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Pharmacology > Pharmacology Infectious Disease > Flashcards

Pharmacology Infectious Disease Flashcards

1
Q

Ethambutol

A

Bacteriostatic antimycobacterial drug used in the treatment of Tb

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2
Q

What is ethambutol often given with for treatment of active Tb

A

Isoniazid, rifampin, and pyrazinamide

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3
Q

MOA ethambutol

A

Blocking bacterial arabinosyltransferase enzyme, which polymerizes carbohydrates in the bacterial cell wall. Therefore, leading to increased permeability of the cell wall

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4
Q

Side effects ethambutol

A

Eyes, optic neuritis, red green color blindness

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5
Q

MOA ethambutol

A

Bacteriostatic
Interfering with bacteria protein production, DNA replication, metabolism without directly harming the organism.

Blocks arabinosyltransferase, which polymerizes carbohydrates in the bacterial cell wall

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6
Q

Side effects ethambutol

A

Red green color blindness and decreased visual acuity. Optic neuritis, which results in color blindness, central scotoma and decreased visual acuity

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7
Q

Discontinuation of ethambutol can lead to what

A

Visual disturbances

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8
Q

Isoniazid

A

Drug used in the treatment of both latent and active tb. It can be used as a mono therapy for the treatment of latent Tb but is commonly used in a four drug regime including pyrazinamide, ethambutol, rifampin for active TB

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9
Q

Isoniazid is a pro drug that required bacterial catalase peroxidase enzyme to activate it and works by inhibiting the synthesis of __ __

A

Myolic acid

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10
Q

Isoniazid is metabolized by the __ via ___

A

Liver

Acetylation

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11
Q

There are two forms of the acetylation enzyme :

A

Fast acetylator

Slow acetylator

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12
Q

People with fast acetylator

A

Metabolize the drug more quickly than the slow acetylator

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13
Q

Side effects osiniazis

A

Vitamin B6 defiency
Hepatotoxicity and neurotoxicity
Drug induced lupus erythematosus

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14
Q

Indications isoniazid

A

TB

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15
Q

MOA isoniazid

A

Inhibits synthesis of mycolic acid

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16
Q

Is isoniazid used for active of latent TB

A

Both

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17
Q

How is isoniazid used for latent TB

A

Monotherapy

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18
Q

How is TB used for active TB

A

Four drug regime

Pyrazinamide, ethambutol, rifampin

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19
Q

MOA isoniazid

A
  1. must be activated by bacterial catalase peroxidase bc it is a pro drug
  2. inhibits synthesis of mycolic acids which is necessary for synthesis of the mycobacterial cell wall
  3. Metabolized in liver fast or slow depending on acetylators
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20
Q

Side effects isoniazid

A

B6 defiency (peripheral neuropathy and sideroblastic anemia)
Neurotoxicity (associated with B6 defiency)
Hepatotoxicity
Drug induced lupus

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21
Q

Rifampin

A

Bactericidal antibiotic commonly used int he treatment of active TB

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22
Q

MOA rifampin

A

Inhibits bacterial RNA stnthesisby inhibiting RNA polymerase.

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23
Q

Why does rifampin resistance develop quickly

A

Due to alteration of the binding sites on RNA polymerase so monotherapy should not be used

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24
Q

Monotherapy rifampin

A

NO

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25
Q

What is rifampin used in combo with

A

Other antibiotics

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26
Q

Indications for rifampin

A

TB
Haemophilus influenza
Leprosy
Meningitis

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27
Q

Rifampin is a p450 inducer….causing what

A

Increased rate of metabolism of other drugs that are cleared by the liver through the p450 system

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28
Q

Side effect rifampin

A

P450. Inducer

Bodily fluids (urine and tears) to become orange red in color which may be alarming but is completely benign

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29
Q

TB rifampin

A

Bactericidal antibiotic used for active TB, but never monotherapy due o high resistance rates

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30
Q

What is rifampin used with to treat active TB

A

Isoniazid, ethambutol, and pyrazinamide

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31
Q

MOA rifampin

A

Blocks RNA polymerization

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32
Q

Indications for rifampin

A

TB, haemophilus influenza, leprosy, Hansen’s disease (rifampin with dapsone and clofazimine)
Meningitis prophylaxis

