2007 First Aid Ch 04 Microbiology

Front 1

Bugs with exotoxins

Back 1

"Some Say Cobra Venom Entering Buttocks Could Cause Complete Blindness So Suck"
[S aureus/pyogenes SuperAgs]
[C. diptheria, V. Cholera, E. coli, B. pertusis----ADP ribosylation/A-B toxin]
[C.perfringens, C. tetani, C. botulinum, B.antrhax, Shigela, S. pyogenes----other toxins]

Front 2

some toxins encoded by lysogenic phages.

Back 2

ABCDE

-shigA-like toxin
-Botulinum toxin
-Cholera toxin
-Diphtheria toxin
-Erythrogenic toxin of -Streptococcus pyogenes

Front 3

examples of Obligate anaerobes

Back 3

Anearobes know their ABC's

-Actinomyces
-Bacterioides
-Clostridium

Front 4

Catalase

what it does and why it's bad

Back 4

Catalase degrades H2O2, an antimicrobial product of PMNs. H2O2 is a substrate for myeloperoxidase.

Front 5

what makes coagulase

Back 5

S. aureus makes coagulase,

whereas S. epidermidis
and S. saprophyticus do not.

Front 6

bacterial cAMP inducers

Back 6

cAMP

-Choerae
-Anthrax
-E.coli (imagine the heat (heat -labile) has caused the E to faint and as fallen over to make an M
-Pertussis

Front 7

Zoonotic bacteria

Back 7

Big Bad Bugs From Yer Pet

-Bartonella henselea
-Borrelia burgdorferi
-Brucella spp.
-Francisella tularensis
-Yersinia pestis
-Pasteurella multocida

Front 8

Cat scratch fever aka

Back 8

Bartonella henselae

Front 9

Bartonella henselae

disease states

Back 9

cat scratch fever
lymphadenopathy (swelling of the lymph nodes) and fever. and Peliosis Hepatis

Front 10

Peliosis Hepatis
describe

Back 10

is an uncommon vascular condition characterised by randomly distributed multiple blood-filled cavities throughout liver.

Front 11

is an uncommon vascular condition characterised by randomly distributed multiple blood-filled cavities throughout liver.

Back 11

Peliosis Hepatis

Front 12

Peliosis Hepatis
causes

Back 12

HIV
bartonella
malignancy
drugs

Front 13

treatment of choice for most
rickettsial infections.

Back 13

Tetracycline is the

Front 14

Rocky Mountain spotted fever

where in the country

Back 14

Endemic to East Coast (in spite of name).

Front 15

Classic cause of atypical “walking” pneumonia

Back 15

Mycoplasma pneumoniae

Front 16

Leptospira interrogans

appearance and where found

Back 16

Question marke shape spirochete bacteria in water contaminated with animal urine

Front 17

Question marke shape spirochete bacteria in water contaminated with animal urine

Back 17

Leptospira interrogans

Front 18

Leptospira interrogans

clinical findings

Back 18

fluelike with fever, headache, stomach pain and jaundace

also Weil's disease - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia

Front 19

Weil's disease

Back 19

aka icterohemorrhagic leptospirosis - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia

Front 20

aka icterohemorrhagic leptospirosis - severe form of jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, and anemia

Back 20

Weil's disease

Front 21

VDRL mech

Back 21

VDRL detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, VDRL detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, but
many biologic false positives

Front 22

detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, VDRL detects nonspecific antibody that reacts with
beef cardiolipin. Used for diagnosis of syphilis, but
many biologic false positives

Back 22

VDRL

Front 23

Systemic mycoses can mimic

Back 23

TB
(granuloma formation).

Front 24

“Tricky T’s”

Back 24

-Typhoid fever=Salmonella typhi
-C.trachomatis=bacteria, STD.
-Trichomonas vaginalis=protozoan, STD.
-Trichinella spiralis=worm in pork.
-Trypanosoma=Chagas’ disease or African ss.
-Treponema=spirochete; causes syphilis (T. pallidum) or yaws (T. pertenue).

Front 25

Rubella aka

Back 25

(German measles)

Front 26

German measles aka

Back 26

Rubella

Front 27

Hepatitis virus families

Back 27

HEP A-picornavirus
HEP B-Hepaddnavirus
HEP C-flavivirus
HEP D-deltavirus
HEP E-Calicivirus/hepivirus

Front 28

Rubella findings

Back 28

fever, lympadenopathy, arthralgias. mild in children, but serious congenital disease)

Front 29

congenital rubella findings

Back 29

# malformations of the heart (especially patent ductus arteriosus), eyes or brain
# deafness
# eye defects (especially cataract and microphthalmia
# thrombocytopenic purpura (presents as a characteristic "blueberry muffin" rash)

Front 30

# malformations of the heart (especially patent ductus arteriosus), eyes or brain
# deafness
# eye defects (especially cataract and microphthalmia
# thrombocytopenic purpura (presents as a characteristic "blueberry muffin" rash)

Back 30

congenital rubella findings

Front 31

"lots of spots"

Back 31

rubella
rubeola
varicella
variola
vaccina

Front 32

TORCHES infection findings

Toxoplasma

Back 32

"clasic triad" of chorioretinitis, intracranial calcifications (ring enhanced lesions) and hydrocephalus

Front 33

TORCHES infection findings

rubella

Back 33

deafness, cataracts, PDA/pulmonary artery stenosis, retardation

Front 34

TORCHES infection findings

CMV

Back 34

petechial rash, intracranial calcifications, mental retardation, hepatosplenomgaly, jaundice. 90% are asymptomatic at birth

Front 35

TORCHES infection findings

HIV

Back 35

hepatosplenomgaly, neurologic problems, and frequent infections

Front 36

TORCHES infection findings

HSV2

Back 36

encephalitis, conjunctivitis, vesicular skin lesions

Front 37

TORCHES infection findings

Syphilis

Back 37

cutaneous lesions, hepatosplenomgaly, jaundice, saddle nose, saber shins, hutchinson teeth, CNVIII deafness,

Front 38

hutchinson teeth

Back 38

teeth that are smaller and more widely spaced than normal and which have notches on their biting surfaces. a sign of congenital syphilis

Front 39

teeth that are smaller and more widely spaced than normal and which have notches on their biting surfaces.

