Question 1

Folic acid synthesis inhibitors (DNA methylation)

Accepted Answer

1. Sulfonamides 
2. Trimethroprim

Question 2

BLOCK Cell wall synthesis by inhibiting

Accepted Answer

1. Peptidoglycan synthesis
2. Peptidoglycan cross-linking

Question 3

Peptidoglycan synthesis inhibitors (BLOCK Cell wall synthesis)

Accepted Answer

Glycopeptides 
1. Vancomycin 
2. Bacitracin

Question 4

Peptidoglycan cross-linking inhibitors (BLOCK Cell wall synthesis)

Accepted Answer

1. Penicillinase-sensitive penicillins
2. Penicillinase-resistant penicillins
3. Antipseudomonals
4. Cephalosporins (I-V)
5. Carbapenems (-penem)
6. Monobactams

Question 5

DNA Topoisomerases inhibitors

Accepted Answer

1. Fluoroquinolones (-xacin)
2.  Quinolone (Nalidixic acid)

Question 6

Damages DNA

Accepted Answer

Metronidazole

Question 7

BLOCKS mRNA synthesis (RNA polymerase)

Accepted Answer

Rifampin

Question 8

BLOCK protein synthesis at 50S SUBUNIT

Accepted Answer

1. Chloramphenicol 
2. Clindamycin 
3. Linezolid 
4. Macrolides (-thromycin)
5. Streptogramins (-pristin)

Question 9

BLOCK protein synthesis at 30S SUBUNIT

Accepted Answer

1. Aminoglycosides 
2. Tetracyclines (-cycline)

Question 10

Penicillinase-sensitive penicillins (BLOCK cell wall synthesis)

Accepted Answer

1. Penicillin G,V
2. Ampicillin 
3. Amoxicillin

Question 11

Penicillinase-sensitive penicillins MOA

Accepted Answer

Bind penicillin-binding proteins (transpeptidases)

Question 12

Penicillinase-sensitive penicillins; clinical use

Accepted Answer

1. Gram-positive organisms
2. Neisseria meningitidis, Treponema pallidum, and syphilis.

Question 13

Penicillinase-sensitive penicillins; TOXICITY

Accepted Answer

Hypersensitivity reactions, hemolytic anemia.

Question 14

Penicillinase-sensitive penicillins RESISTANCE

Accepted Answer

Penicillinase in bacteria (a type of beta-lactamase) cleaves beta-lactam ring.

Question 15

Ampicillin, amoxicillin (aminopenicillins, Penicillinase-sensitive penicillins); CLINICAL USE

Accepted Answer

HELPSS kill enterococci. 
1. Haemophilus influenzae
2. E. coli
3. Listeria monocytogenes 
4. Proteus mirabilis 
5. Salmonella
6. Shigella

Question 16

Ampicillin, amoxicillin (aminopenicillins, Penicillinase-sensitive penicillins); TOXICITY

Accepted Answer

Hypersensitivity reactions; ampicillin rash; PSEUDOMEMBRANOUS COLITIS.

Question 17

PSEUDOMEMBRANOUS COLITIS

Accepted Answer

Ampicillin, amoxicillin

Question 18

Ticarcillin, piperacillin (antipseudomonals); CLINICAL USE

Accepted Answer

1. Pseudomonas  
2. Gram-negative rods; susceptible to penicillinase; use with clavulanic acid.

Question 19

Beta-lactamase inhibitors

Accepted Answer

CAST (-bactam)
1. Clavulanic Acid
2. Sulbactam
3. Tazobactam

Question 20

Often added to penicillin antibiotics to protect the antibiotic from destruction by Beta-lactamase (penicillinase)

Accepted Answer

Beta-lactamase inhibitors

Question 21

Organisms typically not covered by cephalosporins

Accepted Answer

LAME:
1. Listeria
2. Atypicals (Chlamydia, Mycoplasma)
3. MRSA
4. Enterococci. Exception: ceftaroline covers MRSA.