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33
Q

Azoles (ketoconazole)

A

Antifungal medication that work by inhibiting fungal ergosterol synthesis, disabling the fungus from growing

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34
Q

Indications for azoles (ketoconazole)

A

Local and lessserious systemic mycoses

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35
Q

Side effects azoles (ketoconazole)

A

Liver dysfunction and testosterone synthesis inhibition

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36
Q

Azoles suffix

A

Azole

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37
Q

Examples of azoles

A

Fluconazole

Ketoconazole

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38
Q

Indications for azoles

A

Local and less serious systemic mycosis

Exception is fluconazole-used for chronic suppression of cryptococcus, along with candidiasis in AIDS patients

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39
Q

MOA azoles

A

Inhibits ergosterol synthesis leaving to defective cell membrane synthesis in fungi

Inhibits p450 to do this.

In fungus cp450 is responsible for converting lanosterol to ergosterol, and inhibition of it leads to defect cell membrane synthesis

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40
Q

Side effects azoles

A

Liver dysfunction
Inhibition of testosterone synthesis by inhibiting cholesterol desomolase which can lead to gynecomastia and hormone imbalance

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41
Q

Amphotericin B

A

Polyene medication which works by binding to ergosterol in fungal cell membranes.

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42
Q

MOA amphotericin B

A

Bind to ergosterol in fungal cell membrane

Forms membrane pores, causing electrolytes to leak, killing the cell

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43
Q

Indications for amphotericin B

A

Serious systemic mycoses

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44
Q

Side effects emphotericin B

A

Fever, chills, nephrotoxicity, arrhythmias, anemia and IV phlebitis

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45
Q

Indications for amphotericin B

A 
Systemic mycosis (eg crytococcus)
Fungal meningitis (eg cryptococcal meningitis)
Last resort for protozoan infections (eg visceral leishmaniasis and amoebic meningoencephalitis from naegleria Fowleri)
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46
Q

MOA amphotericin B

A

Polyene that binds to ergosterol and forms membrane pores allowing leak of electrolytes, killing the fungal cell

Ergosterol is a component of fungal membranes

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47
Q

Side effects amphotericin B

A

Fever, chills, nephrotoxicity, hypotension, arrhythmias, anemia, IV phlebitis

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48
Q

“Shake and bake” amphotericin B

A

Fever and shaking

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49
Q

How make nephrotoxicity from amphotericin B less

A

Coal minister with liposomes

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50
Q

Hypotension amphotericin B

A

Bc of histamine release

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51
Q

Arrhythmias and amphotericin B

A

Due to Renal tubular damage, potassium and magnesium levels can be altered. Can lead to arrhythmias and ventricular fibrillation and cardiac failure

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52
Q

Flucytosine

A

Antifungal for treating cryptococcal meningitis and candida

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53
Q

What is fluctosine typically combined with

A

Amphotericin B

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54
Q

MOA flucytosine

A

Inhibiting DNA and RNA synthesis by being converted to 5-FU by cytosine deaminase in the fungal cell.

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55
Q

Side effect flucytosine

A

Bone marrow suppression

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56
Q

Indications flucytosine

A

Cryptococcus (cryptococcus meningitis in immunocompromised patients)
, candida (candida cystitis)
, used in combination with amphotericin B or azoles

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57
Q

Why is flucytosine used in combination with amphotericin b or azole antifungal

A

Due to its weak antifungal effects and susceptibility to resistance

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58
Q

MOA flucytosine

A

Inhibits and disrupts DNA and RNA biosynthesis by being converted to 5-FU which is an antimetabolite. In the fungal cel, cytosine deaminase converts fluctosine into 5-FU, which blocks the synthesis of thymidine ( a building block of DNA)

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59
Q

Side effects flucytosine

A

Bone marrow suppression—>anemia, leukopenia, pancytopenia, agranulocytosis

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60
Q

Is flucytosine toxicity reversible

A

None can lead to death, notably in immunocompromised patients

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61
Q

Griseofulvin

A

Oral antifungal medication used to treat infections of the skin.

