Brainscape's Knowledge GenomeTM

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


See full index

Block 6 Week 4 Colt > Chemotherapy and Antibiotic Resistnace - Kozel > Flashcards

Chemotherapy and Antibiotic Resistnace - Kozel Flashcards

1
Q

T/F: Antibiotics are naturally produced chemicals

A

true

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

Is the ideal antimicrobial bacteriocidal or bacteriostatic?

A

bacteriocidal

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

T/F: resistance can be caused by enzymatic inactiavation of the abx or simply a failure to convert it to its active form

A

true

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

T/F: overproduction of an abx target can cause resistance

A

true

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

(Pharmacokinetics/dynamics) describes the interaction between concentration and antimicrobial effect

A

dynamics

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

Concentration vs. time in tissue and other body fluids determines (blank)

A

pharmacologic or toxic effect

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

Concentration vs. time at site of infection determines (blank)

A

antimicrobial effect

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

What are the pharmacokinectic issues that prevent an abx from reaching the bacteria?

A

absorption from the site of administration
transfer from plasma to site of infection
elimination from plasma
elimination from the site of infection

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

What is the difference between bacteriostatic and bacteriocidal?

A 
cidal= KILL the bacteria
static= inhibit growth but does not kill
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some examples of bacteriocidals?

A

beta lactams, vancomycin, fluoroquinolones, metronidazole, aminoglycosides

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

What are some examples of bacteriostatics?

A

tetracyclines, clindamycin, macrolides, sulfonamides

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

What type of abx relies on the host to kill the microbe?

A

bacteriostatics

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

A combination of antibiotics produces a 2-log10 increase in action relative to each agent alone is known as (blank)

A

syngergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

A synergistic relationship between penicillina nd gentamycin is used to treat (blank)

A

viridans streptococcal meningitis

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

What is the post-abx effect

A

suppresion of growth following exposure to abx

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

Hows does the post-abx effect work?

A

slows growth that the sub- minimum inhibitory concentration (MIC) and alters morphology

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

What effects does post-abx leukocyte enhancement have?

A

increases susceptibility to phagocytosis and phagocytic killing

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

Time > MIC is what type of killing?

A

time-dependent killing

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

Describe the persistent effects of time-dependent killing?

A

minimal to moderate

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

The AUC/MIC ratio shows us the (blank)

A

total exposure of microbe to antimicrobial agent

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

Describe the persistent effects of AUC/MIC?

A

prolonged persistent effects

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

Cmax/MIC ratio shows what type of killing?

A

concentration-dependent killing

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

Describe the persistent effects of Cmax/MIC type killing?

A

prolonged persistent effects

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

Absorption, distribution, and elimination are part of pharmaco(blank)

A

kinetics

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

What two ratios are predictors of outcome for concentration dependent mechanisms?

A

AUC/MIC and Cmax/MIC

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

IN plain english, what does it mean if something is concentration dependent when it kills?

A

higher drug concentrations have a higher rate and extent of bacteriocidal activity

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

What are some examples of concentration dependent abx?

A

aminoglycosides, fluoroquinolones, metronidazole

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

What type of killing is relatively slow

A

TIME dependent killing

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

In time dependent killing, (blank) occurs at low multiples of the MIC

A

saturation of killing

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

What are some examples of time dependent abx?

A

B-lactams and vancomycin

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

T/F: bacteriostatic agents have minimal post-abx effect

A

false; prolonged effect

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

What ratio predicts the outcome of bacteriostatic agents?

A

AUC/MIC

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

What are the natural penicillins?

A

B-lactams

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

What other categories of drugs fall under B-lactams besides penicillin?

A

cephalosporins, carbapenems, Beta lactamase inhibitors

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

The spectrum of the natural penicillins includes (blank)

A

ONLY GRAM POSITIVE

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

T/F: natural penicillins provide the starting material for semisynthetic penicillins

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q 
Carboxypeptidases
Endopeptidases
Transglycosylases
Transpeptidases
Are all examples of (blank) binding proteins
A

penicillin binding proteins

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

what is the function of the penicillin binding proteins?

A

construct the pentapeptide-pentaglycine bridges that cross-link peptidoglycan

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

Describe the MOA of penicillin?

