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Antimicrobials and Antibiotics
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Antimicrobials and Antibiotics

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Questions and Answers

What is the primary infectious agent that causes tuberculosis?

Mycobacterium tuberculosis

Which drug is activated on the surface of M.tuberculosis by katG enzyme?

  • Pyrazinamide
  • Ethambutol
  • Isoniazid (correct)
  • Rifampicin

    • Pyrazinamide should be used with caution in patients with hyperuricaemia or gout.

    True

    Ethambutol hydrochloride inhibits the incorporation of _______ into the mycobacterium cell wall.

    <p>mycolic acid</p> Signup and view all the answers

    What chemical group destroys the activity of sulphonamides when substituted for the sulphonamido function?

    <p>–SO3H</p> Signup and view all the answers

    Match the drug with its mode of action:

    <p>Ethionamide = Inhibitory effect on mycolic acid synthesis Rifampicin = Inhibits DNA-dependent RNA polymerase of mycobacteria Amikacin = Semisynthetic aminoglycoside with high activity against mycobacterial species Para-amino-salicylic acid = Inhibitor of bacterial folate metabolism</p> Signup and view all the answers

    Sulphonamides in combination: Trimethoprim with ____________.

    <p>Sulphamethoxazole</p> Signup and view all the answers

    What type of groups bind to the basic centers of proteins according to the text?

    <p>alkyl, alkoxy, halides</p> Signup and view all the answers

    Match the following sulphonamides with their properties and uses:

    <p>Sulphacetamide = Used in the treatment of bacterial infections of urinary tract Sulphasalazine = Used in the treatment of ulcerative colitis Sulphadiazine = Used in the treatment of canceroids and rheumatic fever Sulphadimidine = Less effective in meningeal infection because of poor penetration into cerebrospinal fluid Sulphamerazine = Used as an antibacterial agent</p> Signup and view all the answers

    How are antibiotics different from antiseptics?

    <p>Antiseptics can destroy microorganisms on non-living objects.</p> Signup and view all the answers

    What is the main structural difference between cephalosporins and penicillins?

    <p>Cephalosporins contain a di-hydro meta thiazine ring, while penicillins contain a tetra hydro thiazole ring.</p> Signup and view all the answers

    Match the following cephalosporins with their properties and uses:

    <p>Cephalexin = Recommended for urinary tract infection Cefadroxil = Therapeutic indications similar to cephalexin and cephradine Cefaclor = Used in the treatment of upper respiratory tract infections</p> Signup and view all the answers

    Cephalosporin N is a derivative of 6-aminopenicillanic acid, and Cephalosporin C is a derivative of 7 amino-cephalosporanic acid. Cephalosporin C contains a side-chain derived from ___acid.

    <p>D-α-aminoadipic</p> Signup and view all the answers

    What is the purpose of monitoring therapeutic levels of cyclosporine and tacrolimus?

    <p>To prevent adverse effects and ensure efficacy of treatment.</p> Signup and view all the answers

    Which adverse effect is more prominent with tacrolimus compared to cyclosporine?

    <p>Neurotoxicity</p> Signup and view all the answers

    __________ is a macrolide antibiotic produced by bacteria Streptomyces tsukubaensis.

    <p>Tacrolimus</p> Signup and view all the answers

    Sirolimus is a calcineurin inhibitor.

    <p>False</p> Signup and view all the answers

    Match the drug with its primary usage:

    <p>Azathioprine = Prevents clonal expansion of B and T lymphocytes by inhibiting purine synthesis Mycophenolate Mofetil = Inhibits de novo synthesis of purines, interfering with T and B cell nucleic acid production Methotrexate = Inhibits dihydrofolate reductase, affecting DNA, RNA, and protein synthesis Cyclophosphamide = An alkylating agent that destroys proliferating lymphoid cells</p> Signup and view all the answers

    What is the mechanism of action of IL-2 receptor antagonists?

    <p>Bind to CD25 on activated lymphocytes</p> Signup and view all the answers

    What is the primary use of Type I interferons IFN-α and IFN-β?

    <p>Induced by viral infections</p> Signup and view all the answers

    Loop diuretics inhibit reabsorption of ______ and ______ by inhibiting the Na+ —K+ —2Cl– symport.

    <p>NaCl, KCl</p> Signup and view all the answers

    Match the following diuretics with their site of action:

    <p>Carbonic anhydrase inhibitors = Proximal tubule Osmotic diuretics = Loop of Henle; Proximal tubule Loop diuretics = Thick ascending limb of loop of Henle Thiazides = Distal convoluted tubule</p> Signup and view all the answers

    What is the structure-activity relationship of ethacrynic acid?

