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Pharmacology > Antimircobials > Flashcards

Antimircobials Flashcards

1
Q

Folic acid synthesis (DNA methylation) inhibitors

A

Sulfonamides

Trimethoprim

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2
Q

DNA topoisomerase inhibitor

A

Fluoroquinolones

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3
Q

Damages DNA

A

Metronidazole

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4
Q

mRNA synthesis (RNA polymerase) inhibitor

A

Rifampin

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5
Q

Protein synthesis (50S subunit) inhibitors

A

Chloramphenicol, Clindamycin, Linezolid
Macrolides
Streptogramins

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6
Q

Protein synthesis (30S subunit) inhibitors

A

Aminoglycosides

Tetracyclines

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7
Q

Peptidoglycan cross-linking (of the cell wall) inhibitors

A 
Penicillinase-sensitive penicillins
Penicillinase-resistant penicillins
Antipseduomonals
Cephalosporins (I-V)
Carbapenems
Monobactams (Aztreonam)
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8
Q

Peptidoglycan synthesis (of the cell wall) inhibitors

A

Glycopeptides (bacitracin, vancomycin)

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9
Q

Penicillinase-sensitive penicillins

A

Amoxicillin
Ampicillin
Penicillin G, V

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10
Q

Pencillinase-resistant penicillins

A

Dicloxacillin
Nafcillin
Oxacillin

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11
Q

Antipseudomonals

A

Piperacillin

Ticarcillin

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12
Q

Cephalosporins (I-V)

A 
1st-Cefazolin, Cephalexin
(1 ZObra named LEXI)
2nd-Cefoxitin, Cefaclor, Cefuroxime 
(2 FOXes went into the FACtory and came out as FUR)
3rd-Ceftriaxone
(3 taxidermists TRI to sell a DIMEsaur)
4th-Cefepime
(I'm + 4 PIMEcones turned green/blue)
5th-Ceftaroline
 (5 TARred birds are MRSArible)
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13
Q

Carbapenems

A

Doripenem
Imipenem
Meropenem
Ertapenem

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14
Q

Aminoglycosides

A 
Gentamicin
Neomycin
Amikacin
Tobramycin
Streptomycin
Min (amino) GNATS caNNOT kill anerobes
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15
Q

Tetracyclines

A

Doxycline
Minocyline
Tetracycline

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16
Q

Macrolides

A

Azithromycin
Clarithromycin
Erthyromycin

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17
Q

Streptogramins

A

Dalfopristin

Quinupristin

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18
Q

Fluoroquinolones

A

Ciprofloxacin

Levofloxacin

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19
Q

Sulfonamides

A

Sulfadiazine
Sulfamethoxazole
Sulfisoxazole

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20
Q

Penicillin G, V

A

MOA: B-lactam antibiotics: bind penicillin-binding proteins (transpeptidases that build cell walls)
Use: Mostly used for Gram + (also N. meningitidis, T. pallidum)
Tox: Hypersensitivity reactions, hemolytic anemia
Penicillinase (a B-lactamase) sensitive

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21
Q

Amoxicillin, ampicillin

A

MOA: Broad spectrum B-lactam antibiotics
Oral bioavailability: AmOxicillin>ampicillin
Use: H. influenzae, H. pylori, E. Coli Listeria, Proteus, Salmonella, Shigella, Enterococci (HHELPSS kill enterococci)
Tox: Hypersensitivity reactions, rash, pseudomembranous colitis
Penicillinase sensitive: Combine w/ clavulanic acid to inhibit penicillinase

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22
Q

Dicloxacillin, oxacillin, nafcillin

A

“DON has a narrow mind and only Staphs certain people, even though he is not MRSAble”
MOA: Narrow spectrum B-lactam antibiotics
Use: S. aureus (except MRSA)
Tox: Hypersensitivity reactions, interstitial nephritis
Penicillinase resistant (bulky R-group blocks B-lactamase

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23
Q

Piperacillin, ticarcillin

A

“PIPER and TICA are on an EXTENDED jail sentence for using NEGATIVE language and hurting people with RODS
MOA: Antipseudomonals: Extended spectrum B-lactam antibiotics
Use: Pseudomonas and gram - rods
Tox: Hypersensitivity reactions
Penicillinase sensitive: Combine w/ clavulanic acid to inhibit penicillinase

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24
Q

B-lactamase inhibitors

A

Clavulanic acid, sulbactam, tazobactam (CAST)

