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Microbiology Flashcards

0
Q

Tetracyclines

A

tetracycline, doxycyclne, minocycline

MOA: bacteriostatic
Bind to 30s and prevent attachment of aminoacyl-tRNA-limited CNS penetration

Doxycycline can be used in renal failure (fecal elimination)

Do not take with milk, antacids, or iron containing preparations due to divalent cations (Ca and Mg) inhibit absorption in gut

Clinical: Borrelia burgdorferi, M. pneumoniae, Rickettsia and Chlamydia
Acne

Toxicity: GI distress, discoloration of teeth and inhibition of bone growth in children, photosensitivity-sun burns
Contraindicated in pregnancy

resistance: decrease uptake or increase efflux out of bacterial cells by plasmid encoded transport pumps

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1
Q

3rd gen cephalosporins

A

Ceftriaxone, cefotoxamine, ceftazindime
MOA: Inhibit cell wall synthesis but less susceptible to penicillinases
Bacterocidal
Irreversibly binds to penicillin binding proteins (transpeptidases)

Clinical: serious gram- infections
Cetriaxone-meningitis and gonorrhea
Ceftazidime-Pseudomonas

Toxicity: hypersentivity reactions, vitamin K deficiency, low cross reactivity with penicillins
Increase nephrotoxicity of aminoglycosides

Resistance: change in protein structure in penicillin binding proteins

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2
Q

Macrolides

A

Azithromycin clarithromycin, erythromycin
MOA: inhibit protein synthesis by blocking translocation
Bind to 23S rRNA of the 50s ribosomal subunit
Bacteriostatic

Clinical: Atypical pneumonias, STDS-chlamydia, and gram psotiive cocci-allergtic to penicillin

Toxicity: GI motility issues, arrhytmia caused by prolonged QT, acute Cholestatic hepatitis, Rash, Eosinophilia,
Increases serum concentration of theophyllines, oral anticoagulants

Resistance: Methylation of 23S rRNA-binding site prevents binding of drug

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3
Q

4th gen Cephalosporins

A

Cefepime
MOA: Inhibit cell wall synthesis but less susceptible to penicillinases
Bacterocidal
Irreversibly binds to penicillin binding proteins (transpeptidases)

Clinical: increased activity against pseudomonas and gram+ organisms

Toxicity: hypersentivity reactions, vitamin K deficiency, low cross reactivity with penicillins
Increase nephrotoxicity of aminoglycosides

Resistance: change in protein structure in penicillin binding proteins

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5
Q

Oxacillin, nafcillin, dicloxacillin

A

MOA: bind penicillin binding proteins (transpetptidases)-catalyze cross linking of peptidoglycan cell wall formation specifically joining of amino acids with terminal D-alanine-D-alanine therefore structural analog of D-alanine-D-alanine
Activates autolytic enzymes by weakening cell wall

Clinical: S. aureus-except MRSA due to altered penicillin-binding proteins target site

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

Toxicity: hypersensitivity reactions, interstitial nephritis

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6
Q

Vancomycin

A

MOA: inhibits cell wall peptiodglycan formation by binding D-ala D-ala portion of cell wall precursors
Bacterocidal

Clinical: gram+ only-major resistant organisms (MRSA, enterococci, and Clostridum difficile)

Toxicity: well tolerated in trouble
Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flusing (prevent with antihistamines and slow infusion rate)

resistance: Bacteria have amino acid modification of D-ala Dla to D-ala D-lac

Toxicity:

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7
Q

Ticarcillin, piperacillin

A

MOA: bind penicillin binding proteins (transpetptidases)-catalyze cross linking of peptidoglycan cell wall formation specifically joining of amino acids with terminal D-alanine-D-alanine therefore structural analog of D-alanine-D-alanine
Activates autolytic enzymes by weakening cell wall

Clinical: Pseudomonas and gram - rods

Susceptible to penicillinase-use with B-lactamase inhibitors

Toxicity: hypersensitivity reactions

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8
Q

B-lactamase inhibitors

A

Clavulanic acid, Sulbacam, Tazobactam

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

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9
Q

Aminoglycosides

A

Gentamicin, Neomycin, Amicacin, Tobramycin, Streptomycin

MOA: Bactericidal
Inhibit formation of initiation (bind 30s ribosomal subunit and distorts structure blocking INITIATION) complex and cause misreading of mRNA
Block translocation
Require O2 for uptake; ineffective against anaerobes

