugs : For Roundworm, Hookworm, Pinworm:, Albendazole, Mebendazole, Pyrantel pamoate ,
Piperazine, Levamisole.
For Whipworm, Trichinella spiralis:, Albendazole, Mebendazole. For Tapeworms:, Praziquantel, Niclosamide,
Albendazole. For Threadworm:, Ivermectin, Albendazole. For Filariasis: Diethylcarbamazine. For Hydatid
disease:, Albendazole, Mebendazole
Antimalarial drugs classification: 4,Aminoquinolines:, Chloroquine, Amodiaquine, Piperaquine.
Quinoline methanol: Mefloquine Biguanide: Proguanil (Chloroguanide) Sulfamethopyrazine: Dapsone
Diaminopyrimidine: Pyrimethamine Cinchona Alkaloid:Quinine, Quinidine 8,Aminoquinolines:, Primaquine,
Tafenoquine Sulfonamide/Sulfone: Sulfadoxine Amino alcohols: Halofantrine, Lumefantrine Antibiotics:,
Doxycycline, Clindamycin Naphthyridine:, Artesunate, Pyronaridine Naphthoquinone: Atovaquone.
Sesquiterpine lactones:, Artemether, Arteether, Arterolane
antibacterial drugs classification: Inhibit Cell Wall Synthesis:::, Penicillins, Cephalosporins,
Carbapenems, Monobactams, Vancomycin, Cycloserine, Bacitracin. Inhibit Protein Synthesis:::, Tetracyclines,
Chloramphenicol, Erythromycin (other macrolides), Clindamycin, Linezolid. Cause Leakage from Cell
Membranes:::, Polymyxin, Colistin, Amphotericin B
Cause Misreading of mRNA Affect Permeability:::, Aminoglycosides (Streptomycin, Gentamicin, others).
Inhibit DNA Gyrase:::, Ciprofloxacin (Other fluoroquinolones). Interfere with DNA Function:::, Rifampin.
Interfere with Intermediary Metabolism:::, Sulfonamides, Sulfones, Trimethoprim, Pyrimethamine, Para-
aminosalicylic acid, Metronidazole.
ANTIFUNGAL DRUGS: Antibio: Polyenes, Amphotericin B, Nystatin, Hamycin. Echinocandins:
Caspofungin, Micafungin, Anidulafungin. Heterocyclic benzofuran: Griseofulvin.
Antimetabolite : Flucytosine. Allylamine: Terbinafine. Azoles: Imidazoles : Topical: Clotrimazole,
Econazole, Mico.. , Oxico... . Systemic : Ketoco.. , Triazoles, Fluco... ,Itraco.. , Voricon.. , Posaco... .
Topical agts: Tolnaftate, Undecylenic acid, Benzoic acid ,Ciclopirox, olamine, Butenafine , Thiosulfate.
Treatment of COPD: Chronic obstructive pulmonary disease:
Objectives: To reduce air flow obstruction. To reduce respiratory symptoms and improve quality of life, and.
To prevent and treat secondary complications like hypoxaemia, infections and cor pulmonale (right sided heart
failure). options for the treatment of COPD: •The most important therapeutic intervention is to stop
smoking. •Influenza vaccine may be given to patients of COPD every year and a proper antibiotic therapy
should be provided if patient develops purulent sputum.
•The first line of drug therapy is use of broncho-dilators. Short acting beta_{2} agonists should be tried initially.
Since airway muscle tone is controlled by parasympathetic system, use of anti-muscarinic drugs like
Ipratropium, Oxitropium or Tiotropium is beneficial. •A xanthine like Theophylline may also be
administered orally. It improves respiratory muscle function. In addition, due to ionotropic effects, it is
additionally useful in cor pulmonale. Persistent nocturnal symptoms like cough or wheezing are helped by
night-time use of long acting Theophylline. •Some patients of COPD, receiving broncho-dilator therapy,
exhibit better response to oral corticosteroids (eg Prednisolone 30-40 mg per day for 15 days). If better
responses are achieved, then inhalational corticosteroids should be given. During this time, dose of oral
glucocorticosteroids is gradually tapered. •In patients of severe COPD and persistent hypoxaemia, use of
domiciliary oxygen therapy for 15 hours a day reduces mortality and risk of complications like neuro-
psychological impairment.
