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Quizlets - Antimicrobia Flashcards

1
Q

Antimicrobials by mechanism of action: Block cell wall synthesis by inhibition of peptidoglycan cross-linking

A

Drugs? Penicillin, ampicillin, ticarcillin, piperacillin, imipenem, aztreonam, cephalosporins [#1 below]

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2
Q

Antimicrobials by mechanism of action: Block peptidoglycan synthesis Drugs?

A

Bacitracin, Vancomycin [#2 below]

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3
Q

Antimicrobials by mechanism of action: Disrupt bacterial cell wall membranes Drugs?

A

Polymyxins [#3 below]

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4
Q

Antimicrobials by mechanism of action: Block nucleotide synthesis Drugs?

A

Sulfonamides, Trimethoprim [#4 below]

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5
Q

Antimicrobials by mechanism of action: Block DNA topoisomerases Drugs?

A

Quinolones [#5 below]

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6
Q

Antimicrobials by mechanism of action: Block mRNA synthesis Drugs?

A

Rifampin [#6 below]

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7
Q

Antimicrobials by mechanism of action: Block protein synthesis at 50S ribosomal subunit Drugs?

A

Chloramphenicol, macrolides, clindamycin, streptogramins (quinipristin, dalfopristin), linezolid [#7]

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8
Q

Antimicrobials by mechanism of action: Block protein synthesis at the 30S ribosomal subunit Drugs?

A

Aminoglycosides, tetracyclines [#8 below]

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9
Q

Bacterostatic antibiotics

A

E rythromycin C lindamycin S ulfamethoxazole T rimethoprim T etracylcines C hloramphenicol (We’re ECST aT iC about bacteriostatics )

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10
Q

Bacteriocidal antibiotics

A

V ancomycin F luoroquinolones P enicillin A minoglycosides C ephalosporins M etronidazole V ery F inely P roficient A t C ell M urder

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11
Q

Forms of Penicillin

A

Penicillin G (IV form), Penicillin V (oral form). Prototype Beta-lactam antibiotics.

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12
Q

Mechanism of penicillin

A

1.) Bind penicillin-binding proteins 2.) Block transpeptidase cross-linking of cell wall 3.) Activate autolytic enzymes

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13
Q

Mechanism of penicillinase-resistant penicillins: Methicillin, nafcillin, dicoxacillin

A

Same as penicillin*. Narrow speectrum; penicillinase resistant b/c of bulkier R group. * mechanism of PCN: 1.) Bind penicillin-binding proteins 2.) Block transpeptidase cross-linking of cell wall 3.) Activate autolytic enzymes

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14
Q

Mechanism of aminopenicillins: Ampicillin, amoxicillin

A

Same as penicillin*. Wider spectrum; Penicillinase sensitive. Also combine w/ clavulanic acid (a penicillinase inhibitor) to enhance spectrum. AmO xicillin has greater O ral bioavailability than ampicillin. *Mechanism of PCN: 1.) Bind penicillin-binding proteins 2.) Block transpeptidase cross-linking of cell wall 3.) Activate autolytic enzymes

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15
Q

Mechanism of antipseudomonals: Ticarcillin, carbenicillin, piperacillin

A

Same as penicillin*. Extended spectrum. *Mechanism of penicillin: 1.) Bind penicillin-binding proteins 2.) Block transpeptidase cross-linking of cell wall 3.) Activate autolytic enzymes

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16
Q

Clinical use of penicillin

A

Bactericidal for Gram(+) cocci, Gram(+) rods, Gram(-) cocci, and spirochetes. Not penicillinase resistant.

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17
Q

Toxicity of penicillin

A

Hypersensitivity rxtns. Methicillin: interstitial nephritis.

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18
Q

Clinical use of aminopenicillins (ampicillin, amoxicillin)

A

Extended spectrum penicillin*: certain gram(+) bacteria and gram(-) rods: H aemophilus influenzae, E . coli, L isteria monocytogenes, P roteus mirabilis, S almonella, enterococci (Ampicillin/amoxicillin HELPS kill enterococci) *Think of amp icillin/amoxicillin as AMP ed up penicillin

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19
Q

Toxicity of aminopenicillins (ampicillin, amoxicillin)

A

Hypersensitivity rxtns; Ampicillin rash; Pseudomembranous colitis.

