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Antivirus agents. Agents used in AIDs treatment. Immunomodulators

Antivirus agents. Agents used in AIDs treatment. Immunomodulators. Antivirus agents. Agents used in AIDs treatment. Immunomodulators. Antiviral Agents. Understanding Viruses. Viral Replication A virus cannot replicate on its own. It must attach to and enter a host cell.

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Antivirus agents. Agents used in AIDs treatment. Immunomodulators

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  1. Antivirus agents. Agents used in AIDs treatment. Immunomodulators

  2. Antivirus agents. Agents used in AIDs treatment. Immunomodulators

  3. Antiviral Agents

  4. Understanding Viruses Viral Replication • A virus cannot replicate on its own. • It must attach to and enter a host cell. • It then uses the host cell’s energy to synthesize protein, DNA, and RNA.

  5. Understanding Viruses Viruses are difficult to kill because they liveinside our cells. • Any drug that kills a virus may also kill our cells.

  6. Viral Infections Competent immune system: • Best response to viral infections • A well-functioning immune system will eliminate or effectively destroy virus replication Immunocompromised patients have frequent viral infections • Cancer patients, especially leukemia or lymphoma • Transplant patients, due to pharmacological therapy • AIDS patients, disease attacks immune system

  7. Antivirals Key characteristics of antiviral drugs: • Able to enter the cells infected with virus. • Interfere with viral nucleic acid synthesis and/or regulation. • Some agents interfere with ability of virus to bind to cells. • Some agents stimulate the body’s immune system.

  8. Antivirals Viruses killed by current antiviral therapy: • cytomegalovirus (CMV) • herpes simplex virus (HSV) • human immunodeficiency virus (HIV) • influenza A (the “flu”) • respiratory syncytial virus (RSV)

  9. Antivirals: Mechanism of Action Inhibit viral replication • Inhibit viral attachment • Prevent genetic copying of virus • Prevent viral protein production

  10. Sites of Drug Action

  11. Sites of Drug Action

  12. Antiviral Agents • Block viral entry into the cell or must work inside the cell • Most agents are pyrimidine or purine nucleoside analogs

  13. Antivirals Synthetic Purine Nucleoside Analogues Two types of nucleosides: Purine nucleosides • guanine • adenosine Pyrimidine nucleosides • thymine • cytosine

  14. Antivirals: Purine Nucleosides Agent Antiviral Activity guanines acyclovir HSV 1 & 2, VZV ganciclovir (DHPG) CMV retinitis and systemic CMV infection ribavirin (RTCD) Influenza types A and B, RSV, LV, HV adenosines didanosine (ddl) HIV vidarabine (Ara-A) HSV, herpes zoster

  15. Antivirals: Pyrimidine Nucleosides Agent Antiviral Activity cytosines lamivudine (3TC) HIV zalcitabine (ddC) HIV thymine idoxuridine (IDU) HSV stavudine (d4T) HIV trifluridine HSV zidovudine (AZT) HIV

  16. Other Antivirals amantadine (Symmetrel) and rimantadine (Flumadine) • influenza A foscarnet (Foscavir) • CMV (retinitis and systemic) Neuraminidase Inhibitors: oseltamivir (Tamiflu) and zanamivir (Relenza) • influenza types A and B

  17. Antivirals: Side Effects acyclovir • Burning when topically applied, nausea, vomiting, diarrhea, headache amantadine and rimantadine • Anticholinergic effects, insomnia, lightheadedness, anorexia, nausea didanosine (ddl) • Pancreatitis, peripheral neuropathies, seizures

  18. Antivirals: Side Effects zidovudine (AZT) • Bone marrow suppression, nausea, headache foscarnet (Foscavir) • Headache, seizures, acute renal failure, nausea, vomiting, diarrhea ganciclovir (Cytovene) • Bone marrow toxicity, nausea, anorexia, vomiting