    <p>Designed to mimic mercurial diuretics, with increased activity when an electron withdrawing group is placed ortho to the unstaturated ketone, and ortho and meta positions substituted with chlorine produce the most active compound.</p> Signup and view all the answers

    What is the effect of thiazides on Ca++ reabsorption in the distal convoluted tubule?

    <p>Enhancement of Ca++ reabsorption</p> Signup and view all the answers

    What is the mechanism of action of thiazides?

    <p>Inhibition of a Na+—Cl– symport in the luminal membrane of the epithelial cells in the distal convoluted tubule.</p> Signup and view all the answers

    What is the effect of thiazides on NaCl reabsorption in the distal convoluted tubule?

    <p>Inhibition of NaCl reabsorption</p> Signup and view all the answers

    What is the structure-activity relationship of thiazides?

    <p>These compounds are weakly acidic, with a free sulfamoyl group at position 7 essential for diuretic activity, and an electron-withdrawing group essential at position 6.</p> Signup and view all the answers

    What is the mechanism of action of amiloride and triamterene?

    <p>Inhibition of the sodium channel in the luminal membrane of collecting tubule and collecting duct</p> Signup and view all the answers

    What is the effect of amiloride and triamterene on K+ and H+ secretion?

    <p>Inhibition of K+ and H+ secretion, resulting in conservation of K+ and H+.</p> Signup and view all the answers

    What is the primary function of aldosterone in the kidneys?

    <p>Enhances sodium reabsorption</p> Signup and view all the answers

    Which class of diuretics inhibits the action of carbonic anhydrase?

    <p>Carbonic Anhydrase Inhibitors</p> Signup and view all the answers

    Loop diuretics are considered the most potent type of diuretics.

    <p>True</p> Signup and view all the answers

    _______ is the only available aldosterone antagonist.

    <p>Spironolactone</p> Signup and view all the answers

    Match the diuretic class with its site of action:

    <p>Carbonic Anhydrase Inhibitors = PTC Loop Diuretics = Thick Ascending Limb of Henle Thiazide Diuretics = DCT Potassium Sparing Diuretics = CD</p> Signup and view all the answers

    Which type of diuretic is commonly used to treat hypertension and other conditions?

    <p>Thiazide Diuretics</p> Signup and view all the answers

    Patients with congestive heart failure who are taking cardiac glycosides like digitalis are not at risk of developing hypokalemia.

    <p>False</p> Signup and view all the answers

    What electrolyte imbalance can diuretics lead to, which is characterized by low potassium levels?

    <p>hypokalemia</p> Signup and view all the answers

    Diuretics can affect electrolyte balance, leading to abnormalities such as hypokalemia, hyponatremia, hypomagnesemia, and ____(high potassium) in some cases.

    <p>hyperkalemia</p> Signup and view all the answers

    Match the diuretic type with the correct examples:

    <p>Thiazide Diuretics = Hydrochlorothiazide, Chlorthalidone Loop Diuretics = Furosemide, Bumetanide, Torsemide Potassium-Sparing Diuretics = Spironolactone, Eplerenone, Amiloride, Triamterene Osmotic Diuretics = Mannitol, Glycerol</p> Signup and view all the answers

    Study Notes

    Antimicrobials

    • Antimicrobials reduce the possibility of infection and sepsis
    • Antibiotics are derived from moulds or synthesized, absorbed into the body to kill or prevent bacterial growth
    • Antibiotics can be administered parenterally, orally, or topically
    • Antiseptics are applied to the skin, not absorbed, and reduce infection possibility
    • Disinfectants destroy microorganisms on non-living objects
    • Antifungal agents kill or inhibit fungal growth, administered intravenously, orally, or topically

    Cephalosporins

    • Isolated from Cephalosporium acremonium in 1948
    • β-Lactam antibiotics with similar structure to penicillins, but with a dihydrothiazine ring
    • More acid-stable than penicillins, with a similar mechanism of action
    • Inhibit bacterial cell wall peptidoglycan unit cross-linking by inhibiting transpeptidase enzyme