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20
Q

Clinical use of: Ticarcillin, carbenicillin, piperacillin

A

(antipseudomonals – TCP : T ake C are of P seudomonas) Used for Pseudomonas spp. and gram(-) rods; susceptible to penicillinase; Use w/ clavulinic acid (Beta-lactamase inhibitor).

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21
Q

Toxicity of antipseudomonals (Ticarcillin, carbenicillin, piperacillin)

A

Hypersensitivity rxtns.

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22
Q

Mechanism of cephalosporins

A

Beta-lactam drugs that inhibit cell wall synthesis, but are less susceptible to penicillinases. Bactericidal.

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23
Q

Clinical use of 1st generation cephalosporins (Cefazolin, cephalexin)

A

Gram(+) cocci, P roteus mirabilis, E . c oli, K lebsiella pneumoniae (1st gen = PEcK )

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24
Q

Clinical use of 2nd generation cephalosporins (cefoxitin, cefaclor, cefuroxime)

A

Gram(+) cocci, H aemophilus influenzae, E nterobacter aerogenes, N eisseria spp. P roteus mirabilis, E. c oli, K lebsiella pneumoniae, S erratia marcescens (2nd Gen = HEN PEcKS )

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25
Q

Clinical use of 3rd generation cephalosporins (ceftriaxone, cefotaxime, ceftazidime)

A

Serious gram(-) infxns resistant to other beta-lactams; meningitis (most penetrate the BBB). Examples: Ceftazidime for Pseudomonas Ceftriaxone for gonorrhea

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26
Q

Clinical use of 4th generation cephalosporins (Cefepime)

A

Increased activity against Pseudomonas and gram(+) organisms.

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27
Q

Toxicity of cephalosporins

A

Hypersensitivity rxtn. Cross-hypersensitivvity w/ penicillins occurs in 5-10% of pts. Increased nephrotoxicity of aminoglycosides; disulfiram-like rxtn w/ ethanol (in cephalosporins w/ methylthitetrazole group, e.g., cefamandole)

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28
Q

Mechanism of aztreonam

A

A monobactam resistant to beta-lactamases. Inhibits cell wall synthesis (binds to PBP3). Synergistic w/ aminoglycosides. No cross-allergenicity w/ penicillins.

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29
Q

Clinical use of aztreonam

A

Gram(-) rods - Klebsiella spp., Pseudomonas spp., Serratia spp. No activity against gram(+)’s or anaerobes. For penicillin-allergic pts and those w/ renal insufficiency who cannot tolerate aminoglycosides.

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30
Q

Toxcity of Aztreonam

A

Usually nontoxic; occasional GI upset. No cross-sensitivity w/ penicillins or cephalosporins.

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31
Q

Mechanism of Imipenem/cilastatin, meropenem

A

Imipenem is a broad-spectrum, beta-lactamase-resistant carbapenem. Always administer w/ cilastatin (inhibitor of renal dihydropeptidase I) to decrease inactivation in renal tubules. (With imipenem, the kill is LASTIN’ with ciLASTATIN )

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32
Q

Clinical use of imipenem/cilastatin, meropenem

A

Gram(+) cocci, gram(-) rods, and anaerobes. DOC for Enterobacter. The significant side effects limit use to life-threatening infxns, or after other drugs have failed. Meropenem, howevver, has a reduced risk of seizures and is stable to dihydropeptidase I.

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33
Q

Toxicity of Imipenem/cilastatin, meropenem

A

GI distress, skin rash, and CNS toxicity (seizures) @ high plasma levels

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34
Q

Mechanism of vancomycin

A

Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Resistance occurs w/ AA change of D-ala D-ala to D-ala D-lac

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35
Q

Clinical use of vancomycin

A

Used for serious, gram(+) multidrug-resistant organisms, including S. aureus and Clostridium difficile (pseudomembranous colitis)

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36
Q

Toxicity of vancomycin

A

N ephrotoxicity, O totoxicity, T hromophlebitis, diffuse flushing - red man syndrome (can largely prevent by pretreatment w/ antihistamines and slow infusion rate) Well toleraterd in general – does NOT have many problems.