General principles for the management of poisoning :
1. Resuscitation and Stabilization::.Immediate Action:: Swiftly address life-threatening issues such as
compromised airways, respiratory distress, or cardiovascular collapse to stabilize the patient's condition.
.Personal Protection:: Prioritize the safety of healthcare providers through the use of personal protective
equipment (PPE) to prevent exposure to toxins.
.Early Decontamination Consideration:: Assess the need for decontamination procedures early on to minimize
toxin absorption and prevent secondary contamination.
2. Safety of Staff and Decontamination:: Staff Safety Priority:: Ensure the well-being of healthcare personnel
to maintain an effective response.
.Decontamination Importance:: Prompt decontamination of victims mitigates exposure risks and limits the
spread of toxins.
.Preservation of Critical Facilities:: Effective decontamination procedures contribute to the uninterrupted
functioning of critical facilities, preventing potential closures due to secondary contamination.
3. Resuscitation of Severely Poisoned Patients:: Identification of Toxins:: Thoroughly assess potential toxins
involved to tailor treatment strategies.
.Antidote Administration:: Administer specific antidotes when available, guided by identified toxins and
mechanisms of toxicity.
.Continuous Monitoring:: Monitor vital signs and clinical status closely due to rapid changes in consciousness
and hemodynamics.
4. Toxicological Diagnosis:: Consideration of Toxic Causes:: Maintain a high index of suspicion for toxic
etiologies, especially in ambiguous presentations.
.Comprehensive Assessment:: Conduct a detailed history and physical examination to identify sources of
exposure and toxidromes.
.Collaborative Approach:: Collaborate with poison control centers to enhance diagnostic accuracy and guide
management strategies.
5. Therapeutic Interventions for Poisoning:: Risk-Benefit Evaluation:: Assess the life-threatening nature of
toxic exposures and weigh intervention risks and benefits.
.Dynamic Nature of Poisoning:: Recognize the dynamic nature of poisoning, necessitating frequent
reassessment and adjustment of interventions.
.Individualized Treatment:: Tailor interventions based on specific toxins, route of exposure, and patient's
clinical condition.
6. Decontamination:: Preventing Further Absorption:: Implement decontamination procedures to remove toxins
before absorption into the bloodstream.
.Appropriate Methods:: Select decontamination methods based on the route of exposure.
.Risk Mitigation:: Minimize aspiration or secondary contamination risks during decontamination.
7. Enhanced Elimination of Absorbed Toxins:: Augmenting Toxin Removal:: Consider interventions to enhance
toxin elimination from the bloodstream or tissues.
.Utilization of Modalities:: Employ modalities such as activated charcoal or hemodialysis based on toxin
characteristics.
.Clinical Considerations:: Evaluate benefits and risks of enhanced elimination therapies based on patient's
condition and toxin profile.
8. Supportive Care:: Comprehensive Monitoring:: Monitor vital signs and organ function to assess for delayed
effects and complications.
.Timely Intervention:: Initiate supportive measures promptly to prevent further deterioration.
.Multidisciplinary Approach:: Collaborate with specialists to optimize supportive care and manage
complications effectively.
9. Psychosocial and Workplace Safety Interventions::.Holistic Management:: Address psychosocial aspects and
workplace safety considerations in poisoning management.
.Psychosocial Support:: Offer counseling to patients and families to address psychological distress.
.Workplace Reporting:: Adhere to safety protocols and reporting requirements to prevent future incidents.
.Community Engagement:: Engage stakeholders to raise awareness about poisoning prevention and foster
public health initiatives.
Antitubercular agents: Inhibit the synthesis of mycobacterial cell wall components, such as the inhibition of
enzymes involved in cell wall synthesis like isoniazid.
Antileprotic agents: Work by inhibiting the growth of Mycobacterium leprae, the causative agent of leprosy,
through various mechanisms including inhibition of cell wall synthesis and interference with bacterial
metabolism.
Antifungal agents: Target fungal cell membranes, cell walls, or metabolic processes, inhibiting fungal growth.
Ex include azoles, which inhibit ergosterol synthesis, a key component of fungal cell membranes.
