This document discusses various classes of antifungal and antiviral agents. It provides details on their mechanisms of action, spectra of activity, administration, pharmacokinetics, side effects and uses. The major classes of antifungals discussed are polyenes such as amphotericin B, azoles, allylamines, flucytosine and griseofulvin. The major classes of antivirals discussed are inhibitors of uncoating such as amantadine and rimantadine, inhibitors of nucleic acid synthesis, and inhibitors of release such as neuraminidase inhibitors oseltamivir and zanamivir.
Antifungal drugs work by targeting differences between fungal and human cell membranes and metabolism. Azoles like fluconazole inhibit ergosterol synthesis while polyenes like amphotericin B bind to ergosterol in the fungal cell membrane. Topical antifungals like nystatin and tolnaftate treat superficial infections while systemic drugs like fluconazole and itraconazole treat deep infections. Common adverse effects include nausea, liver toxicity, and drug interactions. The choice of antifungal depends on the infecting organism, infection severity, and route of administration needed.
Entamoeba histolytica is a protozoan parasite that causes amoebiasis. It is transmitted through the oral-fecal route by ingesting cysts from contaminated food or water. In the intestines, cysts excyst into trophozoites which multiply and may invade the intestinal wall, causing dysentery. Trophozoites can spread to other organs through the bloodstream. Metronidazole is effective against both intestinal and tissue infections, as it is activated by anaerobic metabolism and kills the trophozoites. Other nitroimidazole derivatives like tinidazole and ornidazole are also used to treat amoebiasis.
Sulfonamides were the first effective antibacterial drugs, discovered in the 1930s. They work by inhibiting folic acid synthesis in bacteria. Potentiated sulfonamides combine sulfonamides with diaminopyrimidines like trimethoprim for increased efficacy. Sulfonamides are used to treat various bacterial and protozoal infections in animals. While generally safe, they can cause urinary tract disturbances and bone marrow depression if not properly administered and hydration maintained.
This document discusses histamine and antihistamines. It begins by introducing histamine, describing its discovery and roles in allergic reactions and as a neurotransmitter. It then covers histamine's chemistry, distribution in the body, synthesis, storage, and metabolism. The document discusses the four types of histamine receptors (H1-H4) and histamine's pharmacological effects. It also provides details on antihistamines, including their pharmacokinetics, mechanisms of action, side effects, and classifications of first versus second generation antihistamines. The document concludes by mentioning clinical uses of histamine and antihistamines for conditions like allergies and gastric hypersecretions.
This document summarizes a lecture on anthelminthic and anti-protozoal drugs. It discusses how these drugs work, how they are classified based on the organisms they target, and provides examples of specific drugs. Key drugs discussed are albendazole and metronidazole. Albendazole works by paralyzing helminths through binding to microtubule proteins. Metronidazole kills protozoa by interfering with their energy production. Both drugs are generally well tolerated though can cause gastrointestinal side effects.
Histamine is a biogenic amine found in many tissues that is involved in allergic and inflammatory processes as well as gastric acid secretion and neurotransmission. It is synthesized and stored in mast cells and basophils and released during allergic reactions. Histamine exerts its effects through four receptor subtypes (H1-H4), with H1 and H2 receptors having drugs that target them clinically. H1 receptor antagonists are used to treat allergic rhinitis, chronic urticaria, and motion sickness, while H2 receptor antagonists suppress gastric acid secretion. New drugs targeting H3 and H4 receptors may provide treatments for neurological and inflammatory conditions, respectively.
Antiemetics and prokinetics classification with mechansim SONALPANDE5
This document provides information on antiemetics and prokinetics. It discusses nausea, emesis, and the various receptor types involved in vomiting including acetylcholine, dopamine, histamine, serotonin, substance P, and opioid receptors. It covers the etiology, pathophysiology, and classification of conditions causing nausea and vomiting. Various receptor antagonist antiemetics are described including H1 receptor antagonists like cyclizine, muscarinic receptor antagonists like hyoscine, 5-HT3 receptor antagonists like ondansetron, dopamine antagonists like chlorpromazine, and NK1 receptor antagonists like aprepitant. Adjuvant antiemetics including dexamethasone and
This document discusses macrolide antibiotics, including their structure, examples (erythromycin, azithromycin), mechanism of action, spectrum of activity, resistance, pharmacokinetics, adverse effects, drug interactions, and contraindications. Macrolides bind to the bacterial ribosome and inhibit protein synthesis, generally being bacteriostatic. Their spectrum includes many gram-positive bacteria and some intracellular pathogens. Resistance can occur via efflux pumps or ribosomal mutations. Adverse effects include gastrointestinal issues and ototoxicity. Macrolides can interact with drugs metabolized by CYP450 enzymes.
Antifungal drugs work by targeting differences between fungal and human cell membranes and metabolism. Azoles like fluconazole inhibit ergosterol synthesis while polyenes like amphotericin B bind to ergosterol in the fungal cell membrane. Topical antifungals like nystatin and tolnaftate treat superficial infections while systemic drugs like fluconazole and itraconazole treat deep infections. Common adverse effects include nausea, liver toxicity, and drug interactions. The choice of antifungal depends on the infecting organism, infection severity, and route of administration needed.
Entamoeba histolytica is a protozoan parasite that causes amoebiasis. It is transmitted through the oral-fecal route by ingesting cysts from contaminated food or water. In the intestines, cysts excyst into trophozoites which multiply and may invade the intestinal wall, causing dysentery. Trophozoites can spread to other organs through the bloodstream. Metronidazole is effective against both intestinal and tissue infections, as it is activated by anaerobic metabolism and kills the trophozoites. Other nitroimidazole derivatives like tinidazole and ornidazole are also used to treat amoebiasis.
Sulfonamides were the first effective antibacterial drugs, discovered in the 1930s. They work by inhibiting folic acid synthesis in bacteria. Potentiated sulfonamides combine sulfonamides with diaminopyrimidines like trimethoprim for increased efficacy. Sulfonamides are used to treat various bacterial and protozoal infections in animals. While generally safe, they can cause urinary tract disturbances and bone marrow depression if not properly administered and hydration maintained.
This document discusses histamine and antihistamines. It begins by introducing histamine, describing its discovery and roles in allergic reactions and as a neurotransmitter. It then covers histamine's chemistry, distribution in the body, synthesis, storage, and metabolism. The document discusses the four types of histamine receptors (H1-H4) and histamine's pharmacological effects. It also provides details on antihistamines, including their pharmacokinetics, mechanisms of action, side effects, and classifications of first versus second generation antihistamines. The document concludes by mentioning clinical uses of histamine and antihistamines for conditions like allergies and gastric hypersecretions.
This document summarizes a lecture on anthelminthic and anti-protozoal drugs. It discusses how these drugs work, how they are classified based on the organisms they target, and provides examples of specific drugs. Key drugs discussed are albendazole and metronidazole. Albendazole works by paralyzing helminths through binding to microtubule proteins. Metronidazole kills protozoa by interfering with their energy production. Both drugs are generally well tolerated though can cause gastrointestinal side effects.
Histamine is a biogenic amine found in many tissues that is involved in allergic and inflammatory processes as well as gastric acid secretion and neurotransmission. It is synthesized and stored in mast cells and basophils and released during allergic reactions. Histamine exerts its effects through four receptor subtypes (H1-H4), with H1 and H2 receptors having drugs that target them clinically. H1 receptor antagonists are used to treat allergic rhinitis, chronic urticaria, and motion sickness, while H2 receptor antagonists suppress gastric acid secretion. New drugs targeting H3 and H4 receptors may provide treatments for neurological and inflammatory conditions, respectively.
Antiemetics and prokinetics classification with mechansim SONALPANDE5
This document provides information on antiemetics and prokinetics. It discusses nausea, emesis, and the various receptor types involved in vomiting including acetylcholine, dopamine, histamine, serotonin, substance P, and opioid receptors. It covers the etiology, pathophysiology, and classification of conditions causing nausea and vomiting. Various receptor antagonist antiemetics are described including H1 receptor antagonists like cyclizine, muscarinic receptor antagonists like hyoscine, 5-HT3 receptor antagonists like ondansetron, dopamine antagonists like chlorpromazine, and NK1 receptor antagonists like aprepitant. Adjuvant antiemetics including dexamethasone and
This document discusses macrolide antibiotics, including their structure, examples (erythromycin, azithromycin), mechanism of action, spectrum of activity, resistance, pharmacokinetics, adverse effects, drug interactions, and contraindications. Macrolides bind to the bacterial ribosome and inhibit protein synthesis, generally being bacteriostatic. Their spectrum includes many gram-positive bacteria and some intracellular pathogens. Resistance can occur via efflux pumps or ribosomal mutations. Adverse effects include gastrointestinal issues and ototoxicity. Macrolides can interact with drugs metabolized by CYP450 enzymes.