Question 22

Which 5th generation cephalosporin covers MRSA

Accepted Answer

Ceftaroline

Question 23

1st generation (cefazolin, cephalexin); CLINICAL USE

Accepted Answer

PEcK; gram-positive cocci
1. Proteus mirabilis
2. E. coli, 
3. Klebsiella pneumoniae

Question 24

1st generation used prior to surgery to prevent S. aureus wound infections

Accepted Answer

Cefazolin

Question 25

2nd generation (cefoxitin, cefaclor,
cefuroxime); CLINICAL USE

Accepted Answer

HEN PEcKS; gram-positive cocci

1. Haemophilus influenzae
2. Enterobacter aerogenes, 
3. Neisseria
4. Proteus 
5. E. coli
6. Klebsiella 
7. Serratia

Question 26

3rd generation (ceftriaxone, cefotaxime, ceftazidime); CLINICAL USE

Accepted Answer

Serious gram-negative infections resistant to other Beta-lactams.

Question 27

Ceftriaxone (3rd generation Cephalosporin); CLINICAL USE

Accepted Answer

Meningitis and Gonorrhea

Question 28

Ceftazimide (3rd generation Cephalosporin); CLINICAL USE

Accepted Answer

Pseudomonas

Question 29

What antibiotic should always be added to the empiric treatment with Ceftriaxone of Meningitis in children an immuocompromised

Accepted Answer

Ampicillin (to cover for Listeria monocytogenes

Question 30

4th generation (cefepime); CLINICAL USE

Accepted Answer

Increased activity against Pseudomonas and gram-positive organisms

Question 31

5th generation (ceftaroline);CLINICAL USE

Accepted Answer

Broad gram-positive and gram-negative , including MRSA

Question 32

5th generation (ceftaroline) does NOT cover

Accepted Answer

Pseudomonas

Question 33

Cephalosporins; TOXICITY

Accepted Answer

-Hypersensitivity reactions
-Vitamin K deficiency. 
-Increased nephrotoxicity of aminoglycosides.

Question 34

Which medications increase Cephalosporins nephrotoxicity

Accepted Answer

Aminoglycosides

Question 35

Aztreonam (Monobactam); MOA

Accepted Answer

Prevents peptidoglycan cross-linking by binding to PBP3. (Cell wall synthesis inhibitor)

Question 36

Aztreonam (Monobactam); CLINICAL USE

Accepted Answer

1. Gram-negative rods only
2. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosicles.

Question 37

Antibiotic used in those patients with renal insufficiency who cannot tolerate aminoglycosicles.

Accepted Answer

Aztreonam

Question 38

Penicillin-allergic patients

Accepted Answer

Aztreonam

Question 39

Carbapenems are always administered with

Accepted Answer

Cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.

Question 40

Carbapenems (lmipenem, meropenem, ertapenem, doripenem); CLINICAL USE

Accepted Answer

1. Gram-positive cocci
2. Gram-negative rods
3. Anaerobes

Question 41

Which Carbapenem has a reduced risk of seizures and is stable to dehydropeptidase I.

Accepted Answer

Meropenem

Question 42

Carbapenems (lmipenem, meropenem, ertapenem, doripenem); TOXICITY

Accepted Answer

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

Question 43

Vancomycin; MOA

Accepted Answer

Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.

Question 44

Binds D-ala D-ala portion

Accepted Answer

Vancomycin

Question 45

Vancomycin; CLINICAL USE

Accepted Answer

1. Gram positive 
2. MRSA
3. Enterococci
4. Clostridium difficile (oral dose for pseudomembranous colitis).

Question 46

Clostridium difficile (oral dose for pseudomembranous colitis).