Clinical: Severe gram-rod infections
Synergggistic with B-lactams
Neomycin for bowel surgery

Toxicity: Nephrotoxicity (especially with cephalopsporins), Neuromuscular blockade, ototoxicity (especially with loop diuretics), teratogen

Resistance: baceriaal transferase enzymes inactivate the drug by acetylation, phosphorylation or adenylation

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10
Q

2nd gen cephalsporins

A

Cefoxitin, cefaclor, cefuroxime
MOA: Inhibit cell wall synthesis but less susceptible to penicillinases
Bacterocidal
Irreversibly binds to penicillin binding proteins (transpeptidases)

Clinical: gram + cocci, Heamophilus influenza, enterobacteri aerogenes, Neisseria, proteus, E. coli, Kelbseilla, serratia

Toxicity: hypersentivity reactions, vitamin K deficiency, low cross reactivity with penicillins
Increase nephrotoxicity of aminoglycosides

Resistance: change in protein structure in penicillin binding proteins

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11
Q

5th gen Cephalosporins

A

Ceftaroline
MOA: Inhibit cell wall synthesis but less susceptible to penicillinases
Bacterocidal
Irreversibly binds to penicillin binding proteins (transpeptidases)
Toxicity: hypersentivity reactions, vitamin K deficiency, low cross reactivity with penicillins
Increase nephrotoxicity of aminoglycosides

Clinical: broad gram+ and gram-organism coverage including MRSA
DOES NOT cover pseudomonas

Resistance: change in protein structure in penicillin binding proteins

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12
Q

Ampicillin, amoxicillin

A

MOA: bind penicillin binding proteins (transpetptidases)-catalyze cross linking of peptidoglycan cell wall formation specifically joining of amino acids with terminal D-alanine-D-alanine therefore structural analog of D-alanine-D-alanine
Activates autolytic enzymes by weakening cell wall
Wider spectrum than penicillin especially with clavulonic acid

Amoxicillin better oral bioavailiability

Clinical: haemophilus, E. coli, Listeria, proteus, Salmonella, Shigella, H. pylori (amoxicillin)

Toxicity: hypersensitivity reactions, rash, pseudomembranous colitis

Resistance: penicillinase in bacteria cleaves B-lactam ring

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13
Q

H2O2

A

MOA: Destructive free radical production
Oxidize cellular components

IS sporicidal

Used for inanimate objects
Skin cleansing and wound debridement

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14
Q

Aztreonam

A

MOA: monobactam resistant to B-lactamases
Prevents peptidoglycan cross-linking by binding to penicillin binding protein 3
Syngergistic with aminoglycosides
no cross-allergencity with penicillins

Clinical: gram- rods only
For penicillin allergic patients and those with renal insufficiency who cannot tolerate aminoglycosides

Toxicity: usually non-toxic ocasional GI upset

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15
Q

Carbapenems

A

Imipenem, meropenem, ertapenem, doripenem
MOA: imipenem is broad spectrum-B-lactamase resistant
Always admistered with cilistatin (inhibitor or renal dehydropepetdase I) which decreases inactivation of drug in renal tubules

Clinical: gram+ cocci, gram - rods and anaerobes
wide specrum
Side effects limit to to life threatening infections where other drugs have failed

Toxicity: GI distress, skin rash and seizures (meropenem less)

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16
Q

Penicillin G (IV), V (oral)

A

MOA: bind penicillin binding proteins (transpetptidases)-catalyze cross linking of peptidoglycan cell wall formation specifically joining of amino acids with terminal D-alanine-D-alanine therefore structural analog of D-alanine-D-alanine
Activates autolytic enzymes by weakening cell wall

Clinical: gram + organisms, N. meningtidis, and T. pallidum

Toxicity: hypersensitivity, hemolytic anemia

Resistance: Penicillinase in bacteria cleaves B-lactam ring

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16
Q

Alcohol (Disinfectant)

A

MOA: disrupts cell membranes and denatures proteins

Not sporicidal

Disorganizes lipid membranes making them leaky
Denatures cell proteins
Requires water