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62
Q

Indication for griseofulvin

A

Ringworm and tinea infections but has several side effects

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63
Q

Side effects griseofulvin

A

Headache, confusion, teratogenic effects and inducing cytochrome p450

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64
Q

MOA griseofulvin

A

Interferes with mitotic spindle synthesis by binding to tubules and disrupting microtubule formation in fungal cells

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65
Q

Griseofulvin indications

A

Antifungal for superficial infections (ringworm or tinea-hair, nail, or large body surfaces)
INHIBITS DERMATOPHYTES which may cause ringworm or tinea. Can be used for all tineas(Curry’s, pedis, capitis, corporis)

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66
Q

Side effects griseofulvin

A

Teratogen
P450 inducer
Confusion
Headache

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67
Q

Terbinafine

A

Antifungal med which is indicated for use against dermatophytes (tinea cruris, pedis and corporis), as well as onchyomycosis

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68
Q

MOA terbinafine

A

Inhibiting squalene epoxidase, leading to fungal cell lysis and death

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69
Q

Indications terbinafine

A

Dermatophytosis (skin fungal disease-tinea pedis, tinea cruris, tinea corporis)

Onychomycosis (fungal nail infections) bc other topical agents cant penetrate nail beds deeply. It is given orally and acts systemically so can get under the nail bed

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70
Q

MOA terbinafine

A

Inhibits squalene epoxidase which is responsible for ergosterol synthesis. This changing cell membrane permeability leading to fungal cell lysis and death

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71
Q

Side effects terbinafine

A

Hepatotoxicity
GI distress
Taste disturbances
Headache

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72
Q

Chino candies

A

Antifungal meds that work by inhibiting cell wall synthesis

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73
Q

MOA exhinocandins

A

Inhibit the synthesis of beta-glucan

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74
Q

Indications for echinocandins

A

Invasive aspergillosis and candida

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75
Q

Side effects echinocandin

A

GI upset and flushing, due to histamine release

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76
Q

Echinocandins

A

Fungin

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77
Q

Examples of echinocandins

A

Caspofungin

Micafungin

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78
Q

Indications echinocandins

A

Invasive aspergillosis (intolerant. To amphotericin B or itraconazole)

Candida (also invasive candidiasis (abdominal abscesses, peritonitis, pleural cavity infections, esophagitis))

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79
Q

MOA echinocandins

A

Inhibits cell wall synthesis by inhibiting the enzyme that makes beta glucagon, which is an integral part of fungal cell walls

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80
Q

Side effects echinocandins

A

GI distress

Flushing (can promote histamine release)

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81
Q

Nystatin

A

Polyene medication that works by binding ergosterol and forming membrane pores in the fungus it is treating.

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82
Q

Indication for nystatin

A

Candidiasis and administered for topical infections bc it is too toxic for systemic administration

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83
Q

MOA nystatin

A

Amphotericin B same

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84
Q

Indications for nystatin

A

Candidiasis (vaginal, oral, cutaneous)

85
Q

MOA nystatin

A

It is a polyene, so it binds to ergosterol and forms membrane pores , allowing leakage of electrolytes, destroying the fungal cell

86
Q

Topical form of nystatin

A

Polyene and shares same MOA and amphotericin B . Nystatin however is too toxic for systemic use, and works well with cutaneous and topical infections

87
Q

Side effects nystatin

88
Q

Acyclovir (Zovirax)

A

Antiviral medication that inhibits viral replication in organisms of the herpes virus family

89
Q

Indication for acyclovir (zoviraz)

A

Herpes infections and varicella zoster virus

90
Q

Side effects oral acyclovir (Zovirax)

A

Nausea, vomiting, diarrhea and headache

91
Q

Side effects IV acyclovir

A

Nephrotoxicity and neurotoxicity

92
Q

Special considerations acyclovir

A

Preventing recurring episodes of herpes simplex virus and administering IV acyclovir at a slow rate