Added to penicillin antibiotics to protect the antibiotic from destruction by B-lactamase (penicillinase)

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25
Q

Cephalosporin-1st generation

A

Cefazolin, cephaLEXIn (1 ZObra named LEXI)
MOA: B-lactams, peptidoglycan cross-linking inhibitors (bind PBP), less susceptible to penicillinases. Bactericidal.
Use: Gram + cocci, Proteus, E. coli, Klebsiella, Pre-surgery prophylaxis to prevent S. aureus wound infections
Tox: Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency, exhibit cross-reactivity with penicilllins,
increases nephrotoxicity of aminoglycosides

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26
Q

Cephalosporin-2nd generation

A

Cefoxitin, cefaclor, cefuroxime (2 FOXes go to the FACtory and come out as FUR)
MOA: B-lactams, peptidoglycan cross-linking inhibitors (bind PBP), less susceptible to penicillinases. Bactericidal.
Use: Gram + cocci, H. influenzae, Enterobacter aerogenes, Neisseria spp., Proteus mirabilis, E. Coli, Klebsiella, Serratia marcescens
Tox: Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency, exhibit cross-reactivity with penicilllins,
increases nephrotoxicity of aminoglycosides

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27
Q

Cephalosporin-3rd generation

A

Cefotaxime, Ceftriaxone, , cefazidime (3 TAXidermists TRI to sell a DIMEsaur)
MOA: B-lactams, peptidoglycan cross-linking inhibitors (bind PBP), less susceptible to penicillinases. Bactericidal.
Use: Serious gram - infections resistant to other B-lactams
Ceftriazone-meningitis, gonorrhea, disseminated lyme dz
Ceftazidime-Pseudomonas
Tox: Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency, exhibit cross-reactivity with penicilllins,
increases nephrotoxicity of aminoglycosides

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28
Q

Cephalosporin-4th generation

A

CefePIME (I’m +/- (unsure) if 4 PIMEcones turned green/blue)
MOA: B-lactams, peptidoglycan cross-linking inhibitors (bind PBP), less susceptible to penicillinases. Bactericidal.
Use: gram - org., esp Pseudomonas, gram + org.
Tox: Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency, exhibit cross-reactivity with penicilllins,
increases nephrotoxicity of aminoglycosides

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29
Q

Cephalosporin-5th generation

A

CefTARoline (5 TARred birds are MRSArible)
MOA: B-lactams, peptidoglycan cross-linking inhibitors (bind PBP), less susceptible to penicillinases. Bactericidal.
Use: Broad gram + and gram - org., including MRSA
Tox: Hypersensitivity reactions, autoimmune hemolytic anemia, disulfiram-like reaction, vitamin K deficiency, exhibit cross-reactivity with penicilllins,
increases nephrotoxicity of aminoglycosides

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30
Q

Mechanism of resistance to cephalosporins

A

Structural change in penicillin-binding proteins (transpeptidases)

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31
Q

CarbaPENEMs

A

Imipenem, meropenem, ertapenem, doripenem
MOA: B-lactams, peptidoglycan cross-linking inhibitors (bind PBP)
Use: Gram + cocci, gram - rods, anaerobes
Wide spectrum, but side effects that limit use to last resort
Tox: GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels

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32
Q

Meropenem

A

Carbapenem: has a decrease risk of seizures and stable to dehydopeptidase I

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33
Q

Imipenem

A

Carbapenem: broad spectrum, B-lactamase resistant.

Take with cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.

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34
Q

Monobactams

A

Aztreonam
MOA: B-lactam, peptidoglycan cross-linking inhibitors (bind PBP3).
Less susceptible to B-lactamases & synergistic with aminoglycosides.
No cross-allergenicity with penicillins
Use: Gram - rods ONLY. For penicillin-allergic patients and those with renal insufficiency who can’t use aminoglycosides
Tox: Occasional GI upset

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35
Q

Vancomycin

A

MOA: Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. B-lactamase resistant
Use: Gram + ONLY. Serious, multidrug resistant organisms, including MRSA, S. epidermis, sensitive Enterococcus spp, and C. Diff. (oral dose for pseudomembranous colitis)
Tox: Well tolerated except NOT. Nephrotoxicity, Ototoxicity, Thrombophlebitis. Red man syndrome (prevent with H1 antagonist and slow infusion)
Resistance: bacterial aa modification, D-ala D ala-> D-ala D-lac