Anthelmintics | B.Pharm 3rd year 2nd Sem | Medicinal Chemistry-III | History, Classification, Structures & Synthesis of anthelmintics, Synthesis of Diethylcarbamazine citrate, Synthesis of Mebendazole
This document provides an overview of aminoglycoside antibiotics. It discusses that aminoglycosides are a group of bactericidal antibiotics used to treat aerobic Gram-negative bacteria by preventing bacterial protein synthesis. Some key points covered include:
- Aminoglycosides like streptomycin were first discovered in the 1940s from soil bacteria. Common systemic aminoglycosides include gentamicin, tobramycin, and amikacin.
- Their mechanism of action involves binding to the 30S ribosomal subunit of bacteria to prevent proper initiation complex formation and protein synthesis.
- They have concentration-dependent bacterial killing and a post-antibiotic effect. Resistance can develop via enzymatic modification or
synthetic antimicrobials having a quinolone structure that are active primarily against gram-negative bacteria, though newer fluorinated compounds also inhibit gram-positive ones.
This document summarizes various anti-viral drugs used to treat viral infections like herpes, influenza, hepatitis, HIV, and their mechanisms of action and clinical applications. It discusses nucleoside and nucleotide reverse transcriptase inhibitors like acyclovir, valacyclovir, famciclovir for herpes; oseltamivir and zanamivir for influenza; lamivudine for hepatitis B; and protease inhibitors and integrase inhibitors for HIV treatment. It also covers classification, uses, advantages, resistance and adverse effects of these anti-viral medications.
A power point presentation on Pharmacodynamics (what drug does to the body) suitable for undergraduate medical students beginning to study Pharmacology
This document provides an overview of anti-fungal drugs. It begins by classifying antifungals based on their chemical structure, sites of action, and mechanisms of action. The major classes discussed include azoles, polyene macrolides, and other antifungals. Azoles like fluconazole and itraconazole are broad-spectrum and inhibit ergosterol synthesis. Amphotericin B binds to ergosterol and forms pores in fungal membranes. Other antifungals discussed are flucytosine, griseofulvin, and nystatin. The document outlines the mechanisms, therapeutic uses, and adverse effects of the main antifungal drug
This document provides information on various anthelmintic drugs used to treat helminth infections. It discusses the classification, mechanisms of action, pharmacokinetics, efficacy, and side effects of common anthelmintics including mebendazole, albendazole, thiabendazole, pyrantel pamoate, piperazine, diethyl carbamazine citrate, and ivermectin. The document aims to educate on the treatment of helminth infections through different anthelmintic drug options.
1) Aminoglycosides are polybasic amino groups linked glycosidically to aminosugar compounds. They are highly water soluble and excreted unchanged in urine.
2) They are bactericidal, inhibiting protein synthesis by binding to the 30S/50S interface of bacterial ribosomes. This causes misreading of mRNA and nonfunctional protein formation.
3) Common adverse effects include ototoxicity (hearing loss) and nephrotoxicity. Individual drugs vary in their specific toxicities.
Usha Rani Kandula, an assistant professor from Arsi University in Ethiopia, authored this document about expectorants. Expectorants are drugs that increase fluid in the respiratory tract and thin secretions to aid in removal through coughing and cilia action. Common expectorants include guaifensin, potassium iodide, and terpin hydrate elixir. Expectorants are indicated for non-productive coughs, bronchitis, laryngitis, influenza, dry coughs, and productive coughs. Nurses assess lung sounds, cough characteristics, secretions and encourage fluid intake and deep breathing exercises when clients take expectorants.
1. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis and causes the chronic lung infection tuberculosis. It is treated using a combination of antibiotics over a long period of time to prevent drug resistance from developing.
2. First line antibiotics include isoniazid, rifampin, pyrazinamide, and ethambutol. Isoniazid and rifampin are highly effective at killing the bacteria while pyrazinamide and ethambutol prevent resistance. Treatment involves an initial phase to relieve symptoms followed by a continuous phase to fully eliminate the bacteria.
3. Drug resistance is a major problem, requiring longer and more toxic second line treatments. Factors like non-compliance
This document discusses macrolide antibiotics, including their mechanism of action, types, and uses. It describes several macrolide antibiotics like erythromycin, clarithromycin, azithromycin, and roxithromycin. It covers their mechanisms of action, spectra of activity, pharmacokinetics, clinical uses, side effects, and interactions. It also briefly discusses newer macrolides like telithromycin and ketolides, as well as the lincosamide antibiotic clindomycin.
Aminoglycosides are a class of antibiotics that are produced by soil bacteria. They are primarily used to treat infections caused by aerobic gram-negative bacteria and some are used for mycobacterial infections. Aminoglycosides work by binding to bacterial ribosomes which interferes with protein synthesis. They have concentration-dependent bactericidal activity against many gram-negative organisms but limited activity against gram-positive bacteria. Common adverse effects include ototoxicity and nephrotoxicity. Therapeutic drug monitoring is important when using aminoglycosides to minimize toxicity risks.
This document discusses immunomodulators, which are drugs that either suppress (immunosuppressants) or enhance (immunostimulants) the immune system. It describes several classes of immunosuppressants including calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative agents like azathioprine, mTOR inhibitors like sirolimus, glucocorticoids like prednisolone, and biologics like infliximab. Their mechanisms of action, uses, and adverse effects are summarized. Immunostimulants discussed include levamisole, thalidomide, BCG vaccine, and interferons.
Sulfonamides and trimethoprim are antibacterial drugs that work by inhibiting bacterial folic acid synthesis. Sulfonamides were the first antibacterial sulfone drugs discovered in the 1930s. Trimethoprim inhibits a different enzyme in the folic acid pathway. The combination of sulfamethoxazole and trimethoprim is highly synergistic and known as cotrimoxazole. It is used to treat urinary tract, respiratory, and other infections. Both drugs can cause side effects like rash, nausea, and bone marrow suppression if not used carefully, especially in pregnancy, renal impairment, or the elderly.
The document classifies antitubercular drugs into first line, second line, and newer drugs. It provides details on the mechanisms of action, properties, uses and resistance mechanisms of major first line drugs including isoniazid, rifampin, ethambutol, pyrazinamide, and streptomycin. It also briefly discusses some second line drugs like para-aminosalicylic acid, ethionamide, cycloserine, capreomycin, and kanamycin.
The document summarizes key information about aminoglycoside antibiotics. It discusses their discovery, examples currently used, and properties like poor absorption and administration by injection. Mechanisms of action involve binding to bacterial ribosomes to inhibit protein synthesis. Resistance can develop through enzymatic modification of the antibiotics. The structure and functional groups of the different rings that make up aminoglycosides influence their activity, spectrum, and susceptibility to resistance mechanisms.
Hello friends. In this PPT I am talking about anti-fungal drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
This document discusses antifungal drugs. It begins by introducing antifungals and the types of fungal infections they treat. It then describes the most common fungal pathogens and the targets of antifungal therapy. The remainder of the document focuses on specific antifungal drug classes, including polyenes like amphotericin B, azoles like imidazoles and triazoles, and others. It provides details on the mechanisms of action, spectra of activity, pharmacokinetics, uses, and adverse effects of several important antifungal medications.
Antifungals work by exploiting differences between mammalian and fungal cells to kill fungi with fewer side effects, though side effects can still occur. There are three main classes of antifungals: polyenes like nystatin and amphotericin B which attack the fungal cell membrane; azoles like clotrimazole which interfere with ergosterol formation; and griseofulvin which disrupts fungal cell division. Antivirals target various stages of the viral replication cycle by inhibiting viral entry, synthesis of proteins or nucleic acids, or final assembly of new viral particles in order to prevent or treat viral infections. Their mechanisms and side effects vary depending on the specific antiviral drug used
An antifungal medication is a pharmaceutical fungicide used to treat and prevent mycoses such as athlete's foot, ringworm, candidiasis (thrush), serious systemic infections such as cryptococcal meningitis, and others. Such drugs are usually obtained by a doctor's prescription, but a few are available OTC (over-the-counter).
Antifungals work by exploiting differences between mammalian and fungal cells to kill the fungal organism with fewer adverse effects to the host. Unlike bacteria, both fungi and humans are eukaryotes. Thus, fungal and human cells are similar at the biological level. This makes it more difficult to discover drugs that target fungi without affecting human cells. As a consequence, many antifungal drugs cause side-effects. Some of these side-effects can be life-threatening if the drugs are not used properly.