93
Q

MOA acyclovir

A

-it is a nucleoside analog medication. Specifically a guanosine analog, and lacks 3’ group, which is necessary for addition of the next nucleotide. Thus when added to a growing DNA chain, synthesis is halted

Inhibits viral replication . This medication directly targets the thymidine kinase formed by herpesviruses and does not affect human DNA

Uses viral thymidine kinase to convert it into acyclovir monophosphate. This is converted into another compound which then inactivated and competitively inhibits DNA polymerase, halting DNA synthesis in viral cells

94
Q

Indications acyclovir

A

HSV

Varicella zoster

95
Q

Topical acyclovir

A

Initial genital herpes simplex

96
Q

Oral acyclovir

A

Both initial and recurrent oral and genital herpes infections

Varicella within 24 hours of developing rash
High doses if older adult

97
Q

IV acyclovir

A

Severe genital herpes infection, or immunocompromised patients with oral herpes

Immunocompromised patients with varicella zoster

98
Q

Side effects acyclovir oral

A

Headache

GI distress

99
Q

Side efects acyclovir IV

A 
CNS toxicity (esp renal impairment)
Nephrotoxicity (buildup of acyclovir in body can causes neurotoxicity like agitation, tremors, hallucinations, and delirium. Also sudden jerking))

Nephrotoxicity (crystalline nephropathy-increased BUN and creatinine)

100
Q

Ganciclovir

A

Antiviral medication used to treat CMV infections int he immunocompromised

101
Q

MOA ganciclovir

A

Guanosine analog, that is phosphorylation by a viral kinase to form a competitive inhibitor of nucleotide incorporation into DNA)…thus inhibiting viral DNA polymerase

102
Q

Side effects ganciclovir

A

Hematologic also effects, along with renal toxicity

103
Q

Indications ganciclovir

A

CMV

Immunocompromised (HIV, more susceptible to CMV)

104
Q

MOA ganciclovir

A

Guanosine analog which is phosphorylation by a viral kinase encoded by CMV during infection…leading to the formation of ganciclovir triphosphate

Disrupts DNA synthesis-ganciclovir triphosphate is a competitive inhibitor of nucleotide incorporation into DNA, leading to disrupted DNA synthesis

Ganciclovir triphosphate, which is formed by viral processing of ganciclovir, preferentially inhibits viral DNA polymerase, disrupting viral DNA synthesis

105
Q

Side effects ganciclovir

A

Hematologic effects

Nephrotoxicity

106
Q

Foscarnet

A

Antiviral medication used to treat CMV retinitis in immunocompromised that have failed ganciclovir therapy or acyclovir resistant HSV

107
Q

Indications for foscarnet

A

CMV retinitis

Acyclovir resistant HSV

108
Q

MOA foscarnet

A

Inhibiting viral DNA polymerase and does not require activation by a viral kinase

109
Q

Side effect foscarnet

A

Nephrotoxicity

Resistance when their DNA polymerase mutates

110
Q

MOA foscarnet

A
  1. does not require activation by thymidine kinases
  2. Inhibits viral DNA polymerase by binding to pyrophosphate(it is a pyrophosphate analog)-binding site of this enzyme..inhibiting elongation of viral DNA
111
Q

How does foscarnet gain resistance

A

Mutate DNA polymerase so foscarnet cant bind anymore

112
Q

Side effects foscarnet

A

Nephrotoxicity, electrolyte abnormalities

113
Q

What sort of electrolyte abnormalities do you get with foscarnet

A

Hypokalemia, hypocalcemia, hypomagnesemia

114
Q

What level of k is hypokalemia and what are symptoms

A

Under 3.5 mEq/L

Muscle weakness, arrhythmias, presence of U waves, constipation, hyporeflexia

115
Q

What level is hypocalcemia and what are the symptoms

A

8.5 mg/dL

Decreased bone density, muscle spasms, tetany, increased DTR, prolonged QT interval

116
Q

What level is hypomagnesia and what are symptoms

A

1.5mEq/L

Increased DTR, seizures, muscle cramps, tremors, insomnia, and tachycardia

117
Q

Fusion inhibitors / entry inhibitors

A

Medications that are often used in combination therapy to prevent binding, fusion and entry of the HIV vision into the host cell.