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36
Q

Aminoglycosides: names

A

Gentamicin, neomycin, amikacin, tobramycin, streptomycin

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37
Q

Aminoglycosides: MOA

A

Bactericidal. Irreversible inhibition of initiation complex through binding of the 30s subunit. Misreading of mRNA. Ineffective against anaerobes (needs 02)

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38
Q

Aminoglycosides: Use

A

Severe gram - rod infections. Synergistic with B-lactam antibiotics. Neomycin for bowel surgery

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39
Q

Aminoglycosides: Toxicity and resistance

A

Tox: Nephrotoxicity, neuromuscular blockade, ototoxicity, (esp. with loop diuretic), teratogen.
Resistance: Bacterial transferase enzymes inactivate the drug by acteylation, phosphorylation, adenylation

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40
Q

Tertracycline: names

A

Tetracyline, doxycline, minocycline

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41
Q

Tertracycline: MOA

A

Bacteriostatic: binds to 30S and presents tRNA binding.
CNS penetration.
Can’t take with milk (ca2+), anatacids (Ca2+/Mg2+) or iron containing preparations. All inhibit absorption.

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42
Q

Tertracycline: Clinical use

A

Borrelia burgdorferi. M. pneumoniae. Rickettsia. Chlamydia. Acne.
BM CAR makes your teeth YELLOW

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43
Q

Tertracycline: toxicity

A

GI distress, discoloration of teeth, inhibition of bone growth in children, photosensitivity, contraindicated in pregnancy..
Doxycycline is fecally eliminated so can give with renal failure.

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44
Q

Tertracycline: Mechanism of resistance

A

Decrease uptake or ^ efflux out of bacterial cells by plasmid-encoded transport pumps

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45
Q

Chloramphenicol: MOA

A

Blocks peptidyltransferase at 50S ribosomal subunit.

Bacteriostatic

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46
Q

Chloramphenicol: Clinical use

A

Meningitis (H. influ, N. meningitidis, S. pneumo)

Rocky mountain spotted fever (Rickettsia rickettsii)

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47
Q

Chloramphenicol: toxicity

A

Anemia (dose dependent), aplastic anemia (dose independent), gray baby syndrome (premature infants lack UDP-glucuronyl transferase)

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48
Q

Chloramphenicol: Mechanism of resistance

A

Plasmid-encoded acteryltransferase that inactivates the drug

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49
Q

Clindamycin: MOA

A

Blocks peptide transfer at 50S ribosomal subunit.

Bacteriostatic

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50
Q

Clindamycin: Clinical use

A

“Clinda the good witch kills the anaemy (anaerobic) above the diaphragm”
Anaerobic infections (Bacteriodes, C. perfringens) due to aspiration pneumonia, lung abscess, and oral infection.
Also effective against group A strep
*Treats anaerobic infections above the diaphragm. Metronidazole treats anaerobic infections below the diaphragm

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51
Q

Clindamycin: toxicity

A

Pseduomembranous colitis (C. diff overgrowth), fever, diarrhea

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52
Q

Linezolid: MOA

A

Inhibits protein synthesis by binding to 50S subunit and preventing formation of the initiation complex

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53
Q

Linezolid: Clinical use

A

Gram+ species including MRSA and VRE

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54
Q

Linezolid: toxicity

A

Bone marrow suppression (thrombocytopenia)
Peripheral neuropathy
Serotonin syndrome

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55
Q

Linezolid: Mechanism of resistance

A

Point mutation of ribosomal RNA

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56
Q

Macrolides: names

A

Azithromycin, Clarithromycin, Erythromycin

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57
Q

Macrolides: MOA

A

Inhibit protein synthesis by blocking translocation (macroslides). Bind to 23S rRNA of the 50S ribosomal subunit

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58
Q

Macrolides: Clinical use

A

Atypical pneumonias (Mycoplasma, chlamydia, legionella)

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59
Q

Macrolides: toxicity

A

MACRO: Motility issues in GI, Arrhythmia (prolonged QT interval), acute Cholestatic hepatitis, Rash, eOsinophilia
Increases serum theophyllines, oral anticoagulants.
Clarithro and Erythro inhibit p450

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60
Q

Macrolides: mechanism of resistance

A

Methylation of 23S rRNA binding site prevents binding of drug

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61
Q

Trimethoprim: MOA

A

Inhibits bacterial dihydrofolate reductase.