Anthelmintics | B.Pharm 3rd year 2nd Sem | Medicinal Chemistry-III | History, Classification, Structures & Synthesis of anthelmintics, Synthesis of Diethylcarbamazine citrate, Synthesis of Mebendazole
This document provides an overview of aminoglycoside antibiotics. It discusses that aminoglycosides are a group of bactericidal antibiotics used to treat aerobic Gram-negative bacteria by preventing bacterial protein synthesis. Some key points covered include:
- Aminoglycosides like streptomycin were first discovered in the 1940s from soil bacteria. Common systemic aminoglycosides include gentamicin, tobramycin, and amikacin.
- Their mechanism of action involves binding to the 30S ribosomal subunit of bacteria to prevent proper initiation complex formation and protein synthesis.
- They have concentration-dependent bacterial killing and a post-antibiotic effect. Resistance can develop via enzymatic modification or
synthetic antimicrobials having a quinolone structure that are active primarily against gram-negative bacteria, though newer fluorinated compounds also inhibit gram-positive ones.
This document summarizes various anti-viral drugs used to treat viral infections like herpes, influenza, hepatitis, HIV, and their mechanisms of action and clinical applications. It discusses nucleoside and nucleotide reverse transcriptase inhibitors like acyclovir, valacyclovir, famciclovir for herpes; oseltamivir and zanamivir for influenza; lamivudine for hepatitis B; and protease inhibitors and integrase inhibitors for HIV treatment. It also covers classification, uses, advantages, resistance and adverse effects of these anti-viral medications.
A power point presentation on Pharmacodynamics (what drug does to the body) suitable for undergraduate medical students beginning to study Pharmacology
This document provides an overview of anti-fungal drugs. It begins by classifying antifungals based on their chemical structure, sites of action, and mechanisms of action. The major classes discussed include azoles, polyene macrolides, and other antifungals. Azoles like fluconazole and itraconazole are broad-spectrum and inhibit ergosterol synthesis. Amphotericin B binds to ergosterol and forms pores in fungal membranes. Other antifungals discussed are flucytosine, griseofulvin, and nystatin. The document outlines the mechanisms, therapeutic uses, and adverse effects of the main antifungal drug
This document provides information on various anthelmintic drugs used to treat helminth infections. It discusses the classification, mechanisms of action, pharmacokinetics, efficacy, and side effects of common anthelmintics including mebendazole, albendazole, thiabendazole, pyrantel pamoate, piperazine, diethyl carbamazine citrate, and ivermectin. The document aims to educate on the treatment of helminth infections through different anthelmintic drug options.
1) Aminoglycosides are polybasic amino groups linked glycosidically to aminosugar compounds. They are highly water soluble and excreted unchanged in urine.
2) They are bactericidal, inhibiting protein synthesis by binding to the 30S/50S interface of bacterial ribosomes. This causes misreading of mRNA and nonfunctional protein formation.
3) Common adverse effects include ototoxicity (hearing loss) and nephrotoxicity. Individual drugs vary in their specific toxicities.
Usha Rani Kandula, an assistant professor from Arsi University in Ethiopia, authored this document about expectorants. Expectorants are drugs that increase fluid in the respiratory tract and thin secretions to aid in removal through coughing and cilia action. Common expectorants include guaifensin, potassium iodide, and terpin hydrate elixir. Expectorants are indicated for non-productive coughs, bronchitis, laryngitis, influenza, dry coughs, and productive coughs. Nurses assess lung sounds, cough characteristics, secretions and encourage fluid intake and deep breathing exercises when clients take expectorants.
1. Tuberculosis is caused by the bacterium Mycobacterium tuberculosis and causes the chronic lung infection tuberculosis. It is treated using a combination of antibiotics over a long period of time to prevent drug resistance from developing.
2. First line antibiotics include isoniazid, rifampin, pyrazinamide, and ethambutol. Isoniazid and rifampin are highly effective at killing the bacteria while pyrazinamide and ethambutol prevent resistance. Treatment involves an initial phase to relieve symptoms followed by a continuous phase to fully eliminate the bacteria.
3. Drug resistance is a major problem, requiring longer and more toxic second line treatments. Factors like non-compliance
This document discusses macrolide antibiotics, including their mechanism of action, types, and uses. It describes several macrolide antibiotics like erythromycin, clarithromycin, azithromycin, and roxithromycin. It covers their mechanisms of action, spectra of activity, pharmacokinetics, clinical uses, side effects, and interactions. It also briefly discusses newer macrolides like telithromycin and ketolides, as well as the lincosamide antibiotic clindomycin.
Aminoglycosides are a class of antibiotics that are produced by soil bacteria. They are primarily used to treat infections caused by aerobic gram-negative bacteria and some are used for mycobacterial infections. Aminoglycosides work by binding to bacterial ribosomes which interferes with protein synthesis. They have concentration-dependent bactericidal activity against many gram-negative organisms but limited activity against gram-positive bacteria. Common adverse effects include ototoxicity and nephrotoxicity. Therapeutic drug monitoring is important when using aminoglycosides to minimize toxicity risks.
This document discusses immunomodulators, which are drugs that either suppress (immunosuppressants) or enhance (immunostimulants) the immune system. It describes several classes of immunosuppressants including calcineurin inhibitors like cyclosporine and tacrolimus, antiproliferative agents like azathioprine, mTOR inhibitors like sirolimus, glucocorticoids like prednisolone, and biologics like infliximab. Their mechanisms of action, uses, and adverse effects are summarized. Immunostimulants discussed include levamisole, thalidomide, BCG vaccine, and interferons.
Sulfonamides and trimethoprim are antibacterial drugs that work by inhibiting bacterial folic acid synthesis. Sulfonamides were the first antibacterial sulfone drugs discovered in the 1930s. Trimethoprim inhibits a different enzyme in the folic acid pathway. The combination of sulfamethoxazole and trimethoprim is highly synergistic and known as cotrimoxazole. It is used to treat urinary tract, respiratory, and other infections. Both drugs can cause side effects like rash, nausea, and bone marrow suppression if not used carefully, especially in pregnancy, renal impairment, or the elderly.
The document classifies antitubercular drugs into first line, second line, and newer drugs. It provides details on the mechanisms of action, properties, uses and resistance mechanisms of major first line drugs including isoniazid, rifampin, ethambutol, pyrazinamide, and streptomycin. It also briefly discusses some second line drugs like para-aminosalicylic acid, ethionamide, cycloserine, capreomycin, and kanamycin.
The document summarizes key information about aminoglycoside antibiotics. It discusses their discovery, examples currently used, and properties like poor absorption and administration by injection. Mechanisms of action involve binding to bacterial ribosomes to inhibit protein synthesis. Resistance can develop through enzymatic modification of the antibiotics. The structure and functional groups of the different rings that make up aminoglycosides influence their activity, spectrum, and susceptibility to resistance mechanisms.
Hello friends. In this PPT I am talking about anti-fungal drugs. If you like it, please do let me know in the comments section. A single word of appreciation from you will encourage me to make more of such videos. Thanks. Enjoy and welcome to the beautiful world of pharmacology where pharmacology comes to life. This video is intended for MBBS, BDS, paramedical and any person who wishes to have a basic understanding of the subject in the simplest way.
This document discusses antifungal drugs. It begins by introducing antifungals and the types of fungal infections they treat. It then describes the most common fungal pathogens and the targets of antifungal therapy. The remainder of the document focuses on specific antifungal drug classes, including polyenes like amphotericin B, azoles like imidazoles and triazoles, and others. It provides details on the mechanisms of action, spectra of activity, pharmacokinetics, uses, and adverse effects of several important antifungal medications.
Antifungals work by exploiting differences between mammalian and fungal cells to kill fungi with fewer side effects, though side effects can still occur. There are three main classes of antifungals: polyenes like nystatin and amphotericin B which attack the fungal cell membrane; azoles like clotrimazole which interfere with ergosterol formation; and griseofulvin which disrupts fungal cell division. Antivirals target various stages of the viral replication cycle by inhibiting viral entry, synthesis of proteins or nucleic acids, or final assembly of new viral particles in order to prevent or treat viral infections. Their mechanisms and side effects vary depending on the specific antiviral drug used
An antifungal medication is a pharmaceutical fungicide used to treat and prevent mycoses such as athlete's foot, ringworm, candidiasis (thrush), serious systemic infections such as cryptococcal meningitis, and others. Such drugs are usually obtained by a doctor's prescription, but a few are available OTC (over-the-counter).
