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HLSC 220 > Antibacterial Drugs > Flashcards

Antibacterial Drugs Flashcards

1
Q

Invaders

A

-Prokaryotes
-Eukaryotes
-Viruses

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2
Q

Prokaryotes

A

-cell with no nuclei
-Bacteria- cause most infectious diseases

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3
Q

Eukaryotes

A

-Cells with nuclei
-Fungi
-Protozoa
-Helimiths

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4
Q

Viruses

A

-Live off human cells

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5
Q

Chemo therapy

A

-Drugs that are “selectively toxic”
-Minimal effect on host

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6
Q

Antibacterial attack

A

Bacteria

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7
Q

antifungals attack

A

-Fungus
-yeast

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8
Q

antivirals attack

A

viruses

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9
Q

antiparasitic attack

A

parasites

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10
Q

anthelmintics attack

A

helmiths

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11
Q

antiprotozoal attack

A

protozoa

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12
Q

antineoplastics attack

A

tumor cells

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13
Q

Bacterial infections (necrotizing fasciitis)

A

-flash eating disease
-caused by a variety of bacteria

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14
Q

Prokaryotic cells

A

-Average size (1-5 mcm)
-can survive a wide range of environments (hot or cold)
-pathogenic + non-pathogenic

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15
Q

Prokaryotic infections

A

-invasion and multiplication of organisms
-may be caused by bacteria of normal flora (immunocompromised)

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16
Q

prokaryotic colonization

A

-increase in bodies of normal flora colonies
-not usually harmful, can help control growth of potentially pathogenic organisms

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17
Q

Bacteria are described by

A

-Shape
-oxygenation
-Gram + and Gram -

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18
Q

Bacteria shapes

A

-cocci (circular) + bacilli (rod like)
-Staphylococci (cocci in clumps)
-Streptococci (Cocci in chains)

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19
Q

Bacteria oxygenation

A

-Aerobes (oxygenated)
-Anaerobes (deoxygenated)

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20
Q

Bacterial cell wall

A

-Gram + or Gram -
-Does wall stain or not
-fundamental differences in wall structure
-implications for actions with antibacterial

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21
Q

What does the bacterial cell wall do

A

-outside plasma membrane
-structural support
-protection

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22
Q

Gram positive

A

-thick peptidoglycan (up to 40 layers)
-Gram stain (crystal violet) trapped in peptidoglycan layer

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23
Q

Gram Negative

A

-thin peptidoglycan
-outer membrane
-less gram stain is trapped
-LPS layer to some antibacterial

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24
Q

Peptidoglycan

A

-polymer of amino acids and sugars
-not in eukaryotes

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25
Q

Antibacterial is interchangeable with

A

antibiotics

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26
Q

Antibacterial are

A

Meds used to treat bacterial infections
-exploit the differences between human and bacterial cell

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27
Q

antibacterial must

A

legally identify causative organisms before antibacterial therapy
-potential susceptibility

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28
Q

Antibacterial can be effective against

A

-gram neg
-gram pos

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29
Q

Narrow spectrum

A

selective against one class of bacteria
-better

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30
Q

Broad spectrum

A

effective against both classes of bacteria

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31
Q

how do antibacterial effect bacteria (2 ways)

A

Antibacterial either kill or slow bacteria growth so immune system can attack
-bactericidal
-bacteriostatic

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32
Q

Bactericidal

A

lethal to bacteria at clinically achievable concentrations

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33
Q

Bacteriostatic

A

slows bacteria growth so immune system can attack

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34
Q

the immune system

A

is critical to help the body control + eliminate infections

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35
Q

What else is important other than antibacterials

A

host defenses/immune system

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36
Q

Superinfection

A

new microbes take over when antibiotics kill normal flora
-microbes resistant to drug action = difficult to treat

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37
Q

Opportunistic infection

A

infections that wouldn’t normally happen in an immunocompetent person
-immunocompromised
-existing colonization becomes infection

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38
Q

What can become opportunistic infections

A

-virus
-fungi
-protozoa

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39
Q

How many people die due to drug resistance

A

-globally 5 million
-even against last resort drugs
-little resistance to new drugs

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40
Q

Why does resistance occure

A

select mutant bacteria are enhanced due to
-improper choice of antibacterial
-too dose
-dose not continued long enough
-improper treatment
-prophylactic use of antibacterial (animal food)

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41
Q

Host factors to antibacterial therapies

A

-age
-allergies
-organ health
-site of infection
-pregnancy
-persons general health