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17
Q

Chlrohexidine

A

MOA: disrupts cell membranes
Coagulation of cytoplasm

Not sporicidal

Antiseptic of choice for surgical and percutaneous procedures
CI: neurologic, ototoxic, and opthalamologic procedures due to neurotoxicity

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18
Q

Iodine

A

MOA: halogenation of proteins and nucleic acids

IS sporicidal

More skin irritation and toxicity than others
Less effective than chlorohexidine-alcohol combo

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19
Q

Formaldehyde and glutaraldehyde

A

MOA: alkylating and cross linking DNA and proteins

Used for sterilization of hospital instruments that cannot withstand autoclaves

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20
Q

Clindamycin

A

MOA: blocks peptide transfer at 50S ribsomal subunit
Bacteriostatic

Clinical: Anaerobic infections in aspiration pneumonia, lung abscesses, and oral infections
Effective against invasive Group A Strep. infection

Toxicity: psedomembranous colitis (C. difficile overgrowth), fever diarrhea

Treats anaerobes above the diaphragm

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21
Q

Chloramphenicol

A

MOA: blocks peptidyltransferase at 50s ribosomal subunit
Bacteriostatic

Clinical: Meningtis (H. influenzae, N. meningitidis, Strep. pneumo) and Rocky Mountain spotted fever (Rickettsia rickettsii)

Toxicity: anemia, apalstic anemia, gray baby syndrome (premature infants lack liver UDP-glucoronyl transferase)
Reversible cytopenia
Irreversible pancytopenia (without Bone marrow transplantation)

Resistance: plasmid encoded acetyltransferase inactivates the drug

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22
Q

Sulfonamides

A

Sulfamethoxazole, sulfisoxazole, sulfadiazine
MOA: inhibit folate synthesis
para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase
Bacteriostatic

Clinical: gram+, gram-, Nocardia, Chlamydia, simple UTI

Toxicity: hypersensitivity raections, hemolysis if G6PD deficient, nephrotoxicity, photosensitivity, kernicterus in infants, displace other drugs from albumin

Resistance: altered enzyme (bacterial dihydropteroate synthase), decrease uptake, or increase PABA synthesis

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23
Q

Trimethoprim

A

MOA: inhibits bacterial dihydrofolate reductase

Clinical: used in combo with sulfonamides
Causes sequential blockade of folate synthesis
Combo used for UTIs, Shigella, Salmonella, Pneumocystis jirovecii, pneumonia treatment and prophylaxis