Antifungals work by exploiting differences between mammalian and fungal cells to kill the fungal organism with fewer adverse effects to the host. Unlike bacteria, both fungi and humans are eukaryotes. Thus, fungal and human cells are similar at the biological level. This makes it more difficult to discover drugs that target fungi without affecting human cells. As a consequence, many antifungal drugs cause side-effects. Some of these side-effects can be life-threatening if the drugs are not used properly.
Viruses are smaller than bacteria and can only replicate inside host cells. They penetrate cells through various modes of entry and hijack the host's machinery to produce more viruses. This often kills the host cell. Viruses may also integrate dormantly into the host's genome. While not considered living organisms, their ability to reproduce makes them borderline living things. Viruses consist of genetic material surrounded by a protein capsid, and some have an outer envelope. They reproduce by taking over the host cell to produce more viral components, which are then assembled and released to infect new cells. Antiviral drugs target virus-specific enzymes to inhibit viral replication.
The document discusses the sebaceous gland and its role in acne pathogenesis. It describes how sebum composition changes in acne, with increased levels of triglycerides, free fatty acids and other lipids that promote P. acnes bacteria growth and inflammation within pilosebaceous follicles. The four main pathologic features of acne are increased sebum production due to androgens, P. acnes infection, follicular hyperkeratinization, and inflammation.
Ionophores are molecules that transport ions across biological membranes. They contain both hydrophilic regions that bind ions and hydrophobic regions that interact with membrane lipids. Ionophores are classified based on their mechanism of action as either mobile carrier ionophores which transport ion complexes, or channel-forming ionophores which introduce pores for ion passage. Examples include valinomycin which transports potassium ions, gramicidin A which forms channels for cation transport, and ionomycin which carries calcium ions into cells. Ionophores have important applications as antibiotics, in research to manipulate cellular physiology, and as feed additives to improve livestock growth and productivity.
Antifungal agents include both systemic and topical drugs used to treat fungal infections. There are two main types of fungi - yeasts which reproduce by budding and molds which have long branching filaments. Mycotic infections can be cutaneous, subcutaneous, superficial, or systemic and life-threatening in immunocompromised patients. Common antifungal agents include polyenes such as amphotericin B, azoles including fluconazole and ketoconazole, flucytosine, and griseofulvin. These drugs work by various mechanisms including binding to fungal cell membranes, inhibiting DNA synthesis, or disrupting cell division.
Zanamivir is an antiviral drug used to treat and prevent influenza A and B. It works by inhibiting the neuraminidase protein of the influenza virus, preventing it from spreading between cells. Common side effects include weakness, headache, fever, cough, runny nose and sore throat, which may be reduced by 1 to 1.5 days with treatment. It is administered through oral inhalation twice daily for 5 days for treatment or once daily for prevention.
The document discusses several antiviral and antifungal agents, their mechanisms of action, clinical uses, and side effects. It covers agents that target herpes viruses like acyclovir and famciclovir, cytomegalovirus like ganciclovir and cidofovir, and influenza like amantadine and rimantadine. The agents work by inhibiting viral entry, replication, or incorporation into viral DNA. They are used to treat herpes, CMV, influenza and other viral infections. Common side effects include gastrointestinal issues, renal toxicity, and myelosuppression.
This document provides information on various dermatological conditions including:
- Pityriasis versicolor, describing presentation, diagnosis via KOH mount, and treatment with selenium sulfide or ketoconazole.
- Acne vulgaris, outlining exacerbating factors to avoid and medical management approaches for moderate and severe cases including topical and oral medications. Details are given on isotretinoin use and monitoring.
- Rosacea, defining diagnostic criteria and stages, differential diagnosis, and treatment approaches including lifestyle modifications and topical or oral antibiotics.
- Vitiligo, alopecia areata, scabies, lichen planus, and psoriasis, briefly covering presentation, diagnosis
This document provides an overview of viruses and antiviral drugs. It discusses that viruses contain nucleic acid and proteins and live inside host cells. It also categorizes major DNA and RNA viruses that infect humans. The document then describes the mechanisms of several classes of antiviral drugs, including nucleoside analogs, protease inhibitors, and drugs that inhibit viral penetration. It provides examples like acyclovir, ganciclovir, ribavirin, amantadine, and oseltamivir, and discusses their mechanisms of action, spectra of activity, clinical uses, and adverse effects.
This document provides information on antiviral and antiretroviral drugs. It begins by describing viruses and their replication processes. It then discusses several important viruses and the diseases they cause. The document outlines the mechanisms of replication for DNA, RNA, and retroviruses. It proceeds to classify antiviral drugs according to their therapeutic uses and mechanisms of action. Several specific antiviral and antiretroviral drugs are described in detail, including their mechanisms of action, pharmacokinetics, and side effects. The human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS) are also discussed.
This document summarizes different drugs used to treat leprosy. It classifies drugs as sulfones like dapsone, antitubercular drugs like rifampicin and ethionamide, and phenazines like clofazimine. It provides details on how each drug works, common adverse effects, dosage and administration. Dapsone is the main drug used and works by the same mechanism as sulfonamides. Rifampicin is bactericidal and imparts an orange color. Ethionamide acts faster but is more toxic. Clofazimine has anti-inflammatory effects and produces reddish black skin color. Antibiotics like ofloxacin, minocycline and clarithromycin
The document discusses antiviral drugs and their mechanisms and uses. It covers several key points:
1) Viruses require host cells to replicate and antiviral drugs aim to interfere with viral replication mechanisms inside cells without harming cells.
2) Many antiviral drugs are nucleoside/nucleotide analogs that inhibit viral DNA/RNA polymerase after being phosphorylated inside infected cells.
3) Drugs discussed include acyclovir and related drugs for herpes viruses, ribavirin for respiratory viruses, amantadine for influenza, and interferons for hepatitis infections.
4) Optimal antiviral response requires drugs that can achieve inhibitory levels inside infected cells and a competent immune response against
This document discusses various antifungal agents including their classification, mechanisms of action, and uses. It covers several classes of antifungals such as polyenes (e.g. amphotericin B), azoles (e.g. fluconazole, itraconazole), and echinocandins (e.g. caspofungin). It also discusses the antifungal spectra, pharmacokinetics, advantages/disadvantages, and adverse effects of different antifungal drugs. The document provides a comprehensive overview of the major antifungal agents used in clinical practice.
This document discusses various antifungal drugs including polyenes like amphotericin B and nystatin, echinocandins like caspofungin, and the heterocyclic benzofuran griseofulvin. It describes their mechanisms of action, spectra of activity, pharmacokinetics, therapeutic uses, and adverse effects. Amphotericin B is a broad-spectrum antifungal that is fungicidal but highly nephrotoxic. Caspofungin inhibits glucan synthase in fungal cell walls. Griseofulvin binds microtubules to treat dermatophytosis.
This document discusses different classes of antiviral drugs used to treat various viral infections. It begins by outlining the challenges in designing antiviral treatments due to viruses parasitizing host cells and hijacking their metabolic pathways. The document then summarizes the general antiviral strategies of inhibiting viral enzymes, penetration/uncoating, reverse transcription, assembly/maturation, and release. It proceeds to classify specific antiviral drugs for herpes viruses, influenza, hepatitis viruses, and HIV/AIDS. The remainder provides more detailed descriptions of representative drugs in each class, including their mechanisms of action, antiviral spectra, pharmacokinetics, therapeutic uses, and adverse effects.
- Antibiotics selectively target microbial processes without harming human host cells. Proper antibiotic use and hand hygiene have improved patient outcomes.
- Many antibiotics are naturally produced by bacteria and fungi to inhibit competition. Major classes include penicillins, cephalosporins, aminoglycosides, tetracyclines, macrolides, and sulfonamides.
- Antibiotics work by inhibiting bacterial cell wall, protein, or nucleic acid synthesis. However, antibiotic resistance has emerged through various mechanisms and poses a growing challenge.
This document summarizes common fungal infections and the antifungal drugs used to treat them. It discusses both superficial and systemic mycoses caused by fungi like Candida, Dermatophytes, Aspergillus, and Cryptococcus. The main classes of antifungal drugs covered are polyenes like amphotericin B and nystatin, azoles including imidazoles and triazoles, antimetabolites like flucytosine, and allylamines such as terbinafine. Specific drugs discussed in detail include amphotericin B, griseofulvin, ketoconazole, fluconazole, itraconazole, voriconaz
The document discusses various antifungal drugs used to treat fungal infections. It describes the different types of fungal infections including superficial and systemic infections. It provides details on the most common fungal pathogens that cause infections. The mechanisms of action and spectra of various classes of antifungal drugs are summarized, including polyene antibiotics like amphotericin B and azoles like fluconazole and itraconazole. Adverse effects and drug interactions of these antifungals are also mentioned.
