Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

Drugs with highest risk of CDAD

A

clindamycin, ampicillin, cephalosporins and fluoroquinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Drugs to treat CDAD

A

metronidazole or vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What should you use to treat UTI empirically

A

co-trimoxazol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How are most antibiotics cleared

A

excretion by the kidney, consideration for young and elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

antibiotics cleared by the kidney (7)

A

aminoglycosides, vancomycin, cephalosporins, sulfonamides/trimethoprim, extended spectrum penicillins, carbapenems, ethambutol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

antibiotics cleared by the liver (7)

A

Clindamycin, macrolides, chloramphenicol, tetracyclines, metronidazole, isoniazid, rifampin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which drugs are class D for birth defects

A

aminoglycosides and tetracyclins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

antibiotics with placental and breast milk transfer

A

1) aminoglycoside ototoxicity during fetal development

2) sulfonamide induced kernicterus in nursing infants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most common sources of antibiotic allergy (4)

A

beta lactams (penicillin), sulfonamides, trimethoprim, and erythromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the most important difference between gram+ and gram- bacterial

A

gram negative bacteria have an outermembrane which makes them more difficult to penetrate with antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the main MOA of penicillin

A

irreversible inhibition of transpeptidases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

structure of penicillins

A

Beta-lactam ring fused to a 5-member thiazolidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Main mechanisms of penicillin resistance (3)

A
  1. Inability to penetrate G- outermembrane
  2. Acquired mutations in PBPs that lower affinity for B-lactam
  3. Beta-lactamases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the standard, narrow-spectrum penicillins?

A

Penicillin G, penicillin V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which standard, narrow-spectrum penicillin is orally effective?

A

Penicillin V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the DOC for syphilis?

A

Penicillin G,V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the penicillinase-resistant penicillins

A

Nafcillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the aminopenicillins?

A

amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What unique property do aminopenicillins have?

A

Positive charge that makes them effective against G-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Antipseudomonal penicillins

A

ticarcillin, piperacillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which penicillins are prescribed with Beta-lactamases

A

Amoxicillin, ticarcillin, piperacillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Repository prep of penicillin and what it is used for

A

Pen G benzathine, syphilis and rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is a Jarisch-Herxheimer reaction

A

rash, fever, flushing after shot due to death of pathogen, typically syphilis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is a side effect specific to ticarcillin

A

sodium overload can be a problem in CHF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is SJS

A

Steven Johnson’s syndrome is a separation of the dermis from the epidermis covering less than 10% of the body. If it covers more it is called toxic epidermal necrolysis (TEN).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the first generation cephalosporins

A

cefazolin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

First generation cephalosporins have which features (3)

A

1) high activity against G+ MSSA and strep
2) Alternative to penicillin when mild allergy exist
3) Prophylaxis before surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the second generation cephalosporins

A

cefoxitin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Second generation cephalosporins have which features (3)

A

1) Better G- than 1st gen
2) Little CNS penetration
3) Largely replaced by gen 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the third generation cephalosporins

A

ceftriaxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Third generation cephalosporins

A

ceftriaxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Third generation cephalosporins have which features (4)

A

1) higher activity against G-
2) CNS penetration
3) Most widely used
4) meningitis, gonorrhea, empiric chlamydia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Fourth generation cephalosporins

A

cefepime

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Fourth generation cephalosporins have which features (3)

A

1) highly resistant to beta-lactamases
2) good CNS penetration
3) treatment of hospitalized patients when resistance is suspected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is special about 5th gen cephalosporins

A

acitivity against MRSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the carbapenems

A

imipenum, cilastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the important features of carbapenems

A

1) Beta-lactam
2) broad spectrum
3) Highly resistant to beta-lactamases
4) only given parenterally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is a unique toxicity of imipenem?