Toxicity: megaloblastic anemia, leukopenia, granulocytopenia

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24
Fluoroquinolones
``` Ciprofloxacin, norfloxacin, levofloxacin, ofloxacin, sparfoxacin, moxifloxacin, gemifloxacin, enoxacin, Naldixic acid (quinolone) ``` MOA: Inhibit DNA gyrase (topoisomerase II) Bacterocidal Clinical: gram negative rods of urinary and GI tracts (Psudomonas), Niesseria, some gram positive organisms Toxicity: GI upset, superinfections, skin rashes, headache, dizziness Can cause tendonitis, tendon rupture (>60 or taking prednisone), leg cramps and myalgias CI in preganncy, nursing mothers and children under 18 due to cartilage damage Some prolong QT Resistance: Chromosome-encoded mutation in DNA gyrase, plasmid mediated resistance, efflux pumps Do not take with antacids
25
Metronidazole
MOA: forms free radical toxic metabolites in bacterial cell that damage DNA Bacterocidal and antiprotozoal Clinical: Giardia, Entamoeba, Trichomonas, Gardenerlla vaginalis, Anaerobes (below diaphragm) Use with proton pump inhibits and clarythromycin against H. Pylori Toxicity: Disulfuram-like reaction (sever flushing, tachycardia, hypotension) with alcohol, headache, metallic taste Increase acetyladelhyde
26
Isoniazid
MOA: decreases synthesis of mycolic acids Bacterial catalase-peroxidase (encoded by KatG) needed to convert INH to active metabolite Bacteria cannot make cell wall or multiply and lose acid-fastness Clinical: Mycobacterium tuberculosis Solo prophylaxis against TB Toxicity: neurotoxicity (peripheral neuropathy-use pyridoxine-B6), hepatotoxicity, lupus Resistance: 1. decrease in bacterial expresssion of catalase-peroxidase enzyme required for activation 2. modifaction of protein target binding site Can compete with B6 in the synthesis of NTs leading to defective end products Increase urinary excretion of B6 leading to deficiency
27
Rifamycins
Rifampin, rifabutin MOA: Inhibits DNA dependent RNA polymerase Clinical: Mycobacterium tuberculosis delays resistance to dapsone when used for leprosy Used for meingoccal prophylaxis and chemoprophylaxis in children with H. influenza ``` Toxicity: Hepatotoxicity Increases p450 (rifampin) Orange body fludis ``` Rifabutin preferred in HIV patients due to less cytochrome P450 stimulation Resistance: alteration of structure of DNA dependent RNA polymerase
28
Pyrazinamide
MOA: thought to acidify intracellular environment via conversion to pyrazinoic acid Effective in acidic pH of phgaolysosomes where TB is engulfed by macrophages Clinical: Mycobacterium tuberculosis and intracellular organisms Toxicity: hyperuricemia, hepatoxicity Resistance: modified pyrazinamide
29
Echinocandins
Caspofungin, micafungin, anidulafungin MOA: inhibits CELL WALL synthesis by inhibiting synthesis of B glucan (1,3 beta D-glucan) Clinical: invasive aspergillosis, Candida NOT active against crypto Toxicity: GI upset, flushing (histamine release)
30
Suramin and melarsoprol (protozoa)
Trypanosoma brucei
31
Amphotericin B
MOA: binds ergosterol Forms membrane pores that allow leakage of electrolytes Clinical: Serious, systemic mycoses Cryptococcus (with/without flucytosine), Blastomyces, Coccidioides, Histoplasma, Candida, Mucor Intrathecally for fungal meningitis Supplement with K+ and Mg2+ because of altered renal tubular permeability Toxicity: Thrombophlepbitis, Reactions acutely, Electrolyte imbalances (hypokalemia and hypomagnesium), Anemia (decreases erythropoietin), Dose dependent nephrotoxicity (TREAD lightly with Ampho), fevers chills, hypotension renal vasoconstriction leads to decreased GFR Can cause ATN hypokalemia leads to weakness and arrythmias, tachycardia and fibrillation Hydration and liposomal amphotericin decreases toxicity
32
Nystatin
MOA: binds ergosterol Forms membrane pores that allow leakage of electrolytes Topical Clinical: swish and swallow for oral candidiasis topical for diaper rash or vaginal candidasis
33
Flucytosine
MOA: inhibits DNA and RNA biosynthesis by conversion to 5-fluoruracil by cytosine deaminase Clinical: systemic fungal infections (esp. meningitis caused by cryptococcus) in combo with amphotericin B Toxicity: bone marrow suppression
34
Griseofulvin
MOA: interferes with microtubule function Disrupts mitosis Deposits in keratin-containing tissues Clinical: oral treatment for superficial infections, inhibits growth of dermatophytes (tinea, ringworm) Toxicity: Teratogenic, carcinogenic, confusion, headaches, increase P450 and warfarin metabolism
35
Pyrmethamine (protozoa)
Toxoplasmosis
36
Terbinafine