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37
Q

Protein synthesis inhibitors: 30S inhibitors

A

A = A minoglycosides (streptomycin, gentamycin, tobramycin, amikacin) [bacteriostatic] T = T etracyclines [bacteriostatic] (But AT 30 , CCELL (sell) at 50) [*note different specific sites of action of Aminoglycosides and TCNs below]

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38
Q

Protein Synthesis Inhibitors: 50S inhibitors

A

C = C hloramphenicol, C lindamycin [bacteriostatic] E = E rythromycin [bacteriostatic] L = L incomycin [bacteriostatic] L = L inezolid [variable] (But AT 30, CCELL (sell) at 50 ) [note different specific sites of action below]

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39
Q

Aminoglycosides (list)

A

G entamycin N eomycin A mikacin T obramycin S treptomycin (Mean GNATS [mean = amin oglycosides)

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40
Q

Mechanism of aminoglycosides (gentamycin, neomycin, amikacin, tobramycin, streptomycin)

A

Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for uptake; therefore ineffective against anaerobes. (Mean GNATS canNOT kill anaerobes)

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41
Q

Clinical use of aminogyclosides (gentamycin, neomycin, amikacin, tobramycin, streptomycin)

A

Severe gram (-) rod infxns. Synergistic w/ beta-lactam ABX. Neomycin for bowel surgery.

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42
Q

Toxicity of aminoglycosides (gentamycin, neomycin, amikacin, tobramycin, streptomycin)

A

N ephrotoxicity (especially when used w/ cephalosporins) O totoxicity (especially when used w/ loop diuretics) T eratogen. (Mean GNATS canNOT kill anaerobes)

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43
Q

Tetracyclines (list)

A

Tetracylcine Doxycycline Demeclocycline Minocycline

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44
Q

Mechanism of tetracyclines (tetracycline, doxycycline, demeclocyclline, minocycline)

A

Bacteriostatic; bind to 30S and prevent attachment of aminoacyl-tRNA. Limited CNS penetration. Doxycyline is fecally eliminated and can be used in pts w/ renal failure. Must NOT take w/ milk, antacids, or iron-containing preparations b/c divalent cations inhibit absorption in gut. D emeclocycline is an ADH antagonist (acts as a D iuretic in SIADH)

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45
Q

Clinical use of tetracyclines (tetracycline, doxycycline, demeclocyclline, minocycline)

A

V ibrio cholerae A cne C hlamydia U reaplasma U realyticum M ycoplasma pneumoniae T ularemia H . pylori B orrelia burgdorferi (Lyme dz) R ickettsia (VACUUM TH e B edR oom)

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46
Q

Toxicity of tetracyclines (tetracycline, doxycycline, demeclocyclline, minocycline)

A

GI distress Discoloration of teeth and inhibition of bone growth in children Photosensitivity Contraindicated in pregnancy.

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47
Q

Macrolides (list)

A

Erythromycin, azithromycin, clarithromycin

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48
Q

Mechanism of macrolides (Erythromycin, azithromycin, clarithromycin)

A

Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit. Bacteriostatic.

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49
Q

Clinical use of macrolides (Erythromycin, azithromycin, clarithromycin)

A

URIs, pneumonias STDs – gram(+) cocci (streptococcal infxns in pts allergic to penicillin) Mycoplasma Legionella Chlamydia Neisseria

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50
Q

Toxicity of macrolides (Erythromycin, azithromycin, clarithromycin)

A

GI discomfort (most common cause of noncompliance) Acute cholestatic hepatitis Eosinophilia Skin rashes Increases serum concentration of theophyllines, oral anticoagulants.

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51
Q

Mechanism of chloramphenicol

A

Inhibits 50S peptidyltransferase activity. Bacteriostatic.

