This document discusses various antiviral drugs that target different stages of the viral lifecycle. It describes the mechanism of action, pharmacokinetics, uses, and side effects of several nucleoside analogues (acyclovir, cidofovir, famciclovir, ganciclovir), nucleotide analogues (foscarnet, ribavirin), and antisense oligonucleotides (fomivirsen) used to treat infections caused by DNA and RNA viruses like herpesviruses, influenza, hepatitis, and cytomegalovirus. The drugs inhibit viral DNA or RNA synthesis through competitive inhibition or chain termination mechanisms. Many require activation by viral or host kinases to form active triphosphate
This PPT covers Drug therapy for Viral Infection or disease. It includes Viral replication cycle, classification of antiviral drugs, Anti-Herpes drug, Anti Influenza drugs, Anti hepatitis drugs and anti retroviral drugs
medicinal chemistry of Antiviral drugsFatenAlsadek
medicinal chemistry of antiviral drugs with its chemical structures and how they chemically work
Done by: Faten Al-Sadek , Pharmacy student at Mohammed Al-Mana college for Health Sciences -MACHS
This PPT covers Drug therapy for Viral Infection or disease. It includes Viral replication cycle, classification of antiviral drugs, Anti-Herpes drug, Anti Influenza drugs, Anti hepatitis drugs and anti retroviral drugs
medicinal chemistry of Antiviral drugsFatenAlsadek
medicinal chemistry of antiviral drugs with its chemical structures and how they chemically work
Done by: Faten Al-Sadek , Pharmacy student at Mohammed Al-Mana college for Health Sciences -MACHS
Hello friends. In this PPT I am talking about Anti-viral drugs 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.
Antiviral drugs are a class of medication used for treating viral infections. Most antivirals target specific viruses, while a broad-spectrum antiviral is effective against a wide range of viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit its development.
Antiviral Agents,Medicinal Chemistry
•Introduction to Viruses
•Structure of Virus
•Types of Viruses.
•The viral Life cycle.
•Classification of Antiviral Agents
Antiviral Drugs – A Brief (Classification & Mechanism of Actions)Parth Thosani
This presentation gives you an overview of antiviral agents (both retro and non-retro viruses), focusing on the sites of actions, classification and class-wise mechanism of actions.
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.
Antiviral drugs are a class of medication used specifically for treating viral infections.Like antibiotics for bacteria, specific antivirals are used for specific viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit their development.
Antiviral drugs are one class of antimicrobials, a larger group which also includes antibiotic (also termed antibacterial), antifungal and antiparasitic drugs,or antiviral drugs based on monoclonal antibodies. Most antivirals are considered relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from viricides, which are not medication but deactivate or destroy virus particles, either inside or outside the body. Antivirals also can be found in essential oils of some herbs, such as eucalyptus oil and its constituents.
Hello friends. In this PPT I am talking about Anti-viral drugs 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.
Antiviral drugs are a class of medication used for treating viral infections. Most antivirals target specific viruses, while a broad-spectrum antiviral is effective against a wide range of viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit its development.
Antiviral Agents,Medicinal Chemistry
•Introduction to Viruses
•Structure of Virus
•Types of Viruses.
•The viral Life cycle.
•Classification of Antiviral Agents
Antiviral Drugs – A Brief (Classification & Mechanism of Actions)Parth Thosani
This presentation gives you an overview of antiviral agents (both retro and non-retro viruses), focusing on the sites of actions, classification and class-wise mechanism of actions.
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.
Antiviral drugs are a class of medication used specifically for treating viral infections.Like antibiotics for bacteria, specific antivirals are used for specific viruses. Unlike most antibiotics, antiviral drugs do not destroy their target pathogen; instead they inhibit their development.
Antiviral drugs are one class of antimicrobials, a larger group which also includes antibiotic (also termed antibacterial), antifungal and antiparasitic drugs,or antiviral drugs based on monoclonal antibodies. Most antivirals are considered relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from viricides, which are not medication but deactivate or destroy virus particles, either inside or outside the body. Antivirals also can be found in essential oils of some herbs, such as eucalyptus oil and its constituents.
I have tried to provide an outline regarding the general antivirals available in our country..and discussed regarding MOA,indications and Therapeutic uses.
Antiviral drugs are a class of medications used to treat viral infections by inhibiting the replication or growth of viruses in the body. These drugs work by targeting specific components of a virus, such as the viral enzymes, proteins, or nucleic acids, and disrupting their ability to infect or replicate inside host cells. This can help reduce the severity of symptoms, prevent complications, and speed up recovery.
