drug MoAs! Flashcards
(192 cards)
1
Q
name penicillins
A
penicillin G (IV, IM) penicillin V (oral) methicillin
prototype B-lactam antibiotics
2
Q
penicillin: MoA
A
B-LACTAM: binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking
activate autolytic enzymes
3
Q
penicillin: clinical use
A
mostly Gram(+)
also used for: N. meningitidis, T. pallidum, syphilis
not penicillinase resistant
4
Q
penicillin: toxicity
A
hypersensitivity reactions
hemolytic anemia
5
Q
penicillin: resistance
A
B-lactamases cleaves B-lactam ring
6
Q
name penicillinase-resistant penicillins
A
oxacillin, nafcillin, dicloxacillin
**NOD if you’re penicillinase resistant!
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
8
Q
penicillinase-resistant penicillins: clinical use
A
S. aureus (except MRSA, which has an altered PBP)
9
Q
penicillinase-resistant penicillins: toxicity
A
hypersenstivity reactions
interstitial nephritis
10
Q
name aminopenicillins
A
B-LACTAM: ampicillin, amoxicillin
**AMinoPenicillins are AMPed-up penicillin
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
12
Q
aminopenicillins: clinical use
A
H. influenzae, E. coli, Listeria, Proteus, Salmonella, Shigella, enterococci
**ampicillin/amoxicillin HELPSS kill Enterococci.
13
Q
aminopenicillins: toxicity
A
hypersensitivity reactions
ampicillin rash
pseudomembranous colitis
14
Q
aminopenicillins: resistance
A
B-lactamases cleave B-lactam ring
15
Q
name antipseudomonal penicillins
A
B-LACTAM: ticarcillin, piperacillin
16
Q
antipseudomonal penicillins: MoA
A
binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking
wider spectrum
penicillinase sensitive (+clavulanic acid)
17
Q
antipseudomonal penicillins: clinical use
A
Pseudomonas spp. and Gram(-) rods
18
Q
antipseudomonal penicillins: toxicity
A
hypersensitivity reactions
19
Q
name B-lactamase inhibitors
A
CAST
clavulanic acid
sulbactam
tazobactam
20
Q
cephalosporins: MoA
A
B-LACTAM: binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking
less susceptible to penicillinases
21
Q
1st generation cephalosporins: clinical use
A
(cefazolin, cephalexin)
gram(+) cocci, Proteus, E. coli, Klebsiella
**PEcK
22
Q
2nd generation cephalosporins: clinical use
A
(cefoxitin, cefaclor, cefuroxime)
gram(+) cocci, Haemophilus influenzae, Enterobacter, Neisseria, Proteus, E. coli, Klebsiella, Serratia
**HEN PEcKS
23
Q
3rd generation cephalosporins: clinical use
A
(ceftriaxone, cefotaxime, ceftazidime)
serious gram(-) infections resistant to other B-lactams
ceftriaxone: meningitis, gonorrhea
ceftazidime: pseudomonas
24
Q
4th generation cephalosporins: clinical use
A
(cefepime)
increase activity against Pseudomonas and gram(+) organisms
25
cephalosporins: toxicity
hypersensitivity reactions
vitamin K deficiency
low cross-reactivity with penicillins
increase nephrotoxicity of aminoglycosides
26
cephalosporins: resistance
altered structure of PBP's
27
aztreonam: MoA
MONOBACTAM: binds to PBP3 to prevent peptidoglycan cross-linking
B-lactamase resistant
synergistic with aminoglycosides
no cross-allergenicity with penicillins
28
aztreonam: clinical use
gram(-) rods only
use for patients who have:
penicillin allergy
renal insufficiency (can't handle aminoglycosides)
29
aztreonam: toxicity
usually nontoxic
| occasional GI upset
30
name carbapenems
imipenem/cilastatin, meropenem, ertapenem, doripenem
*imipenem always given with cilastatin (inhibits renal dehydropeptidase I) to decrease inactivation of drug in renal tubules
31
carbapenems: MoA
B-LACTAM: binds irreversibly to PBPs (transpeptidases) and inhibits peptidoglycan cross-linking
B-lactamase resistant
32
carbapenems: clinical use
gram(+) cocci
gram(-) rods
anaerobes
broad spectrum but significant side effects limit use to life-threatening infections, or after other drugs have failed
33
carbapenems: toxicity
GI distress
skin rash
CNS toxicity (seizures)
meropenem has less risk of seizures and is stable to dehydropeptidase I
34
vancomycin: MoA
binds to D-ala D-ala portion of cell wall precursors to BLOCK PEPTIDOGLYCAN SYNTHESIS
35
vancomycin: clinical use
gram(+) only
36
vancomycin: toxicity
nephrotoxicity
ototoxicity
thrombophlebitis
diffuse flushing (red man syndrome)
37
what is red man syndrome and how can it be prevented?