This document discusses various types of fungi that cause infections and the antifungal drugs used to treat them. It covers superficial and deep fungal infections, outlines the mechanisms of several commonly used antifungal classes including azoles, polyenes, and echinocandins. It summarizes the pharmacokinetics, uses, and adverse effects of many individual antifungal drugs. New approaches to antifungal treatment and drug development are also briefly mentioned.
This document discusses antifungal drugs and fungal infections. It begins by classifying fungi as either yeasts or molds and describes some common pathogenic fungi in each group. Superficial and deep fungal infections are described. The mechanisms of action and classifications of major antifungal drug classes are discussed, including those that target the fungal cell wall, cell membrane, nucleic acid synthesis, and mitosis. Key drugs from each class like amphotericin B, azoles, and flucytosine are described in detail regarding their mechanisms, spectra of activity, pharmacokinetics, uses, and adverse effects. Resistance development and newer formulations are also mentioned.
This document provides a classification and overview of pathogenic fungi and antifungal drugs. It begins by classifying fungi into yeasts, yeast-like fungi, molds, and dimorphic fungi. It then categorizes fungal infections as superficial, cutaneous, subcutaneous, or systemic/opportunistic. The document further discusses the classification, mechanisms of action, pharmacokinetics, uses, and adverse effects of various antifungal drug classes including polyenes, azoles, allylamines, echinocandins, and others. It provides details on specific drugs like amphotericin B, nystatin, ketoconazole, fluconazole, itraconazole,
LINCOSAMIDES, GLYCOPEPTIDES AND OTHER ANTIBACTERIAL DRUGS.pptxKarthiga M
Clindamycin treatment can lead to Clostridium difficile infection. The described symptoms of severe diarrhea, abdominal pain, and fever after clindamycin treatment are consistent with C. difficile infection. C. difficile infection is a common complication of clindamycin use due to disruption of the normal gut microbiota.
This document discusses various types of fungi and fungal infections. It begins by describing the characteristics of fungi, including their cell structure and cell wall composition. It then classifies fungi and describes the types of infections they can cause, including superficial, subcutaneous, systemic, and opportunistic infections. Specific fungal genera and species that cause different types of infections are identified. The document also categorizes and describes various classes of antifungal drugs, including their mechanisms of action, pharmacokinetics, therapeutic uses, and adverse effects. These drug classes include azoles, polyenes like amphotericin B, and echinocandins.
This document provides an overview of antifungal agents, including their classification, mechanisms of action, pharmacokinetics, indications, contraindications, adverse effects and dosing. It discusses major classes such as azoles, polyenes, echinocandins, allylamines and others. Key antifungal drugs summarized include amphotericin B, fluconazole, terbinafine, griseofulvin and clotrimazole. It describes their uses in treating superficial and systemic fungal infections.
The document discusses various antifungal drugs used to treat fungal infections. It describes different types of fungal infections including superficial infections affecting the skin and mucous membranes, and deep infections affecting internal organs. It then classifies and describes several classes of antifungal drugs including antifungal antibiotics like amphotericin B and nystatin, azoles like imidazoles and triazoles, flucytosine, and squalene epoxidase inhibitors. It provides details on mechanisms of action, pharmacokinetics, clinical uses, and adverse effects of specific antifungal drugs.
This document summarizes antifungal agents used to treat fungal infections. It discusses the classes of fungi and systemic fungal infections. The main classes of antifungal drugs covered are azoles, polyenes, echinocandins, antimetabolites, and allylamines. Each drug's mechanism of action, pharmacokinetics, therapeutic uses, doses, and adverse effects are summarized. The document provides an overview of antifungal treatment options for superficial and systemic fungal infections.
Fungal and anti fungal agents detailed information .pptxRafiaRayanabtbc
This document discusses antifungal agents. It begins by describing fungi and their cell walls, which are made of chitin and ergosterol. It then discusses the classification of fungal infections and organisms like yeasts, molds, and dimorphic fungi. The document covers various antifungal drug classes including azoles, polyenes, echinocandins, and antimetabolites. It provides details on important antifungals like amphotericin B, fluconazole, caspofungin, and their mechanisms of action, uses, and side effects in treating serious fungal infections.
Antifungal drugs work by targeting differences in the cell wall and membrane compositions of fungi compared to human cells. Azoles like fluconazole and itraconazole inhibit fungal ergosterol synthesis while amphotericin B binds to ergosterol in the membrane. Topical antifungals like nystatin and tolnaftate treat superficial infections while systemic drugs like fluconazole and terbinafine treat deep infections. These drugs have various mechanisms of action and are used to treat a wide range of fungal infections based on their spectra, pharmacokinetics and safety profiles.
This document discusses several antifungal drugs including their mechanisms of action, uses, and side effects. It describes how pathogenic fungi contain chitin and ergosterol in their cell walls and membranes. Common antifungal classes mentioned are azoles, polyenes such as amphotericin B, and allylamines like terbinafine. Amphotericin B inserts into fungal membranes to form pores, while griseofulvin disrupts fungal cell division. Flucytosine is converted to a compound interfering with fungal DNA synthesis. The document provides details on administration, metabolism, and adverse effects of these antifungal agents.
The document discusses various aspects of antifungal drugs, including their mechanisms of action, classifications, and uses for treating fungal infections. It describes how echinocandins inhibit fungal cell wall synthesis, while azoles and polyenes like amphotericin B bind to or inhibit ergosterol production in fungal cell membranes. Common antifungals are discussed in more detail, outlining their pharmacokinetics, therapeutic uses, adverse effects, and differences between drugs like fluconazole and itraconazole. The document also covers treatments for systemic versus superficial fungal infections and topically applied antifungals.
This document discusses anti-fungal drugs. It begins by defining fungi and describing their characteristics. It then discusses the structure of fungi including their cell wall, cell membrane, and intracellular components. It notes that anti-fungal drugs target the fungal cell wall, cell membrane, DNA/RNA synthesis, and mitosis. The document categorizes anti-fungal drugs and describes several major classes - polyenes, azoles, echinocandins, griseofulvin, and flucytosine. It provides details on several important anti-fungal drugs, including their mechanisms of action, pharmacokinetics, clinical uses, and side effects.
This document discusses several classes of antifungal drugs, including their mechanisms of action, spectra of activity, pharmacokinetics, uses, and side effects. It covers polyene antibiotics like amphotericin B; pyrimidine antimetabolites like flucytosine; azoles like ketoconazole and fluconazole; echinocandins; and topical agents. Griseofulvin is discussed as a drug that accumulates in fungal cells and disrupts microtubules. The optimal treatments are selected based on the fungal organism and patient factors.
This document discusses several classes of antifungal drugs, including their mechanisms of action, spectra of activity, pharmacokinetics, uses, and side effects. It covers polyene antibiotics like amphotericin B; pyrimidine antimetabolites like flucytosine; azoles like ketoconazole and fluconazole; echinocandins; and topical drugs. It provides details on specific drugs' chemistry, targets in fungi, resistance patterns, formulations, and indications for systemic and superficial fungal infections.
This document discusses anti-fungal drugs. It begins by explaining that anti-fungal drugs are used to treat fungal infections, which can be superficial or systemic. It then classifies major types of anti-fungal drugs and describes several examples in detail. Ketoconazole, clotrimazole, fluconazole and griseofulvin are discussed regarding their mechanisms of action, indications, dosages and side effects. Amphotericin B is described as a broad-spectrum polyene used intravenously to treat serious fungal infections, though it can cause renal toxicity and other side effects. Nystatin is noted as a similar but less toxic polyene used topically for localized candid
This document provides information on anti-fungal drugs, including their classification, mechanisms of action, and therapeutic uses. It discusses several major classes of antifungal medications: azoles like fluconazole and itraconazole which inhibit ergosterol synthesis; amphotericin B which binds to ergosterol in fungal cell membranes; flucytosine an antimetabolite; and griseofulvin which disrupts fungal microtubules. These drugs are used to treat superficial fungal infections caused by dermatophytes and yeasts, as well as more serious systemic mycoses depending on their spectrum of antifungal activity and ability to achieve therapeutic drug concentrations
The document discusses the major histocompatibility complex (MHC) and antigen presentation. It notes that MHC resides on chromosome 6 in humans and is made up of three classes: class I MHC proteins (HLA-A, B, C), class II MHC proteins (HLA-DP, DQ, DR), and class III proteins including tumor necrosis factor and complement components. Class I antigens are expressed on all nucleated cells and present antigens to CD8 T cells, while class II antigens are expressed on antigen-presenting cells and present antigens to CD4 T cells. The MHC is highly polymorphic and plays a key role in transplantation, as matching of MHC proteins between donor and recipient reduces graft rejection.
