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Pharmacology > drug MoAs! > Flashcards

drug MoAs! Flashcards

1
Q

name penicillins

A 
penicillin G (IV, IM)
penicillin V (oral)
methicillin

prototype B-lactam antibiotics

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2
Q

penicillin: MoA

A

B-LACTAM: binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking

activate autolytic enzymes

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3
Q

penicillin: clinical use

A

mostly Gram(+)

also used for: N. meningitidis, T. pallidum, syphilis

not penicillinase resistant

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4
Q

penicillin: toxicity

A

hypersensitivity reactions

hemolytic anemia

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5
Q

penicillin: resistance

A

B-lactamases cleaves B-lactam ring

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6
Q

name penicillinase-resistant penicillins

A

oxacillin, nafcillin, dicloxacillin

**NOD if you’re penicillinase resistant!

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7
Q

penicillinase-resistant penicillins: MoA

A

B-LACTAM: binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking

narrow spectrum

penicillinase resistant because bulky R group blocks access of B-lactamase to B-lactam ring

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8
Q

penicillinase-resistant penicillins: clinical use

A

S. aureus (except MRSA, which has an altered PBP)

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9
Q

penicillinase-resistant penicillins: toxicity

A

hypersenstivity reactions

interstitial nephritis

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10
Q

name aminopenicillins

A

B-LACTAM: ampicillin, amoxicillin

**AMinoPenicillins are AMPed-up penicillin

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11
Q

aminopenicillins: MoA

A

binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking

wider spectrum

penicillinase sensitive (+clavulanic acid)

oral bioavailability: ampicillin > amoxicillin

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12
Q

aminopenicillins: clinical use

A

H. influenzae, E. coli, Listeria, Proteus, Salmonella, Shigella, enterococci

**ampicillin/amoxicillin HELPSS kill Enterococci.

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13
Q

aminopenicillins: toxicity

A

hypersensitivity reactions
ampicillin rash
pseudomembranous colitis

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14
Q

aminopenicillins: resistance

A

B-lactamases cleave B-lactam ring

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15
Q

name antipseudomonal penicillins

A

B-LACTAM: ticarcillin, piperacillin

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16
Q

antipseudomonal penicillins: MoA

A

binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking

wider spectrum

penicillinase sensitive (+clavulanic acid)

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17
Q

antipseudomonal penicillins: clinical use

A

Pseudomonas spp. and Gram(-) rods

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18
Q

antipseudomonal penicillins: toxicity

A

hypersensitivity reactions

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19
Q

name B-lactamase inhibitors

A

CAST

clavulanic acid
sulbactam
tazobactam

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20
Q

cephalosporins: MoA

A

B-LACTAM: binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking

less susceptible to penicillinases

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21
Q

1st generation cephalosporins: clinical use

A

(cefazolin, cephalexin)

gram(+) cocci, Proteus, E. coli, Klebsiella

**PEcK

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22
Q

2nd generation cephalosporins: clinical use

A

(cefoxitin, cefaclor, cefuroxime)

gram(+) cocci, Haemophilus influenzae, Enterobacter, Neisseria, Proteus, E. coli, Klebsiella, Serratia

**HEN PEcKS

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23
Q

3rd generation cephalosporins: clinical use

A

(ceftriaxone, cefotaxime, ceftazidime)

serious gram(-) infections resistant to other B-lactams

ceftriaxone: meningitis, gonorrhea
ceftazidime: pseudomonas

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24
Q

4th generation cephalosporins: clinical use

A

(cefepime)

increase activity against Pseudomonas and gram(+) organisms

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25
Q

cephalosporins: toxicity

A

hypersensitivity reactions
vitamin K deficiency
low cross-reactivity with penicillins
increase nephrotoxicity of aminoglycosides

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26
Q

cephalosporins: resistance

A

altered structure of PBP’s

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27
Q

aztreonam: MoA

A

MONOBACTAM: binds to PBP3 to prevent peptidoglycan cross-linking

B-lactamase resistant

synergistic with aminoglycosides
no cross-allergenicity with penicillins

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28
Q

aztreonam: clinical use

A

gram(-) rods only

use for patients who have:
penicillin allergy
renal insufficiency (can’t handle aminoglycosides)