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42
Q

Allergic reactions

A

-immune response
-GI upset isn’t an allergic reaction

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43
Q

Antibacterial mechanism of action

A

-Disruption of critical metabolic reaction
-interference with cell wall synthesis
-interference with protein synthesis
-interference with DNA replication

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44
Q

Antibiotics that affect cell wall synthesis

A

-penicillins
-vancomycin
-cephalosporins

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45
Q

Antibiotics that impact transcription mechanisms

A

floroquinulones

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46
Q

Antibiotics that affect protein synthesis

A

-macrolides
-tetracyclines
-aminoglycosides

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47
Q

Antibiotics that affect metabolic pathways

A

-sulfamethoxazole
-trimethoprim

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48
Q

Sulfonamides: Metabolic inhibitors

A

-broad spectrum
-sulfa-drug
-bacteriostatic

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49
Q

Sulfonamides: drugs

A

-sulfamethoxazole
-sulfadiazine (prevent synthesis of folic acid)

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50
Q

Sulfonamides: indications

A

-combined with trimethoprim (co-trimoxazole)
-reaches effective concentrations in urinary tract
-Bactrim or septra for URI and otitis media

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51
Q

Sulfonamides: other clinical uses

A

-upper respiratory tract infections
-malaria
-chlamydia

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52
Q

Sulfonamides: contraindications

A

-known allergy: applies to other derivatives of sulfa drugs (antidiabetic agents, thiazide and loop diuretics)
-Pregnant women
-not advised for breast feeding
-not for infants less than 2 months

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53
Q

Sulfonamides: what happens when its given during pregnancy

A

-1st trimester = birth defects

-end of pregnancy increases bilirubin = jaundice
-end of pregnancy kemicterus (brain damage)

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54
Q

Sulfonamides: Adverse effects

A

-integumentary system (allergies/hypersensitivity)
-blood (bone marrow depression = agranulocytosis, thrombopenia, aplastic anemia)
-GI (nausea + vomiting)

55
Q

B-lactam Antibiotics:

A

-sir alexander flemming (1928)
-bacterium staphylococcus aures destroyed by the mold penicillium notatu
-inhibit cell wall enzyme responsible for peptidoglycan synthesis

56
Q

What effect do B-lactam Antibiotics have

A

Bactericidal

57
Q

B-lactam Antibiotics: 4 groups

A

-penicillin
-cephalosporins
-carbapenems
-monobactams

58
Q

B-lactam Antibiotics: characterized by

A

B-lactam ring structure

59
Q

Penicillin: two types

A

-naturally occurring
-semi-synthetic

60
Q

Penicillin: natural

A

sensitive to B-lactamase

61
Q

Penicillin: Semi-synthetic

A

-B-lactamase resistant
-broad spectrum (aminopenicillins)
-extended spectrum (anti-pseudomonal penicillin’s)

62
Q

Penicillin: narrow spectrum

A

-Penicillin G (penicillin/benzylpenicillin)
-penicillin V

63
Q

Penicillin: B-lactamase resistant and penicillinase resistant

A

Cloxacillin

64
Q

Penicillin: broader spectrum

A

-Amoxicillin (acid stable)
-ampicillin

65
Q

Penicillin: Anti-pseudomonal

A

-Extended spectrum
-Ticarcillin
-Piperacillin
-works against pseudomonas aeruginosa infections

66
Q

Penicillin: Pseudomonas aeruginosa infections

A

-in immunocompromised, cystic fibrosis
-Respiratory tract
-ears
- UTIs
-eyes
-CNS
-endocarditis

67
Q

Penicillin: Mechanism of Action

A

-enter bacteria
-in cell bind to penicillin building protein
-normal cell wall synthesis disrupted
-bacteria cell ruptures
-don’t kill other body cells

68
Q

Penicillin: attack method

A

bactericidal
-affects most gram pos and some gram neg

69
Q

Penicillin: Drug Resistance

A

-some bacteria produce penicillin killing enzymes
-Bacteria make B-lactamases

70
Q

Penicillin: beta-lactamases

A

split Beta-lactam rings

71
Q

Penicillin: Beta-lactam inhibitors

A

-used with penicillin’s to combat beta-lactamases
-Clavanic acid
-tazobactam

72
Q

Penicillin: indications

A

-Gram pos bacteria
-broad/extended types kill gram neg

73
Q

Penicillin: Administration

A

-PO
-IM
-IV

74
Q

Penicillin: G is administered

A

IV

75
Q

Penicillin: V is administered

A

PO

76
Q

Penicillin: Adverse Effects

A

-most common drug allergy
~skin rashes
~subcutaneous edema- lips
~can be fatal
-generally well tolerated
-GI problems (nausea, vomiting, diarrhea, abnormal pain)