There are many types of antiviral drugs available, including:
1. Nucleoside or nucleotide analogues: These drugs mimic the structure of the nucleosides or nucleotides needed for viral replication, thereby interfering with virus replication.
2. Protease inhibitors: These drugs block the activity of viral proteases, which are enzymes that are required for the replication and assembly of some viruses.
3. Interferons: These drugs are naturally occurring proteins that help the immune system fight viral infections by boosting the body's antiviral response.
4. Neuraminidase inhibitors: These drugs block the activity of viral neuraminidase, an enzyme that is required for the release of virus particles from infected cells.
5. Fusion inhibitors: These drugs block the fusion of viral and host cell membranes, which is an essential step in viral entry and replication.
Antiviral drugs can be used to treat a variety of viral infections, including influenza, HIV/AIDS, hepatitis B and C, herpes, and Ebola. However, the effectiveness of these drugs can vary depending on the specific virus and the stage of infection. Antiviral drugs may also have side effects, and it is important to consult with a healthcare provider before taking them.
Antiviral drugs are a class of medication used specifically for treating viral infections rather than bacterial ones. Most antivirals are used for specific viral infections, while a broad-spectrum antiviral is effective against a wide range of viruses.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
7. Guanine nucleoside analogue
Effective against HSV-1 and HSV-2,
VZV, CMV, and EBV.
The active metabolite of acyclovir
inhibits herpes virus DNA replication
in two ways.
Acyclovir triphosphate - competitive
Inhibitor deoxyguanosine triphosphate
(dGTP) into the viral DNA.
Acts as a chain terminator -because it lacks the 3 -hydroxy group
necessary for further chain elongation.
8. Pharmacokinetics :Acyclovir absorption is variable
and incomplete following oral administration.
20% bound to plasma protein
Amniotic fluid, placenta, and breast milk.
Acyclovir is both filtered at the glomeruli and
actively secreted.
The plasma half-life of acyclovir is 3 to 4 hours in
patients with normal kidney function and up to 20
hours in patients with renal impairment
9. Oral acyclovir - HSV-1 and HSV-2 infections, such as
genital herpes, herpes encephalitis, herpes keratitis,
herpes labialis, and neonatal herpes.
long-term suppression of recurrent HSV.
Intravenous acyclovir -herpes simplex encephalitis,
neonatal HSV infection, and mucocutaneous HSV
infection in immunocompromised individuals.
Acyclovir ointment is used in the treatment of
initial genital herpes but is not effective for recurrent
disease.
10. Ophthalmic acyclovir formulations are effective in
the treatment of herpes keratoconjunctivitis.
Acyclovir reduces the extent and duration of VZV
lesions
chickenpox treatment and prophylaxis in high- risk
individuals.
Herpes zoster (shingles),
Does not affect post herpetic neuralgia.
11. Headache, nausea, and diarrhea.
Skin rash, fatigue, fever, hair loss, and
depression.
Reversible renal dysfunction (azotemia) and
neurotoxicity (tremor, seizure, delirium) are
dose- limiting toxicities of intravenous acyclovir.
Adequate hydration and slow drug infusion can
minimize the risk of renal toxicity
Thrombotic thrombocytopenic purpura–
hemolytic uremic syndrome (TTP–HUS)
Safe in Pregnancy
12. Drug interaction –Probenacid , cyclosporine
Resistance –Mutations resulting in decrease
in thymidine kinase activity.
Altered substrate specificity
Decreased affinity of viral DNA polymerase
13. - acyclic phosphonate cytosine analogue
- Herpes viruses including CMV, HSV-1, HSV-2, EBV,
and VZV. adenoviruses, papillomaviruses,
polyomaviruses, and poxviruses.
Activation- requires metabolism to a diphosphate.
-competes with deoxycytidine triphosphate (dCTP)
for access to viral DNA polymerase and also acts
as an alternative substrate.
- slows replication
- halts DNA polymerase activity.
14. Pharmacokinetics :
low oral bioavailability. T1/2- 2.6 hours,
the diphosphate form -half life of 17 to 65 hours.
A phosphocholine metabolite half-life 87 hours .
is excreted unchanged by the kidney. Glomerular
filtration and probenecid-sensitive tubular
secretion are responsible for cidofovir elimination
Weekly dosage
15. -Treatment and prophylaxis of
CMV retinitis in AIDS patients.