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52
Q

Clinical use of chloramphenicol

A

Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) Conservative use, owing to toxicities.

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53
Q

Toxicity of chloramphenicol

A

Anemia (dose dependent) Aplastic anemia (dose independent) Gray baby syndrome (in premature infants b/c they lack liver UDP-glucuronyl transferase)

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54
Q

Mechanism of clindamycin

A

Blocks peptide bond formation at 50S ribosomal subunit. Bacteriostatic.

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55
Q

Clinical use of clindamycin

A

Tx anaerobic infxns (e.g., Bacteroides fragilis, Clostridium perfringens) (Treats anaerobes above the diaphragm)

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56
Q

Toxicity of clindamycin

A

Pseudomembranous colitis (C. difficile overgrowth) Fever Diarrhea

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57
Q

Sulfonamides (list)

A

Sulfamethoxazole (SMX) Sulfisoxazole Sulfadiazine

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58
Q

Mechanism of sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine)

A

PABA antimetabolites inhibit dihydropteroate synthetase [see below]. Bacteriostatic.

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59
Q

Clinical use of of sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine)

A

Gram(+), gram(-), Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.

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60
Q

Toxicity of sulfonamides (sulfamethoxazole (SMX), sulfisoxazole, sulfadiazine)

A

Hypersensitivity rxtns Hemolysis if G6PD deficient Nephrotoxicity (tubulointerstitial nephritis) Photosensitivity Kernicterus in infants Displace other drugs from albumin (e.g., warfarin)

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61
Q

Mechanism of trimethoprim (TMP)

A

Inhibits bacterial dihydrofolate reductase. Bacteriostatic.

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62
Q

Clinical use of trimethoprim (TMP)

A

Used in combination w/ sulfonamides (trimethoprim-sulfamethoxazole [TMP-SMX]), causing sequential block of folate synthesis. Combination used for recurrent UTIs, Shigella, Salmonella, Pneumocystis jiroveci pneumonia.

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63
Q

Toxicity of trimethoprim (TMP)

A

Megaloblastic anemia Leukopenia Granulocytopenia (may alleviate w/ supplemental folinic acid) (Trimethoprim = TMP : T reats M arrow P oorly)

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64
Q

Sulfa drug allergies – what do you need to avoid?

A

Pts who do not tolerate sulfa drugs should not be given sulfonamides or other sulf drugs such as: Sulfasalazine Sulfonylureas Thiazide diuretics Acetazolamide Furosemide

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65
Q

Fluoroquinolones (list)

A

Ciprofloxacin Norfloxacin Ofloxacin Sparfloxacin Moxifloxacin Gatifloxacin Enoxacin [above are fluoroquinolones] Nalidixic acid [a quinolone]

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66
Q

Mechanism of fluoroquinolones

A

Inhibit DNA gyrase (topoisomerase II). Bactericidal. Must not be taken w/ antacids.

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67
Q

Clinical use of fluoroquinolones

A

Gram(-) rods of urinary and GI tracts (including Pseudomonas), Neisseria, some gram(+) organisms

68
Q

Toxicity of fluoroquinolones

A

GI upset, superinfections, skin rashes, HA, dizziness. Contraindicated in pregnant women and in children b/c animal studies show damage to cartilage. Tendonitis and tendon rupture in adults; leg cramps and myalgias in kids. (FlouroquinoLONES hur the attachments to your BONES )

69
Q

Mechanism of metronidazole

A

Forms toxic metabolites in the bacterial cell that damage DNA. Bactericidal, antiprotozoal.

70
Q

Clinical use of metronidazole

A

Treats: G iardia E ntamoeba T richomonas G ardnerella vaginalis A naerobes (Bacteroides, Clostridium) Used w/ bismuth and amoxicillin (or TCN) for triple therapy against H. P ylori (GET GAP on the METRO !) Treats anaerobic infxns below the diaphragm.