Bacteriostatic

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62
Q

Trimethoprim: Clinical use

A

Use with sulfonamides (TMP-SMX)–>sequential block of folate synthesis.
UTIs, shigella, Salmonella, P. Jirovecii
Prophylaxis for P. Jirovecii and toxoplasmosis

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63
Q

Trimethoprim: toxicity

A

Megaloblastic anemia, leukopenia, granulocytopenia

TriMethoPrim: Treats Marrow Poorly

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64
Q

Sulfonamides: names

A

Sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

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65
Q

Sulfonamides: MOA

A

Inhibits folate synthesis by inhibiting dihydropteroate synthase (PABA–>dihydropteroic acid)
Bacteriostatic alone. Bacteriocidal with TMP.
Dapsone for leprosy works in a similar way

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66
Q

Sulfonamides: clinical use

A

Gram positives, gram negatives, Nocardia, Chlamydia

Triple sulfas or SMX for simple UTI

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67
Q

Sulfonamides: toxicity

A

Hypersensitivity reactions, hemolysis if G6PD deficient.
Nephrotoxicity (tubulointerstitial nephritis), photosensitivity, kernicterus (bilirubin in the brain) in infants, displace other drugs from albumin (warfarin)

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68
Q

Sulfonamides: Mechanism of resistance

A

Altered enzyme (bacterial dihydropteroate synthase), decrease uptake, ^PABA synthesis

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69
Q

Fluoroquinolones: names

A

Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, moxifloxacin, gemifloxacin, enoxacin

70
Q

Fluoroquinolones: clinical use

A

Gram negative rods or urinary and GI tracts including pseudomonas, Neisseria, some gram +

71
Q

Fluoroquinolones: toxicity

A

GI upset, superinfections, skin rashes, HA, dizziness.
Less common: leg cramps, myalgias
Contraindicated: pregnancy, nursing, children under 18.
May cause tendonitis or tendon rupture in people >60 and those taking prednisone

72
Q

Fluoroquinolones: mechanism of resistance

A

CHromosome-endcoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps

73
Q

Daptomycin: clinical use

A

S. aureus skin infections, esp. MRSA, bacteremia, endocarditis, and VRE

74
Q

Daptomycin: MOA

A

Lipopeptide that disrupts cell membrane of gram + cocci

75
Q

Fluoroquinolones: MOA

A

Inhibit prokaryotic enzymes topoisomerase II (DNA gyrase) and topo. IV.
Bactericidal. Don’t take with antacids!

76
Q

Daptomycin: Toxicity

A

myopathy, rhabdomyolysis

77
Q

Metronidazole: MOA

A

Forms toxic free radical metabolites in the bacterial cell that damage DNA.
Bactericidal and antiprotozoal.

78
Q

Metronidazole: Clinical use

A

GET on the metro: Giardia, Entamoeba, Trichomonas

Mind the GAP: Gardnerella vaginalis, Anaerobes (bacteriodes/C. Diff. , h. Pylori

79
Q

Metronidazole: toxicity

A

Disulfiram-like reaction with alcohol.
HA
Metallic taste
Treats anerobic infections below the diaphragm (vs. clindamycin)

80
Q

M. Tuberculosis prophylaxis

A

Isoniazid

81
Q

M. Tuberculosis treatment

A

RIPE:

Rifampin, isoniazid, pyrazinamide, ethambutal

82
Q

M. avium prophylaxis

A

Azithromycin, rifabutin

83
Q

M. avium treatment

A

Most drug resistant that TB.
Azithromycin or clarithromycin + ethambutol
Can add rifabutin or ciprofloxacin

84
Q

M. leprae treatment

A

Dapsone+ rifampin=tuberculoid form

Dapsone+rifampin+clofazimine=lepromatous form

85
Q

Mycobacterial drugs that target the cell wall

A

Isoniazid-Mycolic acid synthesis

Ethambutol-Arabinogalactan synthessi

86
Q

Mycobacterial drugs that target mRNA synthesis

A

Rifabutin

Rifampin

87
Q

Rifamycins (Rifabutin/Rifampin): MOA

A

Inhibit DNA-dependent RNA polymerase (mRNA synthesis)

88
Q

Rifamycins (Rifabutin/Rifampin): clinical use

A

Mycobacterium tuberculosis
Delay resistance to dapsone when used for leprosy
Meningococcal prophylaxis and chemoprophylaxis in contacts with children with HIB

89
Q

4 R’s of rifampin

A 
RNA polymerase inhibitor
Ramps up microsomal cytochrome p450
Red/orange body fluids
Rapid resistance if used alone
(rifabutin does not ramp up p450
90
Q

Rifamycins (Rifabutin/Rifampin): toxicity

A

Minor hepatotoxicity and drug interactions (^cytochrome p450)
Orange body fluids
Rifabutin flavored over rifampin in HIV patients due to less p450 stimulation

91
Q

Rifamycins (Rifabutin/Rifampin): Mechanism of resistance

A

Mutations reduce drug binding to RNA polymerase.