Back 39

hutchinson teeth-a sign of congenital syphilis

Front 40

"clasic triad" of chorioretinitis, intracranial calcifications (ring enhanced lesions) and hydrocephalus

Back 40

TORCHES infection findings

Toxoplasma

Front 41

TORCHES infection findings

deafness, cataracts, PDA/pulmonary artery stenosis, retardation

Back 41

rubella

Front 42

TORCHES infection findings

petechial rash, intracranial calcifications, mental retardation, hepatosplenomgaly, jaundice. 90% are asymptomatic at birth

Back 42

CMV

Front 43

TORCHES infection findings

hepatosplenomgaly, neurologic problems, and frequent infections

Back 43

HIV

Front 44

TORCHES infection findings

encephalitis, conjunctivitis, vesicular skin lesions

Back 44

HSV2

Front 45

TORCHES infection findings

cutaneous lesions, hepatosplenomgaly, jaundice, saddle nose, saber shins, hutchinson teeth, CNVIII deafness,

Back 45

hutchinson teeth

Front 46

Top three causes of pneumonia in

Children (6 wks–18 yr)

Back 46

-Viruses (RSV)
-Mycoplasma
-Chlamydia pneumoniae

Front 47

Top three causes of pneumonia in

Adults (18–40 yr)

Back 47

-Mycoplasma
-C. pneumoniae
-S. pneumoniae

Front 48

Top three causes of pneumonia in

Adults (40–65 yr)

Back 48

-S. pneumoniae
-H. influenzae
-Anaerobes

Front 49

Top three causes of pneumonia in

Elderly >65

Back 49

-S. pneumoniae
-Viruses
-Anaerobes

Front 50

What age group has this pneumonia pattern

-Viruses (RSV)
-Mycoplasma
-Chlamydia pneumoniae

Back 50

Children (6 wks–18 yr)

Front 51

What age group has this pneumonia pattern

-Mycoplasma
-C. pneumoniae
-S. pneumoniae

Back 51

Adults (18–40 yr)

Front 52

What age group has this pneumonia pattern

-S. pneumoniae
-H. influenzae
-Anaerobes

Back 52

Adults (40–65 yr)

Front 53

What age group has this pneumonia pattern

-S. pneumoniae
-Viruses
-Anaerobes

Back 53

Elderly >65

Front 54

Top three causes of meningitis in

Newborn (0–6 mos)

Back 54

-Group B streptococci
-E. coli
-Listeria

Front 55

Top three causes of meningitis in

Children (6 mos–6 yrs)

Back 55

-Streptococcus pneumoniae
-Neisseria meningitidis
-Haemophilus influenzae type B

Front 56

Top three causes of meningitis in

6–60 yrs

Back 56

-N. meningitidis
-Enteroviruses
- S. pneumoniae

Front 57

Top three causes of meningitis in

60 yrs +

Back 57

-S. pneumoniae
-Gram-negative rods
-Listeria

Front 58

What age group gets this pattern of meningitis

-Group B streptococci
-E. coli
-Listeria

Back 58

Newborn (0–6 mos)

Front 59

What age group gets this pattern of meningitis

-Streptococcus pneumoniae
-Neisseria meningitidis
-Haemophilus influenzae type B

Back 59

Children (6 mos–6 yrs)

Front 60

What age group gets this pattern of meningitis

-N. meningitidis
-Enteroviruses
- S. pneumoniae

Back 60

6–60 yrs

Front 61

What age group gets this pattern of meningitis

-S. pneumoniae
-Gram-negative rods
-Listeria

Back 61

60 yrs +

Front 62

UTI bugs

Back 62

SSEEK PP.

Serratia marcescens, staphylococcus saprophyticus
E. coli, Enterobacter cloacae
Klebsiella, Proteus mirabilis
Pseudomonas aeruginosa

Front 63

Name the Gram + Rods
Anaerobes

Back 63

Anaerobes
p Acne/
Clostridum/
fragilis (is gram but is in the mnemonic)/
a. Israeli /
mobiluncus muleris

Front 64

Name the Gram + Rods
Aerobes

Back 64

-Cornybacterium
-Listeria
-Bacillus
-Erysipelothrix

Front 65

Name the Gram - Rods

Back 65

Yersinia / Haemophilus / vibrio / Helicobacter / Pseudomonas / Campylobacter / Bordatella / Bacteriodes fragilis (the only anaerobe) / Brucella / Legionella / Pasturella / Klebsiella / Shigella / E. coli / Salmonella / Francesella

Front 66

Name the Gram + Cocci

Back 66

Strep
Staph
Enterococcus

Front 67

Name the Gram - Cocci

Back 67

Nissera

Front 68

Name the Gram + Rods
Anaerobes

Back 68

Anaerobes
p Acne/
Clostridum/
fragilis (is gram but is in the mnemonic)/
a. Israeli /
mobiluncus muleris

Front 69

Name the Gram + Rods
Aerobes

Back 69

-Cornybacterium
-Listeria
-Bacillus
-Erysipelothrix

Front 70

Name the Gram - Rods

Back 70

Yersinia / Haemophilus / vibrio / Helicobacter / Pseudomonas / Campylobacter / Bordatella / Bacteriodes fragilis (the only anaerobe) / Brucella / Legionella / Pasturella / Klebsiella / Shigella / E. coli / Salmonella / Francesella

Front 71

Name the Gram + Cocci

Back 71

Strep
Staph
Enterococcus

Front 72

Name the Gram - Cocci

Back 72

Nissera

Front 73

Penicillin

Clinical use

Back 73

-gram-positive cocci,
-gram-positive rods, -gram-negative cocci,
and
-spirochetes.

Front 74

Penicillin

Toxicity

Back 74

Hypersensitivity reactions, hemolytic anemia.