71
Q

Toxicity of metronidazole

A

Disulfiram-like rxtn w/ alcohol Headache Metallic taste

72
Q

Polymyxins (list)

A

Polymyxin B Polymyxin E

73
Q

Mechanism of polymyxins

A

Bind to cell membranes of baccteria and disrupt their osmotic properties. Polymyxins are cationic, basic proteins that act like detergents. (MYXins MIX up membranes)

74
Q

Clinical use of polymyxins

A

resistant gram(-) infxns

75
Q

Toxicity of polymyxins

A

Neurotoxicity, acute renal tubular necrosis

76
Q

Antimycobacterial drugs: for M. tuberculosis

A

Prophylaxis: Isoniazid Tx: R ifampin I soniazid P yrazinamide E thambutol (RIPE for treatment)

77
Q

Antimycobacterial drugs: for M. avium-intracellulare

A

Prophylaxis: Azithromycin Tx: Azithromycin Rifampin Ethambutol Streptomycin

78
Q

Antimycobacterial drugs for M. leprae

A

Tx: Dapsone Rifampin Clofazimine

79
Q

Anti-TB drugs

A

S treptomycin, P yrazinamide, I soniazid (INH ), R ifampin, E thambutol (INH-SPIRE [inspire]) Cycloserine (2nd-line therapy)

80
Q

Side effects of anti-TB drugs

A

Important SE of ethambutol: optic neuropathy (red-green color blindness) For other drugs: hepatotoxicity.

81
Q

Mechanism of isoniazid (INH)

A

Decreases synthesis of mycolic acids. *note that there are different INH half-lives in fast vs. slow acetylators.

82
Q

Clinical use of isoniazid (INH)

A

Mycobacterium tuberculosis. The only agent used as solo prophylaxis against TB.

83
Q

Toxicity of isoniazid (INH)

A

Neurotoxicity, hepatotoxicity. Pyridoxine (Vitamin B6) can prevent neurotoxicity. (INH I njures N eurons and H epatocytes)

84
Q

Mechanism of rifampin

A

Inhibits DNA-dependent RNA polymerase

85
Q

Clinical use of rifampin

A

Mycobacterium tuberculosis. Delays resistance to dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children w/ Haemophilus influenzae type B.

86
Q

Toxicity of rifampin

A

Minor hepatotoxicity and drug interactions (induces P-450) Orange body fluids (nonhazardous side effect)

87
Q

Rifampin’s 4 R’s

A

R NA polymerase inhibitor R evs up microsomal P-450 R ed/orange body fluids R apid resistance if used alone

88
Q

Most common resistance mechanism for: Penicillins/cephalosporins

A

Beta-lactamase cleavage of beta-lactam ring, or altered PBP in cases of MRSA or penicillin-resistant S. pneumoniae.

89
Q

The following is the most common mechanism of resistance for what drug? Beta-lactamase cleavage of beta-lactam ring, or altered PBP in cases of MRSA or penicillin-resistant S. pneumoniae.

A

Penicillins/cephalosporins

90
Q

Most common resistance mechanism for: Aminoglycosides

A

Modification via acetylation, adenylation, or phosphorylation.

91
Q

The following is the most common mechanism of resistance for what drug? Modification via acetylation, adenylation, or phosphorylation.

A

Aminoglycosides

92
Q

Most common resistance mechanism for: Vancomycin

A

Terminal D-ala of cell wall component replaced with D-lac, decreased affinity.

93
Q

The following is the most common mechanism of resistance for what drug? Terminal D-ala of cell wall component replaced with D-lac, decreased affinity.

A

Vancomycin

94
Q

Most common resistance mechanism for: Chloramphenicol

A

Modification via acetylation

95
Q

The following is the most common mechanism of resistance for what drug? Modification via acetylation

A

Chloramphenicol

96
Q

Most common resistance mechanism for: Macrolides

A

methylation of rRNA near erythromycin’s ribosome-binding site

97
Q

The following is the most common mechanism of resistance for what drug? methylation of rRNA near erythromycin’s ribosome-binding site

A

Macrolides

98
Q

Most common resistance mechanism for: Tetracycline

A

Decreased uptake or increased transport out of cell.