118
Q

Two fusion inhibitors

A

Enfuvirtide

Maraviroc

119
Q

MOA enfuviritde

A

Binding gp41 (a HIV protein) and interferes with this ability to fuse CD4 cells

120
Q

MOA maraviroc

A

Binds CCR5 preventing its interaction with viral gp120

121
Q

Indications fusion inhibitors

A

HIW infection, as part of multidrug therapy

122
Q

Maraviroc MOA

A

Binds CCR5 on CD4 (chemokine receptor), preventing its interaction with viral gp120 disallowing viral entry into the human cell

123
Q

Enfuvirtide MOA

A

Binding to gp21 (an HIV protein) and interferes with its ability to fuse with CD4 cells
Inhibits viral entryleading to defective fusion

124
Q

Side effects fusion proteins

A

Skin reactions at injection sites

125
Q

Protease inhibitors

A

Inhibit the maturation of new viruses, by selectively binding to viral proteases and inhibiting replication.

126
Q

Indication for protease inhibitors

A

HIV/AIDS and hepc

127
Q

Side effects protease inhibitors

A

Nephropathy, lidodystrophy, hyperglycemia, and GI distress

128
Q

Suffix protease inhibitors

129
Q

Examples of protease inhibitors

A

Ritonavir and indinavir

130
Q

HIV and protease inhibitors

A

Inhibit HIV-1 protease

131
Q

Protease inhibitors and hepatitis C

A

Treat hepatitis caused by hepatitis C

132
Q

MOA protease inhibitors

A

Inhibit protease, which is required for viral replication. (Viral proteases cleave proteins for viral maturation)

133
Q

Virus maturation

A

Occurs by assembling functional units, which are made from polypeptides that were cleaved by protease. By inhibiting viral protease, these functional protein precursors cant be cleaved, and a new, mature, infectious virus cant be assembled.

134
Q

Side effects protease inhibitors

A

GI distress,
Nephropathy
Lipodystrophy(abnormal degeneration of fat)
Hyperglycemia (insulin resistance

135
Q

Integrate inhibitors

A

Class of antiretroviral medication, which are used to treat HIV.

136
Q

MOA integrate inhibitors

A

Inhibit HIV genome integration into the host DNA, by inhibiting HIV integrate. This medication can lead to insomnia and hypercholestermia.

137
Q

Suffix of integrate inhibitors

138
Q

Example of integrate inhibitors

A

Raltegravir

139
Q

Indications integrate inhibitors

A

HIV, with other meds

140
Q

MOA integrate inhibitors

A

Blocks insertion of HIV viral genome into host chromosome
-block viral genome integration by reversible inhibiting HIV integrate, the viral enzyme which integrate the viral genome

141
Q

Side effects integrate inhibitors

A

Hypercholestermia
Increased LFTs (AST, ALT and bilirubin)
Insomnia
Increased CK (muscle pain)

142
Q

Non nucleoside reverse transcriptase inhibitors (NNRTIs)

A

Class of medication designed to bind to reverse transcriptase to inhibit viral DNA elongation.

143
Q

What are NNRTIs often combined with

A

Other therapies

144
Q

What is different about NNRTI from NRTI

A

Don’t require intracellular metabolism

145
Q

Side effects NNRTIs

A

Hepatotoxicity, vivid dreams and CNS effects

146
Q

NNRTIs contraindicated

A

Pregnant women

147
Q

Indication NNRTI

148
Q

MOA NNRTI

A
  1. dont need intracellular metabolism or phosphorylation

2. inhibit reverse transcriptase(different site from NRTI), preventing viral DNA from being transcripts

149
Q

Side effects NNRTI

A

Rash

Hepatotoxicity, vivid dreams and CNS symptoms

150
Q

Which NNRTI causes vivid dreams and CNS symptoms

151
Q

Why no give NNRTI to pregnant women

A

Delavirdine and efavirenz

Teratogenic

152
Q

Examples of NNRTI

A

Nevirapine, rilpivirine, efavirenze, delavirdine, etravirine

153
Q

Efavirenze

A

Neuropsychiatric effects

154
Q

Delavirdine and efavirenze

A

Teratogenic activity contraindicated in patients

155
Q

Nevirapine (viramune)