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29
Q

aztreonam: toxicity

A

usually nontoxic

occasional GI upset

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30
Q

name carbapenems

A

imipenem/cilastatin, meropenem, ertapenem, doripenem

*imipenem always given with cilastatin (inhibits renal dehydropeptidase I) to decrease inactivation of drug in renal tubules

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31
Q

carbapenems: MoA

A

B-LACTAM: binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking

B-lactamase resistant

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32
Q

carbapenems: clinical use

A

gram(+) cocci
gram(-) rods
anaerobes

broad spectrum but significant side effects limit use to life-threatening infections, or after other drugs have failed

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33
Q

carbapenems: toxicity

A

GI distress
skin rash
CNS toxicity (seizures)

meropenem has less risk of seizures and is stable to dehydropeptidase I

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34
Q

vancomycin: MoA

A

binds to D-ala D-ala portion of cell wall precursors to BLOCK PEPTIDOGLYCAN SYNTHESIS

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35
Q

vancomycin: clinical use

A

gram(+) only

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36
Q

vancomycin: toxicity

A

nephrotoxicity
ototoxicity
thrombophlebitis
diffuse flushing (red man syndrome)

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37
Q

what is red man syndrome and how can it be prevented?

A

diffuse flushing

prevented by pretreatment with antihistamines and slow infusion rate

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38
Q

vancomycin: resistance

A

occurs with amino acid change of D-ala D-ala to D-ala D-lac

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39
Q

bacitracin: MoA

A

BLOCK PEPTIDOGLYCAN SYNTHESIS

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40
Q

group the 2 types of protein synthesis inhibitors

A

buy AT 30, CCEL at 50

30S inhibitors: aminoglycosides, tetracyclines

50S inhibitors: chloramphenicol, clindamycin, erythromycin (macrolides), linezolid

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41
Q

name aminoglycosides

A

gentamicin, neomycin, amikacin, tobramycin, streptomycin

“mean GNATS caNNOT kill anaerobes”

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42
Q

aminoglycosides: MoA

A

INHIBITS PROTEIN SYNTHESIS: inhibit formation of initiation complex causing misreading of mRNA = block transcription/translation

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43
Q

aminoglycosides: clinical use

A

severe gram(-) rod infections

synergistic with B-lactams
neomycin for bowel surgery

require O2 uptake = ineffective against anaerobes

“mean GNATS caNNOT kill anaerobes”

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44
Q

aminoglycosides: toxicity

A

nephrotoxocity (esp with cephalosporin use)
neuromuscular blockade
ototoxicity (esp with loop diuretic use)
teratogenic

“mean GNATS caNNOT kill anaerobes”

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45
Q

aminoglycosides: resistance

A

transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation

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46
Q

name tetracyclines

A

tetracycine, doxycycline, minocycline, demeclocycline

*demeclocycline: ADH antagonist used as a diuretic in SIADH, rarely used as an antibiotic

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47
Q

tetracyclines: MoA

A

INHIBITS PROTEIN SYNTHESIS: binds to 30S and prevents attachment of aminoacyl-tRNA

bacteriostatic

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48
Q

tetracyclines: clinical use

A

Borrelia burgdorferi, Mycoplasma pneumoniae, Rickettsia, Chlamydia

doxycycline is fecally eliminated = can use in patients with renal failure

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49
Q

tetracyclines: toxicity

A

limited CNS penetration

GI distress: do not take with milk, antacids, or iron-containing preps because divalent cations inhibit its absorption in the gut

children: discoloration of teeth and inhibition of bone growth

photosensitivity

contraindicated in pregnancy

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50
Q

tetracyclines: resistance

A

decrease uptake into cells or increase efflux out of cells by plasmid-encoded transport pumps