A

seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the monobactams

A

aztreonam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the structure of monobactams

A

contains beta-lactam ring, but not fused with a second ring. Is not an allergen like penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the features of monobactams (4)

A

1) only active against G- bacteria including pseudomonas
2) Given IV, reduced in renal insufficiency
3) resistant to most beta-lactamases
4) Safe for patients with penicillin allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are the glycopeptides

A

vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are glycopeptides used for

A

Generally serious infections with G+ bacteria
Parenteral- sepsis or endocarditis caused by MRSA or sensitive enterococci
In combination with 3rd gen cephalosporins for meningitis
Oral for CDAD if metronidazole is ineffective
Alternative to penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Route of administration for glycopeptides

A

IV for systemic and viral infections

orally to treat GI infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the adverse reactions to glycopeptides (3)

A

1) Ototoxic
2) red man syndrome (histamine reaction)
3) Thrombophlebitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Which cell wall synthesis inhibitor is commonly used for UTI with G- bacteria

A

Fosfomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What is the MOA of fosfomycin

A

inhibits production of murein monomers by inhibiting enolpyruvate transferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is unique about fosfomycin that allows it to treat G- bacteria

A

It enters through a transporter, but mutations confer resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Which cell wall synthesis inhibitor is a component of Neosporin

A

Bacitracin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why is bacitracin only effective against G+ bacteria

A

It works inside the bacteria to inhibit bactoprenol dephosphorylation, it cannot penetrate G- outer membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Which classes of cell wall inhibitors work inside or outside the bacterial cell

A

inside- fosfomycin and bacitracin

outside- vancomycin and beta lactams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are the classes of beta-lactams (4)

A

Penicillins, cephalosporins, carbapenems, and monbactams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are the sizes of the mammalian and bacterial ribosomes and their subunits

A

Bacterial 70S, 30S and 50S

Mammalian 80S, 40S and 60S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the structure of aminoglycosides and what are the consequences?

A

2 or more amino sugars connected by glycoside linkages. Large bulky, cationic, hydrophilic structure. Does not cross membranes attracted to negative LPS

55
Q

What are the aminoglycosides (4)

A

gentamicin, amikacin, streptomycin, neomycin

56
Q

How do aminoglycosides get into bacteria

A

Concentration dependent, passive diffusion through porins, active transport across membrane is O2 dependent. only effective against aerobes. Can be synergistic with cell wall inhibitors

57
Q

Aminoglycosides MOA (3)

A 
Binding to 30S
1) inhibits formation of initiation complex
2) misreading of mRNA
3) blockade of translocation 
Note: has post antibiotic effect
58
Q

Therapeutic considerations for aminoglycosides

A

Narrow spectrum, diminished therapeutic resistance

59
Q

Aminoglycoside used as second line drug for TB

A

Streptomycin

60
Q

aminoglycoside used in hospitals where resistance is common due to susceptibility to inactivation

61
Q

Aminoglycoside in neosporin effective against G- bacteria

62
Q

What are the two Ototoxic antibiotic classes

A

aminoglycosides and glycopeptides (vancomycin)

63
Q

What are the adverse reactions to aminoglycosides (3) and what is a way to avoid them

A

1) ototoxicity
2) nephrotoxicity (mostly bad due to reduced clearance)
3) Neuromuscular blockade with high doses, respiratory paralysis
Can administer once daily in large dose

64
Q

Tetracyclines (3)

A

tetracycline, tigecycline, doxycycline

65
Q

Which two antibiotic classes bind to the 30S ribosomal subunit

A

tetracyclines and aminoglycosides

66
Q

How are tetracyclines transported into the bacterial cell

A

active transport system only present in bacterial cells

67
Q

Administration of tetracyclines

A

Orally (except tigecycline), do not administer with dairy widely distributed

68
Q

Therapeutic profile of tetracyclines

A

broad spectrum antibiotics, rickettsial infections, peridontal disease, acne, prophylaxix of malaria

69
Q

Adverse reactions of tetracyclines (6)

A

1) GI irritation
2) Deposition in bone and teeth, staining
3) renal toxicity, especially if outdated
4) superinfection
5) hepatotoxicity at high doses, esp in preg women
6) photosensitivity

70
Q

Macrolydes (2)

A

erythromycin, azithromycin

71
Q

MOA of macrolydes

A

binds to 50S inhibits translocation

72
Q

Resistance to macrolydes

A

plasma-encoded methylation of 50S

73
Q

Adverse reactions to macrolydes

A

Generally very safe

1) GI irritation is most common, increases motility
2) Cholestatic hepatitis
3) Prolonged Q-T interval

74
Q

What is the prototype oxizolidinone?