1. The document discusses drugs acting on the gastrointestinal system, focusing on drugs used to treat peptic ulcers and gastroesophageal reflux disease.
2. It describes the physiology of gastric acid secretion and the phases of stimulated secretion. Drugs that reduce acid secretion include H2 receptor blockers, proton pump inhibitors, and anticholinergic agents. Cytoprotective drugs like prostaglandins and sucralfate are also discussed.
3. Causes of peptic ulcers include an imbalance between damaging factors like acid and pepsin and defensive factors like mucus and bicarbonate. Drugs covered for treating ulcers aim to reduce acid, neutralize acid, promote m
This document summarizes various antiparasitic agents used to treat protozoal infections. It discusses the classification, mechanisms of action, administration, pharmacokinetics, side effects, drug interactions, and uses of different classes of drugs including nitroimidazoles, artemisinins, quinine, mefloquine, and halofantrine for treating diseases caused by protozoa such as Entamoeba histolytica, Plasmodium spp., Giardia lamblia, and Trypanosoma spp. The agents described target various protozoa that infect the intestinal tract, blood, and tissues.
The document discusses the autonomic nervous system (ANS) and acetylcholine (Ach) neurotransmission. The ANS controls involuntary functions and is divided into the parasympathetic (PSN) and sympathetic (SNS) systems. Ach is the main neurotransmitter of the PSN and SNS. It binds to muscarinic and nicotinic receptors. Cholinergic drugs like anticholinesterases inhibit Ach breakdown, increasing its effects. They are used to treat conditions like myasthenia gravis but have side effects like excessive secretions. The document covers the synthesis, storage, release and effects of Ach in detail.
This document summarizes skeletal muscle relaxants and neuromuscular blocking agents. It discusses their classification, mechanisms of action, pharmacokinetics, and pharmacological effects. The main types are non-depolarizing competitive blockers like tubocurarine and depolarizing blockers like succinylcholine. The non-depolarizing blockers are competitive inhibitors of acetylcholine, while depolarizing agents cause persistent depolarization at the motor end plate. The document provides details on the properties and clinical uses of commonly used muscle relaxants.
This document discusses cholinergic receptor antagonists, also known as muscarinic receptor antagonists or anticholinergics. It classifies these drugs and describes their mechanisms of action, pharmacological effects, and therapeutic uses in conditions affecting the central nervous system, eye, gastrointestinal tract, bronchial asthma, and more. Precautions are discussed for elderly patients. Adverse reactions from acute poisoning can include central nervous system effects as well as dry mouth and constipation from peripheral antimuscarinic effects.
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
Rasamanikya is a excellent preparation in the field of Rasashastra, it is used in various Kushtha Roga, Shwasa, Vicharchika, Bhagandara, Vatarakta, and Phiranga Roga. In this article Preparation& Comparative analytical profile for both Formulationon i.e Rasamanikya prepared by Kushmanda swarasa & Churnodhaka Shodita Haratala. The study aims to provide insights into the comparative efficacy and analytical aspects of these formulations for enhanced therapeutic outcomes.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
2. SOME PROPERTIES OF FUNGI
1. Yeasts (single cell) or moulds (multicellular)
2. Eukaryotes
3. Cell membrane – has lots of ergosterol
4. Have a rigid cell wall (inner & out layers)- of
mannopeptides, β-glucan, chitin, lipids etc
5. Importance of cell wall: agent of attachment
to host site, stimulate host immune
response, poorly degraded by man
6. Produce spores
3. MYCOSES
1. Most fungal infections are superficial (stratum cornea),
cutaneous (keratinized layers), or subcutaneous; few but
serious infections are systemic (I°) and opportunistic
mycoses
2. Mycoses w/ highest incidence are candidiasis and
dermatophytosis
3. Most mycoses are difficult to treat
Antifungals are few ‘coz
1. Previously disease burden from fungal infections far fewer
than from bacterial infections; increase is due to
immunosuppression (HIV, organ transplant)
2. Differences/targets between fungi and man that can be
exploited are fewer cf to bacteria
3. Fungi turnover is much slower cf to bacteria
7. A) POLYENE ANTIFUNGALS
1. AMPHOTERICIN B (Polyene macrolides)
Mxn: Binds to sterols, forms pores and alters membrane permeability
leading to loss of cellular constituents especially K+
Selectivity: Fungi have ergosterol while mammals have cholesterol
Spectrum: The most broad spectrum antifungal
♦ Most fungi and yeast (**Norcadia and aspergillus are resistant)
♦ Amoeba – Naegleria fowleri ♦ Protozoa: Leishmania Donovani
Adm: IV or intrathecally for systemic effect (not well abs from GIT or muscle)
Local for local effect (e.g. oral for GIT)
Distributn: widely into body tissues and fluids
CSF- adequate if inflamed & (co-adm with Flucytosine)
Protein bound (90%)
Elimination: Largely metabolized, minor renal excretion
8. 1. AMPHOTERICIN B
ADR – is a very toxic drug
1. Nephrotoxic: very common
(i) - A reversible component (pre & post infusion N/Saline
hydration helps)
(ii) -An irreversible component (usually w/ prolonged or
high doses)
♦ Leads to - - - - tubular acidosis, K+ & Mg2+ loss, anemia
Renal toxicity minimized by
1. Hydrating patient
2. Use of low concentrations & compensate by prolonging
infusion time
3. Give drug on alternate days
4. Alkalinize the urine
9. 1. AMPHOTERICIN B - ADR
2. Hepatic dysfunction
3. Thrombocytopenia
4. Anaphylactic rxns
5. Infusion related effects (universal):
- Fever, chills, nausea & vomiting, headache, muscle &
joint pain, hypotension, rare pulmonary involvement
Pre-medication w/ sedatives and antihistamines may
minimize these
- Neurotoxicity (seizures) w/ intrathecal adm
- thrombophlebitis- minimize w/ H/cortisone & heparin
Liposome packed amphotericin B is less toxic (expensive)
D/I – synergistic w/ flucytosine (probably by increasing
permeability)
IV prepared w/dextrose not NS as NS will induce precipitation
10. 1. AMPHOTERICIN B
Uses:
1. (DOC) for serious, acute systemic mycotic
infections e.g. cryptococcal meningitis, fungal
pneumonia, sepsis due to fungi
2. Emperic Rx of fungal infections in patients at
risk in whom if the fungal infection is left
untreated will suffer serious infection e.g. cancer
patients w/ neutropenia
• Local adm:
3. Mycotic infections of – GIT, eye, fungal
arthritis, mycotic infections of the bladder
(bladder irrigation)
11. A) POLYENE ANTIFUNGALS
2. NYSTATIN
Adm; topical or local only (too toxic for systemic use)
Abs: very poor (GIT, other mucus membrane or skin)
Uses
Candida infections – oropharynx, GIT, vagina,
skin
3. NATAMYCIN
Spectrum: Aspergillus, candida
Poor oral abs, given locally (inhalation, topical, oral,
vaginal tablets)
13. 4. AZOLES (imidazoles and triazoles)
Mxn:
Selectivity: different sensitivities
Spectrum: Broad
E.g.