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51
Q

name macrolides

A

azithromycin, clarithromycin, erythromycin

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52
Q

macrolides: MoA

A

INHIBITS PROTEIN SYNTHESIS: binds to 50S (23S rRNA portion) and inhibits translocation

bacteriostatic

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53
Q

macrolides: clinical use

A

atypical pneumonias (Mycoplasma, Chlamydia, Legionella)
STDs (Chlamydia)
gram(+) cocci

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54
Q

macrolides: toxicity

A

MACRO

motility issues
arrhythmia (due to prolonged QT)
acute cholestatic hepatitis
rash
eosinophilia

increases serum concentration of theophyllines, oral anticoagulants

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55
Q

macrolides: resistance

A

methylation of 23S rRNA binding site

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56
Q

chloramphenicol: MoA

A

INHIBITS PROTEIN SYNTHESIS: binds to 50S and blocks peptidyltransferase

bacteriostatic

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57
Q

chloramphenicol: clinical use

A

meningitis (SHiN)

conservative use due to toxicities but often still used in developing countries due to low cost

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58
Q

chloramphenicol: toxicity

A 
anemia (dose-dependent)
aplastic anemia (dose-independent)
gray baby syndrome (premies, who lack liver UDP-glucuronyl transferase)
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59
Q

chloramphenicol: resistance

A

plasmid-encoded acetyltransferase that inactivates drug

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60
Q

clindamycin: MoA

A

INHIBITS PROTEIN SYNTHESIS: binds to 50S and blocks transpeptidation (peptide transfer)

bacteriostatic

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61
Q

clindamycin: clinical use

A

anaerobic infections in aspiration pneumonia or lung abscesses

oral infections with mouth anaerobes

above the diaphragm: clindamycin
below the diaphragm: metronidazole

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62
Q

clindamycin: toxicity

A

pseudomembranous colitis (C. diff overgrowth)
fever
diarrhea

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63
Q

linezolid & streptogramins (quinupristin, dalfopristine): MoA

A

INHIBITS PROTEIN SYNTHESIS at 50S ribosomal subunit

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64
Q

name sulfonamides

A

sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine

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65
Q

sulfonamides: MoA

A

BLOCK NUCLEOTIDE SYNTHESIS BY INHIBITING FOLIC ACID SYNTHESIS: PABA antimetabolites inhibit dihydropteroate synthase

bacteriostatic

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66
Q

sulfonamides: clinical use

A

gram(+)
gram(-)
Nocardia
Chlamydia

UTI: SMX or triple sulfas

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67
Q

sulfonamides: toxicity

A

hypersensitivity reactions
hemolysis if G6PD deficient
nephrotoxicity (tubulointerstitial nephritis)
photosensitivity
kernicterus in infants
displace other drugs from albumin (ie warfarin)

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68
Q

sulfonamides: resistance

A

altered enzyme (bacterial dihydropteroate synthase)
decreased uptake
increased PABA synthesis

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69
Q

trimethoprim: MoA

A

BLOCK NUCLEOTIDE SYNTHESIS BY INHIBITING FOLIC ACID SYNTHESIS: inhibits bacterial dihydrofolate reductase

bacteriostatic

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70
Q

trimethoprim: clinical use

A

combined with sulfonamides (TMX-SMX), causing sequential block of folate synthesis

used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia

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71
Q

trimethoprim: toxicity

A

megaloblastic anemia
leukopenia
granulocytopenia

*TMP treats marrow poorly

(may alleviate with supplemental folinic acid (leucovorin rescue])

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72
Q

name fluoroquinolones

A

ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gatifloxacin, enoxacin, nalidixic acid

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73
Q

fluoroquinolones: MoA

A

BLOCK DNA TOPOISOMERASES: inhibit DNA gyrase (topoisomerase II) and topoisomerase IV = interfere with DNA replication

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74
Q

fluoroquinolones: clinical use

A

gram(-) rods of urinary and GI tracts, Neisseria, some gram(+)