Accepted Answer

Vancomycin

Question 47

Commonly used drugs for MRSA

Accepted Answer

1. Vancomycin
2. Daptomycin 
3. Linezolid

Question 48

Vancomycin; TOXICITY

Accepted Answer

NOT
1. Nephrotoxicity
2. Ototoxicity
3. Thrombophlebitis, diffuse flushing-¨red man syndrome¨

Question 49

Red Man Syndrome caused by Vancomycin can be largely prevented by pretreatment with

Accepted Answer

Antihistamines and slow infusion rate

Question 50

Vancomycin; RESISTANCE

Accepted Answer

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

Question 51

Protein synthesis inhibitors

Accepted Answer

Specifically target smaller bacterial ribosome (70S, made of 30S and 50S subunits)

Question 52

50S inhibitors

Accepted Answer

C = Chloramphenicol, Clindamycin 
￼￼￼￼E = Erythromycin (macrolides) 
L = Linezolid

Question 53

30S inhibitors

Accepted Answer

A = Aminoglycosides 
T = Tetracyclines

Question 54

Protein synthesis inhibitors

Accepted Answer

"Buy AT 30, CCEL (sell) at 50."
A = Aminoglycosides 
T = Tetracyclines 
C = Chloramphenicol, Clindamycin 
￼￼￼￼E = Erythromycin (macrolides) 
L = Linezolid

Question 55

Aminoglycosides (30S inhibitors)

Accepted Answer

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin

Question 56

Aminoglycosides (30S inhibitors); MOA

Accepted Answer

inhibit formation of initiation complex and cause misreading of mRNA. Also block translocation.

Question 57

Require 02 for uptake; therefore ineffective against anaerobes

Accepted Answer

Aminoglycosides (30S inhibitors)

Question 58

Ineffective against anaerobes

Accepted Answer

Aminoglycosides (30S inhibitors)

Question 59

Aminoglycosides (30S inhibitors); CLINICAL USE

Accepted Answer

Severe gram-negative rod infections

Question 60

Used for bowel surgery.

Accepted Answer

Neomycin (Aminoglycoside; 30S inhibitor)

Question 61

Aminoglycosides (30S inhibitors); TOXICITY

Accepted Answer

1.Nephrotoxicity (especially when used with cephalosporins)
2.Neuromuscular blockade
3.Ototoxicity (especially when used with loop diuretics)
4.Teratogen

Question 62

Aminoglycosides produce Ototoxicity, especially when used with

Accepted Answer

Loop diuretics

Question 63

Aminoglycosides (30S inhibitors); RESISTANCE

Accepted Answer

Transferase enzymes inactivate drug by acetylation, phosphorylation, or adenylation.

Question 64

Tetracyclines (-cycline)

Accepted Answer

doxycycline, demeclocycline, minocycline.