Monotherapy rapidly leads to resistance

92
Q

Isoniazid: mechanism of action

A

Decrease synthesis of mycolic acids.

Bacterial catalase peroxidase (encoded by KatG) needed to convert INH to active metabolite

93
Q

Isoniazid: clinical use

A

Mycobacterium tuberculosis

Only prophylaxis against TB

94
Q

Isoniazid: toxicity

A

Neurotoxicity, hepatotoxicity.

Pyridoxine (B6) can prevent neurotoxicity

95
Q

Isoniazid: mechanism of resistance

A

Mutations leading to underexpression of KatG (lack of activation)

96
Q

Pyrazinamide: MOA

A

Uncertain

97
Q

Pyrazinamide: Clinical use

A

Mycobacterium tuberculosis

98
Q

Pyrazinamide: toxicity

A

Hyperuricemia, hepatotoxicity

99
Q

Ethambutol: MOA

A

Decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase

100
Q

Ethambutol: clinical use

A

Mycobacterium tuberculosis

101
Q

Ethambutol: toxicity

A 
Optic neuropathy (colorblindness)
"EYEthembutol"
102
Q

Clinical scenario prophylaxis:

High risk for endocarditis and undergoing surgical/dental procedures

A

Amoxicillin

103
Q

Clinical scenario prophylaxis:

Exposure to gonorrhea

A

Ceftriaxone

104
Q

Clinical scenario prophylaxis:

History of recurrent UTIs

A

TMP-SMX

105
Q

Clinical scenario prophylaxis:

Exposure to meningococcal infection

A

Ceftriaxone, ciprofloxacin, or rifampin

106
Q

Clinical scenario prophylaxis:

Pregnant women carrying group B strep

A

Penicillin G

107
Q

Clinical scenario prophylaxis:

Prevention of gonococcal conjunctivitis in newborn

A

Erythromycin ointment

108
Q

Clinical scenario prophylaxis:

Prevention of post-surgical infection due to S. aureus

A

Cefazolin

109
Q

Clinical scenario prophylaxis:

Prophylaxis of strep pharyngitis in child with prior rheumatic fever

A

Benzathine penicillin G or oral peniCillin V

110
Q

Clinical scenario prophylaxis:

Exposure to syphilis

A

Benzathine penicillin G

111
Q

How do you treat MRSA?

A

Vancomycin, daptomycin, linezolid, tigecycline, ceftaroline

112
Q

How do you treat VRE?

A

Linezolid and streptogramins (50S inhibitors)

113
Q

Amphotericin B: MOA

A 
Binds ergosterol (component of fungal cell membrane)
Forms membrane pores that allow leakage of electrolytes
114
Q

Amphotericin B: clinical use

A

Serious, systemic mycoses:
Cryptococcus (with flucytosine for cryptococcal meningitis)
Blastomyces, Coccidioides, Histoplasma, Candida
INtrathecally for funal meningitis. Supplement K+ and Mg2+ because of altered renal tubule permeability.

115
Q

Amphotericin B: toxicity

A

Fever/chills “shake and bake”
Hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis.
Hydration decreases nephrotoxicity
Liposomal amp decreases toxicity

116
Q

Nystatin: MOA

A

Binds erogsterol and forms membrane pores that allow leakage of electrolytes

117
Q

Nystatin: clinical use

A

Oral candidiasis (thrush), topical for diaper rash or vaginal candidiasis

118
Q

Flucytosine: MOA

A

Inhibits fungal DNA and RNA biosynthesis by conversion of 5-fluorouracil by cytosine deaminase

119
Q

Flucytosine: clinical use

A

Systemic fungal infections (esp. meningitis caused by cryptococcus) in combination with amp B

120
Q

Flucytosine: toxicity

A

Bone marrow suppression

121
Q

-m/nazole: MOA

A

Inhibit fungal ergosterl synthessi by inhibiting the p450 enzyme that converts lanosterol to ergosterol