Imidazoles: Ketoconazole (lipid soluble),
Triazoles: Fluconazole, Itraconazole, Voriconazole
Topical- miconazole, ecnonazole, clotrimazole,
sulconazole etc
Some lipid soluble (keto, itra); water soluble (Fluco, vori)
Adm: oral, parenteral, topical
Abs: variable -ketoconazole and itraconazole but good for
Fluco and vorico; best on acidic medium and w/food,
D/I antacids, proton pump inhibitors, H2-histamine blockers
which reduce gastric pH
Distribution – only Fluco and voriconazole into CSF
Elimination: hepatic metabolism, Fluco -long t1/2
14. B) AZOLES
ADR (dose dependent)
1. GIT irritation
2. Hepatic damage ( usually minor)
3. Inhibition of microsomal enzymes (Ketoco, posaco)–
Endocrine (adrenal, gonads) effects: gynecomastia,
menstrual irregularities, infertility
♦ itraconazole - Less inhibition
♦ Fluconazole and voriconazole -Least effect on hepatic
enzyme, Least effect on GIT irritation, Widest therapeutic
index
4. Itraco- impaired cardiac fxn
5. vorico –reversible, transient visual disturbance
D/I
Increased conc. of other drugs (effect varies w/ individual
member) – cyslosporine, cisapride (arrhythmias)
C/I: 1st trimester of pregnancy
Uses: differ
15. USES
Ketoconazole:
1. Mucocutaneous candidiasis
2. Non-meningeal coccidioidomycosis
3. Off label use: cushing dse, prostate cancer (suppresses steroidogenesis)
Itraconazole
1. Aspergillosis (the main drug with significant activity)
2. DOC for Dermatophytoses
Onychomycosis
Histoplasma
Blastomyces
Sporothrix
3. Candidiasis
Fluconazole and Voriconazole
1. Cryptococcal meningitis (Oral)
2. DOC (oral) prophylaxis of cryptococcal meningitis
3. Systemic candidiasis
4. Mucocutaneus candididiasis
5. Coccidioidal infections (esp meningitis, where it is preferred to intrathecal
amphotericin)
Posaconazole
Infections refractory to other antifungals
17. FUMP - 5-fluorouracil-ribose mono(P),
5-FdUMP -5-fluorodeoxyuridinemono(P)
METABOLISM OF 5-FC
IN A FUNGAL CELL5-FC
Cytosine
permease
5-FC
5-FU
5-FUMP 5-FUDP 5-FUTP
5-FdUMP
dUMP dTMP
RNA
DNA
Cytosine deaminase
Ribonucleotide reductase
Thymydylate
synthetase
Fungal
cytoplasm
18. FLUCYTOSINE
Mxn: …………………+ active uptake via a permease
Selectivity: fungal cytosine deaminase,
Adm: oral, IV
Abs: well
Distribution: into all body tissues and fluids including CSF, lung
Elimination: Renal, thus caution in renal dysfunction
S/E
1. Bone marrow depression– pancytopenia, alopecia (co-adm w/ uracil
ameliorates this effect w/out affecting its antimycotic effect)
2. liver damage
4. Skin rash
3. Toxic enterocolitis
D/I
Synergistic w/ amphotericin B and azoles
Uses: (always combined with others to prevent resistance)
Cryptococcal meningitis, systemic candidiasis
Some dermatophytic infection
19. GRISEOFULVIN
Mxn: Binds to microtubules inhibits and inhibits their function e.g. in
metaphase (no activity on yeast)
Adm; oral,
Abs: erratic, increases w/ fatty foods
Distribution: to skin (keratophilic)
Elimination: metabolized w/ renal excretion of products
D/I - is an enzyme inducer e.g. oral anticoagulants
- potentiates effects of alcohol
S/E
♦ GIT irritation, headache
♦ Photosensitivity
♦ Hypersensitivity rxns e.g. exacerbation of SLE)
♦ Hepatotoxicity (↑ blood & urine pophyrias; C/I in porphyria)
♦ Hematological disorders
♦ Teratogenic risk
Uses
1. Dermatophyte infections of skin, nails
Therapy must be continued till infected keratin is replaced by new keratin
containing the drug
20. GLUCAN SYNTHESIS INHIBITORS
ECHINOCANDINS: Caspofungin, Micafungin, Anidulafungin
Mxn: Inhibitors of β-glucan synthase thus defective fungal cell wall resulting
in osmotic lysis
Adm: IV
Elim: Hepatic metabolism
S/E – few
♦ Infusion related- pruritus, fever, chills
♦ GIT effects – nausea etc
♦ Mild liver damage
♦ Kidney damage (rare)
♦ Embryotoxic
USES; (candida and aspergillus including those resistant to Ampho B)
1. Invasive aspergillosis
2. Fungal infections in neutropenia
3. Candidemia
4. Intra-abdominal, pleural, peritoneal, esophageal candidiasis
21. Minor agents with antifungal activity
THIOCARBAMATES
e.g. Tolnaftate
Inhibits squalene epoxidase
Spectrum: dermatophytes
AMOROLFINE
An ergosterol synthesis inhibitor
Uses: Nail infections - topical
22. Minor agents with antifungal activity
►various acids e.g. Benzoic acid, undecylenic
acid, propionic acid - disrupt cell membranes
► salicylic acid, Triacetin (Glyceryl triacetate)-
are keratolytic
(Benzoic acid + salicylic acid =Whitfield's
ointment)
►Potassium iodide
► Ciclopirox is a fungicidal, inhibits Na+/K+
ATPase and thus transport esp of aminoacids
► Gentian Violet
► Haloprogin
24. ANTIVIRAL AGENTS
CHARACTERISTICS OF VIRUSES
♦ DNA or RNA viruses,
♦ Capsid (protein coat) (nucleic acid + protein coat =
nucleocapsid)
♦ Envelop (lipoprotein, may have antigenic glycoprotein)
♦ Enzymes - that initiate replication
♦ Obligate intracellular parasites,
♦ No cell wall or cell membrane,
♦ No self sustaining metabolic ability - depend on host
metabolic machinery to live & multiply – difficult to get
drugs that are selective for the virus and harmless to
the host
25. ANTIVIRAL AGENTS
1. For all antiviral drugs, the host immune defense is
essential for recovery and complete eradication of the
virus
2. Most drugs don’t act on non-replicating/latent viruses
A few - used for chronic suppression
3. Clinically effective conc. of the active form of the drug
must be achieved at the site of infection (intracellular)
4. Unfortunately most clinical manifestations appear after or
at the peak of viral replication – ideal mngt is prevention
(e.g. w/ vaccines)
27. ACTIVITY SITES OF MAJOR ANTIVIRAL AGENTS
1. Attachment
2. Entry & Uncoating
3. Transfer of (DNA / RNA) to host
nucleus/cytoplasm & early transcription
4. Early viral
protein syn
5. (Genome)
DNA/RNA syn
6. Late protein
syn
7. Late protein
processing
8.Assembly
of virions
Release
-globulins
Amantadine
Formivisen (CMV)
DNA polymerase inhibitors
(Purine, pyrimidine analogues)
Protease inhibitors
Neuraminidase
inhibitors
Reverse transcriptase
inhibitors
28. 1. Inhibitors of uncoating
AMATADINE & RIMATADINE Mxn: inhibit uncoating of
viral mRNA
Spectrum: influenza A (not B)
Adm: oral
Distri: wide (only amantadine into CSF)
Elimination: Amantidine – mainly renal - NB. kidney fxn
Rimantidine –part liver metabolism, part renal
S/E ♦ GIT disturbances
♦ CNS disturbance (amantadine mainly)
♦ Teratogenic and embryotoxic - avoid in pregnancy
♦ Anticholinergic effects
Uses
1. influenza A in patients allergic to the vaccine and in
epidemics
2. Parkinson's diseases (increases availability of dopamine or
has anticholinergic effects)
29. 2. Inhibitors of release
NEURAMINIDASE INHIBITORS (initiate w/in 48hrs of symptoms)
Mxn: Neuraminidase is a viral glycoprotein essential for viral
budding
E.g. Zanamivir, oseltamivir
Zanamivir:
PK: Inhalation (powder), Renal excretion
S/E. - Bronchospasm esp. in patients w/ asthma or COPD
Oseltamivir:
PK: oral, Renal excretion
S/E – GIT (↓if taken w/food)
USES
♦ Acute uncomplicated influenza A and B
32. 3. DNA POLYMERASE INHIBITORS
Acyclic (sugar) Guanosine analogues
1. Acyclovir-
2. Valacyclovir – prodrug of acyclovir
3. Penciclovir –
4. Famciclovir – prodrug or penciclovir –
5. Ganciclovir –
Mxn:
Specificity: - viral kinases phosphorylate them (e.g.x200)
more efficiently than do mammalian enzymes; viral DNA
polymerase also more sensitive
Ganciclovir : specifically phosphorylated by a CMV-
encoded kinase
Resistance:
Cross resistance w/ other drugs activated in a similar
manner
Spectrum: HSV, VZV…………………CMV
33. Uses: Acyclic (sugar) Guanosine analogues
Acyclovir & Valacyclovir, Famcylcovir & pencyclovir
1. Herpes simplex infections – mucocutaneous and genital
2. Herpes simplex encephalitis (DOC, IV)
3. VZV- higher doses (as it is less effective)
Uses: Ganciclovir (intraocular implant, direct intravetreal
injection)
1 CMV infections e.g. retinitis (usually w/ foscarnet), GIT
infections (colitis, esophagitis), pneumonitis, ventriculitis
(CVS)
2. Before organ transplantation to reduce risk of CMV
manifests
34. Nucleoside analogues - INHIBITORS of DNA
POLYMERASE
Adm: oral, parenteral, topical, intra-vitreal injection, intraocular implant
Abs: acyclovir, gancyclovir - small but adequate
Famcyclovir – good
Penciclovir – topical
Distribution: wide including CSF
Elimination: that inside cells - degraded rapidly (by cellular phosphatases)
renal excretion NB. kidney fxn
S/E (well tolerated)
♦ Myelosuppression ♦ GIT irritation (50%)
♦ Headache, vertigo, arthralgia
♦ Renal toxicity esp w/ high dose or rapid infusion of acyclovir
(crystallize)–(esp in those dehydrated)
♦ Phlebitis (IV infusion)
♦ ↑Hepatic enzymes
♦ CNS effects (confusion, hallucinations) w/ valacyclovir
♦ Intraocular adm – retinal detachment, hemorrhage
36. VIDARABINE - Analogue of adenosine
Mxn: triphosphorylated, competitively inhibits DNA
polymerase (not v. selective)
Uses; toxicity Limits its use
HSV infections of the eye (topical, alternative)
IDOXURIDINE (iodinated analogue),
SORIVUDINE, TRIFLURIDINE (fluorinated
analogue) of uridine
Uses: HSV, CMV infections of the eye (topical,
alternative)
41. 5. ACYCLIC NUCLEOSIDE PHOSPHONATES
Mxn: Target viral DNA polymerase;
(i). CIDOFOVIR- CMV retinitis, Progressive multifocal
leukoencephalopathy
Adm: injectable,
Elimination: Renal (active secretion, probenecid) NB. renal fxn
ADR: Nephrotoxic (dose-dependent, reduce by adm w/ probenecid and
hydration) (monitor renal fxn); Others: nausea (48%), fever, allopecia,
myalgia
C/I – other nephrotoxic drugs
(ii). ADEFOVIR – (ntNRT) HBV (hepatitis B)
Adm: oral
ADR: Hepatic damage, lactic acidosis, renal toxicity
(iii). TENOFOVIR- (ntNRT) HIV as part of HAART
Adm: Oral (in combination with other antiretrovirals )
ADR:
Common: nausea, vomiting, diarrhea, and asthenia, headache
Less common: hepatotoxicity, renal failure
42. ANTISENSE THERAPY
Sense sequence –is a nucleotide sequence that contains
information for a protein synthesis.