-Treatment of acyclovir-resistant (viral thymidine
kinase-deficient) HSV infections,
-Polyomavirus associated progressive multifocal
leukoencephalopathy,
condylomata acuminata (anogenital warts), and
molluscum contagiosum.
16. Probenecid with cidofovir . Probenecid carries its own
adverse effects, including gastrointestinal upset.
Nephrotoxic agents (e.g., aminoglycosides, NSAIDs,
amphotericin B, foscarnet) should not be given
within 7 days of cidofovir administration.
ADR-Hypersensitivity reactions, Anterior uveitis and
Neutropenia
Potential human carcinogen- Embryotoxic and
teratogenic effects and to impair fertility .
Nephrotoxicity, Proteinuria, azotemia, glycosuria,
elevated serum creatinine, and
Rarely, Fanconi’s syndrome.
17. -diacetyl ester prodrug of the acyclic guanosine analogue 6-
deoxypenciclovir.
- HSV-1, HSV-2, VZV, and HBV.
- After oral administration, famciclovir is converted to
penciclovir by first-pass metabolism.
Penciclovir triphosphate acts as a competitive inhibitor of
viral DNA polymerase
Resistance : Mutations in DNA polymerase or thymidine
kinase may result in resistance. Acyclovir-resistant HSV strains
18. Penciclovir is available as a topical cream
Famciclovir ->converted to penciclovir by hepatic first-
pass metabolism ->Bioavailability 77%.
Penciclovir-t1/2 is 2 to 3 hours; however, the intracellular
half-life of penciclovir triphosphate is 7 to 20 hours in
infected cells.
Eliminated unchanged by the kidney via glomerular
filtration and active tubular secretion.
The plasma half-life is increased in individuals with renal
insufficiency.
19. Herpes labialis.
Shortens the duration of lesion presence and pain
Famciclovir -acute herpes zoster (shingles)
Famciclovir -treatment of HSV
Famciclovir -Recurrent genital herpes.
For HIV-infected individuals- all recurrent
mucocutaneous HSV infections
20. Headache, nausea, and diarrhea.
Hallucinations and urticaria
Animal studies -Tumorigenic and impair
spermatogenesis.
Dosage adjustment is necessary in individuals with
renal impairment.
Famciclovir interact with probenecid -drugs
eliminated by renal tubular secretion.
Increased blood levels of penciclovir or other
agents.
21. Ganciclovir is an acyclic analogue of 2 de-oxyguanosine
especially CMV.
Valganciclovir is the L-valyl ester prodrug of ganciclovir.
Activation of ganciclovir --ganciclovir monophosphate
Protein kinase pUL97 in CMV or thymidine kinase in
HSV.
additional phosphorylations ganciclovir
triphosphate competes with dGTP incorporation
into DNA chain termination
Ganciclovir triphosphate is up to 100-fold more
concentrated in CMV-infected cells than in normal cells .
22. Resistance : Exposed to the drug for long periods .
-Mutation of the protein kinase gene.
-Mutations in the DNA polymerase .
Pharmacokinetics : - Orally or intravenously
Valganciclovir –orally - rapidly metabolized to
ganciclovir60%
Intravenous -Ganciclovir -vitreous humor
Ganciclovir- eliminated by glomerular filtration and
active tubular secretion.
The T1/2-ganciclovir -3.5 hours (iv)and 4.8 hours (oral)
Oral valganciclovir -4 hours. The intracellular half-life
of ganciclovir triphosphate is over 24 hours.
23. CMV retinitis in immunocompromised
individuals, including those with AIDS, CMV
infection in organ transplant recipients.
-CMV retinitis in AIDS ,
Ganciclovir -intravitreal implant -CMV retinitis
in AIDS patients.
Resistance : Exposed to the drug for long
periods .
-Mutation of the protein kinase gene.
-Mutations in the DNA polymerase .
24. -Myelosuppression
Neutropenia and anemia (25 to 30% ) and
Thrombocytopenia( 5 to 10%).
sperm production, teratogenesis, and tumor formation.
Severe neutropenia -with zidovudine.
Ganciclovir increases serum levels of didanosine,
whereas probenecid decreases ganciclovir elimination.
Nephrotoxicity (e.g., amphotericin B, cyclosporine,
NSAIDs) are administered in conjunction with ganciclovir
25. Idoxuridine -is a water-soluble iodinated derivative of deoxyuridine
-Inhibits several DNA viruses including HSV, VZV, vaccinia, and
polyoma virus.