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75
Q

fluoroquinolones: toxicity

A 
GI upset
superinfections
skin rashes
headaches
dizziness
less common:
tendonitis
tendon rupture
leg cramps
myalgias

contraindicated in pregnant women and children (damage to cartilage)

some may cause prolonged QT interval

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76
Q

fluoroquinolones: resistance

A

chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps

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77
Q

metronidazole: MoA

A

DAMAGE DNA: forms free radical toxic metabolites in bacterial cell that damages DNA

antiprotozoal, bactericidal

78
Q

metronidazole: clinical use

A

Giardia, Entamoeba, Trichomonas, Gardnerella, Anaerobes

used with PPIs and clarithromycin for “triple therapy” against H. pylori

above the diaphragm: clindamycin
below the diaphragm: metronidazole

79
Q

metronidazole: toxicity

A

disulfram-like reaction with alcohol
headache
metallic taste

80
Q

prophylaxis for M. tuberculosis

A

isoniazid

81
Q

treatment for M. tuberculosis

A

RIPE

rifampin
isoniazid
pyrazinamid
ethambutol

82
Q

prophylaxis for M. avium-intracellulare

A

azithromycin

83
Q

treatment for M. avium-intracellulare

A

azithromycin, rifampin, ethambutol, streptomycin

84
Q

treatment for M. leprae

A

long-term treatment with dapsone and rifampin for tuberculoid form

+ clofazimine for lepromatous form

85
Q

isoniazid (INH): MoA

A

decrease synthesis of mycolic acids

bacterial catalase-peroxidase (KatG) needed to convert INH to active metabolite

86
Q

isoniazid (INH): clinical use

A

M. tuberculosis

87
Q

isoniazid (INH): toxicity

A

neurotoxicity
hepatotoxicity

*INH injures neurons + hepatocytes

(vitamin B6 can prevent neurotoxicity, lupus)

88
Q

rifampin: MoA

A

inhibits DNA-dependent RNA polymerase

89
Q

rifampin: clinical use

A

M. tuberculosis

M. leprae: delays resistance to dapsone

meningococcal prophylaxis
chemoprophylaxis in contacts of children with HiB

90
Q

rifampin: toxicity

A

minor hepatotoxicity and drug interactions (increased P450)

orange body fluids

91
Q

4 R’s of Rifampin

A

RNA polymerase inhibitor
Revs up microsomal P450
Red/orange body fluids
Rapid resistance if used alone

92
Q

pyrazinamide: MoA

A

uncertain

theory: acidify intracellular environment via conversion to pyrazinoic acid – effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found

93
Q

pyrazinamide: clinical use

A

M. tuberculosis

94
Q

pyrazinamide: toxicity

A

hyperuricemia

hepatotoxicity

95
Q

ethambutol: MoA

A

decrease carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase

96
Q

ethambutol: clinical use

A

M. tuberculosis

97
Q

ethambutol: toxicity

A

optic neuropathy (red-green color blindness)

98
Q

prophylaxis for meningococcal infection

A

ciprofloxacin (DOC)

rifampin for children

99
Q

prophylaxis for gonorrhea

A

ceftriaxone

100
Q

prophylaxis for syphilis

A

benzathine penicillin G

101
Q

prophylaxis for history of recurrent UTIs

A

TMP-SMX

102
Q

prophylaxis for endocarditis with surgical/dental procedures

A

penicillins

103
Q

prophylaxis for pregnant woman carrying GBS

A

ampicillin

104
Q

prophylaxis for strep pharyngitis in child with prior rheumatic fever

A

oral penicillin

105
Q

prophylaxis for prevention of postsurgical infection due to S. aureus

A

cefazolin

106
Q

prophylaxis for prevention of gonococcal/chlamydial conjunctivitis in newborn

A

erythromycin ointment

107
Q

treatment of MRSA

A

vancomycin

108
Q

treatment of VRE

A

linezolid and streptogramins

109
Q

amphotericin B: MoA

A

binds ergosterol = forms membrane pores that allow leakage of electrolytes

110
Q

amphotericin B: clinical use

A

serious, systemic mycoses

Cryptococcus (+/- flucytosine for meningitis)
Blastomyces
Coccidioides
Histoplasma
Candida
Mucor
111
Q