122
Q

-m/nazole: clinical use

A

Local and less serious systemic mycoses.
Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types.
Itraconazole for Blastomyces, Coccidiodes, Histoplasma.
Clotrimazole and miconazole for topical fungal infections

123
Q

-m/nazole: toxicity

A

Testosterone synthesis inhibition (gynecomastia, esp with ketoconazole), liver dysfunction-inhibits p450

124
Q

Terbinafine: MOA

A

Inhibits the fungal enzyme squalene epoxidase to prevent lanosterol synthesis (precursor of ergosterol)

125
Q

Terbinafine: clinical use

A

Dermatophytoses (esp onychomycosis)

126
Q

Terbinafine: toxicity

A

GI upset, hepatotoxicity, taste disturbance

127
Q

Echinocandins: names

A

Anidulafungin, capofungin, micafungin

128
Q

Echinocandins: MOA

A

Inhibit cell wall synthesis by inhibiting synthesis of B-glucan
*MAC won’t let people discriminate and put up WALLS to ruin the FUNgin

129
Q

Echinocandins: clinical use

A

Invasive aspergillosis, candida

130
Q

Echinocandins: toxicity

A

GI upset, flushing (by histamine release)

131
Q

Griseofulvin: MOA

A

Interferes with microtubule function; disrupts mitosis.

Deposits in keratin-containing tissues (ie nails)

132
Q

Griseofulvin: clinical use

A

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea, ringworm)

133
Q

Griseofulvin: toxicity

A

Teratogenic, carcinogenic, confusion, HA, ^ p450 and warfarin metabolism

134
Q

Antiprotozoan therpy

A

Pyrimethamine (toxoplasmosis), suramin and melarsoprol (Trypanosoma brucei), nifurtimox (t. cruzi), sodium stibogluconate (leishmaniasis)

135
Q

Anti-mite/louse therapy

A

Permethrin (blocks Na+ channels->neurotoxicity)
Malathion (acetylcholinesterase inhibitor)
Lindane (blocks GABA channels->neurotoxicity)
Used to treat scabies (Sarcoptes scabiei) and lice (pediculus and pthirus)

136
Q

Chloroquine: MOA

A

Blocks detoxification of heme into hemozosin. Heme accumulates and is toxic to plasmodia

137
Q

Chloroquine: clinical use

A

Treatment of plasmodial species other than P. falciparum (frequency of resistance in P. falciparum is too high)

138
Q

Antihelminthic therapy

A

Mebendazole, pyrantel pamoate, ivermectin, diethylcarbamazine, praziquantel

139
Q

Cholorquine: toxicity

A

Retinopathy, pruritus

If you’re in the chlorine pool too long your eyes get blurry and your body gets itchy

140
Q

Oseltamivir, zanamivir: MOA

A

Inhibit influenza neuraminidase–> decreased release of progeny virus
Gpa Ose and gma Zana and can’t get the flu out of them every winter

141
Q

Oseltamivir, zanamivir: clinical use

A

Treatment and prevent of Influenza A and B

142
Q

famiciclovir, acyclovir, valacyclovir: MOA

A

My FAV animal is an iGUANA
Guanosine analogs. Monophosphorylated by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells–>few adverse effects.
Triphosphate formed by cellular enzymes.
Preferentially inhibit viral DNA polymerase by chain termination

143
Q

Acyclovir, famiciclovir, valacyclovir: Clinical use

A

HSV (mucocutaneous and genital lesions as well as for encephalitis) and VZV. Prophylaxis in immunocompromised
Weak activity against EBV.
No activity against CMV.
Prophylaxis in immunocompromised patients.
No effects on latent forms of HSV and VZV.
Valacyclovir: prodrug of acyclovir, better oral bioavailability.
Herpes zoster: famciclovir

144
Q

Ganciclovir: MOA

A

Guanosine analog. 5-monophosphate formed by a CMV viral kinase. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase by chain termination.

145
Q

Ganiciclovir: clinical use

A

CMV, esp. in immunocompromised.