    Classification of Cephalosporins

    • Classified based on chemical structure, clinical pharmacology, antibacterial spectrum, or penicillinase resistance
    • Orally administered: cephalexin, cephradine, and cefaclor
    • Parentrally administered: cephalothin, cephapirin, cephacetrile, and cefazedone
    • Resistant to β-lactamase and parentrally administered: cefuroxime, cefamandole, cefoxitin

    Generations of Cephalosporins

    • First-generation: highest activity against gram-positive bacteria, lowest activity against gram-negative bacteria
    • Second-generation: more active against gram-negative bacteria, less active against gram-positive bacteria
    • Third-generation: less active against gram-positive organisms, but with a much expanded spectrum of activity against gram-negative organisms
    • Fourth-generation: cefepime and cefpirome, with a broad spectrum of activity
    • Fifth-generation: ceftobiprole, with anti-pseudomonal activity and less susceptible to resistance

    Structure-Activity Relationship (SAR) of Cephalosporins

    • 7-Acylamino substitution: addition of amino group and hydrogen at α and α1 position produces a basic compound, increasing stability and activity
    • Substitutions on the aromatic ring: increase lipophilicity, providing higher gram-positive activity and generally lower gram-negative activity
    • Modification at C-3 position: affects pharmacokinetics and pharmacodynamics

    Degradation of Cephalosporins

    • In strong acid solutions
    • In the presence of β-lactamase
    • In the presence of acylase

    Anti-TB Drugs

    • First-line drugs: isoniazid, streptomycin, rifampicin, ethambutol, and pyrazinamide
    • Second-line drugs: ethionamide, p-amino salicylic acid, ofloxacin, ciprofloxacin, cycloserine, amikacin, kanamycin, viomycin, and capreomycin

    Isoniazid

    • Prodrug, activated by katG enzyme to isonicotinic acid
    • Inhibits bacterial cell wall mycolic acid, making M.tuberculosis susceptible to reactive oxygen radicals
    • Bacteriostatic or bactericidal, depending on concentration and susceptibility of the organism

    Pyrazinamide

    • Prodrug, activated by M.tuberculosis amidase enzyme to pyrazine carboxylic acid
    • Bactericidal, effective in low pH environments
    • Used to treat tuberculosis and meningitis

    Ethambutol

    • Bacteriostatic, inhibits incorporation of mycolic acid into the mycobacterium cell wall
    • Used in combination with other antitubercular drugs

    Rifampicin

    • Bactericidal, inhibits DNA-dependent RNA polymerase of mycobacteria
    • Used in combination with other antitubercular drugs

    Streptomycin

    • Aminoglycoside, inhibits protein synthesis
    • Used in combination with other antitubercular drugs to treat pulmonary infections

    Ethionamide

    • Inhibits mycolic acid synthesis
    • Used as an antitubercular drug

    Para-amino-salicylic acid

    • Inhibits bacterial folate metabolism
    • Bacteriostatic, highly specific for M.tuberculosis
    • Used to treat tuberculosis### Antibacterial Sulphonamides
    • Para amino benzene sulphonamide (sulphanilamide) is the first effective chemotherapeutic agent used to prevent and treat bacterial infections in humans.
    • Sulphonamides are bacteriostatic antibiotics with a wide spectrum of action against most gram-positive bacteria and many gram-negative organisms.

    Structure-Activity Relationship (SAR) of Sulphonamides

    • Sulphanilamide skeleton is the minimum structural requirement for antibacterial activity.
    • Amino and sulphonyl groups on the benzene ring are essential and should be in the 1 and 4 positions.
    • The N-4 amino group could be modified to be prodrugs, which are converted to free amino function in vivo.
    • Sulphur atom should be directly linked to the benzene ring.
    • Replacement of the –SO2NH group by –CONH reduces the activity.
    • Heterocyclic substituents lead to highly potent derivatives.