amphotericin B: toxicity

A 
fever/chills
hypotension
nephrotoxicity (reduced by hydration)
arrhythmias
anemia
IV phlebitis

supplement K and Mg because of altered renal tubule permeability

liposomal amphotericin reduces toxicity

112
Q

nystatin: MoA

A

binds ergosterol = forms membrane pores that allow leakage of electrolytes

113
Q

nystatin: clinical use

A

“swish and swallow” for oral candidiasis (thrush)
topical for diaper rash or vaginal candidiasis
(only available in topical form - too toxic for systemic use)

114
Q

name azoles

A

fluconazole, ketoconazole, clotrimzole, miconazole, itraconazole, voriconazole

115
Q

azoles: MoA

A

inhibit fungal sterol (ergosterol) synthesis by inhibiting the P450 enzyme that converts lanosterol to ergosterol

116
Q

azoles: clinical use

A

local, less serious systemic mycoses

fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections of all types

itraconazole for blastomyces, coccidioides, histoplasma

clotrimazole and miconazole for topical fungal infections

117
Q

azoles: toxicity

A 
testosterone synthesis inhibition (gynecomastia, esp with ketoconazole)
liver dysfunction (inhibits CYP450)
118
Q

flucytosine: MoA

A

inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase

119
Q

flucytosine: clinical use

A

systemic fungal infections in combination with amphotericin B

(esp with cryptococal meningitis)

120
Q

flucytosine: toxicity

A

bone marrow suppression

121
Q

caspofungin, micafungin, anidulfungin: MoA

A

inhibits cell wall synthesis by inhibiting synthesis of B-glucan

122
Q

caspofungin, micafungin, anidulfungin: clinical use

A

invasive aspergillosis

Candida

123
Q

caspofungin, micafungin, anidulfungin: toxicity

A

GI upset

flushing (histamine release)

124
Q

terbinafine: MoA

A

inhibits squalene epoxidase (fungal enzyme) - lanosterol synthesis

125
Q

terbinafine: clinical use

A

dermatophytoses

esp onychomycosis

126
Q

terbinafine: toxicity

A

abnormal LFTs

visual disturbances

127
Q

naftifine: MoA and clinical use

A

similar to terbinafine: inhibits squalene epoxidase

tinea pedis, cruris, corporis

128
Q

griseofulvin: MoA

A

interferes with microtubule function = disrupts mitosis

129
Q

griseofulvin: clinical use

A

oral treatment of superficial infections

inhibits growth of dermatophytes (tinea, ringworm)

130
Q

griseofulvin: toxicity

A 
teratogenic
carcinogenic
confusion
headaches
increase P450 and warfarin metabolism

deposits in keratin-containing tissues (ie nails)

131
Q

treatment of toxoplasmosis

A

pyrimethamine

132
Q

treatment of T. brucei

A

suramin and melarsoprol

133
Q

treatment of T. cruzi

A

nifurtimox

134
Q

treatment of leishmaniasis

A

sodium stibogluconate

135
Q

chloroquine: MoA

A

blocks detoxification of heme into hemozoin = heme accumulates and is toxic to plasmodia

136
Q

chloroquine: clinical use

A

treatment of plasmodial species, except P. falciparum (frequency of resistance is too high – resistance due to membrane pump that decreases intracellular concentration of drug)

treat P. falciparum with artemether/lumifantrine or atovaquone/proguanil

for life-threatening malaria, use quinidine or artisunate

137
Q

chloroquine: toxicity

A

retinopathy

138
Q

treatment of P. falciparum

vs other plasmodial species

A

artemether/lumifantrine or atovaquone/proguanil

(vs. chloroquine = frequency of resistance is too high – resistance due to membrane pump that decreases intracellular concentration of drug)

