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IBI Test 2 > B3.022 Las Drogas > Flashcards

B3.022 Las Drogas Flashcards

1
Q

how do inhibitors of cell wall synthesis work?

A

B-lactams and vancomycin block enzymatic steps outside of the cell or in the periplasmic space
other ICWS act at intracellular sites

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2
Q

general workings of penicillin

A

very selective toxicity (high chemotherapeutic index)
bactericidal in growing, proliferating cells
primarily used for gram +

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3
Q

mechanism of action of penicillin

A
  1. covalent binding to transpeptidases/penicillin binding proteins
  2. inhibition of transpeptidase reaction (cross linking of cell wall)
  3. activation of murein hydrolases (autolysins)
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4
Q

penicillin absorption

A

oral
acid-sensitive
can also be parenteral (IV, IM)

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5
Q

penicillin distribution

A

good to most tissues and fluids

poor penetration into eye, prostate and CNS

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6
Q

penicillin metabolism

A

variable

not usually significant

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7
Q

penicillin excretion

A

excretes by tubular secretion (organic acid secretory system)
EXCEPTION: nafcillin in bile
oxa-,cloxa- in urine and bile
short half life

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8
Q

which drugs exhibit time dependent killing

A

pens
cephs
vancomycin
time above MBC relates to efficacy

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9
Q

pen G

pen V

A

primarily useful against gram +

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10
Q

anti staph penicllins

A 
nafcillin
methicillin
oxacillin
cloxacillin
B lactamase resistant
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11
Q

extended spectrum penicillins

A 
ampicillin
amoxicillin
ticarcillin
piperacillin
mezlocillin
extended gram - activity
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12
Q

anti-psuedomonal penicilins

A

ticarcillin
piperacillin
mezlocillin
effective against proteus, pseudomonas

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13
Q

problem w anti-pseudomonal penicillins

A

rapid emergence of resistance
use in combo w aminoglycosides or fluoroquinolones
POWERFUL: use only when indicated, protect therapeutic value

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14
Q

ampicillin rash

A

10% incidence
90% for mononucleosis patients
self limiting, often does not recur

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15
Q

hypersensitivity reaction of penicillins

A 
major adverse effect
10-15% claim allergy
complete cross reactivity
not dependent on dose
rapid onset
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16
Q

other adverse effects of penicillins

A

seizures induced by high doses

particularly in renal failure

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17
Q

3 primary resistance mechanisms to penicillin

A
  1. no cell wall, no activation of murein hydrolases, metabolically inactive
  2. inaccessible PBPs
    - gram neg
    - MRSA
  3. B lactamase production
    - plasmid mediated
    - either use B lactamase resistance pens or co administer B lactamase inhibitor
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18
Q

problems associated with penicillin use/overuse

A

sensitization
selection for resistant strains
superinfections by resistant organisms

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19
Q

general overview of cephalosporins in comparison to penicillin

A

structure and function similar to penicillins
less sensitive to B lactamases
broader spectrum of activity
some cross reactivity w pen-sensitive patients
more expensive than pens

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20
Q

absorption of cephs

A

poor oral

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21
Q

toxicity of cephs

A

more toxic than pens

particularly renal

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22
Q

should you use a pen or ceph?

A

if a pen will work, use it

cephs secondary ICWS

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23
Q

describe the ceph classification system

A 
1, 2, 3, 4 generation
chronology of development and use
as they progress you get:
-greater gram - activity
-some with less gram + activity (2)
-less B lactamase sensitivity
-cephalosporinase resistant (4)
-less toxic
-better distribution (especially to CNS)
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24
Q

first gen ceph

A

cefazolin
cephalexin
narrow spectrum
chemoprophylaxis

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25
Q

second gen ceph

A

cefuroxime
cefotetan
cefaclor
intermediate spectrum

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26
Q

third gen cep

A 
cefotaxime
ceftriaxone
ceftazidime
cefpodoxime
broad spectrum
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27
Q

fourth gen ceph

A

cefepime

broad spectrum

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28
Q

adverse effects of cephs

A

local irritation from injection
renal toxicity–tubular necrosis, interstitial nephritis; may be enhanced by aminoglycosides
hypersensitivity - 1% cross reactivity with penicillins, more common in early generation

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29
Q

disulfram effect

A

cefotetan
cefoperazone
bleeding and platelet disorder (give vitamin K)

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30
Q

other B lactams

A 
monobactams - aztreonam
carbapenems - imipenem
meropenem
B lactamase inhibitors:
-clavulanic acid
-sulbactam
-tazobactam
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31
Q

azetreonam

A

monobactam
gram - activity (doesn’t work against gram + or anaerobes)
B lactamase resistant
crosses blood brain barrier
no cross reactivity in penicillin-sensitive patients