MOA: inhibits the fungal enzyme squalene epoxidase (inhibits synthesis of ergosterol) Clinical: dermatophyses (tinea corporis), especially onychomycosis-fungal infection of toes and fingers Toxicity:GI upset, hepatotoxicity, taste disturbance
37
Ehthambutol
MOA: decreases carbohydrate polyemerization of mycobacterium cell wall by blocking arabinosyltransferase Clinical: mycobacterium tuberculosis Toxicity: optic neuropathy (red-green color blindness) Decreased visual acuity, central scotoma, Hepatotoxicity Resistance: increased arabinosyl transferase
38
Nifurtimox (protozoa)
T. cruzi
39
Foscarnet
MOA: viral DNA polymrease inhibitor and RT inhibitor in HIV Binds to pyrophosphate binding site of the enzyme Does not require activation by viral kinase Clinical: CMV retinitis in immunocompromised patietns when gancyclovir fails Acyclovir resistant HSV Toxicity: nephrotoxicity decreased Ca and MG leading to seizures Decreased PTH release Resistance: mutated DNA polymerase
40
Ribarvirin
MOA: inhibits synthesis of guanine nucleotides by competitively inhibiting inosine monophosphate dehydrogenase Pairs with uracil or cytosine causing hypermutation during RNA dependent RNA replication Directly inhibits RNA polymerase Inhibits guanylyltransferase and methyltransferase resulting in defective 5' Cap Enhances TH1 cell mediated immunity while inhibiting TH2 cytokine production Depletes GTP Clinical: RSV (infants), chronic hepatitis C Toxicity: hemolytic anemia, severe teratogen
41
Cidofovir and tenofovir
MOA: preferentially inhibits viral DNA polymerase Does not require phosphorylation by viral kinase Clinical: CMV retinitis in immunocompromised patietns Acycclovir resitant HSV Long half life Toxicity: nephrotoxicity-coadminster with probenecid and IV saline to decrease toxicity
42
Chloroquine
MOA: blocks detoxification of heme into hemozoin Heme accumulates and is toxic to plasmodia Clinical: Treatment of plasmodial species other than P. falciparum Toxicity: retinopathy, pruritus (dark skinned individuals) Resistance: membrane pump that decreases intracellular concentration of drug
43
P. falciparum infection treatment
artermether/lumefantrine | atovaquone/proguanil
44
Life threatening malaria
quinidine or artesunate
45
Zanamivir, Oseltamivir
MOA: inhibit influenza neuraminidase leading to decreased release of virus progeny Clinical: treats and prevents influenza A and B Slows viral penetration of mucus secretions or respiratory epithelium Shortens course and complications of influenza A and B if taken within 48 hours
46
Acyclovir, famciclovir, valacyclovir
MOA: Monophosphorylated (rate limiting) by HSV/VZV thymidine kinase and not phosphorylated in uninfected cells Guanosine analog Triphosphate form is active by cellular enzymes Preferentially inhibits viral DNA polymerase by chain termination Uninfected cells not affected because uptake is poor, phosphorylation in absence of viral thymidine kinaseis minimal and cellular DNA polymerase has less affinity for acyclovir for acyclovir triphosphate than viral DNA polymerase Clinical: HSV and VZV Used for HSV induced mucocutaneous and genital lesions as well as for encephalitis Prophylaxis in immunocompromised patients No effect on latent forms Recurrence suppressed by daily oral intake Valacyclovir has better oral bioavalability Toxicity: obstructive crystalline nephropathy and acute renal failure if not adequately hydrated Resistance: mutated viral thymidine kinase (use foscarnet or cidofiovir for HIV induced resistance-cytidine analog) Does not work in EBV or CMV because they do not use the same thymidine kinase
47
Ganciclovir
MOA: 5'-monophosphate formed by a CMV viral kinase Guanosine analog Triphosphate formed by cellular kinases Preferentially inhibits viral DNA polymerase Valagancicilvoir has better oral bioavailability Clinical: CMV(retinitis)-immunocompromised Toxicity: leukopenia, neutropenia, thrombocytopenia, renal toxicity Resistance: mutated CMV DNA polymerase or lack of viral kinase
48
Protease inhibitors
-navir MOA: assembly of virions depends on HIV-1 protease (pol gene) which cleaves the polypeptide products of HIV mRNA into their functional parts Prevent maturation of new viruses Ritonavir-inhibits cytochrome p450 Toxicity: hyperglycemia, GI intolerance, lipodystophy (ipoared hepatic chylomicron uptake and triglyceride clearance) Nephropathy and hematuria (indinavir)
49
Azoles