75
Q

What is the MOA of oxizolidinones

A

binding to 23S of the 50S subunit, blocks formation of initiation complex. Bacteriostatic

76
Q

What are the Streptogramins?

A

quinupristin-dalfopristin

77
Q

What are the therapeutic uses of oxizolidines

A

MDR G+ pathogens when other agents are not available, due to negative effects like anemia and neuropathy. Have to do blood counts weekly

78
Q

What is the MOA of streptogramins?

A

inhibits Dalfopristin directly inhibits peptidyl transferase center of the 23S rRNA (50S)
Quinupristin binds at the same site as the macrolides
A 30:70 fixed dose combination is bactericidal

79
Q

What is the fluoroquinolones prototype drug

A

ciproflaxin

80
Q

What is the structure of fluoroquinolones

A

fluorinated derivatives of the quinolone, nalidixic acid

81
Q

MOA of fluoroquinolones

A

Inhibits one of the two topoisomerase II enzymes. Bactericidal

82
Q

Pharmacokinetics of fluoroquinolones

A

orally available and widely distributed, cleared renally

83
Q

What is the unique side effect of fluoroquinolones?

A

Tendon rupture, do not give to patients <18

84
Q

What are the therapeutic uses of fluoroquinolones (3)

A

1) Widely used for urogenital, respiratory and GI infections Aerobic G-
2) Prophylaxis for anthrax
3) Respiratory fluoroquinolones

85
Q

Which protein synthesis inhibitor is associated with CDAD?

A

Clindamycin presents in up to 5% patients and may develop weeks after drug withdrawl

86
Q

What other drug class has a similar mechanism to clindamycin?

A

macrolides

87
Q

What type of bacteria is clindamycin used to treat

A

most anaerobic and G+ aerobes

88
Q

Which drug is cheap and effective against a broad spectrum, but not commonly used in the developed world due to toxicities

A

Chloramphenicol

89
Q

Chloramphenicol’s MOA

A

binds to peptidyl transferase center of 50S, prevents attachment of incoming tRNA to A-site

90
Q

What is one condition where chloramphenicol is still used

A

bacterial meningitis

91
Q

What are the main adverse reactions of chloramphenicol (3)

A

1) gray baby syndrome
2) bone marrow suppresion
3) aplastic anemia

92
Q

What are oxizolindones primarily used for therapeutically

A

MDR G+ bacteria, only when others are not effective

93
Q

Adverse reactions to oxizolindones

A

Reversible myelosuppression, blood counts weekly

Neuropathy

94
Q

What drug interaction does linezolid have

A

MAOIs and SSRIs, serotonin syndrome

95
Q

What organisms is quinupristin-dalfopristin affective against

A

G+, G- activity limited

96
Q

Adverse reactions to quinupristin-dalfopristin

A

hyperbilirubinemia (jaundice)
arthralgia /myalgia (joint and muscle pain)
Inhibits CYP3A4

97
Q

Which protein synthesis inhibitors are bacteriocidal

A

aminoglycosides and quinupristin/dalfopristin

98
Q

What are the major resistance mechanisms to protein synthesis inhibitors

A

decreased uptake or efflux

bacterial enzymes that inactivate the drug

99
Q

Major side effects from protein synthesis inhibitors

1) ototoxicity
2) tooth discoloration
3) CDAD
4) aplastic anemia

A

1) aminoglycosides
2) tetracyclines
3) Clindamycin
4) chloramphenicol

100
Q

Protein synthesis that bind the 50S and 30S subunits

A

50S- macrolides and miscellaneous

30S- aminoglycosides and tetracyclins

101
Q

What are the adverse reactions associated with fluoroquinolones

A

1) tendon rupture
2) confusion, visual disturbances in elderly
3) prolong Q-T interval,
4) CDAD

102
Q

What drug interactions do fluoroquinolones have

A

increase theophylline and warfarin

oral absorption reduced if taken with multivalent cations

103
Q

What is the drug of choice to treat CDAD

A

Metronidazole

104
Q

What is the MOA of metronidazole

A

Initiates strand breaks and loss of helical structure, cannot be metabolized by human cells