diffuse flushing
prevented by pretreatment with antihistamines and slow infusion rate
38
vancomycin: resistance
occurs with amino acid change of D-ala D-ala to D-ala D-lac
39
bacitracin: MoA
BLOCK PEPTIDOGLYCAN SYNTHESIS
40
group the 2 types of protein synthesis inhibitors
buy AT 30, CCEL at 50
30S inhibitors: aminoglycosides, tetracyclines
50S inhibitors: chloramphenicol, clindamycin, erythromycin (macrolides), linezolid
41
name aminoglycosides
gentamicin, neomycin, amikacin, tobramycin, streptomycin
"mean GNATS caNNOT kill anaerobes"
42
aminoglycosides: MoA
INHIBITS PROTEIN SYNTHESIS: inhibit formation of initiation complex causing misreading of mRNA = block transcription/translation
43
aminoglycosides: clinical use
severe gram(-) rod infections
synergistic with B-lactams
neomycin for bowel surgery
require O2 uptake = ineffective against anaerobes
"mean GNATS caNNOT kill anaerobes"
44
aminoglycosides: toxicity
nephrotoxocity (esp with cephalosporin use)
neuromuscular blockade
ototoxicity (esp with loop diuretic use)
teratogenic
"mean GNATS caNNOT kill anaerobes"
45
aminoglycosides: resistance
transferase enzymes inactivate the drug by acetylation, phosphorylation, or adenylation
46
name tetracyclines
tetracycine, doxycycline, minocycline, demeclocycline
*demeclocycline: ADH antagonist used as a diuretic in SIADH, rarely used as an antibiotic
47
tetracyclines: MoA
INHIBITS PROTEIN SYNTHESIS: binds to 30S and prevents attachment of aminoacyl-tRNA
bacteriostatic
48
tetracyclines: clinical use
Borrelia burgdorferi, Mycoplasma pneumoniae, Rickettsia, Chlamydia
doxycycline is fecally eliminated = can use in patients with renal failure
49
tetracyclines: toxicity
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
50
tetracyclines: resistance
decrease uptake into cells or increase efflux out of cells by plasmid-encoded transport pumps
51
name macrolides
azithromycin, clarithromycin, erythromycin
52
macrolides: MoA
INHIBITS PROTEIN SYNTHESIS: binds to 50S (23S rRNA portion) and inhibits translocation
bacteriostatic
53
macrolides: clinical use
atypical pneumonias (Mycoplasma, Chlamydia, Legionella)
STDs (Chlamydia)
gram(+) cocci
54
macrolides: toxicity
MACRO
```
motility issues
arrhythmia (due to prolonged QT)
acute cholestatic hepatitis
rash
eosinophilia
```
increases serum concentration of theophyllines, oral anticoagulants
55
macrolides: resistance
methylation of 23S rRNA binding site
56
chloramphenicol: MoA
INHIBITS PROTEIN SYNTHESIS: binds to 50S and blocks peptidyltransferase
bacteriostatic
57
chloramphenicol: clinical use
meningitis (SHiN)
conservative use due to toxicities but often still used in developing countries due to low cost
58
chloramphenicol: toxicity
```
anemia (dose-dependent)
aplastic anemia (dose-independent)
gray baby syndrome (premies, who lack liver UDP-glucuronyl transferase)
```
59
chloramphenicol: resistance
plasmid-encoded acetyltransferase that inactivates drug
60
clindamycin: MoA
INHIBITS PROTEIN SYNTHESIS: binds to 50S and blocks transpeptidation (peptide transfer)
bacteriostatic
61
clindamycin: clinical use
anaerobic infections in aspiration pneumonia or lung abscesses
oral infections with mouth anaerobes
---------
above the diaphragm: clindamycin
below the diaphragm: metronidazole
62
clindamycin: toxicity
pseudomembranous colitis (C. diff overgrowth)
fever
diarrhea
63
linezolid & streptogramins (quinupristin, dalfopristine): MoA
INHIBITS PROTEIN SYNTHESIS at 50S ribosomal subunit
64
name sulfonamides
sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine
65
sulfonamides: MoA
BLOCK NUCLEOTIDE SYNTHESIS BY INHIBITING FOLIC ACID SYNTHESIS: PABA antimetabolites inhibit dihydropteroate synthase
bacteriostatic
66
sulfonamides: clinical use
gram(+)
gram(-)
Nocardia
Chlamydia
UTI: SMX or triple sulfas
67
sulfonamides: toxicity
hypersensitivity reactions
hemolysis if G6PD deficient
nephrotoxicity (tubulointerstitial nephritis)
photosensitivity
kernicterus in infants
displace other drugs from albumin (ie warfarin)
68
sulfonamides: resistance
altered enzyme (bacterial dihydropteroate synthase)
decreased uptake
increased PABA synthesis
69
trimethoprim: MoA
BLOCK NUCLEOTIDE SYNTHESIS BY INHIBITING FOLIC ACID SYNTHESIS: inhibits bacterial dihydrofolate reductase
bacteriostatic
70
trimethoprim: clinical use
combined with sulfonamides (TMX-SMX), causing sequential block of folate synthesis
used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii pneumonia
71
trimethoprim: toxicity
megaloblastic anemia
leukopenia
granulocytopenia
*TMP treats marrow poorly
(may alleviate with supplemental folinic acid (leucovorin rescue])
72
name fluoroquinolones
ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfloxacin, moxifloxacin, gatifloxacin, enoxacin, nalidixic acid
73
fluoroquinolones: MoA
BLOCK DNA TOPOISOMERASES: inhibit DNA gyrase (topoisomerase II) and topoisomerase IV = interfere with DNA replication
74
fluoroquinolones: clinical use
gram(-) rods of urinary and GI tracts, Neisseria, some gram(+)
75
fluoroquinolones: toxicity
```
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
76
fluoroquinolones: resistance
chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps
77
metronidazole: MoA
DAMAGE DNA: forms free radical toxic metabolites in bacterial cell that damages DNA
antiprotozoal, bactericidal
78
metronidazole: clinical use
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
metronidazole: toxicity
disulfram-like reaction with alcohol
headache
metallic taste
80
prophylaxis for M. tuberculosis
isoniazid
81
treatment for M. tuberculosis
RIPE
rifampin
isoniazid
pyrazinamid
ethambutol
82
prophylaxis for M. avium-intracellulare
azithromycin
83
treatment for M. avium-intracellulare
azithromycin, rifampin, ethambutol, streptomycin
84
treatment for M. leprae
long-term treatment with dapsone and rifampin for tuberculoid form
+ clofazimine for lepromatous form
85
isoniazid (INH): MoA
decrease synthesis of mycolic acids
bacterial catalase-peroxidase (KatG) needed to convert INH to active metabolite
86
isoniazid (INH): clinical use
M. tuberculosis
87
isoniazid (INH): toxicity
neurotoxicity
hepatotoxicity
*INH injures neurons + hepatocytes
(vitamin B6 can prevent neurotoxicity, lupus)
88
rifampin: MoA
inhibits DNA-dependent RNA polymerase
89
rifampin: clinical use
M. tuberculosis
M. leprae: delays resistance to dapsone
meningococcal prophylaxis
chemoprophylaxis in contacts of children with HiB
90
rifampin: toxicity
minor hepatotoxicity and drug interactions (increased P450)
| orange body fluids
91
4 R's of Rifampin
RNA polymerase inhibitor
Revs up microsomal P450
Red/orange body fluids
Rapid resistance if used alone
92
pyrazinamide: MoA
uncertain
theory: acidify intracellular environment via conversion to pyrazinoic acid -- effective in acidic pH of phagolysosomes, where TB engulfed by macrophages is found
93
pyrazinamide: clinical use
M. tuberculosis
94
pyrazinamide: toxicity
hyperuricemia
| hepatotoxicity
95
ethambutol: MoA
decrease carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase
96
ethambutol: clinical use
M. tuberculosis
97
ethambutol: toxicity
optic neuropathy (red-green color blindness)
98
prophylaxis for meningococcal infection
ciprofloxacin (DOC)
| rifampin for children
99
prophylaxis for gonorrhea
ceftriaxone
100
prophylaxis for syphilis
benzathine penicillin G
101
prophylaxis for history of recurrent UTIs
TMP-SMX
102
prophylaxis for endocarditis with surgical/dental procedures
penicillins
103
prophylaxis for pregnant woman carrying GBS
ampicillin
104
prophylaxis for strep pharyngitis in child with prior rheumatic fever
oral penicillin
105
prophylaxis for prevention of postsurgical infection due to S. aureus
cefazolin
106
prophylaxis for prevention of gonococcal/chlamydial conjunctivitis in newborn
erythromycin ointment
107
treatment of MRSA
vancomycin
108
treatment of VRE
linezolid and streptogramins
109
amphotericin B: MoA
binds ergosterol = forms membrane pores that allow leakage of electrolytes
110
amphotericin B: clinical use
serious, systemic mycoses
```
Cryptococcus (+/- flucytosine for meningitis)
Blastomyces
Coccidioides
Histoplasma
Candida
Mucor
```
111
amphotericin B: toxicity
```
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
nystatin: MoA
binds ergosterol = forms membrane pores that allow leakage of electrolytes
113
nystatin: clinical use
"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
name azoles
fluconazole, ketoconazole, clotrimzole, miconazole, itraconazole, voriconazole
115
azoles: MoA
inhibit fungal sterol (ergosterol) synthesis by inhibiting the P450 enzyme that converts lanosterol to ergosterol
116
azoles: clinical use
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
azoles: toxicity
```
testosterone synthesis inhibition (gynecomastia, esp with ketoconazole)
liver dysfunction (inhibits CYP450)
```
118
flucytosine: MoA
inhibits DNA and RNA biosynthesis by conversion to 5-fluorouracil by cytosine deaminase
119
flucytosine: clinical use
systemic fungal infections in combination with amphotericin B
(esp with cryptococal meningitis)
120
flucytosine: toxicity
bone marrow suppression
121
caspofungin, micafungin, anidulfungin: MoA
inhibits cell wall synthesis by inhibiting synthesis of B-glucan
122
caspofungin, micafungin, anidulfungin: clinical use
invasive aspergillosis
| Candida
123
caspofungin, micafungin, anidulfungin: toxicity
GI upset
| flushing (histamine release)
124
terbinafine: MoA
inhibits squalene epoxidase (fungal enzyme) - lanosterol synthesis
125
terbinafine: clinical use
dermatophytoses
| esp onychomycosis
126
terbinafine: toxicity
abnormal LFTs
| visual disturbances
127
naftifine: MoA and clinical use
similar to terbinafine: inhibits squalene epoxidase
tinea pedis, cruris, corporis
128
griseofulvin: MoA
interferes with microtubule function = disrupts mitosis
129
griseofulvin: clinical use
oral treatment of superficial infections
| inhibits growth of dermatophytes (tinea, ringworm)
130
griseofulvin: toxicity
```
teratogenic
carcinogenic
confusion
headaches
increase P450 and warfarin metabolism
```
deposits in keratin-containing tissues (ie nails)
131
treatment of toxoplasmosis
pyrimethamine
132
treatment of T. brucei
suramin and melarsoprol
133
treatment of T. cruzi
nifurtimox
134
treatment of leishmaniasis
sodium stibogluconate
135
chloroquine: MoA
blocks detoxification of heme into hemozoin = heme accumulates and is toxic to plasmodia
136
chloroquine: clinical use
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
chloroquine: toxicity
retinopathy
138
treatment of P. falciparum
| vs other plasmodial species
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
name 5 antihelminthic treatments
and 1 specific for trematodes
```
immobilize helminths:
mebendazole
pyrantel pamoate
ivermectin
diethylcarbamazine
praziquantel
```
praziquantel for trematodes
140
zanamivir, oseltamivir: MoA
inhibit influenza neuraminidase = decreases release of progeny virus
141
zanamivir, oseltamivir: clinical use
treatment/prevention of influenza A and B
142
ribavirin: MoA
inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase
143
ribavirin: clinical use
RSV, chronic hepatitis C
144
ribavirin: toxicity
hemolytic anemia
| severe teratogen
145
acyclovir: MoA
guanosine analog - monophosphorylated by HSV/VZV thymidine kinase; triphosphate formed by cellular enzymes
preferentially inhibits viral DNA polymerase by chain termination
146
acyclovir: clinical use
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
acyclovir: resistance
mutated viral thymidine kinase
148
ganciclovir: MoA
guanosine analog - 5'-monophosphate formed by a CMV viral kinas; triphosphate formed by cellular kinases
preferentially inhibits viral DNA polymerase
149
ganciclovir: clinical use
CMV, esp in ICM
valganciclovir (prodrug) has better oral bioavailability
150
ganciclovir: toxicity
leukopenia
neutropenia
thrombocytopenia
renal toxicity
more toxic to host enzymes than acyclovir
151
ganciclovir: resistance
mutated CMV DNA polymerase
| lack of viral kinase
152
foscarnet: MoA
viral DNA polymerase inhibitor that binds to pyrophosphate-binding site of enzyme
does not require activation by viral kinase
*FOScarnet = pyroFOSphate analog
153
foscarnet: clinical use
CMV retinitis in ICM when ganciclovir fails
| acyclovir-resistant HSV
154
foscarnet: toxicity
nephrotoxicity
155
foscarnet: resistance
mutated DNA polymerase
156
cidofovir: MoA
preferentially inhibits viral DNA polymerase
does not require phosphorylation by viral kinase
157
cidofovir: clinical use
CMV retinitis in ICM
acyclovir-resistant HSV
long half-life
158
cidofovir: toxicity
nephtrotoxicity (coadminister with probenecid and IV saline to reduce toxicity)
159
3 situations in which HAART is initiated
when patient presents with:
1. AIDS-defining illness
2. low CD4 cell counts (<500)
3. high viral load
160
what does the HAART regimen consist of?
2 NRTIs
+
1 NNRTI or 1 protease inhibitor or 1 integrase inhibitor
161
name protease inhibitors
-navir
lopinavir, atazanavir, darunavir, fosamprenavir, saquinavir, ritonavir, indinavir
162
protease inhibitors: MoA
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
protease inhibitors: toxicity
hyperglycemia
GI intolerance
lipodystrophy
ritonavir: inhibits CYP450 = can increase other drugs
indinavir: nephropathy, hematuria
164
name NRTIs
nucleoside reverse transcriptase inhibitor
```
tenofovir (TDF)
emtricitabine (FTC)
abacavir (ABC)
lamivudine (3TC)
zidovudine (ZDV)
didanosine (ddI)
stavudine (d4T)
```
165
NRTIs: MoA
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
which NRTI is used for general prophylaxis and during pregnancy to reduce risk of fetal transmission?
zidovudine
167
NRTIs: toxicity
```
bone marrow suppression (reverse with G-CSF and EPO)
peripheral neuropathy
lactic acidosis (nucleosides)
rash (non-nucleosides)
anemia (ZDV)
```
168
name NNRTIs
non-nucleoside reverse transcriptase inhibitor
nevirapine
efavirenz
delavirdine
169
NNRTIs: MoA
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
NNRTIs: toxicity
```
bone marrow suppression (reverse with G-CSF and EPO)
peripheral neuropathy
lactic acidosis (nucleosides)
rash (non-nucleosides)
anemia (ZDV)
```
171
name integrase inhibitor
raltegravir
172
raltegravir: MoA
integrase inhibitor
inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase
173
raltegravir: toxicity
hypercholesterolemia
174
interferons: MoA
glycoproteins synthesized by virus-infected cells
blocks replication of both RNA and DNA viruses
175
interferons: clinical use
IFNa: chronic heptatitis B and C, kaposi's sarcoma
IFNb: MS
IFNy: NAPDH oxidase deficiency
176
interferons: toxicity
neutropenia
| myopathy
177
name 5 immunosuppressant drugs
```
cyclosporine
tacrolimus (FK-506)
sirolimus (rapamycin)
azathioprine
muromonab-CD3 (OKT3)
```
178
cyclosporine: MoA
binds to cyclophilins => complex blocks the differentiation and activation of T cells by inhibiting calcineurin = prevents production of IL-2 and its receptor
179
cyclosporine: clinical use
suppresses organ rejection after transplantation
also used for select autoimmune disorders
180
cyclosporine: toxicity
```
nephrotoxicity
HTN
hyperlipidemia
hyperglycemia
tremor
gingival hyperplasia
hirsutism
```
181
tacrolimus: MoA
binds to FK-binding protein => inhibits calcineurin and secretion of IL-2 and other cytokines
182
tacrolimus: clinical use
potent immunosuppressive used in organ transplant recipients
183
tacrolimus: toxicity
```
nephrotoxicity
HTN
hyperlipidemia
hyperglycemia
tremor
```
184
sirolimus: MoA
inhibits mTOR = inhibits T cell proliferation in response to IL-2
185
sirolimus: clinical use
immunosuppression after KIDNEY transplantation
used in combo with cyclosporine and corticosteroids
also used with drug-eluting stents
186
sirolimus: toxicity
hyperlipidemia
thrombocytopenia
leukopenia
187
azathioprine: MoA
antimetabolite precursor of 6-MP = interferes with metabolism and synthesis of nucleic acids
toxic to proliferating lymphocytes
188
azathioprine: clinical use
KIDNEY transplantation
| autoimmune disorders
189
azathioprine: toxicity
bone marrow suppression
toxic effects may be increased by allopurinol due to active metabolite mercaptopurine being metabolized by xanthine oxidase
190
muromonab-CD3: MoA
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
muromonab-CD3: clinical use
immunosuppression after KIDNEY transplantation
192
muromonab-CD3: toxicity
cytokine release syndrome
| hypersensitivity reaction