MOA:The triphosphorylated metabolite of idoxuridine inhibits
both viral and cellular DNA synthesis
Host cytotoxicity,
Pharmacokinetics: Idoxuridine topical ophthalmic use
Uses : treatment of herpes simplex infections of the eyelid,
conjunctiva, and cornea. soft tissue sarcoma
Adverse Events: local irritation, mild edema, itching, and
photophobia. Corneal clouding and small punctate defects
in the corneal epithelium .
26. Trifluridine is a fluorinated pyrimidine nucleoside
-HSV-1 and HSV-2, vaccinia, adenoviruses.
MOA: Activation of trifluridine 5
monophosphate inhibits the conversion of
deoxyuridine monophosphate (dUMP) to
deoxythymidine monophosphate (dTMP) by
thymidylate synthetase.
Resistance alterations in thymidylate synthetase
specificity.
27. Pharmacokinetics :- topical instillation of trifluridine into
the eyes. Its half-life is approximately 12 minutes.
Uses:
Trifluridine (topical ophthalmic solution)- primary
keratoconjunctivitis, recurrent keratitis due to HSV-1 or
HSV-2.
Unresponsive or intolerant to topical idoxuridine or
vidarabine.
Adverse effects:Transient burning or stinging and
palpebral edema.
-Superficial punctate keratopathy, epithelial keratopathy,
hypersensitivity, stromal edema, irritation, keratitis
sicca, hyperemia, and increased intraocular pressure.
28. Foscarnet is an inorganic pyrophosphate analogue
HSV-1, HSV-2, VZV, CMV, EBV, HBV, and HIV.
Noncompetitive inhibitor of viral DNA polymerase
and reverse transcriptase
Resistance -mutation of viral DNA polymerase.
Pharmacokinetics : IV -14 to 17% bound to plasma
proteins.
-accumulates in bone bimodal initial half-life of 4
to 8 hours and prolonged terminal elimination half-life
of 45 to 130 hours.
- eliminated as unchanged drug glomerular
filtration and active tubular secretion.
29. Uses
CMV retinitis in AIDS patients.
refractory retinitis, Kaposi’s sarcoma
Acyclovir- resistant mucocutaneous HSV infections in
immunocompromised individuals.
Acyclovir-resistantVZV and nonretinitis forms of CMV
infection
Adverse effects
Nephrotoxicity -second week of induction therapy
Serum creatinine levels may be elevated in up to 33 to 50%
of patients;
Dehydration, previous renal impairment, and concurrent
administration of other nephrotoxic drugs increase the
risk of renal toxicity.
30. -synthetic guanosine analogue
-Influenza A and B, parainfluenza, RSV, HCV, HIV-1, and
various herpesviruses, arena viruses, and paramyxo viruses.
-inhibits the synthesis of viral mRNA
ribavirin monophosphate, diphosphate, and
triphosphate forms.
Ribavirin monophosphate-- inhibits the guanosine
triphosphate (GTP) synthesis Ribavirin triphosphate
inhibits the 5 capping of viral mRNA with GTP increasing
the mutation rate of RNA viruses nonviable progeny virions
31. Resistance has not been documented in clinical isolates.
Pharmacokinetics : Aerosol respiratory tract secretions
approximately 100 times
Oral absorption is rapid, and first-pass metabolism is
extensive;
Ribavirin’s oral bioavailability is 64% -high-fat meal.
Steady-state levels are reached after 4 weeks.
Ribavirin triazole carboxylic acid metabolite urine
The plasma half-life -9.5 hours
The drug accumulates in erythrocytes, with a half-life of 40
days.
32. Uses :
Severe bronchiolitis or pneumonia due to RSV infection.
Oral ribavirin in combination with interferon- α
Intravenous ribavirin -Hantaan virus infection, Crimean or
Congo virus hemorrhagic fever, Lassa fever, and severe
adenovirus infection.
Ribavirin monotherapy
Adverse effects
Local adverse effects.
Pulmonary function -chronic obstructive lung disease or
asthma.
Headache, conjunctivitis, rash, and rarely, bronchospasm.
Oral and intravenous- hemolytic anemia
33. With interferon-α - fatigue, nausea, insomnia,
depression, and anemia, fatal or nonfatal
pancreatitis.
Ribavirin is mutagenic, teratogenic, and embryotoxic
C/I- pregnant women ,Effective forms of
contraception during ribavirin treatment .
Sickle cell anemia and other
hemoglobinopathies,coronary disease ,severe renal
impairment.
D/I-In vitro, ribavirin inhibits the phosphorylation
reactions zidovudine and stavudine
34. First antisense oligonucleotide immediate early
region 2 (IE2) of CMV mRNA.