Antiviral drugs: Act by interfering with viral replication at various stages of the viral life cycle, such as
inhibition of viral entry, viral replication, or viral assembly/release. Examples include nucleoside analogs like
acyclovir, which inhibit viral DNA synthesis.
Anthelmintics: Work by disrupting the nervous system or metabolic processes of parasitic worms (helminths),
leading to paralysis and expulsion of the worms from the body. Examples include benzimidazoles like
albendazole.
Antimalarial drugs: Target different stages of the Plasmodium parasite lifecycle, inhibiting its growth and
replication. Examples include chloroquine, which interferes with heme detoxification in the parasite.
Antiamoebic agents: Act by damaging the cell membrane or inhibiting essential metabolic pathways of
amoebae, leading to their death. Ex include metronidazole, which disrupts DNA synthesis in the parasite.
Immunostimulants: Boost the immune response by enhancing the activity of immune cells, such as
macrophages and T cells. Ex include interferons, which stimulate the immune system’s.
Immunosuppressants: Suppress the activity of the immune system, often by inhibiting the function of T cells
or reducing the production of inflammatory cytokines. Examples include corticosteroids like prednisone and
immunosuppressive drugs like cyclosporine.
Antiulcer agents: Work by reducing the production of gastric acid, enhancing mucosal defense mechanisms, or
promoting healing of ulcers. Examples include proton pump inhibitors like omeprazole and H2 receptor
antagonists like ranitidine.
Anti-asthmatic drugs: Act by reducing airway inflammation, bronchoconstriction, and mucus production,
helping to relieve symptoms of asthma. Examples include bronchodilators like β2-agonists and anti-
inflammatory agents like corticosteroids.
Emetics and anti-emetics: Emetics induce vomiting by stimulating the vomiting center in the brain or irritating
the stomach lining, while anti-emetics work by blocking signals to the vomiting center or by acting on recpter
involved in the emetic reflex. Ex apomorphine (emetic) and ondansetron (anti-emetic).
Drugs used for constipation: Laxatives: they work by increasing the frequency and ease of bowel
movements. They may do this by drawing water into the bowel, softening the stool, or stimulating the muscles
of the intestines to push the stool through. Examples include: - Stimulant laxatives (e.g., bisacodyl): These
stimulate the muscles of the intestines, promoting bowel movements.
- Bulk-forming laxatives (e.g., psyllium): These increase the bulk of the stool, making it easier to pass.
- Osmotic laxatives (e.g., polyethylene glycol): These draw water into the bowel, softening the stool &
promoting bowel movements.
Drug used for diarrhea: Antidiarrheal agents: This work by reducing intestinal motility and fluid secretion,
helping to control diarrhea. They may also have additional effects such as adsorbing toxins or pathogens in the
intestines. Examples include: - Loperamide: Loperamide works by slowing down the movement of the
intestines, allowing more time for water and electrolytes to be absorbed, thus reducing the frequency and
fluidity of bowel movements.
- Bismuth subsalicylate: This agent has antimicrobial and anti-inflammatory properties, helping to reduce
diarrhea by killing or inhibiting the growth of bacteria and reducing intestinal inflammation.
Sulfonamides and Cotrimoxazole: Sulfonamides inhibit bacterial growth by blocking the synthesis of folic
acid, which is essential for bacterial DNA and protein synthesis.
Cotrimoxazole is a combination of sulfamethoxazole and trimethoprim, which work synergistically to inhibit
sequential steps in the folic acid syntsis pathway, providing a broader spectrum of antibacterial.
Penicillins: Penicillins interfere with bacterial cell wall synthesis by inhibiting the activity of enzymes called
penicillin-binding proteins (PBPs). This leads to weakened cell walls and eventual cell lysis. Penicillins are
bactericidal against actively growing bacteria.
Cephalosporins: Cephalosporins also target bacterial cell wall synthesis by binding to PBPs, leading to cell
wall weakening and bacterial cell lysis. They are structurally similar to penicillins but have a broader spectrum
of activity and increased resistance to some bacterial enzymes that inactivate penicillins.
Chloramphenicol: Chloramphenicol inhibits bacterial protein synthesis by binding to the 50S ribosomal
subunit, thereby preventing the formation of peptide bonds during translation. It is bacteriostatic and inhibits
the growth of a wide range of bacteria.