A

Penicllin binds to penicillin binding proteins. PDG cross-linking blocked; cell lysis due to autolytic enzymes that destroy the cell wall

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

T/F: beta lactamase is carried by a plasmid

A

ture

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

T/F: beta lactamase is carried by a transposable chromosome gene

A

true

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

Gram (blank) have an intrinsic ability to block the access of penicillin to PBPs

A

gram negative

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

An altered (blank) protein in N. gonorrheoeae creates penicillin resistance

A

porin

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

Newly resistant strains of S. pneumoniae have what changes to their abx binding site?

A

reduction in number or affinity to the PBP

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

S. pneumoniae, N. gonorrheoeae, and MRSA are all examples of what type of abx resistance?

A

alteration in abx binding site

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

Penicillinase resistant penicillins work by (blank)

A

introducing a bulky R group near the site of hydrolysis

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

What are two examples of penicillinase resistant PCN?

A

methicillin and nafcillin

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

What is the trade off when using a PCNase resistant PCN?

A

they are 1/10th as potent as penicillin G

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

Where is lipoteichoic acid found in the gram pos wall?

A

in the PDG layer above the PM

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

Where is lipid A and O polysacc found in the gram neg wall?

A

OUTER layer of the OUTER membrane

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

Where is PDG found in gram neg?

A

in between the two membranes

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

Where are porins found in the gram neg wall?

A

outer layer of the outer membrane

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

What does O polysacc attach to in the gram neg wall?

A

Lipid A

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

The outer membrane of gram neg resists penetration of (hyrophobic/philic) molecules

A

hydrophobic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

How do you enchance the penetration of PCN thru outer membrane porins?`

A

add a hydrophilic charged group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

T/F: broad spectrum PCNs like ampicillin and carbenicillin have the same sensitivity to PCNases as natural PCN

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

T/F: PCN forms a covalent irreversible bond with PBPs

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

How do PBPs prep the PDG for crosslinking?

A

they remove the D-alanine precursor from PDG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Where in the bacteria do you find PBPs?

A

membrane bound and in the cytosol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How do PBPs aid in abx resistance?

A

overproduction of PBPs and formation of PBPs that have low affinity for PCN; b-lactamase production as well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Which PBP is responsible for causing MRSA ?

A

PBP 2A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Generally speaking, are PCNs cleared rapidly or slowly from the kidneys?

A

rapid secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Are PCNs generally distributed to most tissues?

A

yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Do PCNs penetrate the blood brain barrier?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How do you maximize drug exposure for PCN that use time-dependent killing?

A

optimize your dosing strategy; lower doses more frequently; keep the dose above the MIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Opening of the b-lactam ring allows for binding to host proteins causing the (blank) reaction and creating an allergic reaction

A

hapten

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Disturbances of GI flora is most prominent with what abx?

A

ampicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

An allergic reaction can occur with reactivity to the (blank) ring within PCN

A

thiazolidine ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

T/F: cephalosporins have high immunological cross reactivity with PCN

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

cephalosporins are resistant to what enzyme?

A

b-lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Describe the characterization of the spectrum of cephalosporins from gen’s 1-4?

A
  1. narrrow
  2. expanded
  3. Broad
  4. Extended
    MRSA-active
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What generation of cephalosporin includes gram neg activity that will kill Pseudomonas?

A

3rd gen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

High affinity for (blank) allows for MRSA-active cephalosporin

A

PBP 2A’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Which penicillins are acid labile?

A

PCN G, methicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

which PCNs are acid stable?

A

PCN V; most semi-synthetic PCNs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Differences between acid labile or stable PCNs creates a large variation in (blank)

A

oral absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

T/F: cephalosporins generally have good tissue distribution

A

false; distribution and metabolism varies widely from one to the other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

T/F: cephaolosporins are capable of CNS penetratioN

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How are cephalosporins excreted? In what patients do you need to alter the dosage?

A

Renal excretion; pt’s with renal insufficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the most common side effect of cephalosporins?

A

diarrhea and nausea (GI symptoms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

(blank)-infections are possible with broad spectrum cephalosporins

A

superinfections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What are the three mechanisms by which N. gonorrheoeae is resistant to cephalosporins?

A

altered PBP2A
overexpression of efflux pump
mutation in porin reduces uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Carbapenems, imipenem, and muropenem have what structure?

A

B-lactam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

the modified alpha ring in carbapenems eliminates (blank)

A

sulfur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is the spectrum of carbapenems?