Front 75

penicillinase-resistant penicillins

names

Back 75

Methicillin, nafcillin, dicloxacillin

Front 76

Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)

Mechanism

Back 76

Same as penicillin

Front 77

Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)

Clinical use

Back 77

S. aureus (except MRSA; resistant because of altered penicillin-binding protein target site).

Front 78

Methicillin, nafcillin, dicloxacillin (penicillinase-resistant penicillins)

Toxicity

Back 78

Hypersensitivity reactions; methicillin––interstitial nephritis.

Front 79

aminopenicillins
names

Back 79

Ampicillin, amoxicillin

Front 80

Ampicillin, amoxicillin (aminopenicillins)

Mechanism

Back 80

Same as penicillin. Wider spectrum; penicillinase
sensitive. Also combine with clavulanic acid

Front 81

Ampicillin, amoxicillin (aminopenicillins)

Clinical use

Back 81

Extended-spectrum penicillin––certain gram-positive bacteria and gram-negative rods "HELPS" (Haemophilus influenzae, E. coli, Listeria monocytogenes, Proteus mirabilis, Salmonella, enterococci).

Front 82

Ampicillin, amoxicillin (aminopenicillins)

Toxicity

Back 82

Hypersensitivity reactions; ampicillin rash;
pseudomembranous colitis.

Front 83

combine with clavulanic acid
(penicillinase inhibitor) to enhance spectrum.

Back 83

Ampicillin, amoxicillin (aminopenicillins)

Front 84

Ampicillin, amoxicillin (aminopenicillins)

wrt combinations

Back 84

combine with clavulanic acid
(penicillinase inhibitor) to enhance spectrum.

Front 85

penicillin forms

Back 85

Penicillin G (IV form), penicillin V (oral)

Front 86

aminopenicillins

aka

Back 86

Ampicillin, amoxicillin

Front 87

Ampicillin, amoxicillin

aka

Back 87

aminopenicillins

Front 88

anti-pseudomonals

aka

Back 88

TCP: Takes Care of
Pseudomonas.

Ticarcillin, carbenicillin, piperacillin

Front 89

Ticarcillin, carbenicillin, piperacillin

aka

Back 89

TCP: Takes Care of
Pseudomonas.

anti-pseudomonals

Front 90

use with clavulanic acid.

Back 90

Ticarcillin, carbenicillin, piperacillin (anti-pseudomonals)

Ampicillin, amoxicillin (aminopenicillins)

Front 91

Ticarcillin, carbenicillin, piperacillin (anti-pseudomonals)

use wit

Back 91

clavulanic acid (penicillinase inhibitor) to enhance spectrum.

Front 92

Ticarcillin, carbenicillin, piperacillin

Mechanism

Back 92

Same as penicillin. Extended spectrum.

Front 93

Ticarcillin, carbenicillin, piperacillin

Clinical use

Back 93

Pseudomonas spp. and gram-negative rods;

Front 94

Ticarcillin, carbenicillin, piperacillin

Toxicity

Back 94

Hypersensitivity reactions.

Front 95

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

Back 95

Cephalosporins

Front 96

Cephalosporins

Mechanism

Back 96

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

Front 97

1st generation Cephalosporins

Clinical use

Back 97

PEcK.

gram-positive cocci, Proteus mirabilis, E. coli, Klebsiella
pneumoniae.

Front 98

2nd generation Cephalosporins

Clinical use

Back 98

HEN PEcKS.

gram-positive cocci, Haemophilus influenzae,
Enterobacter aerogenes, Neisseria spp., Proteus, E. coli, Klebsiella , Serratia.

Front 99

3rd generation Cephalosporins

Clinical use

Back 99

serious gram-negative infections resistant to other
β-lactams; meningitis (most penetrate the blood-brain
barrier). Examples: ceftazidime for Pseudomonas;
ceftriaxone for gonorrhea.

Front 100

4th generation Cephalosporins

Clinical use

Back 100

↑ activity against Pseudomonas and gram-positive organisms.

Front 101

Cephalosporins

Toxicity

Back 101

Hypersensitivity reactions. Cross-hypersensitivity with
penicillins occurs in 5–10% of patients. nephrotoxicity of aminoglycosides; Disulfiram type reaction with ethanol

Front 102

which Cephalosporins

Disulfiram type reaction with ethanol

Back 102

with a methylthiotetrazole group, e.g., cefamandole

Front 103

1st generation Cephalosporins

Names

Back 103

1st generation...All cephalosporin sounds like CEF except 1st generation in 1st generation there is PH rather CEF like..->CePHalothin ,CePHaprin, CePHradine, CePHalexin

dont be FAZed, this exception is out O' LINe ..CeFAZOLIN

Front 104

2nd generation Cephalosporins

Names

Back 104

FOXes have FACe FUR

ceFOXitin, ceFAClor, ceFURoxime)–

Front 105

3rd generation Cephalosporins

names

Back 105

TRI to TAX TAZ
cefTRIaxone, cefoTAXime, cefTAZidime

Front 106

4th generation Cephalosporins

names

Back 106

Cefepime is the only one

Front 107

what generation Cephalosporin is

cephalexin

Back 107

1st generation

Front 108

what generation Cephalosporin is

cefazolin

Back 108

1st generation

Front 109

what generation Cephalosporin is

cefuroxime

Back 109

2nd generation

Front 110

what generation Cephalosporin is

cefaclor

Back 110

2nd generation

Front 111

what generation Cephalosporin is

cefoxitin

Back 111

2nd generation

Front 112

what generation Cephalosporin is

ceftriaxone

Back 112

3rd generation

Front 113

what generation Cephalosporin is

cefotaxime

Back 113

3rd generation

Front 114

what generation Cephalosporin is

ceftazidime

Back 114

3rd generation

Front 115

what generation Cephalosporin is

cefepime

Back 115

4th generation

Front 116

Aztreonam

Mechanism

Back 116

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

Front 117

Aztreonam

Clinical use

Back 117

Gram-negative rods––Klebsiella spp., Pseudomonas spp., Serratia spp. No activity against
gram-positives or anaerobes. For penicillin-allergic patients and those with renal
insufficiency who cannot tolerate aminoglycosides.