By binding to IE2 mRNA, fomivirsen prevents its
translation to protein and thereby blocks viral
replication. Because this mechanism of action is
different from that of other antiviral agents, cross-
resistance with other drugs used to treat CMV is
unlikely.
Pharmacokinetics: Fomivirsen is injected directly
into the vitreous humor of the eye.-->retina and iris
over 3 to 5 days and is cleared from the vitreous
humor within 7 to 10 days.
35. Fomivirsen exhibits minimal systemic absorption
and is degraded locally by cellular exonucleases.
Uses
Fomivirsen -CMV retinitis in patients with AIDS.
Adverse effects: Iritis, (25%) -topical
corticosteroids.
- Vitreitis IOT
C/I- with cidofovir
36. Amantadine is a synthetic tricyclic amine, and
rimantadine is its α -methyl derivative. Both drugs
inhibit the replication of the three antigenic
subtypes of influenza A (H1N1, H2N2 and H3N2) ,
less activity against influenza B.
Mechanism Of Action
- involves inhibition of the viral M2 protein, (H
channel) Blockade acid-mediated dissociation
of the ribonucleoprotein complex -inhibited
The pH changes M2 inhibition alter the
hemagglutinin inhibit viral assembly.
37. -Viral resistance -30% ,-failure of drug prophylaxis
-Mutation in the transmembr- M2 protein
Pharmacokinetics : Amantadine -2 to 5 hours.
T1/2- 17 hours -29 hours in the elderly.
Eliminated unchanged by glomerular filtration and
tubular secretion. Rimantadine -5 to 7 hours.
Its elimination half-life averages 25- 32 hours in the
elderly. -25% -unchanged drug ,75%- hydroxylated or
conjugated metabolites.
38. Uses :-influenza A strains
Adverse effects:- Nausea, anorexia, dizziness, and insomnia
Dose-related effects - amantadine than rimantadine.
-Depression, impaired coordination, confusion, anxiety,
Cardiac arrhythmias, delirium, hallucinations
long-term treatment may cause peripheral edema, Abrupt
withdrawal -neuroleptic malignant syndrome.
-Seizures or worsen preexisting seizure disorders.
Amantadine is teratogenic and Rimantadine - embryotoxic.
Pregnancy and lactation.
39. Drug interactions:- Anticholinergic drugs,
Thiazide–triamterene, trimethoprim–
sulfamethoxazole, quinine, and quinidine
increase plasma amantadine levels.
Cimetidine decreases rimantadine clearance,
and aspirin and acetaminophen decrease
rimantadine plasma levels.
40. Docosanol is a long-chain saturated alcohol
HSV. CMV, influenza virus, and respiratory syncytial
virus.
-Blocks the entry of the virion
Docosanol cream -herpes labialis.
Adverse effects -Skin irritation occurs infrequently.
41. Oseltamivir phosphate is the ethyl ester prodrug of
oseltamivir carboxylate
- competitive antagonist of influenza A and B
neuraminidase.
Neuraminidase -then destroys these hemagglutinin
receptors cleavage of hemagglutinin receptors is
required for the release of progeny virus from the host
cell-inhibited
Spread of infection by allowing viral particles to
penetrate the neuraminic acid–rich respiratory mucus
and by preventing the clumping of virus that results from
the binding of hemagglutinins to neuraminic acid residues
on neighboring viral particles –inhibited
Resistant strains –mutations- neuraminidase
42. P/KOrally -80%- 2.5 to 5 hours.
Plasma t1/2 -7 to 9 hours.
Elimination -active tubular secretion and glomerular
filtration.
Uses :Oseltamivir - uncomplicated acute influenza in
patients aged 1 year and older. --Prophylaxis of influenza in
individuals aged 13 and older.
Post- exposure prophylaxis
Adverse effects:
-Nausea and vomiting, Bronchitis, insomnia, and vertigo
-Chronic cardiac or respiratory disease renal insufficiency;
-Probenecid decreases the elimination of oseltamivir,
No interference with antibody production in response to
the influenza vaccine.
43. Zanamivir is a neuraminidase inhibitor with activity
against influenza A and B strains. - reversible
competitive antagonist of viral neuraminidase.
- inhibits the release of progeny virus,
Resistant variants with hemagglutinin and/or
neuraminidase mutations
Pharmacokinetics : bioavailability < 5% oral.
breath-actuated inhaler device- 12 to 17%, -1.5
hours.