A

HIGH AFFINITY for essential PBPs of gram pos and neg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Carbapenems can penetrate the gram neg outer membrane via a specific (blank)

A

OMP (outer membrane protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Are carbapenems effective against MRSA?

A

NOPE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

The hydroxyethyl at C-6 in carbapenem makes it highly resistant to (blank)

A

beta lactamase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

T/F: carbapenems are only used when the specific microbe is known

A

false; used in empirical therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What is the preferred route of administration of carbapenem? why?

A

pareneterally; poor absorption after oral ingestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Carbapenem is rapidly hydrolyzed by (blank) in the renal tubule

A

peptidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the peptidase inhibitor that blocks renal degradation of imipenem?

A

Cilastatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the side effects of carbapenems?

A

generally well tolerated; can cause allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

NDM-1 plasmid encoding extended spectrum beta lacatamase confers resistance to which abxs?

A

imipenems, all B-lactams, aminoglycosides, tetracyclines, and fluoroquinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

T/F: NDM-1 plasmid is found in common enteric bacilli

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

In what setting do you typically see NDM-1 cause problems?

A

Pts getting elective surgery in SE asia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What are two common b lacatamase inhibitors?

A

clavulanic acid and sulbactam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Why do we use b lactamase inhibitors?

A

used with b lactams with little direct antibacterial action to improve their power

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

what is the MOA of b lactamase inhibitors?

A

SUICIDE INHIBITION; clavulanate will bind to the b-lactamase IRREVERSIBLY (suicide) to prevent it from functioning; forms an acyle enzyme intermediate that is hydrolyzed VERY slowly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

B-lactamase inhibitors are used in conjuction with (blank)ase sensitive b-lactams

A

PCNase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What humongous class of abx inhibits cell wall synthesis?

A

b-lactams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

what drug is used against M. tuberculosis that inhibits cell wall synthesis

A

cycloserine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What class of abx is vancomycin?

A

glycopeptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Where does vancomycin bind on the cell wall?

A

terminal D-ala-D-ala

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What function does vancomycin block?

A

transpeptidation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Is vancoymycin bactericidal or bacteriostatic?

A

bacteriocidal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Vancomycin resistance is (blank) mediated

A

plasma mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are two bugs that are vancomycin resistant?

A

enterococcus spp. and S. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

How do VRE and VRSA avoid vancomycin?

A

they substitute lactate for alanine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

VISA avoids vancomycin how?

A

multiple free ala-ala to act as decoys for vancomycin

111
Q

What is the spectrum of vancomycin and glycopeptide abx?

A

gram pos ONLY

112
Q

T/F: vancomycin is a firstline drug

A

false; drug of LAST RESORT

113
Q

What is the usual route of administration of glycopeptide abx?

A

IV

114
Q

What bug is vancomycin especially useful for?

A

C. diff

115
Q

What is the mode of excretion of vancomycin? what kind of pts should you alter dose for?

A

renal; renal insufficiency

116
Q

vancomycin is (blank)-toxic at high doses

A

ototoxic, nephrotoxic

117
Q

Red Man syndrome is associated with what abx?

A

vancomycin; rapid IgE mediated mast cell degranulation causing red rash

118
Q

Is VRSA or VISA the most common form of resistant S. aureus?

A

VISA

119
Q

Is polymyxin useful againt gram pos or gram neg bacteria? why?

A

gram neg; fatty acid tail penetrates the phospholipid bilyater

120
Q

What is the MOA of polymyxin?

A

leakage of metabolites and disruption of membrane function

121
Q

Is polymyxin bacteriocidal or static?

A

cidal

122
Q

The toxicity of polymyxin limits its use to (blank)

A

topical applications

123
Q

highly resistant strains of Pseudomonas, Klebsiella, and Acinetobacter warrant of use of parenteral (blank)

A

polymyxin

124
Q

Why is polymyxin given in parenterally?

A

not absorbed after oral administration

125
Q

Polymyxin shows dose-related (blank)toxicity

A

nephrotoxicity

126
Q

What abx should be used when an enteric carries that fucking god-awful NDM b lactamase plasmid?

A

Poly-fuckin-myxins

127
Q

P. aeruginosa, A. baumanii, and enterobacteriacaeae that are resistant to all b-lactams, fluoroquinolones, and aminoglycosides should be treated with (blank)

A

polymyxins

128
Q

What is the MOA of quinolones?

A

inhibits DNA synth via inhibition of DNA gyrase

129
Q

are quinolones cidal or static?

