Antiviral-Antifungai-Antihemintics Flashcards
Explain life cycle of Viruses , types of viral infected cell ,
—virus life cycle :
1-Start with attachment : the virus endocyite to the cell
2-Uncouting : by the M2 proton channel
3-Replaction phase : in the nucleus the virus gets 2 pathways
3.1: viral genome to form a new virus
3.2 mRNA : which is for inhibition of host cell raibosm and start synthesis the virus proteins
4-Translation : in the ribosm and synthesis polyproteins of the virus
5-Processing : by enzyne called proatase : and its cutting the polyproteins into proteins
6-Assembly
7-release : normally virus released without enzymes but in influnza its need enzyme called Nueruaminadase
——faith of viral cell infection:
1-Apoptosis
2-Servival
3-Cancer
Explain Virus replication in RNA virus , DNA virus , Retrovirus
1-RNA virus : in the nucleus host cell with help of RNA polymarese synthesis mRNA and viral genom
2-DNA viruses : in the neuclus of host cell with help of Integrase enzyme the virus integrate with Host cell DNA and becoma letant virus , then every-time the immune system becomes week the virus activated and with help of enzyme DNA polymerse synthesis mRNA and viral genome
3-Retroviruses :before entering the nucleus with help of enzyme called Reverse transcriptase its transform from RNA into DNA then enters the nucleus and integrate with host cell DNA with enzyme called integrase , then every time the immune system get week the virus activates and synthesis mRNA and viral genome by enzyme called DNA polymers
Explain Treatment of HIV ( retrovirus) fusion inhibitors,RT inhibitors ,integratese inhibitors,Protease inhibitors
1-Fusion inhibitors
-Drugs :
-Enfuvirtide : binds to Gp41 subunit of HIV-1 viral envalople that attaches to receptors on CD4 of host cell membranes and prevent the attachment
——-
2-RT inhibitors :
-Drug :
-zidovudine : its nucloside analogue so its competitive inhibtitor of Reverse transcriptase enzyme duo to similar structural components
-Side effect : Animea and myopathy
————
3-Integrase inhibitors :
-Drug : Raltegravir tab
-they inhibit the insertion of proviral DNA into host cell genomes by inhibiting the integrase enzyme
————-
4-Protase inhibitors:
-Drug : Saquinavir Caps
-its peptied like analog that binds to protase enzyme in active site and inhibits the activity of the protase enzyme which is the processing of polyproteins resulting if formation of immature non fractional virus particles
-side effect : metabolism side effect such as hypoglycaemia, hypolipidemia
Explain treatment of HBV , Drugs , mechanism, side effect
-Drugs :
1-Lamivudine tab : its inhibit HBV DNA polymarase by converting inter-cellularly to triphospah form then it competes with cytosine triphosphate for incorporation into developing viral DNA strains resulting of termination of Viral DNA replication
2-Interferon-a A/3milin IU
-mechanism: the exact mechanism are unknown but its through these 3 mechanisms:
1-interfere with viral replication
2-stimulate of apoptosis
3-regulation of immune response
—Side effect :
1-Immune distrbance
2-Fatuge
3-neurotoxicity
4-Anemia and BM depression
Treatment of Herpes virus ,Drugs , mechanism,uses
-Drugs :
1-Acyclovir tab/oint
2-Ganciclovir tab/A
-mechanism: they are purine analogues, they are pro drugs that are activated inside the viral infected cell Aciclovir is converted by viral
thymidine kinase to aciclovir monophosphate
✔Aciclovir monophosphate is then converted to aciclovir triphosphate by host kinases
✔Aciclovir triphosphate inhibit HSV-specified DNA-polymerases and prevent viral DNA synthesis
-Uses :
1-Acyclovir : Herpes V 1-2
2-Ganciclovir : cytomegalovirus
Treatment of influenza virus , uncouting inhibitors, release inhibitors
1-Uncoating inhibitors:
-Drugs: Rimantadine tab
-its bind to the M2 proton channel of the virus which lead to inhibition of virus uncoating and its active exassivly aginst influza A only
-uses : Influenza A
————-
2-Release inhibitors
-Drug : oseltamivir Caps 0,075
-mechanism: its inhibit the nuroaminadse enzyme with is responsible for budding of the virus
-side effect : neurpsychtric effect ,livedo reticularis
-uses : influenzaA,B
Type of fungal infection, list of fungais caused diseases
-type of infection:
1-Superficial: candida , onychimycosis , dermatophytes