Question	Answer
Folic acid synthesis inhibitors (DNA methylation)	1. Sulfonamides 2. Trimethroprim
BLOCK Cell wall synthesis by inhibiting	1. Peptidoglycan synthesis 2. Peptidoglycan cross-linking
Peptidoglycan synthesis inhibitors (BLOCK Cell wall synthesis)	Glycopeptides 1. Vancomycin 2. Bacitracin
Peptidoglycan cross-linking inhibitors (BLOCK Cell wall synthesis)	1. Penicillinase-sensitive penicillins 2. Penicillinase-resistant penicillins 3. Antipseudomonals 4. Cephalosporins (I-V) 5. Carbapenems (-penem) 6. Monobactams
DNA Topoisomerases inhibitors	1. Fluoroquinolones (-xacin) 2. Quinolone (Nalidixic acid)
Damages DNA	Metronidazole
BLOCKS mRNA synthesis (RNA polymerase)	Rifampin
BLOCK protein synthesis at 50S SUBUNIT	1. Chloramphenicol 2. Clindamycin 3. Linezolid 4. Macrolides (-thromycin) 5. Streptogramins (-pristin)
BLOCK protein synthesis at 30S SUBUNIT	1. Aminoglycosides 2. Tetracyclines (-cycline)
Penicillinase-sensitive penicillins (BLOCK cell wall synthesis)	1. Penicillin G,V 2. Ampicillin 3. Amoxicillin
Penicillinase-sensitive penicillins MOA	Bind penicillin-binding proteins (transpeptidases)
Penicillinase-sensitive penicillins; clinical use	1. Gram-positive organisms 2. Neisseria meningitidis, Treponema pallidum, and syphilis.
Penicillinase-sensitive penicillins; TOXICITY	Hypersensitivity reactions, hemolytic anemia.
Penicillinase-sensitive penicillins RESISTANCE	Penicillinase in bacteria (a type of beta-lactamase) cleaves beta-lactam ring.
Ampicillin, amoxicillin (aminopenicillins, Penicillinase-sensitive penicillins); CLINICAL USE	HELPSS kill enterococci. 1. Haemophilus influenzae 2. E. coli 3. Listeria monocytogenes 4. Proteus mirabilis 5. Salmonella 6. Shigella
Ampicillin, amoxicillin (aminopenicillins, Penicillinase-sensitive penicillins); TOXICITY	Hypersensitivity reactions; ampicillin rash; PSEUDOMEMBRANOUS COLITIS.
PSEUDOMEMBRANOUS COLITIS	Ampicillin, amoxicillin
Ticarcillin, piperacillin (antipseudomonals); CLINICAL USE	1. Pseudomonas 2. Gram-negative rods; susceptible to penicillinase; use with clavulanic acid.
Beta-lactamase inhibitors	CAST (-bactam) 1. Clavulanic Acid 2. Sulbactam 3. Tazobactam
Often added to penicillin antibiotics to protect the antibiotic from destruction by Beta-lactamase (penicillinase)	Beta-lactamase inhibitors
Organisms typically not covered by cephalosporins	LAME: 1. Listeria 2. Atypicals (Chlamydia, Mycoplasma) 3. MRSA 4. Enterococci. Exception: ceftaroline covers MRSA.
Which 5th generation cephalosporin covers MRSA	Ceftaroline
1st generation (cefazolin, cephalexin); CLINICAL USE	PEcK; gram-positive cocci 1. Proteus mirabilis 2. E. coli, 3. Klebsiella pneumoniae
1st generation used prior to surgery to prevent S. aureus wound infections	Cefazolin
2nd generation (cefoxitin, cefaclor, cefuroxime); CLINICAL USE	HEN PEcKS; gram-positive cocci 1. Haemophilus influenzae 2. Enterobacter aerogenes, 3. Neisseria 4. Proteus 5. E. coli 6. Klebsiella 7. Serratia
3rd generation (ceftriaxone, cefotaxime, ceftazidime); CLINICAL USE	Serious gram-negative infections resistant to other Beta-lactams.
Ceftriaxone (3rd generation Cephalosporin); CLINICAL USE	Meningitis and Gonorrhea
Ceftazimide (3rd generation Cephalosporin); CLINICAL USE	Pseudomonas
What antibiotic should always be added to the empiric treatment with Ceftriaxone of Meningitis in children an immuocompromised	Ampicillin (to cover for Listeria monocytogenes