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32
Q

imipenem

A 
carbapenems
broad spectrum (gram +, Gram -, and anaerobes)
B lactamase resistant
IV only
crosses blood-brain barrier
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33
Q

discuss the resistance mechanisms to imipenem

A

pseudomonas develops resistance rapidly, use with aminoglycosides
inactivated by renal dipeptidase in host (co administer Cilastatin)

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34
Q

meropenem

A

dipeptidase-resistant carbapenem

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35
Q

vancomycin mechanism

A 
inhibits transglycosylation (step before transpeptidation)
bactericidal for gram +
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36
Q

vancomycin administration

A

IV for systemic use

oral for C.diff

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37
Q

vancomycin uses

A

MRSA
synergistic w aminoglycosides
vancomycin dependent enterococci

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38
Q

vancomycin excretion

A

IV drug cleared through kidney

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39
Q

vancomycin adverse effects

A

enhances oto- and renal toxicity of aminoglycosides
red neck syndrome - histamine release
misuse/overuse issues

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40
Q

fosfomycin

A

newest ICWS

gram + and gram -

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41
Q

fosfomycin mechanism

A

inhibits cytoplasmic step in cell wall precursor synthesis

active uptake by G6P transporter

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42
Q

fosfomycin administration

A

oral and parenteral
oral only in US
single dose therapy for UTI

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43
Q

fosfomycin metabolism and excretion

A

excreted by kidney

synergistic w B-lactams, aminoglycosides, or fluororquinolones

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44
Q

bacitracin

A

markedly nephrotoxic
topical ONLY
OTC

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45
Q

B lactamase inhibitors:

A
  • clavulanic acid
  • sulbactam
  • tazobactam
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46
Q

membrane active drugs

A

polymixin B

polymixin E

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47
Q

polymixin mechanism

A

basic peptides, act as detergents

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48
Q

polymixin uses

A

gram - EXCEPT proteus and Neisseria
limited to topical use due to systemic toxicity (renal)
salvage therapy for highly resistant Acinetobacter, Pseudomonas, and Enterobacterieae

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49
Q

give an overview of the inhibitors of protein synthesis (IPS) drug class as a whole

A

target is “different” in pathogen than host due to differing ribosome sizes
different sites for different drugs (30S vs 50S)
different steps in protein synthesis blocked by different drugs
most reversible and bacteriostatic (except aminoglycosides)
less selective toxicity than ICWS

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50
Q

tetracyclines mechanism

A

reversible binding to 30S subunit
bacteriostatic
selectivity based on bacterial uptake

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51
Q

tetracyclines pharmacokinetics

A

urually oral, but absorption variable
chelate metal ions
not absorbed (do not administer w food)
rarely given IV

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52
Q

tetracyclines distribution

A

well distributed, except to CNS and synovial fluid
concentrates in teeth, bone, liver, kidney
cross the placenta and are excreted in milk

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53
Q

tetracyclines excretion

A

doxycycline mostly fecal

others mostly urine

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54
Q

clinical uses of tetracyclines

A

first broad spectrum antibiotic
gram + and gram -
mycoplasma, chlamydia, rickettsiae
Lyme disease

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55
Q

tetracycline adverse effects

A

GI irritation
superinfections
impaired liver function (high doses, during pregnancy, pre existing liver disease)
photosensitization
calcium chelation (discoloration, growth retardation, deformity)

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56
Q

resistance to tetracyclines

A

decreased uptake, efflux pumps are major mediators
altered ribosomal proteins or RNA are secondary mechanisms (pseudomonas, proteus)
indiscriminate use/overuse has fostered emergence of resistance

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57
Q

new tetracyclines

A

glycylcyclines (tigecycline)
retain antibacterial spectrum but overcome resistance
not affected by efflux pump
black box warning due to increased risk of death

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58
Q

other tetracyclines

A

tetracycline
doxycycline
minocycline

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59
Q

macrolide antibiotics

A

erythromycin
clarithromycin
azithromycin
bacteriostatic or cidal depending on dose

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60
Q

macrolide pharmacokinetics

A 
absorbed from GI tract, but acid labile
use enteric coating or erythromycin esters
also administered IV
excellent distribution except to CNS
crosses placenta
excreted in bile
half life 1-5 hours EXCEPT azithromycin
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61
Q

clinical uses of macrolides

A

gram + bacteria, same gram - some mycobacteria
backup for penicillins in pen–sensitive patients
azithro and clarithro are broader spectrum
mycoplasma pneumonia, Legionnaires, chlamydia

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62
Q

macrolides adverse effects

A
  1. GI distress
  2. microsomal enzyme inhibition (drug-drug interactions, oral anticoagulant, digoxin, non sedating antihistamines)
  3. hepatotoxicity
63
Q

macrolide resistance

A

staph resistant, some strepto and pneumococci

  • altered rRNA
  • efflux pump
  • esterase which hydrolyzes erythromycins
64
Q

clarithromycin

A

less GI effects

longer half life (6 hours)

65
Q

azithromycin

A

minimal p450 based interactinos
tissue levels 10-100 x higher than plasma levels
t0.5= 2-4 days

66
Q

newer macrolides in general

A

clarith and azith
both higher availability
active against mycobacterium avium-intracellulare in AIDS patients

67
Q

macrolide like: ketolide

A

telithromycin (semi synthetic macrolide)

68
Q

telithromycin administration

A

oral
well absorbed and distributed
metabolized in liver and excreted in bile and urine
once daily dosing

69
Q

telithromycin uses

A

resp tract infections (CAP, bronchitis, sinusitis)

poor substrate for efflux pump

70
Q

telithromycin adverse effects

A

inhibits CYP3A4

QT prolongation

71
Q

aminoglycosides mechanism

A

bactericidal irreversible inactivation of 30S ribosome

multiple effects on translation, misreading of mRNA, interference with initiation, breaking up polysomes

72
Q

aminoglycosides pharmacokinetics

A 
poor oral absorption, usually IV or IM
good distribution, except eye and CNS
 no significant host metabolism
excreted unchanges
very high conc in proximal tubule cells
73
Q

aminoglycosides cell killing type

A 
concentration dependent (also fluoroquinolones)
peak serum concentration related to extent of killing
higher peak = increased efficacy
74
Q

aminoglycoside drugs

A 
gentamycin (older)
tobramycin
amikacin
streptomycin (older)
neomycin
spectinomycin
75
Q

aminoglycoside uses

A

non resistant gram - infections
E.coli, proteus, pseudomonas
use older first, save newer for when they’re needed

76
Q

when treating pseudomonas w aminoglycosides…

A

use gentamicin > tobramycin >amikacin

77
Q

spectinomycin use

A

used against pen resistant gonococci

78
Q

adverse effects of aminoglycosides

A 
nephrotoxicity
-high concentration in renal cortes
-5-25% receiving more than 3 days show renal impairment
-usually reversible
ototoxicity
-high conc in inner ear
5-25% of patients
-may be reversible
-loss of vestibular and/or auditory function
79
Q

dose and time dependency of aminoglycosides

A

plasma conc and time at high conc are critical factors in adverse effects
monitor closely
once daily dosing

80
Q

neuromuscular blockade of aminoglycosides

A

very high dose phenomenon
most common during surgery
also in myasthenia gravis patients

81
Q

aminoglycosides resistance

A

emerges rapidly is used alone
increased bacterial metabolism
alteration in bacterial uptake
altered target

82
Q

chloramphenicol mechanism

A

bacteriostatic

broad spectrum

83
Q

chloramphenicol pharmacokinetics

A

well absorbed from all routes
CNS levels = serum levels
100% excreted in urine
glucuronidation in liver is rate limiting step for inactivation/clearance

84
Q

chloramphenicol resistance

A

plasmid mediated
chloramphenicol acyl transferase
slow development
only slight resistance

85
Q

chloramphenicol adverse effects

A

GI disturbances followed by fungal superinfections
anemia due to bone marrow depression
aplastic anemia (irreversible and often fatal)
gray baby syndrome (cant clear drug)
drug-drug interactions

86
Q

chloramphenicol clinical uses

A

powerful, but use limited by toxicity and resistance
typhoid fever
rocky mountain spotted fever

87
Q

clindamycin mechanism

A

lincosamide antibiotic
bacteriostatic
well absorbed and distributed

88
Q

clindamycin uses

A

bacteroides fragilis, other anaerobes
MRSA
endocarditis prophylaxis

89
Q

clindamycin adverse effects

A

GI upset
C. difficile
superinfections
hepatotoxicity

90
Q

what are the streptogramins

A

quinupristin

dalfopristin

91
Q

streptogramins mechanism

A

peptide macrolactones
potent inhibitor of CYP 3A4
block sites affected by macrolides and clindamycin

92
Q

streptogramins uses

A

bacteriostatic against enterococcus faecium
bactericidal against others
approved for use against vanco- and multi drug resistant enterococcus faecium, and MRSA

93
Q

streptogramins administration

A

IV
80% excreted in bile, 20% excreted in urine
no cross resistance with any other IPS

94
Q

oxazolidinones (linezolid) mechanism

A

prevents formation of 70S ribosome

no cross resistance with other IPS

95
Q

linezolid administration

A

IV or oral

good distribution to tissues

96
Q

linezolid uses

A

bactericidal against streptococci
bacteriostatic against staphylococci and enterococci
primary indication - vancomycin resistant E. faecium

97
Q

linezolid adverse effects

A

bone marrow suppression

thrombocytopenia (reversible and mild)

98
Q

what are the two classes of anti-folates

A

inhibitors of folate synthesis
-p-Aminobenzoic acid analogs (PABA)
inhibitors of folate use
-dihydrofolate reductase inhibitors

99
Q

sulfonamides

A

sulfamethoxazole
sulfasalazine (salicylazosulfapyridine)
silver sulfadiazine
co-trimoxazole

100
Q

sulfonamides mechanism

A

PABA analogs
enter into a normal metabolic pathway, but then block the pathway
competitive inhibitor of dihydrofolate synthesis
bacteriostatic

101
Q

sulfonamide pharmacokinetics

A 
oral, some topical (burns), rarely IV
well absorbed from GI, well distributed including to CNS
variable metabolism
acetylation yields inactive metabolite
excreted in urine
10-20x blood conc in urine
102
Q

clinical uses of sulfonamides

A

topical for burns (silver)
UTI
ulcerative colitis (sulfasalazine)
rarely used as single agents (combine with trimethoprim)

103
Q

sulfonamide adverse effects

A 
allergic reactions: fever, rash
-up to 5% incidence
-may cross react with other sulfonamides
stevens-johnson syndrome
-fever, malaise, rare but can be fatal
crystalluria/hematuria
hematopoietic effects
hemolytic anemias
104
Q

sulfonamide resistance

A

overproduction of PABA
loss of permeability
new form of dihydropteroate synthetase (discriminated between PABA and sulfonamide)

105
Q

which drug exhibits dihydrofolate reductase inhibition activity?

A

trimethoprim- blocks bacterial enzyme

106
Q

trimethoprim administration

A

readily absorbed from GI
wide distribution, including CNS
excreted in urine

107
Q

trimethoprim uses

A

can be used alone for UTI, but usually combined with a sulfonamide
trimethoprim-sulfamethoxazole (co-trimoxazole)
pneumocystis pneumonia
combo is bactericidal

108
Q

trimethoprim adverse effects

A 
10000x more effective against bacterial DHFR than mammalian, but still may see "anti-folate" effects
megaloblastic anemia
leukopenia
granulocytopenia
treat with folinic acid
109
Q

AIDS patients receiving co-trimoxazole

A 
much higher incidence of adverse effects
fever
rashes
leukopenia
diarrhea
110
Q

DNA gyrase inhibitors

A 
quinolones
-nalidixic acid
fluoroquinolones
-ciprofloxacin
-levofloxacin
111
Q

DNA gyrase inhibitor mechanism

A

nalidixic acid:
-inhibits bacterial topoisomerase II; transcription, and DNA replication
-inhibits bacterial topoisomerase IV; DNA replication
fluoroquinolones:
-fluorinated analogues of nalidixic acid

112
Q

fluoroquinolones pharmacokinetics

A

well absorbed and distributed
oral (parenteral forms available too)
20% is metabolized in liver
excreted in urine

113
Q

fluoroquinolones use

A

excellent for gram -
moderate for gram +
gram - in GI and UTIs
promise for resp, skin, and soft tissue infections – especially for multi drug resistant organisms

114
Q

fluoroquinolones adverse effects

A 
some GI
Less:
-headaches
-dizziness
-insomnia
-abnormal liver function
connective tissue disorder?
115
Q

drugs used as urinary tract antiseptics

A

use systemic agents which are efficiently cleared in urine

-pens, aminoglycosides, sulfas, fluoroquinolones

116
Q

issues w urinary tract antiseptics

A

resistance and reinfection common

may need to suppress bacteria for a long time

117
Q

alternative drug for urinary tract

A

nitrofurantoin

118
Q

nitrofurantoin mechanism

A

unknown, maybe oxidative stress

bacteriostatic or cidal depending on organism

119
Q

nitrofurantoin pharmacokinetics

A

rapidly absorbed, metabolized and excreted in urine
oral
NOT systemic even as IV

120
Q

clinical use of nitrofurantoin

A

UTI, gram + or gram -

most effective if urine pH < 5.5

121
Q

nitrofurantoin adverse effects

A

anorexia
GI distrubances
occasional hemolytic anemia, leukopenia, hepatotoxicity

122
Q

nitrofurantoin resistance

A

all pseudomonas

some proteus

123
Q

when is anti-mycobacterial chemotherapy used

A

tuberculosis and leprosy
chronic infections with long dormant period separating intermittent active (symptomatic) periods
intracellular pathogens

