Anti: Virals, Fungals, Tubercular Agents Flashcards
Varicella-zoster Virus (VSV)
chicken pox, and herpes zoster (Shingles)
Herpes Simplex Virus (HSV)
Infections of mouth, face, genitalia
Meds for HSV: acyclovir/ Zovirax
MOA: Inhibits viral production by suppressing synthesis of viral DNA, activated by enzyme - enzyme converts acyclovir into a compound that inhibits viral DNA polymerase.
IND: Oral herpes simplex, Genital herpes simplex, Varicella, Herpes zoster
AE: Oral: GI upset, HA
IV: Irritation at site of infusion, Nephrotoxicity
DI : Any Nephrotoxic drug
NURS: infuse IV slowly, increase fluid intake
Cytomegalovirus (CMV)
Member of Herpes virus family, remains dormant within cells for life. Reactivated in immune compromised patients. Causes infections in GI tract, lungs, eyes (retinitis)
Ganciclovir/ Cytovene
MOA: Suppresses synthesis of Viral DNA, Like Acyclovir but more toxic
IND: CMV retinitis in immunocompromised pts. (also used prophyl)
CMV prevention in transplant pts.
AE: Bone marrow suppression
Reproductive toxicity in both men and women
NURS: Monitor WBC count, Platelet count
Hepatitis
Inflammation of the liver, viral infection. Five strains: A, B, C, D, E
Paltho: Widespread inflammation of the liver tissue causing hepatic cell scaerring, necrosis and degeneration, may also interrupt bile flow. Lead to liver failure.
Interferon Alpha
MOA: Binds to receptors on host cell membrane and blocks viral entry into cells. Also blocks synthesis of viral mRNA, viral proteins, Blocks viral assembly and release.
IND: Chronic Hepatitis B and C
AE: Flu like symptoms, Depression, Heart Damage, Bone Marrow Suppression
Influenza
Respiratory tract infection - Fever, chills, cough, sore throat, muscle aches. Two influenza viruses: A & B
Oseltamvir/ Tamiflu
MOA: Stops viral spread by inhibiting enzyme needed for replication.
IND: Prophylaxis/treatment for Influenza A & B
Treatment of H1N1 and H5N1
AE: N/V
DI: Live influenza vaccine, Tamiflu will interfere with vaccine.
HIV
Causes AIDS, Immune system becomes incompetent due to depletion of T-cells, Leads to risk for opportunistic infections.
Patho: HIV-RNA virus = retrovirus. HIV enters cell when gp120 knobs on viral envelope bind to specific CD4 receptor sites on cells. Viral genetic material enters cell and viral RNA is transcribed into DNA with reverse transcriptase. Viral DNA enters Nucleus of cell and becomes permanent part of genetic structure. HIV infects T-cells, monocyites, brain cells, and nerve cells. Destruction of T-cells causes immune dysfunction. Immune problems start when counts < 500 and severe problems (AIDS) <200
Meds for HIV: HAART (Highly Active Anti-Retroviral Therapy)
1: Reverse transcriptase Inhibitors
a: Nucleoside/Nucleotide reverse transcriptase inhibitors (NRTIs)
b: non-Nucleoside reverse transcriptase inhibitors (NNRTIs)
2: Protease inhibitors
3: HIV fusion inhibitors
NRTIs
First drugs, similar structure to nucleosides, nucleotides that make up DNA
ex) zidovudine/Retrovir, AZT
Zidovudine/ Retrovir
MOA: Inhibits HIV replication by suppressing synthesis of viral DNA by reverse transcriptase, inhibits activity of viral enzyme.
IND: HIV
AE: Bone marrow suppression, Syndrome of lactic acidosis with hepatomegaly, GI
DI: Gancyclovir, any drug that causes bone marrow suppression.