A

For HIV AIDS

Used in triplecombination due to viral resistance

156
Q

Rilpivirine (edurant)

A

Second generation NNRTI

Higher potency and longer half life and less side effects

157
Q

Delavirdine (DLV, rescriptor)

A

Not HAART bc lower efficacy than other NNRTI. Associated with teratogenic effects and contraindicated in pregnancy

158
Q

Efavirenz (EFV, sustiva)

A

Part of HAART
Also combined with other for prophylaxis of HIV transmission. Has dopaminergic and serotonergic activity, leading to neuropsychiatric adverse effects

159
Q

What CNS effects do you get with efavirenz

A

Depression, anxiety, hallucinations, aggression, suicidal ideation, sleep disturbances)

160
Q

How can you alleviate CNS side effects from efavirenz

A

Cyproheptadine

161
Q

Etravirine (ETR, intelence)

A

Second generation NNRTI designed to be active against HIV with mutations that display resistance to the two most commmonly prescribed first generation NNRTI

162
Q

NRTI (nucleoside reverse transcriptase inhibitors)

A

Antiretroviral drugs used for HIV work by competitively inhibiting nucleotide binding to reverse transcriptase, and also terminate the elongating DNA chain

163
Q

Adverse

A

General prophylaxis and during pregnancy to decrease transmission

164
Q

NRTI activation

A

Int he cel, requiring phosphorylation

165
Q

Indication for NRTI

A 
HIV 
zidovudine (Zdz) for general prophylaxis and pregnant women to reduce transmission
166
Q

MOA NRTI

A

1.activation in the cell by phosphorylation2.competitively inhibit nucleotide binding to reverse transcriptase, preventing the virus from making a DNA copy of its RNA
Chain termination
-lack of 3’-OH group in the incorporated nucleotide analogue prevents DNA chain elongation and therefore, the viral DNA growth is terminated

167
Q

What are the two groups of NRTI

A

Nucleoside reverse transcriptase inhibitors

Nucleotide reverse transcriptase inhibitors

168
Q

Nucleoside reverse transcriptase inhibitors

A 
Didanosine (DDI)
Emtricitabine (FTC)
Abacavir (ABC)
Lamivudine (3TC)
Stavudine (d4T)
Zidovudine (Zdv)

DEALSZ

169
Q

Nucleoside analog medication

A

Tenofivir (TDF)

170
Q

Didanosine DDI

A

Adenosine analog

171
Q

Adverse reaction didanosine

A

Diarrhea, nausea, vomiting, abdominal pain, fever, headache rash, peripheral neuropathy

172
Q

Emtricitabine (FTC)

A

Analog to cytidine
Treat HIV and hep B
Rare side effects-may get hepatotoxicity or lactic acidosis

173
Q

Abacavir (ABC)

A

Nucleoside analog reverse transcriptase inhibitor analog of guanosine
Oral-high bioavailability

174
Q

Side effects abacavir

A

Nausea, headache, fatigue, vomiting, hypersensitivity reaction, diarrhea, fever/chills , depression, rash , anziety, URI, ALT, AST up, hypertriglyceridemia, lipodystrophy

175
Q

Lamivudine (3TC)

A

Cytidine analogue

Inhibit HIV reverse transcriptase and hep b reverse transcriptase

176
Q

Stavudine (d4T)

A

Thymidine analogue which inhibits HIV RT by competing with natural substrate, thymidine triphosphate. Then leads to termination of DNA replication by incorporating into the DNA strand

177
Q

Side effects stavudine (d4T)

A

Peripheral neuropathy and lipodystrophy, so less commonly used in developing countries)

178
Q

Zidovudine (Zdv)/AZt

A

For selectively inhibiting HIVs reverse transcriptase, the enzyme that the virus uses to make a DNA copy of its RNA.