4th generation (cefepime); CLINICAL USE	Increased activity against Pseudomonas and gram-positive organisms
5th generation (ceftaroline);CLINICAL USE	Broad gram-positive and gram-negative , including MRSA
5th generation (ceftaroline) does NOT cover	Pseudomonas
Cephalosporins; TOXICITY	-Hypersensitivity reactions -Vitamin K deficiency. -Increased nephrotoxicity of aminoglycosides.
Which medications increase Cephalosporins nephrotoxicity	Aminoglycosides
Aztreonam (Monobactam); MOA	Prevents peptidoglycan cross-linking by binding to PBP3. (Cell wall synthesis inhibitor)
Aztreonam (Monobactam); CLINICAL USE	1. Gram-negative rods only 2. For penicillin-allergic patients and those with renal insufficiency who cannot tolerate aminoglycosicles.
Antibiotic used in those patients with renal insufficiency who cannot tolerate aminoglycosicles.	Aztreonam
Penicillin-allergic patients	Aztreonam
Carbapenems are always administered with	Cilastatin (inhibitor of renal dehydropeptidase I) to decrease inactivation of drug in renal tubules.
Carbapenems (lmipenem, meropenem, ertapenem, doripenem); CLINICAL USE	1. Gram-positive cocci 2. Gram-negative rods 3. Anaerobes
Which Carbapenem has a reduced risk of seizures and is stable to dehydropeptidase I.	Meropenem
Carbapenems (lmipenem, meropenem, ertapenem, doripenem); TOXICITY	GI distress, skin rash, and CNS toxicity (seizures) at high plasma levels.
Vancomycin; MOA	Inhibits cell wall peptidoglycan formation by binding D-ala D-ala portion of cell wall precursors.
Binds D-ala D-ala portion	Vancomycin
Vancomycin; CLINICAL USE	1. Gram positive 2. MRSA 3. Enterococci 4. Clostridium difficile (oral dose for pseudomembranous colitis).
Clostridium difficile (oral dose for pseudomembranous colitis).	Vancomycin
Commonly used drugs for MRSA	1. Vancomycin 2. Daptomycin 3. Linezolid
Vancomycin; TOXICITY	NOT 1. Nephrotoxicity 2. Ototoxicity 3. Thrombophlebitis, diffuse flushing-¨red man syndrome¨
Red Man Syndrome caused by Vancomycin can be largely prevented by pretreatment with	Antihistamines and slow infusion rate
Vancomycin; RESISTANCE	Occurs with amino acid change of D-ala D-ala to D-ala D-lac
Protein synthesis inhibitors	Specifically target smaller bacterial ribosome (70S, made of 30S and 50S subunits)
50S inhibitors	C = Chloramphenicol, Clindamycin E = Erythromycin (macrolides) L = Linezolid
30S inhibitors	A = Aminoglycosides T = Tetracyclines
Protein synthesis inhibitors	"Buy AT 30, CCEL (sell) at 50." A = Aminoglycosides T = Tetracyclines C = Chloramphenicol, Clindamycin E = Erythromycin (macrolides) L = Linezolid
Aminoglycosides (30S inhibitors)	Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin
Aminoglycosides (30S inhibitors); MOA	inhibit formation of initiation complex and cause misreading of mRNA. Also block translocation.
Require 02 for uptake; therefore ineffective against anaerobes	Aminoglycosides (30S inhibitors)
Ineffective against anaerobes	Aminoglycosides (30S inhibitors)
Aminoglycosides (30S inhibitors); CLINICAL USE	Severe gram-negative rod infections
Used for bowel surgery.	Neomycin (Aminoglycoside; 30S inhibitor)
Aminoglycosides (30S inhibitors); TOXICITY	1.Nephrotoxicity (especially when used with cephalosporins) 2.Neuromuscular blockade 3.Ototoxicity (especially when used with loop diuretics) 4.Teratogen