Front 118

Aztreonam

Toxicity

Back 118

Usually nontoxic; occasional GI upset.

Front 119

Synergistic with aminoglycosides. No cross-allergenicity with penicillins.

Back 119

Aztreonam

Front 120

Gram-negative rods––Klebsiella spp., Pseudomonas spp., Serratia spp. No activity against
gram-positives or anaerobes. For penicillin-allergic patients and those with renal
insufficiency who cannot tolerate aminoglycosides.

Back 120

Aztreonam

Front 121

Imipenem/cilastatin, meropenem

Mechanism

Back 121

Imipenem is a broad-spectrum, β-lactamase-resistant
carbapenem.

Front 122

Imipenem/cilastatin, meropenem

Clinical use

Back 122

Gram-positive cocci, gram-negative rods, and
anaerobes. Drug of choice for Enterobacter (esp UTI)

Front 123

Imipenem/cilastatin, meropenem

Toxicity

Back 123

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

Front 124

Always administered with cilastatin

Back 124

Imipenem

Front 125

Imipenem Always administered with what and why

Back 125

Always administered with cilastatin (inhibitor of renal dihydropeptidase I) to ↓
inactivation in renal tubules.

With imipenem, “the kill is
LASTIN’ with ciLASTATIN.”

Front 126

Drug of choice for Enterobacter.

Back 126

Imipenem/cilastatin, meropenem

Front 127

Vancomycin

Mechanism and resistance

Back 127

Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Resistance occurs with amino acid change of D-ala D-ala to
D-ala D-lac.

Front 128

Vancomycin

Clinical use

Back 128

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

Front 129

Vancomycin

Toxicity

Back 129

Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing––“red man syndrome”
(can largely prevent by pretreatment with antihistamines and slow infusion rate). Well tolerated in general––does NOT have many problems.

Front 130

Nephrotoxicity, Ototoxicity, Thrombophlebitis, diffuse flushing

Back 130

“red man syndrome” Vancomycin

Front 131

Inhibits cell wall mucopeptide formation by binding D-ala D-ala portion of cell wall precursors. Bactericidal. Resistance occurs with amino acid change of D-ala D-ala to
D-ala D-lac.

Back 131

Vancomycin

Front 132

30S inhibitors:

Back 132

A = Aminoglycosides [bactericidal]
T = Tetracyclines [bacteriostatic]

Front 133

50S inhibitors:

Back 133

C = Chloramphenicol, Clindamycin
E = Erythromycin [bacteriostatic]
L = Lincomycin [bacteriostatic]
L = Linezolid [bacteriostatic]

Front 134

Aminoglycosides

names

Back 134

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin.

“Mean” GNATS canNOT
kill anaerobes.

Front 135

Aminoglycosides

Mechanism and resistance

Back 135

Bactericidal; inhibit formation of initiation complex and cause misreading of mRNA. Require O2 for
uptake; therefore ineffective against anaerobes.

Front 136

Aminoglycosides

Clinical use

Back 136

Severe gram-negative rod infections. Synergistic with
β-lactam antibiotics. Neomycin for bowel surgery.

Front 137

Aminoglycosides

Toxicity

Back 137

Nephrotoxicity (especially when used with cephalosporins ,Ototoxicity (especially when
used with loop diuretics). Teratogen.
-“Mean” GNATS canNOT kill anaerobes.

Front 138

Severe gram-negative rod infections. Synergistic with
β-lactam antibiotics.

Back 138

Aminoglycosides

Front 139

Bactericidal; inhibit formation of initiation complex
and cause misreading of mRNA. Require O2 for
uptake; therefore ineffective against anaerobes.

Back 139

Aminoglycosides

Front 140

Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin.

Back 140

Aminoglycosides

Front 141

Tetracyclines

names

Back 141

-CYCLINE

TetracCYCLINE, doxyCYCLINE, demecloCYCLINE, minoCYCLINE.

Front 142

Tetracyclines

Mechanism

Back 142

bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.

Front 143

Tetracyclines

Clinical use

Back 143

VACUUM THe BedRoom.
Vibrio cholerae, Acne, Chlamydia, Ureaplasma
Urealyticum, Mycoplasma pneumoniae, Tularemia,
H. pylori, Borrelia burgdorferi (Lyme disease), Rickettsia.

Front 144

Tetracyclines

Toxicity

Back 144

GI distress, discoloration of teeth and inhibition of
bone growth in children, photosensitivity.

Front 145

bind to 30S and prevent attachment of aminoacyl-tRNA; limited CNS penetration.

Back 145

Tetracyclines

Front 146

Tetracyclines

contraindications

Back 146

-Doxycycline is fecally eliminated and can be used
in patients with renal failure.
-Contraindicated in pregnancy.

Front 147

Must NOT take with milk, antacids, or iron-containing
preparations because divalent cations inhibit its
absorption in the gut.

Back 147

Tetracyclines

Front 148

GI distress, discoloration of teeth and inhibition of
bone growth in children, photosensitivity.

Back 148

Tetracyclines

Front 149

Macrolides

names

Back 149

Erythromycin, azithromycin, clarithromycin.

Front 150

Macrolides

Mechanism

Back 150

Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S

Front 151

Macrolides

Clinical use

Back 151

URIs, pneumonias, STDs––gram-positive cocci (streptococcal infections in patients
allergic to penicillin), Mycoplasma, Legionella, Chlamydia, Neisseria.

Front 152

Macrolides

Toxicity

Back 152

GI discomfort (most common cause of noncompliance), acute cholestatic hepatitis,
eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral
anticoagulants.

Front 153

eosinophilia, skin rashes. Increases serum concentration of theophyllines, oral
anticoagulants.

Back 153

Macrolides

Front 154

Inhibit protein synthesis by blocking translocation; bind to the 23S rRNA of the 50S

Back 154

Macrolides

Front 155

Clindamycin

Mechanism

Back 155

Blocks peptide bond formation at 50S ribosomal subunit.