77
Q

Cephalosporins

A

-semi-synthetic derivatives from cephalosporium fungus
-structurally + pharmacologically related to penicillin’s

78
Q

Cephalosporins: attack method

A

bactericidal

79
Q

Cephalosporins: are ___ antibiotics

A

Beta-lactam

80
Q

Cephalosporins: are organized into___ ranging from

A

Divided into groups generations, ranging from better gram negative coverage to better Beta-lactamase resistance

81
Q

Cephalosporins: Generation 1 vs. 5

A

-1: best gram neg coverage, worst beta-lactam resistance
- Middle generations gradually change
-5: worse gram neg coverage, best beta-lactam resistance

82
Q

Cephalosporins: first gen

A

-Cefazolin (IV)
-Cephalexin (PO)
-Cefadroxil
-Surgical prophylaxis, UTIs, Otitis media

83
Q

Cephalosporins: Second gen

A

-good gram pos coverage
-better gram neg coverage then gen 1
-Cefuroxime (PO) -surgical prophylaxis
-Cefoxitin (IV + IM)

84
Q

Cephalosporins: Third gen

A

-Broader spectrum (better gram neg)
-Cefotaxime (IV + IM) -easily passes meninges into CSF
-Cefixime (PO) -best oral cephalosporin against gram neg

85
Q

Cephalosporins: Third gen is best for

A

Treating meningitis

86
Q

Cephalosporins: fourth gen

A

-broader spectrum of antibacterial activity (especially against gram neg)
-Cefepime

87
Q

Cephalosporins: fifth gen

A

-Broadest spectrum (kills gram neg well)
-Ceftaroline (MRSA infections)

88
Q

Cephalosporins: Adverse Effects

A

-generally well tolerated
-GI problems (nausea, vomiting, diarrhea, abnormal pain)
-Allergies

89
Q

Carbapenems: action is

A

Broad spectrum

90
Q

Carbapenems: Broad spectrum attacks

A

-gram pos
-gram neg
-anerobic
-effective for mixed infections

91
Q

Carbapenems: Don’t affect what infections

A

MRSA infections

92
Q

Carbapenems: must be given __ not __

A

must be given IV not PO

93
Q

Carbapenems: drugs, are used in

A

-imipenem
-meropenem
- used in combination therapy

94
Q

Carbapenems: reserved for

A

severe complicated body cavity and connective tissue infections

95
Q

Carbapenems: are classified as __ for infections ___

A

last resort antibacterial for infections that can’t be treated by narrow drugs

96
Q

Carbapenems: Drug resistance

A

-Carbapenem-resistant entero-bacteriaceae (CRE)
-Klebsiella pneumonia carbapenemases (KPC) and New-dehli metallo-beta lactamase (NDM)- enzymes that break down Carbapenems

97
Q

Carbapenems: opportunistic infections

A

are veery hard to treat

98
Q

Carbapenems: treat bacteria that are

A

resistant to most antibacterial

99
Q

Macrolides: size and drugs

A

-Very large
-Erythromycin
-Azithromycin
-Clarithromycin

100
Q

Macrolides: Mechanism of action

A

-Inhibit protein synthesis
-Broad spectrum
-Bacteriostatic and Bactericidal (depending on concentration)

101
Q

Macrolides: Given to people with what allergies/resistances

A

-allergies to Beta-lactam antibacterial
-Penicillin resistances

102
Q

Macrolides: Azithromycin
and Clarithromycin are used

A

in combination therapy for those with HIV/AIDs to stop opportunistic infections

103
Q

Macrolides: Treat infections of

A

-Respiratory, skin, soft tissues
-Strep
-Streptococcus pyogenes (group A beta-hemolytic streptococci)
-Mild to moderate upper respiratory tract infections
-Hemophilus influenzae
-Spirochetal infections
-Syphilis + Lyme disease
-Gonorrhea
-Chlamydia
- Mycoplasma

104
Q

Macrolides: Adverse Effects

A

-GI Disturbances (Nausea, Vomiting, diarrhea)
-Provoke cardiac dysrhythmias (long Q-T)

105
Q

Macrolides: Azithromycin
and Clarithromycin adverse efects

A

-Fewer drug-drug interactions (Theophylline, warfarin, cyclosporin)
-little to no inhibition of CYP enzymes