124
Q

duration of anti-tuberculosis therapies

A 
uncomplicated - 6-9 mo
chemoprophylaxis - 1 year
TB meningitis - 2 years
resistance develops rapidly to single drugs
combo is the general rule
125
Q

1st line anti-mycobacterials

A 
isoniazid
ethambutol
rifampin
streptomycin
pyrazinamide
dapson
126
Q

2nd line anti-mycobacterials

A

cycloserine
ethionamide
capreomycin
para-aminosalicylic acid (PAS)

127
Q

isoniazid mechanism

A

blocks synthesis of mycolic acids for cell wall

bactericidal in growing cells only

128
Q

isoniazid pharmacokinetics

A

well absorbed and distributed
oral
CNS 20-100% of serum; intracellular = extracellular
acetylated in liver
fast acetylators require higher doses
-50% of US blacks and whites, most Asians, native americans
excreted in urine

129
Q

isoniazid clinical uses

A

prophylaxis - used alone

combo therapy for TB - w ethambutol, rifampin, or pyrazinamide

130
Q

isoniazid adverse effects

A

dose and duration dependent
hepatotoxicity
peripheral and central neuropathy (treat with pyridoxine)

131
Q

isoniazid resistance

A

rapid development
10% of US isolates
higher in Caribbean and asia (20%)
deletion of katG gener in mycobacterium

132
Q

rifampin mechanism

A

inhibits bacterial RNA synthesis

bactericidal

133
Q

rifampin pharmacokinetics

A

well absorbed and distributed

excreted in bile

134
Q

rifampin adverse effects

A

inducer of microsomal enzymes (alters t0.5 of anticoagulants, oral contraceptives, other drugs)
hepatotoxic
flu like syndrome
orange body fluids

135
Q

clinical use of rifampin

A

combination chemo for active disease

single agent prophylaxis for INH intolerant patients or INH resistant bug

136
Q

ethambutol mechanism

A

inhibits synthesis of mycobacterial cell wall glycan

137
Q

ethambutol pharmacokinetics

A

well absorbed and distributed
CNS levels variable, but usually therapeutic
most excreted in urine

138
Q

ethambutol adverse effects

A

dose dependent optic neutitis
decreased acuity
loss of red green differentiation

139
Q

pyrazinamide pharmacokinetics

A

oral
absorbed and distributed
bacteriostatic

140
Q

pyrazinamide mechanism

A

activated by mycobacterium
blocks membrane functions
rapid resistance if used alone

141
Q

pyrazinamide adverse effects

A

causes hyperuricemia (gouty arthritis) in up to 40%
1-5% incidence of hepatotoxicity
contraindicated in pregnancy

142
Q

what is characteristic of 2nd line anti-TB drugs?

A

toxicity outweighs therapeutic effects except for highly resistant strains
-PAS, cycloserine, ethionamide
currently a resurgence in TB, highly resistant strains are common

143
Q

what drug is used to treat leprosy?

144
Q

dapsone pharmacokinetics

A

well absorbed and distributed
concentrates in skin, muscle, liver, and kidney
acetylated and excreted in feces and urine

145
Q

dapsone adverse effects

A

hemolysis

methemoglobinemia

146
Q

dapsone uses

A

used in combo with rifampin and clofazimine for M. leprae

P. jroveci pneumonia

147
Q

bactericidal drugs

A 
aminoglycosides
bacitracinB lactams
isoniazid
metronidazole
polymixins
pyrazinamide
quinolones
quinpristin-dalfopristin
rifampin
vancomycin
148
Q

bacteriostatic drugs

A 
chloramphenicol
clindamycin
ethambutol
linezolid
macrolides
nitrofurantoin
sulfonamides
tetrcyclines
trimethoprim
149
Q

why shouldn’t you combine static and cidal drugs?

A

cidal inhibit cells that are growing

if you stop growth with a static agent, there is nothing for the cidal agent to kill

150
Q

ototoxic drugs

A

aminoglycosides

vancomycin

151
Q

hematopoietic toxic drugs

A

chloramphenicol

sulfonamides

152
Q

hepatotoxic drugs

A

tetracyclines
isoniazid
erythromycin
clindamycin

153
Q

renal toxic drugs

A

cephalosporins
vancomycin
aminoglycosides
sulfonamides

IBI Test 2 (10 decks)

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