Eliminated -by the kidneys t1/2.5 to 5 hours.
44. Uses :- Uncomplicated acute influenza A and B virus
Effective prophylaxis against influenza.
Adverse effects:
-Bronchospasm and impaired lung function -
underlying pulmonary disease.
- Allergic reactions, including angioedema,
C/I -Severe or decompensated chronic obstructive lung
disease or asthma
-serious adverse pulmonary reactions. Moderate
asthma
Severe renal insufficiency
45. Other antiviral drugs
Immunoglobin ->( γ-globulin, immunoglobulin [Ig] G)
-primarily of IgG and contains trace amounts of IgA
and IgM.
inhibit viral penetration of host cells, opsonize viral
particles, activate complement, and stimulate cell-
mediated immunity.
Pharmacokinetics: γ-Globulin im/iv - viral disorders.
Protection lasts for 2 to 3 weeks after a single
injection, although for prolonged infections,
injections can be repeated every 2 to 3 weeks.
46. Uses :- CMV, HBV, rabies, RSV , and VZV
- heterogeneous human immune globulin solution- measles,
varicella, or rubella infection
- adjunctive form of therapy with other therapeutic
approaches.
Adverse effects : Hypersensitivity reactions
-Anaphylactoid reaction, urticaria, angioedema, fever, and
injection site reactions.
- flushing, dizziness, blood pressure changes, palpitations,
abdominal cramps, and dyspnea; Aseptic meningitis
Interference- live virus vaccines (e.g., measles mumps,
rubella).
47. -Potent antiviral, immunoregulatory, and
antiproliferative effects
Interferon-α (type I, leukocyte) and
Interferon - β (type I, fibroblast)
Interferon- γ (type II, immune) -natural killer (NK)
cells and T lymphocytes
inhibition of viral penetration, uncoating, mRNA
synthesis, translation, and/or virion assembly and
release.
48. Initiate the JAK-STAT signal transduction
pathway 2 -5 –oligo adenylate synthetase (2 -5
OAS)- initiates the activation of a cellular
ribonuclease that cleaves single-stranded RNAs,
Protein kinase phosphorylates and inactivates an
elongation factor (eIF-2)
Interferons inflammatory cytokines, biological
oxidants immune response.
49. Natural interferons ,recombinant interferons
,Monomethoxy polyethylene glycol (PEG; pegylated
interferons).
Subcutaneously, intramuscularly, intravenously, or
intralesionally (e.g., into genital warts).
-peak plasma levels within 4 to 8 hours within 16
to 36 hours.
Pegylated interferons 15 to 44 hours 48 to 72
hours.
Eliminated cellular uptake and catabolism in the
kidney and liver
50. Interferon- α -2a chronic hepatitis C, hairy cell
leukemia, AIDS- related Kaposi’s sarcoma, and
chronic phase Philadelphia chromosome–positive
chronic myelogenous leukemia.
Interferon-α -2b Hairy cell leukemia, malignant
melanoma, follicular lymphoma, condylomata
acuminata, AIDS-related Kaposi’s sarcoma, and
chronic hepatitis B and C.
Interferon-α -2b and RibavirinChronic hepatitis C.
Interferon- α -n3 condylomata acuminata by
intralesional injection.
51. Interferon alfacon-1 5 times Interferon α -
2a or -2b.
Interferon alfacon-1 and peg interferon- α -
2b chronic hepatitis C.
Interferon β -1a and interferon β -1b
multiple sclerosis.
Interferon -1b chronic granulomatous
disease , malignant osteopetrosis.
52. Flu like symptoms fever, chills, weakness,
fatigue, myalgia, and arthralgia, (50% )of
patients CNS complaints headache,
dizziness, impaired memory and concentration,
agitation, insomnia, and anxiety occur with
regularity.
Depression interferon-α and interferon- β .
Myelosuppression dose limiting
Gastrointestinal symptoms nausea, vomiting,
Elevation of hepatic enzymes
Injection site reaction alopecia, fertility, cause
miscarriage .
53. Palivizumab is a humanized monoclonal antibody F
protein on the surface of RSV.
It contains 95% human and 5% murine antibody
sequences
inhibits its ability to fuse with host cell membranes.
Pharmacokinetics : prophylactically IM/monthly—RSV
season. T1/2- 20 days.
Uses : Serious LRTI due to RSV.
bronchopulmonary dysplasia or chronic lung disease
Premature infants (less than 32 weeks gestation)
Adverse effects : Mild erythema and pain
Anaphylactoid reactions –protein.