Aminoglycosides produce Ototoxicity, especially when used with	Loop diuretics
Aminoglycosides (30S inhibitors); RESISTANCE	Transferase enzymes inactivate drug by acetylation, phosphorylation, or adenylation.
Tetracyclines (-cycline)	doxycycline, demeclocycline, minocycline.
Tetracyclines; MOA	bind to 30S and prevent attachment ofaminoacyl-tRNA; limited CNS penetration.
Tetracycline fecally eliminated and can be used in patients with renal failure	Doxycycline
Do not take Tetracyclines with	milk, antacids, or iron containing preparations because divalent cations inhibit its absorption in the gut.
Tetracyclines (30S inhibitors); CLINICAL USE	1. Borrelia burgdorferi 2. M. pneumnoniae 3. Rickettsia and Chlamydia
Tetracyclines (30S inhibitors); TOXICITY	1. Gl distress 2. Discoloration of teeth 3. Inhibition of bone growth in children, 4. Photosensitivity. Contraindicated in pregnancy.
PHOTOSENSITIVITY	SAT for PHOTO: 1. S= Sulfonamides 2. A= Amiodarone 3. T= Tetracyclines
Discoloration of teeth and inhibition of bone growth in children	Tetracyclines
Tetracyclines (30S inhibitors); RESISTANCE	DECREASED uptake into cells or INCREASED efflux out of cell by plasmid-encoded transport pumps.
Macrolides (50S inhibitors)	Azithromycin, clarithromycin, erythromycin.
Macrolides (50S inhibitors); MOA	Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S ribosomal subunit.
Bind to the 23S rRNA of the 50S ribosomal subunit	Macrolides
Macrolides (50S inhibitors); CLINICAL USE	1. Atypical pneumonias (Mycoplasma, Chlamydia, Legionella) 2. STDs (for Chlamydia) 3. Gram positive cocci (streptococcal infections in patients allergic to penicillin).
Macrolides (50S inhibitors); TOXICITY	MACRO: 1. M= Motility issues, 2. A= Arrhythmia caused by prolonged QT, 3. C= Cholestatic hepatitis (acute) 4. R= Rash 5. eOsinophilia
Increases serum concentration oftheophyllines, oral anticoagulants	Macrolides (50S inhibitors)
Macrolides (50S inhibitors); RESISTANCE	Methylation of 23S rRNA binding site.
Chloramphenicol; MOA	Blocks peptidyltransferase at 50S ribosomal subunit
Chloramphenicol (50S inhibitors); CLINICAL USE	1. Meningitis (Haemophilus influenzae, Neisseria meningitidis, Streptococcus pneumoniae) 2. Rocky Mountain spotted fever (Rickettsia ricketsii)
Rocky Mountain spotted fever (Rickettsia ricketsii) TREATMENT	Chloramphenicol (50S inhibitors)
Chloramphenicol (50S inhibitors); TOXICITY	1. Anemia (dose dependent) 2. Aplastic anemia (dose independent) 3. Gray baby syndrome (in premature infants because they lack liver UDP-glucuronyl transferase).
50S inhibitor that causes Gray baby syndrome	Chloramphenicol
50S inhibitor that causes Aplastic anemia (dose independent)	Chloramphenicol
Chloramphenicol (50S inhibitors); RESISTANCE	Plasmid-encoded acetyltransferase that inactivates drug by acetylation
Clindamycin; MOA	Blocks peptide transfer (transpeptidation) at 50S ribosomal subunit.
Clindamycin; CLINICAL USE	1. Anaerobic infections (e.g., Bacteroides fragilis, Clostridium perfringens) in aspiration pneumonia or lung abscesses. 2. Oral infections with mouth anaerobes. 3. Invasive Group A streptococcal (GAS) infection.
Treats anaerobes ABOVE the diaphragm	Clindamycin
Treats anaerobes BELOW the diaphragm	Metronidazole
Clindamycin;TOXICITY	Pseudomembranous colitis (C. difficile overgrowth), fever, diarrhea.