Front 156

Clindamycin

Clinical use

Back 156

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

Front 157

Clindamycin

Toxicity

Back 157

Pseudomembranous colitis (C. difficile overgrowth),
fever, diarrhea.

Front 158

Sulfonamides

names

Back 158

Sulfamethoxazole (SMX), sulfisoxazole, triple sulfas, sulfadiazine.

Front 159

Sulfonamides

Mechanism

Back 159

PABA antimetabolites inhibit dihydropteroate synthase.

Front 160

Sulfonamides

Clinical use

Back 160

Gram-positive, gram-negative, Nocardia, Chlamydia. Triple sulfas or SMX for simple UTI.

Front 161

Sulfonamides

Toxicity

Back 161

Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (TIN), kernicterus in infants, displace other drugs from albumin (e.g., warfarin).

Front 162

Hypersensitivity reactions, hemolysis if G6PD deficient, nephrotoxicity (TIN), kernicterus in infants, displace other drugs from albumin (e.g., warfarin).

Back 162

Sulfonamides

Front 163

Trimethoprim

Mechanism

Back 163

Inhibits bacterial dihydrofolate reductase.

Front 164

Trimethoprim

Clinical use

Back 164

Combination TMP-SMX used for recurrent UTIs, Shigella,Salmonella, Pneumocystis carinii pneumonia.

Front 165

Trimethoprim

Toxicity

Back 165

Trimethoprim = TMP:
“Treats Marrow Poorly.”

Megaloblastic anemia, leukopenia, granulocytopenia.
(May alleviate with supplemental folinic acid.)

Front 166

Why TMP with SMX

Back 166

synergy

Front 167

Trimethoprim

Toxicity Tx

Back 167

Megaloblastic anemia, leukopenia, granulocytopenia.
(May alleviate with supplemental folinic acid.)

Front 168

Fluoroquinolones

names

Back 168

-Floxacin (fluoroquinolones)

and

nalidixic acid (a quinolone).

Front 169

Fluoroquinolones

Mechanism

Back 169

Inhibit DNA gyrase (topoisomerase II)

Front 170

Fluoroquinolones

Clinical use

Back 170

Gram-negative rods of urinary and GI tracts (including Pseudomonas), Neisseria,

Front 171

Fluoroquinolones

Toxicity

Back 171

GI upset, superinfections, skin rashes, headache,
dizziness.
Contraindicated in pregnant women and in children damage to cartilage. Tendonitis and tendon rupture in adults;
leg cramps and myalgias in kids.
FluoroquinoLONES hurt
attachments to your
BONES.

Front 172

GI upset, superinfections, skin rashes, headache,
dizziness.
Contraindicated in pregnant women and in children damage to cartilage. Tendonitis and tendon rupture in adults;
leg cramps and myalgias in kids.

Back 172

Fluoroquinolones

Front 173

Inhibit DNA gyrase (topoisomerase II)

Back 173

Fluoroquinolones

Front 174

Metronidazole

Mechanism

Back 174

Forms toxic metabolites in the bacterial cell.

Front 175

Metronidazole

Clinical use

Back 175

GET GAP on the Metro!
Anaerobic infection below
the diaphragm.

Antiprotozoal. Giardia, Entamoeba, Trichomonas,
Gardnerella vaginalis, anaerobes (Bacteroides,
Clostridium). Used with bismuth and amoxicillin (or tetracycline) for “triple therapy” against H. Pylori.

Front 176

Metronidazole

Toxicity

Back 176

Disulfiram-like reaction with alcohol; headache, metallic taste.

Front 177

Disulfiram-like reaction with alcohol; headache, metallic taste.

Back 177

Metronidazole

Front 178

Polymyxins

names

Back 178

Polymyxin B, polymyxin E.

Front 179

Polymyxins

Mechanism

Back 179

’MYXins MIX up membranes.

Bind to cell membranes of bacteria and disrupt
their osmotic properties. Polymyxins are cationic, basic proteins that act like detergents.

Front 180

Polymyxins

Clinical use

Back 180

Resistant gram-negative infections.

Front 181

Polymyxins

Toxicity

Back 181

Neurotoxicity, acute renal tubular necrosis.

Front 182

Anti-TB drugs

names and complications

Back 182

INH-SPiRE (inspire). 2C

-Isoniazid (INH),
-Streptomycin,
-Pyrazinamide,
-Rifampin,
-Ethambutol.
-Cycloserine (2nd-line therapy).

All are hepatotoxic.

Front 183

Isoniazid aka

Back 183

INH

Front 184

INH aka

Back 184

Isoniazid

Front 185

Isoniazid (INH)

Mechanism

Back 185

↓ synthesis of mycolic acids.

Front 186

Isoniazid (INH)

Clinical use

Back 186

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

Front 187

Isoniazid (INH)

Toxicity

Back 187

"INH Injures Neurons and
Hepatocytes"

Hemolysis if G6PD deficient, neurotoxicity, hepatotoxicity, SLE-like syndrome.
Pyridoxine (vitamin B6) can prevent neurotoxicity.

Front 188

Isoniazid (INH)

half-life

Back 188

Different INH half-lives in fast
vs. slow acetylators.

Front 189

Rifampin

Mechanism

Back 189

Inhibits DNA-dependent RNA polymerase.

Front 190

Rifampin

Clinical use

Back 190

Mycobacterium tuberculosis; delays resistance to
dapsone when used for leprosy. Used for meningococcal prophylaxis and chemoprophylaxis in contacts of children with
Haemophilus influenzae type B.

Front 191

Rifampin

Toxicity

Back 191

Minor hepatotoxicity and drug interactions (↑ P-450).

orange body fluids

Front 192

Inhibits DNA-dependent RNA polymerase.

Back 192

Rifampin

Front 193

↓ synthesis of mycolic acids.