Fluconazole, ketoconazole, clotrimazole, miconazole, itraconazole, voriconazole MOA: inhibit fungal sterol (ergosterol) synthesis by inhibiting cytochrome p450 enzyme that converts lanosterol to ergosterol Clinical: local and less serious systemic mycoses Fluconazole for chronic suppression of cryptococcal meningitis in AIDS patients and candidal infections Itraconazole for balstomyces, coccidiodes, histoplasma Clotrimazole and miconazole for topical fungal infections Toxicity: testerosterone synthesis inhibition (gynecomastia esp. ketoconazole), liver dysfunction (inhibits cytochrome p450)
50
Daptomycin
MOA: depolarization of the cellular membrane Creates cell membrane channels causing leakage of intracellular ions and inhibition of DNA, RNA, and Protein syntesis Treats: skin infections and bacteremia (with or without endocarditis), due to S. Aureus including MRSA Inactivated by pulmonary surfactant-don't use in pneumonia Toxicity: increased CPK and myopathy
51
don't use in pregnancy and adverse effect
``` Sulfonamides-kernicterus Aminoglycosides-ototoxicity Fluroquinolones-cartilage damage Clarithromycin-embryotoxic Tetracyclines-discolored teeth, inhibition of bone growth Ribavirin-tertogenic Griseofulvin-terotogenic Chlroramphenicol-gray baby ```
52
Sodium stibogluconate (protozoa)
leishmaniasis
53
Typical HIV therapy regimen
2 nucleoside RT inhibitors + | 1 non-nucleoside RT inhibitor or 1 protease inhibitor or 1 integrase inhibitor
54
NRTIs
LT DAZES Lamivudine, Tenofovir, Didanosine, Abacavir, Zidovudine, Emtricitabine, Stavudine MOA: competitively inhibit nucleotide binding to reverse transcription and terminate the DNA chain Disrupts 3'-5' phosphodiester bond formation Tenofovir is the only nucleotide Nucleosides need to be phosphorylated to be active ZDV is used for prophylaxis and during pregnancy to decrease risk of fetal transmission ZDV inhibits cellular and mitochondrial DNA polymerases-watch with gancyclovir co-adminstration Toxicity: bone marrow suppression (reversed with G-CSF and erythropoietin), peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleoside), anemia (ZDV), pancreastitis (didanosine)
55
NNRTIs
Efavirenz, nevirapine, Delavirdine (END) MOA: bind to reverse transcriptase at site different than NRTIs Do not require phosphorylation to be active Toxicity: flu like symptoms, abdominal pain, jaundice, steven johnsons syndrome, or toxic epidermial necorlysis Rash and hepatoxicity Vivid dreams and CNS symptoms with efavirenz Delvirdine and efavirenz CI in pregancy
56
Raltegravir
Integrase inhibitor MOA: inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase Inhibiting mRNA transcription Toxicity: hypercholesterolemia
57
Enfurvirtide
Fusion inhibitor MOA: binds gp41 inhibiting viral entry Toxicity: skin reactions at injection site
58
Maraviroc
Fusion inhibitor MOA: binds CCR5 on surface of T cells/monocytes inhibiting interaction with gp120
59
1st gen Cephalosporins
Cefazolin, cephalexin) MOA: Inhibit cell wall synthesis but less susceptible to penicillinases Bacterocidal Irreversibly binds to penicillin binding proteins (transpeptidases) Clinical: Gram+ cocci, Proteus, E. Coli, Klebsiella Cefazolin used prior to surgery to prevent S. aureus wound infections Toxicity: hypersentivity reactions, vitamin K deficiency, low cross reactivity with penicillins Increase nephrotoxicity of aminoglycosides Resistance: change in protein structure in penicillin binding proteins
60
Interferons
MOA: Glycoproteins normally synthesized by virus-infected cells Wide range of antiviral and antitumoral properties Clinical: IFN-a: chronic hep B and C, Kaposi, hairy cell luekemia, condolyloma acurmintum, renal cell carcinoma, malignant melanoma IFN-B: MS IFN-y: CGD Toxcity: neutropenia, myopathy
61
Dapsone
MOA: inhibits bacterial synthesis of dihydrofolic acid through competitive inhibition of dihydropteroate synthetase Clinical: second line prophylaxis for pneumocystis pneumonia Toxicity: fever, rash, methehemoglobinemia, agranuolocytosis Causes hemolysis in G6PD
62
Fidaxomicin
Inhibits RNA polymerase Given orally with minimal systemic absorption Used for recurring C. Difficile
63
Palvizumab
Ab against F protein used to prevent pneumonia caused by RSV in premature infants
64
Specific indinavir (protease inhibitor) side effect
Nephrotoxicity and nephrolithiasis | Adequately hydrate to avoid
65
Specific didanosine side effect
Pancreatitis
66
Specific abacavir side effect
Hypersensitivity
67
NRTIs specific side effect
Lactic acidosis
68
Specific NNRTIs
Stevens Johnson syndrome
69
Specific nevirapine side effect
Liver failure

Step 1 Drugs (15 decks)

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