Sulfonamides	1. Sulfamethoxazole (SMX) 2. Sulfisoxazole 3. Sulfadiazine.
Acne vulgaris (topical antimicrobial)	Tetracyclines (1st line) Erythromycin (2nd line)
work on Aerobes	Aminoglycosides
Used in Hepatic Encephalopathy	Neomycin (Aminoglycoside; 30S inhibitor)
Sulfonamides; MOA	Inhibit Folate synthesis. Para-aminobenzoic acid (PABA) antimetabolites inhibit dihydropteroate synthase.
Sulfonamides; CLINICAL USE	1. Gram-positive 2. Gram-negative 3. Nocardia 4. Chlamydia
simple UTI´s	Triple sulfas or Sulfamethoxazole (SMX)
Sulfonamides; TOXICITY	1. Hypersensitivity reactions 2. Hemolysis if G6PD deficient 3. Nephrotoxicity (tubulointerstitial nephritis) 4. Photosensitivity 5. Kernicterus in infants
Antimicrobial that displaces other drugs from albumin (e.g., warfarin) .	Sulfonamides
Antimicrobial that produces hemolysis if G6PD deficient	Sulfonamides
Sulfonamides; RESISTANCE	Altered enzyme (bacterial dihydropteroate synthase), DECREASED uptake, or INCREASED PABA synthesis.
Inhibit dihydropteroate synthase	Sulfonamides
Inhibits bacterial dihydrofolate reductase	Trimethoprim
Trimethoprim; MOA	Inhibits bacterial dihydrofolate reductase
Trimethoprim-sulfamethoxazole [TMP SMX]; CLINICAL USE	1. UTI´s 2. Shigella 3. Salmonella 4. Pneumocystis jirovecii pneumonia (treatment and prophylaxis).
Trimethoprim is used in combination with	Sulfonamides (trimethoprim-sulfamethoxazole [TMP SMX]), causing sequential block of folate synthesis
Block folate synthesis	Trimethoprim-sulfamethoxazole [TMP SMX]
Pneumocystis jirovecii pneumonia (treatment and prophylaxis)	Trimethoprim-sulfamethoxazole [TMP SMX]
UTI´s	Trimethoprim-sulfamethoxazole [TMP SMX]
Toxoplasmosis prophylaxis	Trimethoprim-sulfamethoxazole [TMP SMX]
Trimethoprim; TOXICITY	Megaloblastic anemia, leukopenia, granulocytopenia. (May alleviate with supplemental folinic acid [leucovorin rescue].)
Granulocytopenia caused by Trimethoprim may alleviate with	supplemental folinic acid [leucovorin rescue].)
Fluoroquinolones; MOA	Inhibit DNA gyrase (Topoisomerase II) and Topoisomerase IV.
Inhibit DNA gyrase	Fluoroquinolones
Fluoroquinolones must NOT be taken with	Antacids
Fluoroquinolones; CLINICAL USE	1. Gram-negative rods urinary and GI tracts (including Pseudomonas) 2. Neisseria 3. Some gram-positive organisms
Fluoroquinolones; TOXICITY	1. GI upset, superinfections, skin rashes, headache, dizziness. 2. Tendonitis, tendon rupture, leg cramps, myalgias. 3. Prolonged QT interval. 4. Tendon rupture in people > 60 years old and in patients taking prednisone.
Fluoroquinolones contraindicated due possible damage to cartilage.	1. Pregnant women 2. Nursing mothers 3. Children under 18
Tendon rupture in people > 60 years old and in patients taking prednisone.	Fluoroquinolones
Antimicrobial that prolongs QT interval.	Fluoroquinolones
Fluoroquinolones; RESISTANCE	Chromosome-encoded mutation in DNA gyrase, plasmid-mediated resistance, efflux pumps.
Metronidazole; MOA	Forms free radical toxic metabolites in the bacterial cell that damage DNA.
Bactericidal, antiprotozoal	Metronidazole
Metronidazole; CLINICAL USE	GET GAP on the Metro with metronidazole! G= Giardia E= Entamoeba T= Trichomonas G= Gardnerella vaginalis A= Anaerobes (Bacteroides, C. difficile). P= H. Pylori.
Used with a proton pump inhibitor and clarithromycin for "triple therapy" against H. Pylori.	Metronidazole