99
Q

The following is the most common mechanism of resistance for what drug? Decreased uptake or increased transport out of cell.

A

Tetracycline

100
Q

Most common resistance mechanism for: Sulfonamides

A

Altered enzyme (bacterial dihydropteroate synthetase), decreased uptake, or increased PABA synthesis.

101
Q

The following is the most common mechanism of resistance for what drug? Altered enzyme (bacterial dihydropteroate synthetase), decreased uptake, or increased PABA synthesis.

A

Sulfonamides

102
Q

Most common resistance mechanism for: Quinolones

A

Altered gyrase or reduced uptake.

103
Q

The following is the most common mechanism of resistance for what drug? Altered gyrase or reduced uptake.

A

Quinolones

104
Q

Nonsurgical antimicrobial prophylaxis of: meningococcal infxn

A

Rifampin (DOC), minocycline

105
Q

Nonsurgical antimicrobial prophylaxis of: gonorrhea

A

Ceftriaxone

106
Q

Nonsurgical antimicrobial prophylaxis of: syphilis

A

Benzathine penicillin G

107
Q

Nonsurgical antimicrobial prophylaxis of: Hx of recurrent UTIs

108
Q

Nonsurgical antimicrobial prophylaxis of: Pneumocystis jiroveci pneumonia

A

TMP-SMX (DOC), aerosolized pentamidine.

109
Q

Nonsurgical antimicrobial prophylaxis of: endocarditis w/ surgical or dental procedures

A

Penicillins.

110
Q

Tx of highly resistant bacteria

A

MRSA: vancomycin VRE: linezolid and streptogramins (quinupristin/dalfopristin)

111
Q

Mechanism of Amphotericin B

A

Binds ergosterol (unique to fungi); Forms membrane pores that allow leakage of electrolytes. (Amphotear acin ‘tears’ holes in fungal membranes by forming pores) [on left, below]

112
Q

Clinical use of Amphotericin B

A

Use for wide spectrum of systemic mycoses. Cryptococcus, Blastomyces, Coccidioides, Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross BBB.

113
Q

Toxicity of Amphotericin B

A

Fever/chills (shake and bake), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis (amphotericin = amphoterrible). Hydration reduces nephrotoxicity. Liposomal amphotericin reduces toxicity.

114
Q

Mechanism of Nystatin

A

Binds to ergosterol, disrupting fungal membranes. Too toxic for systemic use. [on left w/ amphotericin, below]

115
Q

Clinical use of nystatin

A

Swish and swallow for oral candidiasis (thrush); topical for diaper rash or vaginal candidiasis.

116
Q

Azoles (list)

A

Fluconazole Ketoconazole, Clotrimazole, miconazole, itraconazole, voriconazole

117
Q

Mechanism of azoles

A

Inhibit fungal sterol (ergosterol) synthesis [below, top/middle]

118
Q

Clinical use of azoles

A

Systemic mycoses. Fluconazole for cyptococcal meningitis in AIDS pts (b/c it can cross the BBB) and candidal infxns of all types (i.e., yeast infxns). Ketoconazole for Balstomyces, Coccidioides, Histoplasma, Candida albicans, hypercortisolism. Clotrimazole and miconazole for topical fungal infxns.

119
Q

Toxicity of azoles

A

Hormone synthesis inhibition (gynecomastia), liver dysfunction (inhibits cytochrome P-450), fever, chills

120
Q

Flucytosine mechanism

A

Inhibits DNA synthesis by conversion to 5-fluorouracil [below, middle]

121
Q

Clinical use of flucytosine

A

Used in systemic fungal infxns (e.g., Candida, Cryptococcus) in combination w/ amphotericin B

122
Q

Toxicity of flucytosine

A

Nausea, vomiting, diarrhea, bone marrow suppression

123
Q

Mechanism of Caspofungin

A

Inhibits cell wall synthesis by inhibiting synthesis of beta-glucan. [not included in image of anti-fungal mechanisms]

124
Q

Clinical use of caspofungin

A

Invasive aspergillosis

125
Q

Toxicity of caspofungin

A

GI upset, flushing.