    Classification of Sulphonamides

    • Based on the site of action:
      • Sulphonamides for general infections (e.g. Sulphanilamide, Sulphapyridine, Sulphadiazine, Sulphamethoxazole).
      • Sulphonamides for urinary tract infections (e.g. Sulphaisoxazole, Sulphathiazole).
      • Sulphonamides for intestinal infections (e.g. Phthalylsulphathiazole, Succinyl sulphathiazole, Sulphasalazine).
      • Sulphonamides for local infections (e.g. Sulfacetamide, Mafenide, Silver sulphadiazine).
      • Sulphonamides for dermatitis (e.g. Dapsone, Solapsone).
      • Sulphonamides in combination (e.g. Trimethoprim with Sulphamethoxazole).
    • Based on pharmacokinetic properties:
      • Poorly absorbed sulphonamides (locally acting sulphonamides, e.g. Sulphasalazine, Phthalylsulphathiazole, Sulphaguanidine, Salicylazo sulphapyridine, Succinyl sulphathiazole).
      • Rapidly absorbed and rapidly excreted sulphonamides (systemic sulphonamides, e.g. Sulphamethoxazole, Sulphaisoxazole, Sulphadiazine, Sulphadimidine, Sulphafurazole, Sulphasomidine, Sulphamethiazole, Sulphacetamide, Sulphachlorpyridazine).
      • Topically used sulphonamides (e.g. Sulphacetamide, Mafenide, Sulphathiazole, Silver sulphadiazine).
    • Based on duration of action:
      • Extra long-acting sulphonamides (e.g. Sulphasalazine, Sulphaclomide, Sulphalene).
      • Long-acting sulphonamides (e.g. Sulphadoxine, Sulphadimethoxine, Sulphamethoxy pyridazine, Sulphamethoxydiazine, Sulphaphenazole, Sulphamethoxine).
      • Intermediate-acting sulphonamides (e.g. Sulphasomizole, Sulphamethoxazole).
      • Short-acting sulphonamides (e.g. Sulphamethiazole, Sulphaisoxazole).
    • Based on chemical structure:
      • N-substituted sulphonamides (e.g. Sulphadiazine, Sulphacetamide, Sulphadimidine).
      • N-4 substituted sulphonamides (prodrugs, e.g. Prontosil).
      • Both N-1 and N-4 substituted sulphonamides (e.g. Succinyl sulphathiazole, Phthalylsulphathiazole).

    Specific Sulphonamides

    • Sulphacetamide: used to treat bacterial infections of the urinary tract, exists as a white crystalline powder, bitter in taste.
    • Sulphasalazine: used to treat ulcerative colitis, exists as a bright yellow or brownish-yellow fine powder.
    • Sulphadiazine: used to treat canceroids and rheumatic fever, exists as a white or yellowish-white crystalline powder or crystals.
    • Sulphadimidine: used to treat bacterial infections, exists as a white crystalline powder with a bitter taste.
    • Sulphamerazine: used as an antibacterial agent, exists as a white or almost white crystalline powder.
    • Trimethoprim: used as a dihydrofolate reductase inhibitor, effective against chloroquine and pyrimethamine-resistant strains of Plasmodium falsiparum.

    Immunosuppressant Drugs

    • Inhibitors of cytokine (IL-2) production or action:
      • Calcineurin inhibitors (e.g. Cyclosporine, Tacrolimus).
      • Sirolimus (rapamycin).
    • Inhibitors of cytokine gene expression:
      • Corticosteroids (e.g. Prednisone, Prednisolone, Methylprednisolone, Dexamethasone).
    • Cytotoxic drugs:
      • Inhibitors of purine or pyrimidine synthesis (antimetabolites, e.g. Myclophenolate Mofetil, Leflunomide, Azathioprine, Methotrexate).
      • Alkylating agents (e.g. Cyclophosphamide).
    • Immunosuppressive antibodies:
      • Antilymphocyte globulins (ALG).
      • Antithymocyte globulins (ATG).
      • Rho (D) immunoglobulin.
      • Muromonab-CD3.
      • Basiliximab.
      • Daclizumab.

    Cyclosporine

    • A fungal polypeptide composed of 11 amino acids.
    • Mechanism of action: inhibits interleukin-2 production, decreases proliferation and differentiation of T cells.
    • Pharmacokinetics: given orally or i.v., slowly and incompletely absorbed, peak levels reached after 1-4 hours, elimination half-life 24 hours.
    • Therapeutic uses: organ transplantation, autoimmune disorders, graft-versus-host disease.
    • Adverse effects: nephrotoxicity, hypertension, hyperkalemia, liver dysfunction, hyperglycemia, viral infections, lymphoma, hirsutism, neurotoxicity.

    Tacrolimus (FK506)

    • A macrolide antibiotic, chemically not related to cyclosporine.
    • Mechanism of action: similar to cyclosporine, inhibits calcineurin.
    • Kinetics: given orally or i.v., variable and incomplete absorption, half-life 9-12 hours.
    • Uses: similar to cyclosporine, organ and stem cell transplantation, prevention of rejection of liver and kidney transplants.
    • Toxic effects: nephrotoxicity, neurotoxicity, hyperglycemia, GIT disturbances, hypertension, anaphylaxis.