A

cidal

130
Q

How can a bug have resistance to quinolones?

A

mutation to DNA gyrase

131
Q

what is the spectrum of quinolones?

A

gram neg and pos

132
Q

what are the clinical uses of quinolones?

A

UTIs and other bacterial infections

133
Q

do quinolones have good oral absorption?

A

yes

134
Q

What is the method of clearance of quinolones?

A

renal

135
Q

What is the most common cause of C. diff colitis?

A

Ciproflaxin!

136
Q

What are the three classes of side effects with quinolones?

A

GI, CNS, and achilles tendon damage

137
Q

what is the trade name of metronidazole?

A

flagyl

138
Q

what is the MOA of metronidazole?

A

PRODRUG reduced to active form by electron transport protein

139
Q

(aerobic/anaerobic) bacteria are able to convert metronizadole prodrug to active form

A

anaerobic via electron transport, strangely

140
Q

T/F: some protozoa have a mechanism that makes them susceptible to metronizadole?

A

true

141
Q

What does metronizadole do once it is converted to its active form?

A

produces cytotoxic compounds that DAMAGE DNA

142
Q

What is the spectrum of mentronidazole

A

obligate anaerobes and many protozoa

143
Q

Does metronidazole work in facultative anerobes or obligate aerobes?

A

nope

144
Q

is metronidazole cidal or static?

A

cidal

145
Q

What drug is given as a prophylaxis in colorectal surgery?

A

metronidazole

146
Q

Trichomonas vaginalis is commonly treated with (blank)

A

flagyl

147
Q

T/F: flagyl has roughly similar blood levels following oral and IV administration

A

true

148
Q

What is the most common side effect of flagyl?

A

GI upset; mutagenic effects UNPROVEN, but possible

149
Q

What is the mechanism of Rifampin?

A

binds to DNA-dependent RNA pol, blocks CHAIN INITIATION and RNA transription

150
Q

T/F: Rifampin is active on eukaryotic polymerases

A

false; only on bacterial!

151
Q

T/f: Rifampin is cidal or static depending on the concentration of the BACTERIUM

A

TRUE

152
Q

How do bugs become resistant to Rifampin?

A

single step mutation in the beta subunit of RNA Pol; very rapid mutation

153
Q

what are the clinical uses of Rifampin?

A

Tx of TB, leprosy, prophylaxis of N. meningitidis

154
Q

What is the normal route of administration of Rifampin?

A

oral

155
Q

Describe the distribution of Rifampin?

A

good throughout the body, limited CNS penetration

156
Q

what is method of elimination of Rifampin?

A

30% urine and 60-70% feces!

157
Q

What drug causes ORANGE DISCOLORATION of tears, sweat, and urine?

A

Rifampin

158
Q

What are the most common side effects of Rifampin?

A

GI

159
Q

Rifampin is (blank)toxic

A

hepatotoxic

160
Q

Rifampin upregulates CYP450 and therefore decreases hormone and drug (blank)

A

half lives; need to check to see if there is a potential med interaction!

161
Q

Is streptomycin cidal or static?

A

cidal

162
Q

what is the MOA of streptomycin?

A

irreversibly binds to 30S unit
depletes ribosome pool
misreads the message
premature release from the ribosome

163
Q

Aminoglycosides like streptomycin are syngergistic with (blank), that facilitate their uptake by gram pos bacteria

A

cell wall-active antimicrobials

164
Q

What is the method that a bacteria becomes resistant to streptomycin?

A

Plasmid mediated enzymatic alteration: acetylation, phosphorylation, adenylation (most common) or reduced uptake or intrinsic resistance

165
Q

Do aerobes or anaerobes have intrinsic resistance to aminoglycosides?

A

anaerobes

166
Q

what is the spectrum of streptomycin?

A

BROAD spectrum: gram pos and neg, and TB

167
Q

Streptomycin is a (first/second)line drug in TB Tx

A

second line

168
Q

what other terrible diseases do you use streptomycin to treat?

A

tularemia, plague; more toxic than newer agents

169
Q

Gentamycin, tobramycin, and amikacin are used in empiric therapy of (blank)

A

suspected aerobic, gram NEG bacteria

170
Q

Once starting pt on empiric gentamycin and you get cultures back, do you continue therapy or switch abx?

A

switch abx

171
Q

What is needed to make aminoglycosides more effective against gram pos bacteria?