Valganciclovir, a prodrug of ganciclovir with ^ bioavailability

146
Q

Ganiciclovir: Toxicity

A

Leukopenia, neutropenia, thrombocytopenia, rental toxicity.
More toxic to host enzymes than acyclovir.
Resistance: mutated viral kinase

147
Q

Foscarnet: MOA

A

Viral DNA/RNA polymerase inhibitor and HIV reverse transcriptase inhibitor. Binds pyrophosphate binding site of enzyme. No activation required.
“binds to PyroFOSphate binding site of polymerase analog”

148
Q

Foscarnet: clinical use

A

CMV retinitis in immunocompromised when ganciclovir fails.

Acyclovir resistant HSV.

149
Q

Foscarnet: toxicity

A

Nephrotoxicity, electrolyte abnormalities can lead to seizures
Mech. of resistance: mutated DNA polymerase

150
Q

Cidofovir: MOA

A

Inhibits viral DNA polymerase. Does not require activation by viral kinase.

151
Q

Cidofovir: clinical use

A

CMV retinitis in immunocompromised patients.

Acyclovir-resistant HSV.

152
Q

Cidofovir: toxicity

A

Nephrotoxicity (give with probenecid and IV saline to decrease toxicity)

153
Q

What drugs do you give for acyclovir-resistant HSV?

A

Foscarnet or cidofovir

154
Q

HIV therapy

A

HAART: Highly active antiretroviral therapy initiated at the time of HIV diagnosis.
Strongest indication for patients present with AIDS defining illness, low CD4 cell counts or high viral load.
2 NRTIs +
1 NNRTI OR protease inhibitor OR integrase inhibitor

155
Q

Protease inhibitor: MOA

A

-navir

Prevents maturation of new viruses by cleaving HIV1 protease, preventing required mRNA cleaving.

156
Q

Protease inhibitor: toxicity

A 
Hyperglycemia, GI intolerance, lipodystrophy
Nephropathy, hematuria 
Rifampin contraindicated (decreased protease inhibitor concentration)
157
Q

NTRIs: MOA

A

Competitively inhibit nucleotide binding to reverse transcriptase and terminate the DNA chain.
Tenofavir is the nucleoTide and does not need to be virally activated like the others.
“Have you dined (vudine) with my nuclear(side) family?

158
Q

NTRI: toxicity

A

Bone marrow suppression-reverse with G-CSF and EPO.

Peripheral neuropathy, lactic acidosis, anemia (ZDV), and pancreatitis

159
Q

NNRTIs: names

A

Delavirdine, Efavirenz, Nevirapine

“Okay, DEN, we gotta get rid of this HIV with one of DEmN NNRTI’s

160
Q

NNRTIs: MOA

A

Bind reverse transcriptase at site different from NRTIs. No activation needed.

161
Q

NNRTIs: toxicity

A

Rash and hepatotoxicity.
Efavirenz: vivid dreams, CNS symptoms
NOT with pregnancy: delavirdine and efavirenz

162
Q

Integrase inhibitor: MOA and toxicity

A

Raltegravir
Inhibits HIV genome intergration into host cell Cr by reversibly inhibiting HIV integrase
^creatine kinase

163
Q

Enfuvirtide: MOA and toxicity

A

Fusion inhibitor

Binds p41: inhibits viral fusion (skin reaction at injection site)

164
Q

Maraviroc: MOA and toxicity

A

Binds CCR-5 on surface T cells/monocytes and inhibits interaction with gp120

165
Q

Interferons: MOA

A

Glycoproteins normally synthesized by virus-infected cells, exhibiting a wide range of antiviral and antitumoral properties

166
Q

Interferons: clinical use

A

IFN-a: chronic hepatitis B/C, kaposi sarcoma, hairy cell uekemia, condyloma acuminatum, RCC, malignant melanoma
IFN-B: Multiple sclerosis
IFN-g: CGD

167
Q

Interferons: toxicity

A

Neutropenia and myopathy

168
Q

Hepatitis C therapy

A

Ribavirin
Simeprevir
Sofosbuvir

169
Q

Antibiotics to avoid in pregnancy

A 
SAFe Children Take Really Good Care
Sulfonamides- Kernicterus
Aminoglycosides- Otoxicity
Fluoroquinolones- Cartilage damane
Clarithromycin-Embryotoxic
Tetracyclines- Discolored teeth, inhibition of bone growth
Ribarvirin (antiviral)- teratogenic
Griseofulvin (antifungal)- teratogenic
Chloamphenicol- grey baby syndrome
170
Q

What viral drugs do not need to be activated?

A

Foscarnet, cidofovir, Tenofovir (NRTI)

Pharmacology (6 decks)

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