139
Q

name 5 antihelminthic treatments

and 1 specific for trematodes

A 
immobilize helminths:
mebendazole
pyrantel pamoate
ivermectin
diethylcarbamazine
praziquantel

praziquantel for trematodes

140
Q

zanamivir, oseltamivir: MoA

A

inhibit influenza neuraminidase = decreases release of progeny virus

141
Q

zanamivir, oseltamivir: clinical use

A

treatment/prevention of influenza A and B

142
Q

ribavirin: MoA

A

inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase

143
Q

ribavirin: clinical use

A

RSV, chronic hepatitis C

144
Q

ribavirin: toxicity

A

hemolytic anemia

severe teratogen

145
Q

acyclovir: MoA

A

guanosine analog - monophosphorylated by HSV/VZV thymidine kinase; triphosphate formed by cellular enzymes

preferentially inhibits viral DNA polymerase by chain termination

146
Q

acyclovir: clinical use

A

HSV, VZV

used for HSV-induced mucocutaneous and genital lesions as well as encephalitis; no affect on latent HSV/VZV

prophylaxis in ICM

weak activity against EBC
no activity against CMV

valacyclovir (prodrug) has better oral availability
for herpes zoster, use famciclovir

147
Q

acyclovir: resistance

A

mutated viral thymidine kinase

148
Q

ganciclovir: MoA

A

guanosine analog - 5’-monophosphate formed by a CMV viral kinas; triphosphate formed by cellular kinases

preferentially inhibits viral DNA polymerase

149
Q

ganciclovir: clinical use

A

CMV, esp in ICM

valganciclovir (prodrug) has better oral bioavailability

150
Q

ganciclovir: toxicity

A

leukopenia
neutropenia
thrombocytopenia
renal toxicity

more toxic to host enzymes than acyclovir

151
Q

ganciclovir: resistance

A

mutated CMV DNA polymerase

lack of viral kinase

152
Q

foscarnet: MoA

A

viral DNA polymerase inhibitor that binds to pyrophosphate-binding site of enzyme

does not require activation by viral kinase

*FOScarnet = pyroFOSphate analog

153
Q

foscarnet: clinical use

A

CMV retinitis in ICM when ganciclovir fails

acyclovir-resistant HSV

154
Q

foscarnet: toxicity

A

nephrotoxicity

155
Q

foscarnet: resistance

A

mutated DNA polymerase

156
Q

cidofovir: MoA

A

preferentially inhibits viral DNA polymerase

does not require phosphorylation by viral kinase

157
Q

cidofovir: clinical use

A

CMV retinitis in ICM
acyclovir-resistant HSV

long half-life

158
Q

cidofovir: toxicity

A

nephtrotoxicity (coadminister with probenecid and IV saline to reduce toxicity)

159
Q

3 situations in which HAART is initiated

A

when patient presents with:

  1. AIDS-defining illness
  2. low CD4 cell counts (<500)
  3. high viral load
160
Q

what does the HAART regimen consist of?

A

2 NRTIs
+
1 NNRTI or 1 protease inhibitor or 1 integrase inhibitor

161
Q

name protease inhibitors

A

-navir

lopinavir, atazanavir, darunavir, fosamprenavir, saquinavir, ritonavir, indinavir

162
Q

protease inhibitors: MoA

A

prevents maturation of new viruses by inhibiting HIV-1 protease (pol gene), which cleaves the polypeptide products of HIV mRNA into their functional parts = can’t assemble new virions

163
Q

protease inhibitors: toxicity

A

hyperglycemia
GI intolerance
lipodystrophy

ritonavir: inhibits CYP450 = can increase other drugs
indinavir: nephropathy, hematuria

164
Q

name NRTIs

A

nucleoside reverse transcriptase inhibitor

tenofovir (TDF)
emtricitabine (FTC)
abacavir (ABC)
lamivudine (3TC)
zidovudine (ZDV)
didanosine (ddI)
stavudine (d4T)
165
Q

NRTIs: MoA

A

competitively inhibits nucleotide binding to RT and terminate the DNA chain (lack 3’OH group)

these nucleoside analogs need to be phosphorylated to be active
(with the exception of tenofovir, a nucleotide)

166
Q

which NRTI is used for general prophylaxis and during pregnancy to reduce risk of fetal transmission?