Back 193

Isoniazid (INH)

Front 194

Minor hepatotoxicity and drug interactions (↑ P-450).

orange body fluids

Back 194

Rifampin

Front 195

Rifampin mnemonic

Back 195

Rifampin’s 4 R’s:
RNA polymerase inhibitor
Revs up microsomal P-450
Red/orange body fluids
Rapid resistance if used
alone

Front 196

Resistance mechanisms for various antibiotics

Penicillins/
cephalosporins

Back 196

β-lactamase cleavage of β-lactam ring

Front 197

Resistance mechanisms for various antibiotics

β-lactamase cleavage of β-lactam ring

Back 197

Penicillins/
cephalosporins

Front 198

Resistance mechanisms for various antibiotics

Aminoglycosides

Back 198

Modification via acetylation, adenylation, or phosphorylation

Front 199

Resistance mechanisms for various antibiotics

Modification via acetylation, adenylation, or phosphorylation

Back 199

Aminoglycosides
and
Chloramphenicol (acetylation only)

Front 200

Resistance mechanisms for various antibiotics

Vancomycin

Back 200

Terminal D-ala of cell wall component replaced with D-lac; ↓ affinity.

Front 201

Resistance mechanisms for various antibiotics

Terminal D-ala of cell wall component replaced with D-lac; ↓ affinity.

Back 201

Vancomycin

Front 202

Resistance mechanisms for various antibiotics

Chloramphenicol

Back 202

Modification via acetylation

Front 203

Resistance mechanisms for various antibiotics

Macrolides

Back 203

Methylation of rRNA near erythromycin’s ribosome-binding site

Front 204

Resistance mechanisms for various antibiotics

Methylation of rRNA near erythromycin’s ribosome-binding site

Back 204

Macrolides

Front 205

Resistance mechanisms for various antibiotics

↓ uptake or ↑ transport out of cell

Back 205

Tetracycline

Front 206

Resistance mechanisms for various antibiotics

Tetracycline

Back 206

↓ uptake or ↑ transport out of cell

Front 207

Resistance mechanisms for various antibiotics

Sulfonamides

Back 207

Altered enzyme (bacterial dihydropteroate synthetase), ↓ uptake, or ↑ PABA synthesis

Front 208

Resistance mechanisms for various antibiotics

Altered enzyme (bacterial dihydropteroate synthetase), ↓ uptake, or ↑ PABA synthesis

Back 208

Sulfonamides

Front 209

Nonsurgical antimicrobial prophylaxis

Meningococcal infection

Back 209

Rifampin (drug of choice), minocycline.

Front 210

Nonsurgical antimicrobial prophylaxis

Rifampin (drug of choice), minocycline.

Back 210

Meningococcal infection

Front 211

Nonsurgical antimicrobial prophylaxis

Gonorrhea

Back 211

Ceftriaxone.

Front 212

Nonsurgical antimicrobial prophylaxis

Ceftriaxone.

Back 212

Gonorrhea

Front 213

Nonsurgical antimicrobial prophylaxis

penicillin.

Back 213

Syphilis (Benzathine penicillin G)

Endocarditis with surgical or dental procedures (penicillin)

Front 214

Nonsurgical antimicrobial prophylaxis

Syphilis

Back 214

Benzathine penicillin G.

Front 215

Nonsurgical antimicrobial prophylaxis

TMP-SMX.

Back 215

-History of recurrent UTIs

Pneumocystis jiroveci
pneumonia

Front 216

Nonsurgical antimicrobial prophylaxis

-History of recurrent UTIs

Back 216

TMP-SMX.

Front 217

Nonsurgical antimicrobial prophylaxis

Back 217

TMP-SMX (DOC) , aerosolized pentamidine.

Front 218

Nonsurgical antimicrobial prophylaxis

Endocarditis with surgical or dental procedures

Back 218

Penicillins.

Front 219

Amphotericin B

Mechanism

Back 219

Amphotericin “tears” holes in
the fungal membrane by forming pores.

Binds ergosterol (unique to fungi); forms membrane
pores that allow leakage of electrolytes and
disrupt homeostasis.

Front 220

Amphotericin B

Clinical use

Back 220

Used for wide spectrum of systemic mycoses.
Cryptococcus, Blastomyces, Coccidioides,
Aspergillus, Histoplasma, Candida, Mucor (systemic mycoses). Intrathecally for fungal meningitis; does not cross blood-brain barrier.

Front 221

Amphotericin B

Toxicity

Back 221

Fever/chills (“shake and bake”), hypotension, nephrotoxicity, arrhythmias, anemia, IV phlebitis
(“amphoterrible”). Hydration reduces nephrotoxicity.

Front 222

Nystatin

mechanism

Back 222

Binds to ergosterol, disrupting fungal membranes

Front 223

Nystatin

Clinical use

Back 223

Too toxic for systemic use.

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

Front 224

Binds to ergosterol, disrupting fungal membranes. Too toxic for systemic use.

Back 224

Nystatin

Front 225

-AZOLES

Mechanism

Back 225

Inhibit fungal steroid (ergosterol) synthesis. by blocking the final step from Lanosterol to ergosterol

Front 226

-AZOLES

Clinical use and which ones

Back 226

Systemic mycoses. Fluconazole for cryptococcal meningitis in AIDS patients and candidal
infections of all types (i.e., yeast infections). Ketoconazole for Blastomyces, Coccidioides,
Histoplasma, Candida albicans; hypercortisolism.

Front 227

-AZOLES

Toxicity

Back 227

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

Front 228

Inhibit fungal steroid (ergosterol) synthesis. by blocking the final step from Lanosterol to ergosterol

Back 228

-AZOLES

Front 229

Flucytosine

Mechanism

Back 229

Inhibits DNA synthesis by conversion to fluorouracil, which competes with uracil.

Front 230

Flucytosine

Clinical use

Back 230

Used in systemic fungal infections (e.g., Candida, Cryptococcus).

Front 231

Flucytosine

Toxicity

Back 231

Nausea, vomiting, diarrhea, bone marrow suppression.