106
Q

Tetracyclines: Mechanism of action

A

-Broad spectrum
-Inhibit protein synthesis
-Bacteriostatic

107
Q

Tetracyclines: Drugs

A

-Tetracycline
-Doxycycline
-Minocycline
-Demeclocycline

108
Q

Tetracyclines: Indications

A

-Gram neg and gram pos
-Bind to metal ions

109
Q

Tetracyclines: Bind to what metal ions

A

-Bind to Ca2+, Mg2+, Iron, and aluminum

110
Q

Tetracyclines: Don’t take at the same time as what products

A

-Don’t take at the same time as any metal ion products
-Milk, supplements, laxatives, antacids

111
Q

Tetracyclines: why can’t you take these with metal ions

A

-form insoluble complexes (Chelation)
-Which passes out of the body reducing absorption

112
Q

Tetracyclines: Adverse effects

A

-Strong affinity for calcium
-GI disturbances
-Gut flora disturbances (Candida, Colitis/C-diff)
-Photosensitivity
-Antagonistic to bactericidal antibiotics (Time 1h apart)

113
Q

Tetracyclines: Do NOT give to, why

A

-Pregnant people
-Breastfeeding moms
-Children younger then 8 years
-Due to calcium binding (Tooth discoloration, bone deformities)

114
Q

Aminoglycosides:

A

-Amino Sugars
-Natural and synthetic (produced from streptomyces)
-First effective bacteria against gram neg

115
Q

Aminoglycosides: mechanisms of action

A

-Bactericidal
-Prevents abnormal protein synthesis
-Attack mostly gram neg and some gram pos

116
Q

Aminoglycosides: Drug types

A

-Gentamicin
-Neomycin
-Streptomycin
-Tobramycin
-Amikacin

117
Q

Aminoglycosides: Indicators

A

-Acts against gram neg
-used best in combination

118
Q

Aminoglycosides: are given, because

A

-Parenterally due to poorly absorbed through GI given parenterally (IM or IV)
-Given orally or as enema to decontaminate prior to surgery

119
Q

Aminoglycosides: Adverse effects

A

Serious toxicities
-Ototoxicity
-Nephrotoxicity

120
Q

Aminoglycosides: Ototoxicity

A

Hearing or balancing loss
-Irreversible
-Ringing (tinnitus)
-Deafness
-Vestibular (balance)

121
Q

Aminoglycosides: What makes ototoxicity worse

A

-Made worse if other ototoxic drugs are given

122
Q

Aminoglycosides: Nephrotoxicity

A

-Reversable
-Extreme neonates + existing renal conditions
-Measure protein, urea, serum creatine levels, BUN

123
Q

Aminoglycosides: Nephrotoxicity steps to limit

A

-Time each dose and test blood to limit effects
-Monitor drug plasma levels

124
Q

Aminoglycosides: What increases nephrotoxicity risk

A

-Vancomycin (antibacterial)
-Cyclosporine (Immunosuppressant)
-Amphotericin B (Antifungal)

125
Q

Quinolone’s or Fluroquinolones: Drug types

A

-Ciprofloxacin (Effective and most common)
-Norfloxacin
-Gemifloxacin
-Levofloxacin
-Gemifloxacin

126
Q

Quinolone’s or Fluroquinolones: Mechanism of Action

A

-Bactericidal
-Gram neg and some gram pos
-Alters DNA of bacteria

127
Q

Quinolone’s or Fluroquinolones: Indications

A

-UTI
-Lower respiratory tract infection
-Bone and Joint infections
-Infectious diarrhea
-Skin infections
-STD
-Anthrax

128
Q

Quinolone’s or Fluroquinolones: Adverse Effects

A

-GI (Nausea, Vomiting, Diarrhea)
-Skin (Rashes)
-CNS (Headaches, dizziness)

129
Q

Quinolone’s or Fluroquinolones: Interactions

A

-Drug-Drug (CYP inhibition)-Theophylline (asthma), Warfarin
-Oral absorption reduced by (antacids, iron, zinc, calcium containing preparations)- give 1-2h prior to drugs

130
Q

Vancomycin: methods of action

A

-Inhibits cell wall synthesis
-Bactericidal
-Only protein target to Beta-lactams

131
Q

Vancomycin: Administration

A

-IV

132
Q

Vancomycin: Indications

A

-MRSA and other gram pos infections
-Oral for Pseudomembranous colitis

133
Q

Vancomycin: Adverse Effects

A

-Resistance increasing
-Infusion rate-related (infuse over 1h)
-Fever, chills, phlebitis
-Ototoxicity
-Nephrotoxicity

134
Q

Vancomycin: What do you do to reduce adverse effects

A

Blood drug monitoring

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