Macrolides: Macrolides inhibit bacterial protein synthesis by binding to the 50S ribosomal subunit, blocking
the translocation step of protein synthesis. This prevents the elongation of the peptide chain. Macrolides are
bacteriostatic & are effective against a variety of Gram +ve and some Gram-ve bacteria.
Quinolones and fluoroquinolones: Quinolones and fluoroquinolones target bacterial DNA gyrase
(topoisomerase II) and topoisomerase IV, enzymes involved in DNA replication and repair. By inhibiting these
enzymes, they interfere with DNA synthesis, replication, and repair, leading to bacterial cell death.
Fluoroquino..: are a newer generation of quinolones with enhanced activity & broader spectrum activity.
Tetracyclines: Tetracyclines inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit,
blocking the attachment of aminoacyl-tRNA molecules to the ribosome. This prevents the elongation of the
peptide chain. Tetracyclines are bacteriostatic and are effective against a wide range of Gram +ve and Gram-
negative bacteria, as well as some atypical pathogens.
Aminoglycosides: Aminoglycosides inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit,
causing misreading of the genetic code and inhibition of protein synthesis. They are bactericidal and are
effective against a wide range of Gram-negative bacteria, as well as some Gram +ve bacteria.
Drug Acting on UTI (Urinary Tract Infection):Most antibiotics used to treat UTIs work by inhibiting
bacterial cell wall synthesis, disrupting bacterial DNA replication, or interfering with bacterial protein
synthesis. Examples include sulfonamides, fluoroquinolones, and beta-lactams.
Antitussives (Cough Suppressants):Antitussives typically work by acting on the cough center in the
brainstem or by numbing the cough receptors in the respiratory tract. Common antitussives include opioids like
codeine and non-opioids like dextromethorphan.
Anti Cancer :
Antimetabolites:Antimetabolites are drugs that mimic natural substances within the cell, such as nucleotides,
and interfere with DNA and RNA synthesis. By doing so, they disrupt the normal processes of cell division and
proliferation, which are necessary for cancer growth. Examples include methotrexate, 5-fluorouracil (5-FU),
and gemcitabine.
Alkylating Agents: Alkylating agents are compounds that directly damage the DNA of cancer cells by forming
covalent bonds with the DNA strands, leading to cross-linking between DNA strands or within a single DNA
strand. This interferes with DNA replication and transcription, ultimately triggering apoptosis (programmed cell
death) in the cancer cells. Examples include cyclophosphamide, cisplatin, and temozolomide.
Topoisomerase Inhibitors: Topoisomerases are enzymes involved in the regulation of DNA topology,
including DNA replication, transcription, and repair. Topoisomerase inhibitors interfere with the action of these
enzymes, leading to the accumulation of DNA strand breaks and ultimately causing cell death. There are two
classes of topoisomerase inhibitors: Topoisomerase I inhibitors (e.g., irinotecan, topotecan) and Topoisomerase
II inhibitors (e.g., etoposide, doxorubicin).
Microtubule Inhibitors: Microtubules are structures essential for cell division, serving as tracks along which
chromosomes move during mitosis. Microtubule inhibitors disrupt the dynamic assembly and disassembly of
microtubules, leading to mitotic arrest and cell death. They can be further classified into two groups:
microtubule-stabilizing agents (e.g., paclitaxel, docetaxel) and microtubule-destabilizing agents (e.g., vinca
alkaloids like vincristine, vinblastine).
Tyrosine Kinase Inhibitors (TKIs):Tyrosine kinases are enzymes that play crucial roles in cell signaling
pathways involved in cell growth, proliferation, and survival. TKIs block the activity of specific tyrosine
kinases that are often overactive or mutated in cancer cells, thereby inhibiting the downstream signaling
cascades that promote cancer growth. Examples include imatinib, erlotinib, and crizotinib.
Monoclonal Antibodies: Monoclonal antibodies (mAbs) are designed to target specific proteins that are
overexpressed or aberrantly expressed on the surface of cancer cells. By binding to these proteins, mAbs can
induce various anti-cancer effects, including antibody-dependent cellular cytotoxicity (ADCC), complement-
dependent cytotoxicity (CDC), and inhibition of signaling pathways essential for cancer cell survival. Examples
include trastuzumab, rituximab, and pembrolizumab.