    Sirolimus (Rapamycin)

    • A macrolide antibiotic, not a calcineurin inhibitor.
    • Mechanism of action: inhibits the response of T cells to IL-2, blocks activation of T- and B-cells.
    • Pharmacokinetics: given orally, reduced by fat meal, extensively bound to plasma proteins, metabolized by CYP3A4, excreted in feces.
    • Uses: synergistic action with cyclosporine, solid organ allografts, hematopoietic stem cell transplant recipients.
    • Toxic effects: hyperlipidaemia, thrombocytopenia, leukopenia, hepatotoxicity, hypertension, GIT dysfunction.Here are the study notes for the text:

    Glucocorticoids

    • Lead to decreased eicosanoid production and cyclooxygenase expression
    • Decrease production of inflammatory mediators, such as prostaglandins, leukotrienes, histamine, platelet-activating factor, and bradykinin
    • Inhibit gene transcription of many inflammatory genes
    • Suppress cell-mediated immunity, decreasing production of cytokines (IL-1, IL-2, interferon, TNF) and T lymphocyte proliferation
    • Suppress humoral immunity, reducing both B cell clone expansion and antibody synthesis

    Kinetics

    • Can be administered orally, parenterally, topically, and by inhalation (for asthma)
    • Dynamics include:
      • Anti-inflammatory and immunosuppressive effects
      • Suppression of response to infection
      • Metabolic effects

    Indications

    • Solid organ allografts and hematopoietic stem cell transplantation
    • Autoimmune diseases, such as refractory rheumatoid arthritis, systemic lupus erythematosus, and asthma
    • Acute or chronic rejection of solid organ allografts

    Adverse Effects

    • Adrenal suppression
    • Osteoporosis
    • Hypercholesterolemia
    • Hyperglycemia
    • Hypertension
    • Cataract
    • Infection

    Cytotoxic Drugs

    • Antimetabolites:
      • Leflunomide
      • Azathioprine
      • Mycophenolate mofetil
      • Methotrexate
    • Alkylating agents:
      • Cyclophosphamide

    Azathioprine

    • Derivative of mercaptopurine
    • Prodrug
    • Inhibits de novo synthesis of purines required for lymphocyte proliferation
    • Prevents clonal expansion of both B and T lymphocytes
    • Pharmacokinetics:
      • Orally or intravenously administered
      • Widely distributed but does not cross the blood-brain barrier
      • Metabolized in the liver to thiouric acid
      • Excreted primarily in urine
    • Drug interactions:
      • Co-administration with allopurinol may lead to toxicity due to inhibition of xanthine oxidase
    • Uses:
      • Acute glomerulonephritis
      • Systemic lupus erythematosus
      • Rheumatoid arthritis
      • Crohn's disease
      • Autoimmune hemolytic anemia
    • Adverse effects:
      • Bone marrow depression
      • Leukopenia
      • Thrombocytopenia
      • Gastrointestinal toxicity
      • Hepatic dysfunction
      • Increased risk of infections

    Mycophenolate Mofetil

    • Semisynthetic derivative of mycophenolic acid
    • Prodrug
    • Inhibits de novo synthesis of purines
    • Inhibits inosine monophosphate dehydrogenase, crucial for purine synthesis
    • Pharmacokinetics:
      • Given orally, intravenously, or intramuscularly
      • Rapidly and completely absorbed after oral administration
      • Undergoes first-pass metabolism to give the active moiety, mycophenolic acid
      • Extensively bound to plasma protein
      • Metabolized in the liver by glucuronidation
      • Excreted in urine as glucuronide conjugate
    • Clinical uses:
      • In solid organ transplantation
      • In hematopoietic stem cell transplant patients
      • In autoimmune disorders, such as rheumatoid arthritis and dermatologic disorders
    • Adverse effects:
      • Gastrointestinal toxicity
      • Leukopenia
      • Neutropenia
      • Lymphoma

    Leflunomide

    • Antimetabolite immunosuppressant
    • Inhibits pyrimidine synthesis
    • Can be given orally
    • Prodrug
    • Active metabolite undergoes enterohepatic circulation
    • Has a long duration of action
    • Approved only for rheumatoid arthritis
    • Adverse effects:
      • Elevation of liver enzymes
      • Renal impairment
      • Teratogenicity
      • Cardiovascular effects (tachycardia)