126
Q

Mechanism of terbinafine

A

Inhibits the fungal enzyme squalene epoxidase. [below, top/right]

127
Q

Clinical use of terbinafine

A

Used to Tx dermatophytoses (especially onychomycosis)

128
Q

Mechanism of griseofulvin

A

Interferes w/ microtubule fxn; disrupts mitosis. Deposits keratin-containing tissues (e.g., nails). [below, bottom/right]

129
Q

Clinical use of griseofulvin

A

Oral Tx of superficial infxns; inhibits growth of dermatophytes (tinea, ringworm)

130
Q

Toxicity of griseofulvin

A

Teratogenic, ccarcinogenic, confusion, HA, induces P-450 (increasing warfarin metabolism).

131
Q

Mechanism of amantadine

A

Blocks viral penetration/uncoating (M2 protein); may buffer pH of endosome. (A man to dine [amantadine] takes of his coat .) Also causes the release of dopamine from intact nerve terminals. [below, top/right]

132
Q

Clinical use of amantadine

A

Prophylaxis and Tx for influenza A; Parkinson’s Dz. (A mantadine blocks influenza A and rubellA , and causes problems w/ the cerebellA )

133
Q

Toxicity of amantadine

A

Ataxia, dizziness, slurred speech. (A mantadine blocks influenza A and rubellA , and causes problems w/ the cerebellA ) Rimantidine is a derivative w/ fewer CNS side effects (does not cross BBB)

134
Q

Mechanism of resistance to amantadine

A

Mutated M2 protein. 90% of all influenza A strains are resistant to amantadine, so not used.

135
Q

Mechanism of: Zanamivir, oseltamivir

A

Inhibit influenza neuraminidase, decreasing the release of progeny virus. [below, bottom/left: Neuraminidase inhibitors]

136
Q

Clinical use of Zanamivir, oseltamivir

A

Both influenza A and B

137
Q

Mechanism of ribavirin

A

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase. [not included in figure, but acts at point of NA synthesis, bottom/right]

138
Q

Clinical use of ribavirin

A

RSV Chronic hepatitis C

139
Q

Toxicity of ribavirin

A

Hemolytic anemia. Severe teratogen.

140
Q

Mechanism of acyclovir

A

Monophosphorylated by HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular enzymes. Preferentially inhibits viral DNA polymerase by chain termination. [fits w/ NA analogs below, bottom/right]

141
Q

Clnicial use of acyclovir

A

HSV, VZV, EBV. Used for HSV-induced mucocutaneous and genital lesions as well as for encephalitis. Prophylaxis in immunocompromised pts. For herpes zoster, use a related agent (famciclovir). No effect on latent forms of HSV and VZV.

142
Q

Toxicity of acyclovir

A

Generally well-tolerated.

143
Q

Mechanism of resistance to acyclovir

A

Lack of thymidine kinase

144
Q

Mechanism of ganciclovir

A

5’-monophosphate formed by a CMV viral kinase or HSV/VZV thymidine kinase. Guanosine analog. Triphosphate formed by cellular kinases. Preferentially inhibits viral DNA polymerase. [fits in w/ NA analogs below, bottom/right]

145
Q

Clinical use of ganciclovir

A

CMV, especially in immunocompromised pts

146
Q

Toxicity of ganciclovir

A

Leukopenia, neutropenia, thrombocytopenia, renal toxicity. More toxic to host enzymes than acyclovir.

147
Q

Mechanism of resistance to ganciclovir

A

Mutated CMV DNA polymerase or lack of viral kinse.

148
Q

Mechanism of foscarnet

A

Viral DNA polymerase inhibitor that binds to the pyrophosphate-binding site of the enzyme. Does not require activation by viral kinase. (FOS carnet = pyroFOS phate analog) [would fit into DNA synthesis on bottom/right]

149
Q

Clinical use of foscarnet

A

CMV retinitis in immunocompromised pts when ganciclovir fails; acyclovir-resistant HSV.