  19. Antiherpes Agents • Acyclovir- prototype • Valacyclovir • Famciclovir • Penciclovir • Trifluridine • Vidarabine

  20. Mechanism of Action Acyclovir • an acyclic guanosine derivative • Phosphorylated by viral thymidine kinase • Di-and tri-phosphorylated by host cellular enzymes • Inhibits viral DNA synthesis by: • 1) competing with dGTP for viral DNA polymerase • 2) chain termination

  21. Types of allergic reactions (according to Gell and Cumbs): 1. I type reactions (anaphylactic) 2. II type reaction (humoral cytotoxic immune reactions) 3 III type reactions 4. IV type reactions 5. V type reactions (autosensibilization)

  22. Classification of allergic reactions in clinic: • reactions of immediate type • (I, II, III, V types after Cumbs) • 2. reactions of delayed type (IV type after Cumbs)

  23. General principles of prevention and treatment of allergic reactions 1) Avoiding contact with the allergen 2) Performing specific desensitization by repeated introduction of small doses of specific antigen 3) Performing nonspecific desensitization through administration of drugs which depress immune reactions (immune depressants) 4) Using antiallergic drugs which are able to prevent releasing the mediators of allergic reaction through stabilization of mast sells’ membranesor to block receptors with which these mediators interact in tissues 5) Symptomatic treatment of allergic reactions manifestations which have already developed

  24. Directions of therapy of hypersensitivity reactions of immediate type 1) Antiallergic drugs : а) drugs which stabilize membranes of mast cells and basophiles and slow down releasing of mediators of hypersensitivity reaction (sodium-cromolin, ketotifen) б) antihistamine drugs – block receptors with which histamine binds in the tissues ( dimedrol, suprastin etc.) 2) Drugs which decrease damage of the tissues (glucocorticosteroids) 3) Drugs of symptomatic treatment (adrenalin, euphyllin)

  25. Antihistamine drugs R1 CH3 CH2-CH2-N R1 CH3 Structure of nucleus of Н1 histamine-receptors antagonists (H1 histamine-blockers)

  26. According to chemical structure blockers of Н1histamine-receptors are divided into derivatives of: 1) ethylendiamin (suprastin) 2) ethanolamin (dimedrol, klemastin) 3) piperasin (cetyrisin) 4) alkilamins (feniramin) 5) phenothiasin (diprasin, teralen) 6) oxycam (meloxycam, pyroxycam) 6) different structure (diasolin, peritol, fenkarol)

  27. Comparative antiallergic activity Н1histamine blockers of 1st generation diprasine>tavegil>dimedrol>suprastin> fenkarol>diasoline Н1 histamine blockers of 2nd and 3rd generations cetirizine>ebastin> terfenadine=fexofenadine> astemizole>loratadine

  28. Indications for administration of antihistamine drugs: 1. Nettle-rash 2. Hay fever 3. Vasomotor rhinitis 4. Contact dermatitis 5. Angionevrotic edema 6. Serum diseases 7. Anaphylactic shock 8. Others

  29. Side effects of Н1-histamine receptors blockers of 1st generation 1) Depression of CNS (disorders of coordination, increased tiredness, dizziness,diplopia, tremor, euphoria, nervousness, insomnia) 2) Disturbance of GI functioning : decreasing of appetite, nausea, vomiting, pain in epigastria, constipation of diarrhea 3) As a result of M-cholinoblocking activity – dryness of mucous membranes, eye disorders - blurred vision, impotence, ischuria, tachycardia, headache, psychosis, in case of repeated administration - tachyphylaxia

  30. Properties of Н1- histamine receptors blockers of 2nd and 3rd generations: 1) Blockage Н1-histamine receptors 2) Stabilizing mast cells 3) Decreasing histamine secretion 4) Possessing anti-inflammatory activity