2-Systemic or deep : such as fungal pneumonia , fungal siptecemia , fungal meningitis , its not common and only happens with patients who immune comprised such as Chemotherapy,immunosuppressants
——-List of fungal and its diseases:
1-Yeast : candida , cryptococcal
2-mold fungi. : aspergilles
3-Dimorphic , histoplasm capselutum ,blasyimycosis
Explain anti fungal drugs , on scheme , Outer membrane , Ergostrerol pathway and its drugs , DNA drugs
1-Outer membrane : its synthsis by enzyme called B-glucan synthase
-Drug effect on this phase is : Echinocandins ( fungin )
2-Ergosterol pathway :
2.1 start with Squlene transform into squlene epoxide by enzyme called squlene epoxidase : drug effecting this enzyme is Allymines
2.2 then from squlene epoxide transform into Lanosterol by enzyme called 14-a-Demithylase : drug effecting this enzyme ( Azoles )
2.3 From lanosterol transform into ergosterol and here the effect on the ergosterol directly by drugs called ( Polynes )
3-Drug effecting the DNA its Griseofulvin
classification of antifungal according to Action , Chimical steructur
1- Action :
Fungicidal - cause death of fungi
Fungistatic - delay and stop the growth of fungi
2- By chimical structre :
2.1 Antifungal antibiotcs : Polyenes ,Echinocandins
2.1 Synthatics : Azoles ,Allylamines
Explain Echinocandine ,( outer membrane inhibitors) , drugs , mechanism,spectrum , Pharmcokintics,side effect ,uses
-Drugs :
1-Caspofungin
2-micafungin Pwoder ( systemic use )
-mechanism: they are outer membrane synthesis inhibitors by inhibition of B-(1-3)-D-glucan synthase which is lead to disruption of the glucan formation and destroy cell intergtry
-Spectrums :
1-Candida ; fungcidal
2-Aspergills : Fungostatic
-Pharmcokintics:
-Abs : poor
2-Dist : high concentration in tissue and organ
3-metabolism: in liver without cyp450 ( no drug drug interaction )
-Side effect : Fever , Dyspepsia
-uses :
1-invasive Candida
2-Invasive Asprgillosis ( which resistant to standard therapy )
explain Allymines , Drugs , Mechanism , Spectrum , Pharmacokintics , Uses
-Drugs terbinafine tab / oint
-mechansim : Inhibition of squalene epoxidase
whch is lead to decrease synthesis of ergosterol in the early stages and accumulation of toxic squalene result of abnormality of the cytoplasmic membrane
-Spectrum : Dermatophytes, Candida
-Pharmacokintics :
-abs : 70%
-Dist : high concentraion in skin and nalis
-Metabolsim : in liver
-uses :
1.onychomycosis caused by dermatophytes
2.skin candidiasis
explain Azoles , Drugs , Mechnasim
-Drugs :
1-imidazol dervativs : miconazole ( systamic)
, ketoconazole (local )
2-triazol dervativs : Fluconazole , itraconazole (systmic )
-Mechaims : they are Selective inhibition CypP450-dependent
α-dimethylase which lead to Inhibit conversion of lanosterol to ergosterol and result of Disruption of growth and death of fungal cells
explain Ketoconazole ,spectrum , pharmacokintics , side effect , uses,
-Spectrum of action : broad spectrum
1.dermatophytes (Trichophyton, Microsporum, Epidermophyton )
2.Candida .
3.dimorphic fungi
-Pharmacokinetics
-abs : Variable absorption
-metabolism : Biotransformation in the liver with cytP450
-Dist : Poor penetration through the BBB
-side effect : High toxicity (hepatotoxicity, ↓ adrenal cortex, ↓ testosterone, gynecomastia, oligospermia, sexual dysfunction). After itraconazole development - only topically!
-Uses :
1.candidiasis
2.dermatomycosis
3-Prostate cancer
explain itraconazole ,spectrum , pharmacokintics , side effect , uses,
-spectrum : Broad spectrum
yeast and mold fungi
-Pharmacokinetics
-abs : bioavailability is variable
metabolsim : biotransformation in the liver, inhibit cytP450 (drug interaction)
-Dist : high concentrations in the skin
-side effect : Less side effects (hepatotoxicity, etc.) than in ketoconazole.
-uses :
1.onychomycosis (main application)
2.candidiasis,
3.apergillosis, .
4.blastomycosis
explain fluconazole ,spectrum , pharmacokintics ,uses,
-Spectrum of action
Yeast (Candida spp., Cryptococcus spp.)
NB! Does not work against mold fungi (Aspergillus spp.)
-Pharmacokinetics
-Abs : food does not affect bioavailability
-Dist : penetrates the BBB , high [C] in CSF, skin and urine
-Metabolsim : biotransformation in the liver, inhibit of cytP450 (interaction)
-uses:
1. superficial and invasive candidiasis
2.cryptococcosis