A

zidovudine

167
Q

NRTIs: toxicity

A 
bone marrow suppression (reverse with G-CSF and EPO)
peripheral neuropathy
lactic acidosis (nucleosides)
rash (non-nucleosides)
anemia (ZDV)
168
Q

name NNRTIs

A

non-nucleoside reverse transcriptase inhibitor

nevirapine
efavirenz
delavirdine

169
Q

NNRTIs: MoA

A

bind to reverse transcriptase at site different from NRTIs = inhibits nucleotide binding to RT and terminate the DNA chain (lack 3’OH group)

doesn’t require phosphorylation to be active or compete with nucleotides

170
Q

NNRTIs: toxicity

A 
bone marrow suppression (reverse with G-CSF and EPO)
peripheral neuropathy
lactic acidosis (nucleosides)
rash (non-nucleosides)
anemia (ZDV)
171
Q

name integrase inhibitor

A

raltegravir

172
Q

raltegravir: MoA

A

integrase inhibitor

inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase

173
Q

raltegravir: toxicity

A

hypercholesterolemia

174
Q

interferons: MoA

A

glycoproteins synthesized by virus-infected cells

blocks replication of both RNA and DNA viruses

175
Q

interferons: clinical use

A

IFNa: chronic heptatitis B and C, kaposi’s sarcoma

IFNb: MS

IFNy: NAPDH oxidase deficiency

176
Q

interferons: toxicity

A

neutropenia

myopathy

177
Q

name 5 immunosuppressant drugs

A 
cyclosporine
tacrolimus (FK-506)
sirolimus (rapamycin)
azathioprine
muromonab-CD3 (OKT3)
178
Q

cyclosporine: MoA

A

binds to cyclophilins => complex blocks the differentiation and activation of T cells by inhibiting calcineurin = prevents production of IL-2 and its receptor

179
Q

cyclosporine: clinical use

A

suppresses organ rejection after transplantation

also used for select autoimmune disorders

180
Q

cyclosporine: toxicity

A 
nephrotoxicity
HTN
hyperlipidemia
hyperglycemia
tremor
gingival hyperplasia
hirsutism
181
Q

tacrolimus: MoA

A

binds to FK-binding protein => inhibits calcineurin and secretion of IL-2 and other cytokines

182
Q

tacrolimus: clinical use

A

potent immunosuppressive used in organ transplant recipients

183
Q

tacrolimus: toxicity

A 
nephrotoxicity
HTN
hyperlipidemia
hyperglycemia
tremor
184
Q

sirolimus: MoA

A

inhibits mTOR = inhibits T cell proliferation in response to IL-2

185
Q

sirolimus: clinical use

A

immunosuppression after KIDNEY transplantation

used in combo with cyclosporine and corticosteroids

also used with drug-eluting stents

186
Q

sirolimus: toxicity

A

hyperlipidemia
thrombocytopenia
leukopenia

187
Q

azathioprine: MoA

A

antimetabolite precursor of 6-MP = interferes with metabolism and synthesis of nucleic acids

toxic to proliferating lymphocytes

188
Q

azathioprine: clinical use

A

KIDNEY transplantation

autoimmune disorders

189
Q

azathioprine: toxicity

A

bone marrow suppression

toxic effects may be increased by allopurinol due to active metabolite mercaptopurine being metabolized by xanthine oxidase

190
Q

muromonab-CD3: MoA

A

monoclonal antibody that binds to CD3 on the surface of T cells = blocks cellular interaction with CD3 protein responsible for T cell signal transduction

191
Q

muromonab-CD3: clinical use

A

immunosuppression after KIDNEY transplantation

192
Q

muromonab-CD3: toxicity

A

cytokine release syndrome

hypersensitivity reaction

Pharmacology (10 decks)

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