  31. Advantages of Н1-histamine receptors blockers of 2nd and 3rd generations over classical Н1-antagonists 1) High specificity and affinity to Н1-receptors 2) Short onset 3) Long duration of action (over 24 hours) 4) Absence of blockade of other types of receptors 5) Nonpenetrable through HEB in therapeutic doses 6) Absence of tachyphylaxia

  32. Anti-inflammatory drugs

  33. Groups of anti-inflammatory agents and mechanism of action: 1) nonsteroidal anti-inflammatory drugs - NSAI 2) glucocorticosteroids (GCS) + - Phospholipids Arachidonic acid Cyclic endoperoxydases glucocorticosteroids LK Phospholipase А2 - Cyclooxygenases (COG-1, COG-2, COG-3) NSAID ProstaglandinsThromboxan InflammationPainFeverVasoconstriction Increasing of platelets aggregation - depressing effect - stimulating effect - +

  34. Classification of nonsteroid anti-inflammatory drugs according to mechanism of action: • Selective inhibitors of COG-1 (acetylsalicylic acid in small doses) • II.Nonselective inhibitors of COG-1 and COG-2 (most of NSAID) • III.Drugs with dominant influence on COG-2 • (meloxycam, nimesulid) • IV.High selective inhibitors of COG-2 • (celecoxyb,rofecoxyb)

  35. Classification of nonsteroid anti-inflammatory drugs according to their chemical structure: 1) Derivatives of salicylic acid (acetylsalicylic acid) 2) Derivatives of fenamic acid - fenamates(flufenamic and mefenamic acids) 3) Derivatives of propion acid (ibuprofen, naproxen, ketoprofen, surgam) 4) Derivatives of pyrasolon (butadion) 5) Derivatives of acetic acid (dyclofenac, indometacyn, sulindac, nabumethon) 6) Derivatives of oxycam (pyroxycam, meloxycam)

  36. Properties of nonsteroid anti-inflammatory drugs • Anti-inflammatory action • indometacyn> flurbiprofen>dyclofenac>meloxycam>nimesulid>pyroxycam>ketoprofen>naproxen>butadion>ibuprofen>acetylsalicylic acid • Analgesic action • Febrifugal (antipyretic) action

  37. Indications for administration of nonsteroid anti-inflammatory drugs 1. Rheumatism 2. Infectious-allergic myocarditis 3. Rheumatoid polyarthritis 4. System lupus erythematosus 5. Anchilizing spondilitis (Bechterev’s disease) 6. Gout 7. Deformating osteoarthrosis(DOA) 8. Thrombophlebitis 9. Inflammation diseases of connective tissue, osseous-muscular system 10. Neuralgia 11. Meningoencephalitis 12. Chronic bronchitis 13. Virus hepatitis

  38. Doses in which NSAID are used as anti-inflammatory agents

  39. Acetylsalicylic acid

  40. Aspirin С

  41. Aspirin

  42. Butadion

  43. Indometacin (methyndol)

  44. Ibuprofen (brufen)

  45. Piroxicam

  46. Sodium diclofenac

  47. Voltaren

  48. Side effects of nonsteroid anti-inflammatory drugs

  49. Prevention of development of GI complications while administering NSAID: 1) Administer simultaneously with gastric protectors sucralfat, misoprostol, ranitidin, famotidin, omeprasol 2) Create and introduce NSAID which selectively inhibit COG-2 meloxycam, nimesulid

  50. Directions of medical treatment ofrheumatoid illnesses: • NSAIDwith the aim of depression of inflammatory process, pain, rigidness of muscles and joints • 2) Basis drugs(disease modifying) • Methotrexat, hydroxychloroquin, sulfasalazin, gold containing drugs, penicillamin, , • purin derivatives (asathioprin and mercaptopurin) • Alkilying drugs (chlorbutin and cyclophosphamid), • cyclosporin • 3) GCSare administered if there’s a lack of effect of NSAID and basis drugs in case of very severe currency of inflammatory process

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