"triple therapy" against H. Pylori.	Proton pump inhibitor + Clarithromycin + Metronidazole
Metronidazole; TOXICITY	1. Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with ALCOHOL 2. Headache 3. MetaIIic taste.
MetaIIic taste	Metronidazole
Disulfiram-like reaction (severe flushing, tachycardia, hypotension) with ALCOHOL	Metronidazole
M. tuberculosis; PROPHYLAXIS	Isoniazid
M. avium-intracellulare; PROPHYLAXIS	Azythromycin, Rifabutin
M. tuberculosis; TREATMENT	RIPE R= Rifampin I= Isoniazid P= Pyrazinamide E= Ethambutol
M. avium-intracellulare; TREATMENT	Azithromycin, rifampin, ethambutol, streptomycin
M. leprae; TREATMENT	Tuberculoid form: dapsone and rifampin Lepromatous form: add clofazimine
Isoniazid; MOA	Decreases synthesis of mycolic acid. Bacterial catalase-peroxidase (KatG) needed to convert INH to active metabolite.
ONLY agent used as SOLO prophylaxis against TB	Isoniazid
Isoniazid; CLINICAL USE	Mycobacterium tuberculosis
Isoniazid; TOXICITY	1. Neurotoxicity 2. Hepatotoxicity 3. Lupus
Can prevent neurotoxicity produced by Isoniazid	Pyridoxine (vitamin B6)
Rifamycins (Rifampin, rifabutin); MOA	Inhibits DNA-dependent R A polymerase.
Rifampin's 4 R's	1. RNA polymerase inhibitor 2. Ramps up microsomal cytochrome P-450 3. Red/orange body fluids 4. Rapid resistance if used alone
Used for MONOTHERAPY in Meningococcal prophylaxis	Rifampin
Red/orange body fluids	Rifampin
Rifamycins (Rifampin, rifabutin); CLINICAL USE	1. Mycobacterium tuberculosis 2. Delays resistance to dapsone when used for leprosy. 3. Meningococcal prophylaxis 4. Chemoprophylaxis in contacts of children with Haemophilus influenzae type B.
Chemoprophylaxis in contacts of children with Haemophilus influenzae type B	Rifamycins (Rifampin, rifabutin)
Rifamycin prefered in patients with HIV infection due to less cytochrome P-450 stimulation	Rifabutin
Ethambutol; MOA	Decreases carbohydrate polymerization of mycobacterium cell wall by blocking arabinosyltransferase
Blocks arabinosyltransferase	Ethambutol
Ethambutol; CLINICAL USE	M. tuberculosis; RIPE R= Rifampin I= Isoniazid P= Pyrazinamide E= Ethambutol
Ethambutol; TOXICITY	Optic neuropathy (red-green color blindness)
Optic neuropathy (red-green color blindness)	Ethambutol
Endocarditis with surgical or dental procedures; Antimicrobial prophylaxis	Penicillins
Meningococcal infection; Antimicrobial prophylaxis	Ciprofloxacin (drug of choice), rifampin for children
Gonorrhea; Antimicrobial prophylaxis	Ceftriaxone (3rd generation Cephalosporin)
Syphilis; Antimicrobial prophylaxis	Benzathine penicillin G (IV and IM form)
History of recurrent UTI´s; Antimicrobial prophylaxis	TMP-SMX
Pregnant woman carrying group B strep; Antimicrobial prophylaxis	Ampicillin
Prophylaxis of strep pharyngitis in child with prior rheumatic fever	Oral penicillin
Prevention of postsurgical infection clue to S. aureus	Cefazolin (1st generation Cephalosporin)
Prevention of gonococcal or chlamydial conjunctivitis in newborn	Erythromycin ointment
HIV Prophylaxis	1. CD4 < 200 cells/mm3, Pneumocystis pneumonia: TMP-SMX 2. CD4 < 100 cells/mm3, Pneumocystis pneumonia + Toxoplasmosis: TMP-SMX 3. CD4 < 50 cells/mm3, MAC: Azithromycin
Treatment of Vancomycin- Resistant Enterococcus (VRE)	Linezolid and Streptogramins (quinupristin/dalfopristin)

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ANTIMICROBIALS