105
Q

Therapeutic uses of metronidazole (5)

A

1) anaerobic bacterial infections
2) bacterial vaginosis
3) CDAD
4) with tetracycline and bismuth subsalicylate for H.pylori in peptic ulcer disease
5) antiparasitic agent

106
Q

Adverse reactions to metronidazole

A

headache, GI, metallic taste, dark brown urine

107
Q

Drug interactions with metronidazole

A

disulfiram-like reaction with ethanol

inhibits metabolism of warfarin-bleeding

108
Q

Sulfonamine prototype

A

sulfamethoxazole

109
Q

Sulfonamine MOA

A

Structural analog of PABA, bacteriostatic

110
Q

Resistance mechanisms to sulfonamine

A

1) synthesis of PABA to overcome inhibition
2) mutation in dihydropteroate synthase
3) decreased uptake

111
Q

Therapeutic uses of sulfonamides

A

Broad specturm against G-/G+
diminished due to development of resistance and safer alternatives
Mostly in combination with trimethoprim

112
Q

Adverse reactions to sulfonamides

A

1) kernicterus
2) hypersensitivity- Stevens-Johnson syndrome
3) Hemolytic anemia

113
Q

What are the 2 types of folic acid inhibitors

A

sulfonamides, trimethoprim (TMP)

114
Q

What is the MOA of trimethoprim

A

inhibits dihydrofolate reductase (DHFR)

115
Q

Resistance to Trimethoprim

A

1) increased synthesis of DHFR
2) mutated DHFR
3) reduced uptake

116
Q

Adverse reactions to trimethoprim

A

Bone marrow suppression in folate deficient patients

Fatal fetal malformations in experimental animals

117
Q

What is co-trimoxazole

A

Fixed-dose combination of trimethoprim and sulfamethoxazole that has a synergistic bactericidal effect due to inhibition of sequential steps of folate biosynthesis.

118
Q

Therapeutic uses of co-trimoxazole (5)

A

1) UTI, chronic and recurrent
2) oportunistic pneumonia
3) ear infections
4) MSSA + MRSA
5) Shigellosis (diarrhea)

119
Q

What is the third line drug for CDAD

A

Fidoxomicin after metronidozol and vancomycin.

120
Q

What features does fidoxomicin have relative to other treatments for CDAD

A

minimally disruptive to normal GI flora and lowers risk of recurrence.

121
Q

What Nucleic acid synthesis inhibitor is a pro-drug

A

Metronidazol causes DNA strand breaks in anaerobic bacteria

122
Q

Which drug class inhibits bacterial DNA gyrase

A

Fluoroquinolones

123
Q

Which drugs inhibit bacterial RNA polymerase

A

Fidoxamicin and rifampin

124
Q

Major side effects of nucleic acid synthesis inhibitors and their causative agents

A

1) tendon rupture- fluoroquinolones
2) kernicterus, hemolytic anemia- sulfonamides
3) Myelosuppression- SMX and TMP

125
Q

What is the prototype Lipopeptide

A

daptomycin

126
Q

What is the MOA of lipopeptides

A

Calcium dependent insertion of lipophilic tail into plasma membrane forms an ion-permeable channel that permits efflux of intracellular K+

127
Q

Therapeutic uses for daptomycin

A

administered IV, complicated skin, bacteremia and right-sided endocarditis with resistant microbes

128
Q

Adverse reactions to daptomycin

129
Q

What are the polymyxins?

A

colistin, polymyxin B

130
Q

MOA of polymyxins

A

Binds to neg charged LPS in G- bacteria , disrupts plasma membranes

131
Q

What are the two formulations of colistin?

A 
Colistin sulfate (cationic)- oral and GI
Colistimethate (anionic)- parenteral use, prodrug
132
Q

What are the therapeutic uses of colistimethate

A

treatment of last resort for serious MDR G- infections

133
Q

Colistin sulfate therapeutic uses

A

topical for infection of skin, mucous membranes, eye, ear

134
Q

What are the side effects of colistin

A

reversible nephrotoxicity and neurotoxicity

Pharmacology (35 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions