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GT BSN/CNL PHARM > Antibiotics > Flashcards

Antibiotics Flashcards

1
Q

definition: bactericidal

A

lethal to bacterial

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2
Q

definition: bacteriostatic

A

slows bacterial growth

(allows for host defenses to eliminate bacteria)

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3
Q

definition: broad spectrum antibiotic

A

active against a wide variety of bacteria

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4
Q

definition: narrow spectrum antibiotic

A

active only against a few species of microorganisms

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5
Q

How does antibiotic resistance develop?

A

Spontaneous (RANDOM) mutation occurs that prevents bacteria from being killed by antibiotic.

Remainder of bacteria are killed by antibiotic, resistant organism remains and replicates freely (unless killed by host)

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6
Q

definition: superinfection

A

new infection that appears during course of treatment for primary infection

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7
Q

What we do that can result in development of resistant bacteria

A
  1. use antibiotics unnecessarily
  2. use broad spectrum instead of narrow spectrum antibiotics
  3. too long of an antibiotic course
  4. stopping the full course too early
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8
Q

Prior to starting antibiotics, what should be done first?

A

obtain cultures

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9
Q

List drugs/drug classes that disrupt bacterial cell walls

A

penicillins
cephalosporins
vancomycin
lipoglycoproteins
daptomycin

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10
Q

are drugs that disrupt bacterial cell walls bacteriostatic or bactericidal?

A

bactericidal

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11
Q

mechanism of action of drugs that disrupt bacterial cell walls

A

allow for H2O influx into bacteria –> cell bursts & dies

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12
Q

What is the significance of a drug containing a beta lactam ring?

A

Some bacterial strains can develop beta lactamase enzymes that break open the beta lactam ring = inactive antibiotic

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13
Q

Mechanism of action of penicillins

A

bind penicillin binding proteins (PBPs) on bacterial cell = weakening of bacterial cell wall

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14
Q

How can resistance develop to penicillins?

A

beta lactamase
alteration of PBP expression (drug cant bind)

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15
Q

List some penicillins.

A

PCN G, PCN V
nafcillin
oxacillin
ampicillin
amoxicillin
piperacillin

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16
Q

Route of administration of PCN G

A

IV or IM

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17
Q

adverse effects PCN G

A

allergy reactions
injection site reactions

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18
Q

Which drug results in the most anapylaxis

A

PCN

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19
Q

Treatment of PCN induced anaphylaxis

A

supportive care: cardiopulmonary support
epinephrine

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20
Q

If your patient is allergic to PCN G, which other drugs may be of concern

A

Other PCNs
cephalosporins (maybe!)

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21
Q

What is a beta lactamase inhibitor

A

drug that inhibits the enzyme that inactivates PCN

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22
Q

Name some beta lactamase inhibitors (never available to be given alone though!)

A

subactam
clavulanate
tazobactam

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23
Q

List three drugs that are PCNs combined with beta lactamase inhibitors

A

unasyn
augmentin
zosyn

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24
Q

Do PCNs have a beta lactam ring

A

yes

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25
Q

Do cephalosporins have a beta lactam ring

A

yes

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26
Q

mechanism of action of cephalosporins

A

bind PBPs and disrupt cell wall synthesis

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27
Q

Two trends in cephalosporins as the generations go from 1–>5 are:

A
  1. increased ability to reach the CSF
  2. increased resistance to beta lactamases
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28
Q

Excretion of cephalosporins

A

unchanged by kidneys (lower the dose in ESRD or CKD)

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29
Q

Name some commonly used cephalosporins

A

ceftriaxone
cefazolin
cefepime
cephalexin

30
Q

List the carbapenems

A

imipenem
meropenem
ertapenem

31
Q

Do carbapenems contain a beta lactam ring?

A

yes

32
Q

Mechanism of action of carbapenems

A

same as PCN
(bind PBPs, disrupt cell wall = lysis)

resistant to beta lactamase

33
Q

What is MRSA

A

staph infection that is resistant to all beta lactam antibiotics

(this bacterial strain produces a PBP that has a low affinity for antibiotics)

34
Q

Drug of choice for MRSA

A

vancomycin

35
Q

Does vancomycin contain a beta lactam ring

A

no

36
Q

Mechanism of action of vancomycin

A

inhibit cell wall synthesis by binding & inhibiting precursors to cell wall

(NOT PBP binding)

37
Q

elimination of vancomycin

A

unchanged by kidneys (decreased dose in ESRD/CKD)

38
Q

Adverse effects of vancomycin

A

renal failure
ototoxicity (rare)
rapid infusion can = histamine release
red man syndrome

(histamine release
–> flushing/rash/itching
–> tachycardia/hypotension/angioedema)

39
Q

Max rate of infusion of vancomycin

A

1g/hr

40
Q

What is red man syndrome

A

allergic reaction to vancomycin
- flushing
- hypotension & tachycardia
- N/V
- itching
- angioedema
- rash: face, neck, upper torso

41
Q

Treatment of red man syndrome

A

supportive
antihistamines

42
Q

mechanism of action of daptomycin

A

insert self in bacterial cell membrane & allow for K+ efflux
proteins can’t be manufactured & cell death occurs

43
Q

adverse effects of daptomycin

A

+/- muscle injury

44
Q

List drugs that affect bacterial protein synthesis

A

tetracyclines
macrolides
clindamycin
linezolid
aminoglycosides

45
Q

Are drugs that affect bacterial protein synthesis bactericidal or bacteriostatic?

A

bacteriostatic

46
Q

List some tetracyclines

A

tetracycline
doxycycline

47
Q

mechanism of action of tetracyclines

A

prevent addition of further amino acids (inhibit bacterial protein synthesis)

48
Q

Adverse effects of tetracyclines

A

GI irritation
teeth discoloration
hepatotoxicity
renal toxicity
photosensitivity

49
Q

Who to avoid tetracyclines in?

A

Pregnancy >4m
Peds <8yrs

50
Q

List some macrolides

A

erythromycin
azithromycin
clarithromycin

51
Q

mechanism of action of macrolides

A

block addition of new amino acids (prevents synthesis of bacterial proteins)

52
Q

adverse effects of macrolides

A

epigastric pain, N/V, diarrhea

can prolong QT interval in high [ ]

53
Q

mechanism of action of clindamycin

A

prevents addition of amino acids on bacterial proteins

54
Q

mechanism of action of linezolid

A

prevents addition of amino acids on bacterial proteins

55
Q

adverse effects of linezolid

A

reversible myleosuppression (monitor CBC)
rarely neuropathy with prolonged therapy

56
Q

List some aminoglycosides

A

gentamicin
tobramycin
amikacin

57
Q

Mechanism of action of aminoglycosides

A

inhibit bacterial protein synthesis + aid in production of abnormal (inactive) proteins

58
Q

route of administration of aminoglycosides

A

at the site of infection (cannot be absorbed from GI tract)

PO if GI infection
IV if systemic infection
topical if skin infection

59
Q

goal peak & trough of aminoglycosides

A

peak = high enough to kill bacteria
trough = low (avoid toxicity)

60
Q

adverse effects of aminoglycosides

A

irreversible ototoxicity (tinnitus/HA –> hearing loss)

nephrotoxicity (usually reversible)

**monitor trough levels for prevention of both

61
Q

List two drugs/classes that disrupt bacterial DNA function

A

fluoroquinolones
metronidazole

62
Q

Are drugs that disrupt bacterial DNA function bactericidal or bacteriostatic

A

bactericidal

63
Q

List some fluoroquinolones

A

ciprofloxacin
ofloxacin
moxifloxacin
levofloxacin

64
Q

adverse effects of fluoroquinolones

A

GI effects
CNS effects (rare)
phototoxicity
tendon rupture

65
Q

Risks for tendon rupture w/ fluoroquinolones

A

age >60
on glucocorticoids
transplant history

66
Q

mechanism of action of metronidazole

A

breaks helical DNA structure –> cell death

67
Q

Mechanism of action of sulfonamides

A

compete with PABA (para-aminobenzoic acid) to decrease DNA/RNA/protein synthesis

68
Q

adverse effects of sulfonamides

A

hypersensitivity reactions (can be severe)
hematologic effects (decrease in all blood levels)
kernicterus
renal damage

69
Q

In which patient ages should sulfonamides be avoided

A

<2m old or >32 weeks gestation

**due to deposition of bilirubin in brain resulting in various neuro deficits and death

70
Q

what is bactrim

A

TMP/SMZ
trimethoprim/sulfamethoxazole

71
Q

adverse effects of trimethoprim

A

itching, rash, GI effects
rare hematologic suppression

72
Q

What is bactrim primarily used for?

A

UTIs

GT BSN/CNL PHARM (26 decks)

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