Antisense sequence - is the nucleotide chain that is
complementary to the sense sequence.
Antisense molecules recognize and bind to the nucleotide
sense sequence of specific RNA molecules, preventing the
synthesis of specified proteins.
e.g. Formivirsen Sodium –is complementary to a sequence
of CMV mRNA.
Adm: direct injection into the vitreous body
Uses; CMV retinitis (alternative)
49. NRTI- USES
1. HIV
HAART regimen
PMTCT: Monotherapy – ZDV (not DOC)
2. Lamivudine – Hepatitis B
NON-NUCLEOSIDE REVERSE TRANSCRIPTASE
INHIBITORS (NNRTIS)
Mxn:
Resistance: rapid; There is little cross-resistance amongst
these drugs
There is no cross resistance w/ NRTIs nor w/ protease
inhibitor
E.g. Nevirapine, efavirenz, delavirdine, etravirine
50. NNRTIs - General PK
(NB. Delavirdine – not in current HIV use ‘coz of
efficacy issues)
Adm: oral
Abs: good;
♦ Efavirenz - avoid taking w/ fatty meals
Distribution: wide including CSF, Placenta
Elimination: metabolized (CYP 450) (NB. liver fxn)
T1/2- long for Efavirenz
♦ Nevirapine – Inducer & Substrate of CYP3A4
enzymes
♦ Efavirenz – Mixed inducer & inhibitor of CYP3A4
51. NNRTIs S/E in general
1. Hypersensitivity rxns e.g. SJS (NVP, DLV, EFV)
Highest w/NVP, corticosteroid use- no help
Discontinue use if severe
2. CNS toxicity (EFV) (↓if taken at bedtime)
Avoid in- unstable psychiatric disorders, or
concomitant use of most CNS drugs
3. Hepatitis (NVP,± fatal, monitor liver)
4. GIT irritation – nausea, vomiting, diarrhea
5. Fetotoxic (EFV- avoid in pregnancy)
52. PROTEASE INHIBITORS
Mxn:
Specificity:
Resistance: Some cross –resistance amongst protease
inhibitors may occur
E.g Lopinavir, Ritonavir, saquinavir, Indivavir, Nelfinavir,
Amprenavir, darunavir
General S/E of protease inhibitors
1. GIT irritation (most common) – e.g. diarrhoea
2. Insulin resistance-hyperglycemia, DKA, new or worse
diabetes mellitus
3. Lipodystrophy - altered body fat distribution – (buffalo
hump, truncal obesity, breast enlargment, facial and
peripheral atrophy), and
4. Lipid abnormalities
5. Osteopenia
53. PROTEASE INHIBITORS – General PK
(Ritonavir – not used ‘coz of toxicities unless as PK
enhancer – lopinavir, kelatra)
Adm: oral
Abs: many affected by food
Distr: saquinavir -wide but not CSF,
●Indinavir – wide and highest (of proteases) CSF
conc.
Elimination: all fecal
●Saquinavir – sig. 1st pass metabolism
● All inhibitors of cyp 450 enzymes – increase
conc. of drugs e.g. benzodiazepines
55. INTERGRASE INHIBITORS
Mxn: intergrase - integrates HIV genetic material into the
DNA of human thus the drug prevents HIV genome from
being intergrated into the host genome
E.g. Raltegravir, Elvitegravir
Adm: oral
Elimination: glucuronidation
ADR:
Common: nausea, dizziness, headache, diarrhea, & pyrexia
Less common: creatinine kinase elevations, myopathy, and
rhabdomyolysis
56. ENTRY and FUSION INHIBITORS
Mxn:
HIV binds to CD4 receptors by the protein gp120. Upon
binding GP120 deforms facilitating the viral protein gp41 to
embed itself into the host cell's plasma membrane to form
a pore.
Entry Inhibitors: bind and inhibit either the surface proteins
present on HIV particle that are necessary for attachment
to specific host receptors e.g. gp 120
Or bind to the specific receptors present on host cells
e.g.CD4, CXCR4 or CCR5 (Selzentry -maraviroc®)
Fusion inhibitors: bind to gp41 thus prevent fusion with cell
membrane and the formation of a pore that the capsid
needs to enter the cell.
e.g. Enfuvirtide (T-20, Fuzeon®)
57. ENFUVIRTIDE
Adm: Subcutaneous
S/E
♦ Hypersensitivity
♦ Local injection site rxns
♦ Peripheral neuropathy
INTERFERONS
Mxn: bind to specific receptors on host cell membrane, act by
inducing the synthesis of enzymes that interfere with
translation of mRNA into viral proteins
S/E
Flu-like syndrome, fever, fatigue, myalgia, anorexia, diarrhea
CNS effects
IMMUNOGLOBULINS (vaccines)
58. GOALS OF ARV THERAPY (it is part of a
Comprehensive Care)
1. suppression of HIV replication - maximal &
durable
2. Restore & preserve immune fxn
3. Improve quality of life
4. Reduce morbidity and mortality
Factors to consider before initiating ARV Therpy
. Adherence
Avalability, accessibility and affordability of RX
Supporting services- clinical (e.g. diagnostic),
social, nutrition, counseling,
59. GENERAL CONSIDERATIONS IN THE CLINICAL USE
OF ANTIMICROBIAL AGENTS
Emperic (presumptive) Rx
-Indications - ● when disease is severe, ● if withholding Rx will
result in life-threatening infection, ● or if early intervention
will improve the outcome
- requires knowledge of likely infecting microorganism
(history, site of infection) and their sensitivity to particular
antimicrobials
-give broad spectrum coverage (either singe drug broad in
spectrum or combine)
- Always collect appropriate specimens for identification and
sensitivity tests before instituting Rx
- Change to more narrow spectrum and specific after
identification of microbe
60. GENERAL CONSIDERATIONS IN THE CLINICAL USE
OF ANTIMICROBIAL AGENTS
Drug combinations - indications
● Emperic Rx when broad coverage is necessary
● Rx of polymicrobial infections e.g. intra-abdominal infections
● To decrease rate of emergence of resistance - antivirals,
antimycobacterials
● To minimize dose-related adverse effects (flucytosine +
amphotericin B)
61. E.g. Indications for prophylactic use of
antimicrobial agents
1.Some surgical procedures/conditions - before,
during (sterilizing the area) and after
2. Persons at risk of developing serious infections
because of underlying conditions –
● Rheumatic heart disease patients or
● Patients w/ prosthetic valves undergoing
certain medical procedures e.g. dental
procedures,
● Close contacts of TB patients,
● Prevention of mother to child HIV transmission