NURS: Monitor Blood cell count, hemoglobin, hematocrit
Monitor arterial blood gas if suspected acidosis
Monitor Liver Function
NNRTIs (Non-nucleoside reverse transcriptase inhibitors)
Not structurally related to nucleosides
ex) Efavirenz/ Sustiva, EPV
Efavirenz/ Sustiva
MOA: Binds directly to HV reverse transcriptase, suppresses enzyme activity.
IND: HIV - Usually in combo with zidovudine and another NRTI
AE: CNS Symptoms, Rash, Liver Damage, Teratogenic
DI: Competes with other drugs for metabolism by P450
Induces P450 - accelerates own metabolism along with others
NURS: MUST TAKE ON EMPTY STOMACH
High fat meals increase plasma levels
Monitor Liver function.
Protease Inhibitors
Are not used alone, risk of drug resistance. Combined with reverse transcriptase inhibitors.
ex) Lopinavir-ritonavir/ Kaletra
Lopinavir-ritonavir/ Kaletra
MOA: Binds to HIV protease, prevents enzyme from cleaving HIV polyproteins–> virus remains immature and noninfectious.
IND: HIV
AE: Hyperglycemia
Fat maldistribution, more fat distribution to torso
Hyperlipidemia
Reduced bone mineral density –> Osteoporosis
Hepatotoxicity
DI: P450 inhibitors: Grapefruit juice, Ketoconazole (anti-fungal)
P450 inducers: Rifampin, anti-seizure meds
NURS: Monitor blood sugar, teach pt S&S of hyperglycemia,
Monitor LFT (Liver Function Tests)
HIV Fusion Inhibitors:
Enfuvirtide/ Fuzeion, T-20 (sq)
MOA: Prevents HIV from fusing with cell membrane of CD4 cells. blocks entry.
IND: HIV Infections that are resistant to other antiretrovirals
AE: Injection site reaction - pain/tenderness
Pneumonia - Bacterial
Hypersensitivity reaction
Types of Fungal infections
Systemic Infections:
a: opportunistic - Candidiasis, aspergillosis, cryptoccosis, mucormycosis b: Non-opportunistic - sporotrichosis, blastomycosis, histoplasmosis, coccidiodomycosis
Superficial Infections:
a: candidiasis - mouth, vaginal, any moist area b: dermatophytic infections - Tinea pedis, tinea corporus, tinea cruris, tinea captis
Types of antifungals:
Polyenes -Bind to ergosterol, a component of the fungal cell membrane, causes increase in cell permeability, cells leak intracellular components, no longer viable
Azoles- inhibits synthesis of ergosterol, w/o ergosterol there is leakage of cellular components
Amphotericin B
Polyene, Given IV
MOA: Binds to ergosterol - component of the fungal cell membrane, causes increase in cell permeability, cells leak intracellular components, no longer viable.
IND: Broad spectrum for systemic fungal infections
AE: Infusion reactions - Fever, chills, rigors, shaking, inflammation
Neprotoxicity
hypokalemia
bone marrow suppression
DI: other nephrotoxic agents
NURS: Monitor creatinine, K levels, I&O, RBC count.
Nystantin
Polyene
IND: Candidiasis:
Oral, esophageal: suspension, lozenges, tablet
Skin: cream, ointment, powder
Vaginal: Vaginal tablet
AE: Oral and Topical
Azoles;
Itraconazole (Neg Inotropic agent)
MOA: Inhibits synthesis of ergosterol. without ergosterol leakage of cellular components.
IND: Broad spectrum for systemic fungal infections. Alternative to Ampho B
AE: Hepatotoxicity
Cardiac SUppression
DI: Azoles are P450 inhibitors,
Warfarin, digoxin, oral hypoglycemic agents, antacids
Tuberculosis
Infectious disease caused by Mycobacterium tuberculosis.
Patho: Airborne droplets. Bacillus inspired into lungs causes inflammation, which causes neutrophil and macrophage activity. Engulf bacilli, sealed off, forming tubercle lesion. Infected tissue within tubercle dies, scar tissue grows around the lesion.