    Methotrexate

    • Folic acid antagonist
    • Can be given orally or parenterally
    • Excreted in urine
    • Inhibits dihydrofolate reductase required for folic acid activation
    • Inhibits DNA, RNA, and protein synthesis
    • Interferes with T-cell replication
    • Used in treatment of many neoplastic disorders, including acute lymphoblastic leukemia
    • Used in autoimmune disorders, such as rheumatoid arthritis, psoriasis, and Crohn's disease
    • Adverse effects:
      • Pulmonary fibrosis
      • Nausea, vomiting, diarrhea
      • Alopecia
      • Bone marrow depression
      • Teratogenicity

    Cyclophosphamide

    • Alkylating agent
    • Destroys proliferating lymphoid cells
    • Anticancer agent in lymphomas
    • Effective in autoimmune diseases, such as rheumatoid arthritis and systemic lupus erythematosus
    • Adverse effects:
      • Alopecia
      • Hemorrhagic cystitis
      • Bone marrow suppression
      • Gastrointestinal disorders
      • Sterility

    Antibodies

    • Used as a quick and potent immunosuppressive therapy to prevent acute rejection reactions
    • Types:
      • Polyclonal antibodies:
        • Antilymphocyte globulins (ALG)
        • Antithymocyte globulins (ATG)
      • Monoclonal antibodies:
        • Rho (D) immunoglobulin
        • Basiliximab
        • Daclizumab

    Antilymphocyte Globulins (ALG) and Antithymocyte Globulins (ATG)

    • Obtained by immunizing either horses or rabbits with human lymphoid cells
    • Produces mixtures of polyclonal antibodies directed against a number of lymphocyte antigens
    • Bind to the surface of circulating T lymphocytes, which are phagocytosed in the liver and spleen, giving lymphopenia and impaired T-cell responses and cellular immunity
    • Kinetics:
      • Given intramuscularly or slowly infused intravenously
      • Half-life extends from 3-9 days
    • Uses:
      • Combined with cyclosporine for bone marrow transplantation
      • To treat acute allograft rejection
      • Steroid-resistant rejection
    • Adverse effects:
      • Antigenicity
      • Anaphylactic and serum sickness reactions
      • Leukopenia
      • Thrombocytopenia
      • Risk of viral infection

    Muromonab-CD3

    • Murine monoclonal antibody
    • Prepared by hybridoma technology
    • Directed against the glycoprotein CD3 antigen of human T cells
    • Given intravenously
    • Metabolized and excreted in the bile
    • Mechanism of action:
      • Binds to CD3 proteins on T lymphocytes
      • Leads to transient activation and cytokine release
      • Followed by disruption of T-lymphocyte function
      • Decreased immune response
      • Block killing by cytotoxic T cells
    • Uses:
      • Used for treatment of acute renal allograft rejection
      • Steroid-resistant acute allograft rejection
      • To deplete T cells from bone marrow donor prior to transplantation
    • Adverse effects:
      • Anaphylactic reactions
      • Fever
      • CNS effects (seizures)
      • Infection
      • Cytokine release syndrome

    Basiliximab and Daclizumab

    • Obtained by replacing murine amino acid sequences with human ones
    • Have less antigenicity and longer half-lives than murine antibodies
    • Mechanism of action:
      • Interleukin-2 receptor antagonists
      • Bind to CD25 (α-subunit chain of IL-2 receptor on activated lymphocytes)
      • Block IL-2-stimulated T-cell replication and T-cell response system
    • Given intravenously
    • Half-life: Basiliximab (7 days), Daclizumab (20 days)
    • Uses:
      • Given with CsA and corticosteroids for prophylaxis of acute organ rejection in renal transplantation
    • Adverse effects:
      • Gastrointestinal disorders

    Interferons

    • Families:
      • Type I IFNs (IFN-α, β): induced by viral infections
      • Type II IFN (IFN-γ): produced by activated T lymphocytes
    • Interferon types and uses:
      • IFN-α:
        • Hepatitis B and C infections
        • Treatment of cancer (malignant melanoma)
      • IFN-β:
        • Multiple sclerosis
      • IFN-γ:
        • Treatment of chronic granulomatous diseases

    Diuretics

    • Increase the rate of urine flow
    • Also increase excretion of Na+ and an accompanying anion (negatively charged ion) like Cl–
    • Reduce extracellular fluid volume (decrease in edema) by decreasing total body NaCl content
    • Classes of diuretics:
      • Carbonic anhydrase inhibitors
      • Osmotic di

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