Front 232

Terbinafine
Mechanism

Back 232

Inhibits the fungal enzyme squalene epoxidase. by blocking the initial step from squaline to Lanosterol (in ergesterol synthesis)

Front 233

Terbinafine

Clinical use

Back 233

Used to treat dermatophytoses (especially onychomycosis).

Front 234

Inhibits the fungal enzyme squalene epoxidase. by blocking the initial step from squaline to Lanosterol (in ergesterol synthesis)

Back 234

Terbinafine

Front 235

Caspofungin

Mechanism

Back 235

Inhibits cell wall synthesis.

Front 236

Caspofungin

Clinical use

Back 236

Invasive aspergillosis.

Front 237

Caspofungin

Toxicity

Back 237

GI upset, flushing.

Front 238

Tx for Invasive aspergillosis.

Back 238

Caspofungin

Front 239

Griseofulvin

Mechanism

Back 239

Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing
tissues (e.g., nails).

Front 240

Griseofulvin

Clinical use

Back 240

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea,
ringworm).

Front 241

Griseofulvin

Toxicity

Back 241

Teratogenic, carcinogenic, confusion, headaches, ↑ P-450 and warfarin metabolism.

Front 242

antifunfal that is Teratogenic, carcinogenic, confusion, headaches, ↑ P-450 and warfarin metabolism.

Back 242

Griseofulvin

Front 243

Oral treatment of superficial infections; inhibits growth of dermatophytes (tinea,
ringworm).

Back 243

Griseofulvin

Front 244

Interferes with microtubule function; disrupts mitosis. Deposits in keratin-containing tissues

Back 244

Griseofulvin

Front 245

Amantadine

Mechanism

Back 245

“A man to dine” takes off his
coat.

Blocks viral penetration/uncoating (M2 protein); may buffer pH of endosome. Also causes the
release of dopamine from intact nerve terminals.

Front 246

Amantadine

Clinical use

Back 246

Prophylaxis and treatment for influenza A and rubellA; Parkinson’s disease.

Front 247

Amantadine

Toxicity

Back 247

Ataxia, dizziness, slurred speech.

Front 248

Amantadine

Mechanism of resistance

Back 248

Mutated M2 protein. In 2006, 90% of influenza A were resistant to amantadine.

Front 249

Amantadine

mnemonic

Back 249

Amantadine blocks influenza
A and rubellA and causes problems with the cerebellA.

Front 250

Rimantidine

Back 250

a derivative of Amantadine with fewer CNS side effects. Does not cross the BBB.

Front 251

a derivative of Amantadine with fewer CNS side effects. Does not cross the BBB.

Back 251

Rimantidine

Front 252

Zanamivir, oseltamivir

Mechanism

Back 252

Inhibit influenza neuraminidase. So release of progeny virus is decreased.

Front 253

Zanamivir, oseltamivir

Clinical use

Back 253

Both influenza A and B.

Front 254

Blocks viral penetration and uncoating (M2 protein);

Back 254

Amantadine

Front 255

Inhibit influenza neuraminidase

Back 255

Zanamivir, oseltamivir

Front 256

Ribavirin

Mechanism

Back 256

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.

Front 257

Ribavirin

Clinical use

Back 257

RSV, chronic hepatitis C.

Front 258

Ribavirin

Toxicity

Back 258

Hemolytic anemia. Severe teratogen.

Front 259

drug for

RSV, chronic hepatitis C.

Back 259

Ribavirin

Front 260

Inhibits synthesis of guanine nucleotides by competitively inhibiting IMP dehydrogenase.

Back 260

Ribavirin

Front 261

Acyclovir

Mechanism

Back 261

Preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine
kinase.

Front 262

Acyclovir

Clinical use

Back 262

HSV, VZV, EBV. Mucocutaneous and genital herpes lesions. Prophylaxis in
immunocompromised patients.

Front 263

Acyclovir

Toxicity

Back 263

Delirium, tremor, nephrotoxicity.

Front 264

Acyclovir

Mechanism of resistance

Back 264

Lack of thymidine kinase.

Front 265

drug for

Prophylaxis and treatment for influenza A;
Parkinson’s disease.

Back 265

Amantadine

Front 266

drug for

Both influenza A and B.

Back 266

Zanamivir, oseltamivir

Front 267

drug for

CMV, especially in immunocompromised patients.

Back 267

Ganciclovir

Front 268

Ganciclovir

Mechanism

Back 268

Phosphorylation by viral kinase; preferentially inhibits CMV DNA polymerase.

Front 269

Ganciclovir

Clinical use

Back 269

CMV, especially in immunocompromised patients.

Front 270

Ganciclovir

Toxicity

Back 270

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

Front 271

Ganciclovir

Mechanism of resistance

Back 271

Mutated CMV DNA polymerase or lack of thymidine kinase.

Front 272

Preferentially inhibits viral DNA polymerase when phosphorylated by viral thymidine kinase.

Back 272

Acyclovir

Front 273

Phosphorylation by viral kinase; preferentially inhibits CMV DNA polymerase.

Back 273

Ganciclovir

Front 274

Foscarnet

Mechanism

Back 274

FOScarnet = pyroFOSphate
analog.

Viral DNA polymerase inhibitor that binds to the
pyrophosphate binding site of the enzyme. Does not require activation by viral kinase.

Front 275

Foscarnet

Clinical use

Back 275

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

Front 276

Foscarnet

Toxicity

Back 276

Nephrotoxicity.

Front 277

Foscarnet

Mechanism of resistance

Back 277

Mutated DNA polymerase.

Front 278

drug for

CMV retinitis in immunocompromised patients
when ganciclovir fails;

Back 278

Foscarnet

Front 279

drug for

acyclovir-resistant HSV.

Back 279

Foscarnet

Front 280

HIV therapy
Protease inhibitors

names

Back 280

SaquiNAVIR, ritoNAVIR, indiNAVIR, nelfiNAVIR, ampreNAVIR.

NAVIR (navir) tease a pro—
pro-tease inhibitors.

