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Step 1 Drugs > Microbiology > Flashcards

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
Q

Fluoroquinolones

A 
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

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25
Q

Metronidazole

A

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

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26
Q

Isoniazid

A

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

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27
Q

Rifamycins

A

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

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28
Q

Pyrazinamide

A

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
Q

Echinocandins

A

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
Q

Suramin and melarsoprol (protozoa)

A

Trypanosoma brucei

31
Q

Amphotericin B

A

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
Q

Nystatin

A

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
Q

Flucytosine

A

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
Q

Griseofulvin

A

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
Q

Pyrmethamine (protozoa)

A

Toxoplasmosis

36
Q

Terbinafine

A

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
Q

Ehthambutol

A

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
Q

Nifurtimox (protozoa)

A

T. cruzi

39
Q

Foscarnet

A

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
Q

Ribarvirin

A

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
Q

Cidofovir and tenofovir

A

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
Q

Chloroquine

A

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
Q

P. falciparum infection treatment

A

artermether/lumefantrine

atovaquone/proguanil

44
Q

Life threatening malaria

A

quinidine or artesunate

45
Q

Zanamivir, Oseltamivir

A

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
Q

Acyclovir, famciclovir, valacyclovir

A

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
Q

Ganciclovir

A

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
Q

Protease inhibitors

A

-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
Q

Azoles

A

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
Q

Daptomycin

A

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
Q

don’t use in pregnancy and adverse effect

A 
Sulfonamides-kernicterus
Aminoglycosides-ototoxicity
Fluroquinolones-cartilage damage
Clarithromycin-embryotoxic
Tetracyclines-discolored teeth, inhibition of bone growth
Ribavirin-tertogenic
Griseofulvin-terotogenic
Chlroramphenicol-gray baby
52
Q

Sodium stibogluconate (protozoa)

A

leishmaniasis

53
Q

Typical HIV therapy regimen

A

2 nucleoside RT inhibitors +

1 non-nucleoside RT inhibitor or 1 protease inhibitor or 1 integrase inhibitor

54
Q

NRTIs

A

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
Q

NNRTIs

A

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
Q

Raltegravir

A

Integrase inhibitor
MOA: inhibits HIV genome integration into host cell chromosome by reversibly inhibiting HIV integrase
Inhibiting mRNA transcription

Toxicity: hypercholesterolemia

57
Q

Enfurvirtide

A

Fusion inhibitor
MOA: binds gp41 inhibiting viral entry

Toxicity: skin reactions at injection site

58
Q

Maraviroc

A

Fusion inhibitor
MOA: binds CCR5 on surface of T cells/monocytes
inhibiting interaction with gp120

59
Q

1st gen Cephalosporins

A

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
Q

Interferons

A

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
Q

Dapsone

A

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
Q

Fidaxomicin

A

Inhibits RNA polymerase

Given orally with minimal systemic absorption

Used for recurring C. Difficile

63
Q

Palvizumab

A

Ab against F protein used to prevent pneumonia caused by RSV in premature infants

64
Q

Specific indinavir (protease inhibitor) side effect

A

Nephrotoxicity and nephrolithiasis

Adequately hydrate to avoid

65
Q

Specific didanosine side effect

A

Pancreatitis

66
Q

Specific abacavir side effect

A

Hypersensitivity

67
Q

NRTIs specific side effect

A

Lactic acidosis

68
Q

Specific NNRTIs

A

Stevens Johnson syndrome

69
Q

Specific nevirapine side effect

A

Liver failure

Step 1 Drugs (15 decks)

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