150
Q

Toxicity of foscarnet

A

Nephrotoxicity.

151
Q

Mechanism of resistance to foscarnet

A

Mutated DNA polymerase.

152
Q

HIV therapy: Protease inhibitors (list)

A

Saquinavir Ritonavir Indinavir Nelfinavir Amprenavir [all protease inhibitors end in -avir ] (NAVIR (never) TEASE a proTEASE )

153
Q

HIV therapy: Mechanism of protease inhibitors

A

Inhibit maturation of new virus by blocking protease in progeny of virus.

154
Q

HIV therapy: Toxicity of protease inhibitors

A

GI intolerance (nausea, diarrhea) Hyperglycemia Lipodystrophy Thrombocytopenia (indinavir)

155
Q

HIV therapy: Reverse transcriptase inhibitors –> nucleosides (list)

A

Zidovudine (ZDV, formerly AZT) Didanosine (ddI) Zalcitabine (ddC) Stavudine (d4T) Lamivudine (3TC) Abacavir (Have you dined (vudine ) with my nuclear (nucleosides ) family?)

156
Q

HIV therapy: Reverse transcriptase inhibitors –> non-nucleosides (list)

A

N evirapine, E favirenz, D elaviridine (N ever E ver D eliver nucleosides.)

157
Q

HIV therapy: Mechanism of reverse transcriptase inhibitors

A

Preferentially inhibit reverse transcriptase of HIV; prevent incorporation of DNA copy of viral genome into host DNA. [below, bottom/right]

158
Q

HIV therapy: Toxicity of reverse transcriptase inhibitors

A

Bone marrow suppression* (neutropenia, anemia) Peripheral neuropathy Lactic acidosis (nucleosides) Rash (non-nucleosides) Megaloblastic anemia (ZDV) *GM-CSF and erythropoietin can be used to reduce BM suppression.

159
Q

HIV therapy: Clinical use of reverse transcriptase inhibitors

A

Highly active antiretroviral therapy (HAART) generally entails combination Tx w/ protease inhibitors and reverse transcriptase inhibitors. Initiated when pts have low CD4 counts (<500 cells/mm^3) or high viral load. ZDV is used for general prophylaxis and during pregnancy to reduce risk of fetal transmission.

160
Q

HIV therapy: Fusion inhibitor (there’s one – what is it?)

A

Enfuvirtide

161
Q

HIV therapy: Mechanism of fusion inhibitors (enfuvirtide)

A

Bind viral gp41 subunit; inhibit conformational change required for fusion w/ CD4 cells. Therefore block entry and susequent replication.

162
Q

HIV therapy: Toxicity of fusion inhibitors (enfuvirtide)

A

Hypersensitivity rxtns Rxtns at subcutaneous injection site Increased risk of bacterial pneumonia

163
Q

HIV therapy: Clinical use of fusion inhibitors (enfuvirtide)

A

In pts w/ persistent viral replication in spite of antiretroviral Tx. Used in combination w/ other drugs.

164
Q

Mechanism of interferons (as antimicrobials)

A

Glycoproteins from human leukocytes that block various stages of viral RNA and DNA synthesis. Induce ribonuclease that degrades viral mRNA.

165
Q

Clinical use of interferons

A

IFN-alpha: chronic hepatitis B and C, Kaposi’s sarcoma IFN-beta: MS IFN-gamma: NADPH oxidase deficiency

166
Q

Toxicity of interferons

A

Neutropenia

167
Q

Antibiotics to avoid in pregnancy (list – what are they, and why for each one?)

A

(SAFE M oms T ake R eally G ood C are.) S ulfonamides – kernicterus A minoglycosides – ototoxicity F luoroquinolones – cartilage damage E rythromycin – acute cholestatic hepatitis in mom (and clarythromycin – embryotoxic) M etronidazole – mutagenesis T etracyclines – discolored teeth, inhibition of bone growth R ibavirin (antiviral) – teratogenic Griseofulvin (antifungal) – teratogenic Chloramphenicol – gray baby

First AID (6 decks)

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