179
Q

Side effects zidovudine AZt

A

Anemia, neutropenia, hepatotoxicity, cardiomyopathy, myopathy

180
Q

Why is AZt given as part of HAART

A

Resistance

181
Q

Tenofovir

A

Nucleoside analogue reverts transcriptase inhibitor

HIV hep b

182
Q

Side effects tenofovir

A

Nausea, comiting, diarrhea, weakness

Renal complications-acute renal failure, falcon I syndrome, proteinuria, tubular necrosis

183
Q

NRTI toxicity

A

Medications that inhibit RT in HIV

184
Q

Toxicities of NRTI

A

Bone marrow suppression, rash, neuropathy, lactic acidosis, pancreatitis, anemia

185
Q

Which NRTI cause pancreatitis with alcohol

A

DIDANOSINE

186
Q

How reverse bone marrow suppression with NRTI

A

G-CSF and erythropoietin

187
Q

Cidofovir

A

Antiviral med for CMV retinitis in immunocompromised patients and is also indicated for acyclovir resistant HSV

188
Q

MOA cidofovir

A

Long half life and works by preferentially inhibit viral DNA polymerase
Active and doesn’t require phosphorylation

189
Q

Side effect cidofovir

A

Nephrotoxicity, which can be decreased when co administered with probenecid and IV saline

190
Q

Indications cidofovir

A

CMV retinitis in immunocompromised patients

Acyclovir resistant HSV

191
Q

MOA cidofovir

A

Inhibits viral DNA polymerase by selectively inhibiting viral DNA polymerases thus inhibiting viral DNA synthesis during its reproduction cycle

192
Q

Side effects cidofovir

A

Nephrotoxicity

193
Q

How prevent nephrotoxicity with cidofovir

A

Administer with probenecid and IV saline

194
Q

HAART

A

Highly active antiretroviral therapy
Medication regime for patients who display AIDS defining lesions or have CD4 count below 350 internationally or 500 in US

195
Q

What is HAART

A

2 NRTI+1 of the following: a NNRTI, a protease inhibitor or an integrate inhibitor

196
Q

When initiate HAART

A

When HIV diagnosis

To reduce disease progression and prevent transmission

197
Q

How many drugs are in HAART

198
Q

What are the 2NRTIs(nucleoside reverse transcriptase inhibitors)

A

Inhibit binding of nucleotides to reverse transcriptase and by terminating the DNA chain

199
Q

What is the 3rd HAART drug

A 
NNRTI
Treats HIV by inhibiting nucleotide binding to reverse transcriptase at a different site of action than NRTI
Or
Protease inhibitor
Or
Integrate inhibitor
200
Q

Ribavirin

A

Antiviral medication with activity against both RNA and DNA viruses.

201
Q

Indication for ribavirin

A

Hep c and viral hemorrhagic fevers, off label RSV

202
Q

Side effect ribavirin

A

Teratogen, hemolytic anemia

203
Q

MOA ribavirin

A

Hypermutation in RNA viruses-incorporated into RNA base pairs guanine and adenosine. Induces hypermutations in RNA dependent replication, leading to virus death

Inhibits inosine monophosphate dehydrogenase-inhibits cellular inosine monophosphate dehydrogenase, depleting intracellular GTP which may play a role

204
Q

Indications ribavirin

A

Hep c
Viral hemorrhagic fever
RSV

205
Q

Side effects ribavirin

A

Hemolytic anemia

Teratogen

206
Q

Zanamivir (relenza) and oseltamivir (tamiflu)

A

Antiviral medications used to treat and provide prophylaxis against influenza A and B.

207
Q

MOA zanamivir and oseltamivir

A

Bind to neuraminidase, preventing the virus from escaping its host cell and infecting others

208
Q

Indications zanamivir and oseltamivir

A

Influenza a and b

Prophylaxis for people exposed to flu

209
Q

MOA zanamivir and oseltamivir

A

Inhibits release of new virus 9render virus unable to escape from the host cell that it has infected. Thus unable to infect other cells)

Work to inhibit viral transmission by binding to the active site of viral neuraminidase. This makes the infected host cell unable to bud

Pharmacology (52 decks)

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