Front 281

HIV therapy
Protease inhibitors

Mechanism

Back 281

Inhibit assembly of new virus by blocking protease
in progeny virions.

Front 282

HIV therapy
Protease inhibitors

Toxicity

Back 282

GI intolerance (nausea, diarrhea), hyperglycemia,
lipodystrophy, thrombocytopenia (indinavir).

Front 283

HIV therapy
Reverse transcriptase inhibitors
Nucleosides

names

Back 283

DINE , SINE, and BINE

Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC),
stavudine (d4T), lamivudine (3TC),

Front 284

Zidovudine (AZT), didanosine (ddI), zalcitabine (ddC),
stavudine (d4T), lamivudine (3TC),

Back 284

HIV therapy
Reverse transcriptase inhibitors
Nucleosides

Front 285

SaquiNAVIR, ritoNAVIR, indiNAVIR, nelfiNAVIR, ampreNAVIR.

Back 285

HIV therapy
Protease inhibitors

NAVIR (navir) tease a pro—
pro-tease inhibitors.

Front 286

HIV therapy
Reverse transcriptase inhibitors
Non-nucleosides

names

Back 286

Nevirapine, efavirenz, delavirdine.

Never Ever Deliver nucleosides.

Front 287

Nevirapine, efavirenz, delavirdine.

Back 287

HIV therapy
Reverse transcriptase inhibitors
Non-nucleosides

Never Ever Deliver nucleosides.

Front 288

HIV therapy
Reverse transcriptase inhibitors

Mechanism

Back 288

Preferentially inhibit reverse transcriptase of HIV;
prevent incorporation of viral genome into host DNA.

Front 289

HIV therapy
Reverse transcriptase inhibitors

Toxicity

Back 289

Bone marrow suppression (neutropenia, anemia),
peripheral neuropathy, lactic acidosis (nucleosides), rash (non-nucleosides), megaloblastic anemia (AZT).

Front 290

HIV therapy
Reverse transcriptase inhibitors

Clinical use

Back 290

Highly active antiretroviral therapy (HAART) generally entails combination therapy with protease inhibitors and reverse transcriptase.
AZT is used during pregnancy to reduce risk of fetal
transmission.

Front 291

HAART

when initiated

Back 291

protease inhibitors and reverse transcriptase
inhibitors. Initiated when patients have low CD4
counts (< 500 cells/mm3) or high viral load.

Front 292

HIV therapy

what is used during pregnancy to reduce risk of fetal
transmission.

Back 292

AZT

Front 293

Interferons

Mechanism

Back 293

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

Front 294

Interferons

Clinical use

Back 294

IFN-α––chronic hepatitis B and C, Kaposi’s sarcoma.
IFN-β––MS.
IFN-γ––NADPH
oxidase deficiency.

Front 295

Interferons

Toxicity

Back 295

Neutropenia.

Front 296

Antibiotics to avoid in pregnancy

just names

Back 296

SAFE Moms Take Really Good Care.

Sulfonamides, Aminoglycosides,
Fluoroquinolones, Erythromycin, Metronidazole, Tetracyclines, Ribavirin,
Griseofulvin, Chloramphenicol

Front 297

Antibiotics to avoid in pregnancy problem/cause

Sulfonamides

Back 297

kernicterus

Front 298

Antibiotics to avoid in pregnancy problem/cause

kernicterus

Back 298

Sulfonamides

Front 299

Antibiotics to avoid in pregnancy problem/cause

Aminoglycosides

Back 299

ototoxicity

Front 300

Antibiotics to avoid in pregnancy problem/cause

ototoxicity

Back 300

Aminoglycosides

Front 301

Antibiotics to avoid in pregnancy problem/cause

Fluoroquinolones

Back 301

cartilage damage.

Front 302

Antibiotics to avoid in pregnancy problem/cause

cartilage damage.

Back 302

Fluoroquinolones

Front 303

Antibiotics to avoid in pregnancy problem/cause

Erythromycin

Back 303

acute cholestatic hepatitis in mom

Front 304

Antibiotics to avoid in pregnancy problem/cause

acute cholestatic hepatitis in mom

Back 304

Erythromycin

Front 305

Antibiotics to avoid in pregnancy problem/cause

Metronidazole

Back 305

mutagenesis.

Front 306

Antibiotics to avoid in pregnancy problem/cause

mutagenesis.

Back 306

Metronidazole

Front 307

Antibiotics to avoid in pregnancy problem/cause

teratogenic.

Back 307

Ribavirin
Griseofulvin

Front 308

Antibiotics to avoid in pregnancy problem/cause

Tetracyclines

Back 308

discolored teeth, inhibition of bone growth.

Front 309

Antibiotics to avoid in pregnancy problem/cause

discolored teeth, inhibition of bone growth.

Back 309

Tetracyclines

Front 310

Antibiotics to avoid in pregnancy problem/cause

Ribavirin

Back 310

teratogenic.

Front 311

Antibiotics to avoid in pregnancy problem/cause

Griseofulvin

Back 311

teratogenic.

Front 312

Antibiotics to avoid in pregnancy problem/cause

“gray baby.”

Back 312

Chloramphenicol

Front 313

Antibiotics to avoid in pregnancy problem/cause

Chloramphenicol

Back 313

“gray baby.”

Front 314

uses of Antiparasitic drugs

Ivermectin

Back 314

Onchocerciasis (rIVER blindness treated with IVERmectin).

Front 315

uses of Antiparasitic drugs

Praziquantel

Back 315

Trematode/fluke (e.g., schistosomes, Paragonimus, Clonorchis)

cysticercosis (tania solium)
Diphilobotorum latum

Front 316

uses of Antiparasitic drugs

Primaquine

Back 316

Latent hypnozoite (liver) forms of malaria (Plasmodium vivax, P. ovale).

Front 317

uses of Antiparasitic drugs

Nifurtimox

Back 317

Chagas’ disease, American trypanosomiasis (Trypanosoma cruzi ).

Front 318

uses of Antiparasitic drugs

Suramin

Back 318

African trypanosomiasis (sleeping sickness).