A

combo therapy with cell wall active agents

172
Q

T/F: aminoglycosides are minimally absorbed from the GI tract

A

true; must give IM or IV

173
Q

what is the clearance mechanism of aminoglycosides?

A

renal

174
Q

What pharmacodynamic ratio is a predictor of efficacy?

A

Cmax/MIC; CONCENTRATION DEPENDENT EFFECT

175
Q

What type of toxicity is most common with aminoglycosides? 2nd most common? Any other side effects?

A
  1. Nephrotoxicity 5-25%
  2. ototoxicity –IRREVERSIBLE 2-10%
  3. neuromuscular blockade: rare
176
Q

To what ribosomal subunit does tetracycline bind?

A

30s

177
Q

Where on the 30s does tetracycline bind?

A

A-site, blocks binding of aminoacyl tRNA

178
Q

is tetracycline binding reversible?

A

yes!

179
Q

is tetracycline bacteriostatic or cidal?

A

STATIC

180
Q

What is the most common mechanism for tetracycline resistance? Next most common?

A

Active efflux pump; ribosomal protection: cytoplasmic proteins bind to the ribosome to protect it

181
Q

What is the spectrum of tetracylcine?

A

VERY BROAD; gram pos and neg, many anaerobes, spirochetes, mycoplasma, rickettsiae and chlamydia

182
Q

(blank) is firstline Tx in chlamydia, rickettsia, and spirochetes,

A

tetracycline

183
Q

What factors make tetracycline a second line choice?

A

toxicity, resistance, and availability of alternatives

184
Q

What factors play into oral absorption of tetracyline?

A

varies from person to person and amongst various types, also impaired by MILK and divalent/trivalent cations

185
Q

What are the two methods that tetracycline is excreted?

A

kidney and bile

186
Q

T/F: tetracycline can cause superinfection

A

true

187
Q

T/F: tetracyline may stain teeth and bones in early years

A

true

188
Q

what are the side effects of tetracyline?

A

photosensitivity, GI problems, nephrotoxicity, bone/tooth staining, superinfection

189
Q

Is chloramphenicol used in the US?

A

nope

190
Q

What is the more common name for lincosamides?

A

clindamycin

191
Q

to what ribosomal unit does clindamycin bind?

A

50s

192
Q

what is the MOA of clindamycin?

A

blocks peptidyl transferase

193
Q

is clindamycin static or cidal?

A

static

194
Q

Describe the mechanism of resistance to clindamycin

A

plasmid mediated methylation of ribosome reducing abx binding

195
Q

what is the spectrum of clindamycin?

A

Aerobic GRAM POSITIVE COCCI

ANAEROBES

196
Q

Is clindamycin effective against gram negative?

A

nope

197
Q

what is the clinical use for clindamycin?

A

anaerobic infections, alternative to PCN if allergy, MRSA is susceptible!

198
Q

How do you deliver clindamycin?

A

Oral and pareneteral

199
Q

how is clindamycin excreted?

A

urinary and fecal

200
Q

The (blank) of clindamycin increases with renal failure

A

half life

201
Q

Pseudomembranous colitis is associated with what bug?

A

C. diff; intrinsically resistant to clindamycin

202
Q

What is the most common side effect of clindamycin?

A

GI disturbances

203
Q

what part of the ribosome does linezolid bind to?

A

50s unit

204
Q

what is the MOA of linezolid?

A

prevents formation of the 70s complex; unusual mechanism makes it SUPER EFFECTIVE! against resistant bacteria

205
Q

is linezolid static or cidal?

A

static

206
Q

what is the spectrum of linezolid?

A

most clinically important gram pos; limited with gram neg

207
Q

What drugs do you use linezolid for?

A

MRA, multi-drug resistant strep pneumoniae, VRE, and as a reserve abx for difficult bacteria

208
Q

What are the ways to give linezolid?

A

IV or orally

209
Q

What is the bioavailability of linezolid?

A

FUCKING OUTSTANDING

210
Q

how is linezolid excreted?

A

broken down in vivo and excreted in urine

211
Q

Long term use of linezolid results in (blank)

A

myelosuppresion

212
Q

What is the most common side effect of linezolid?

A

GI upset

213
Q

Linezolid is a weak nonspecific inhibitor of monoamine oxidase and should therefore not be given with (blank)

A

SSRIs!!

214
Q

What are the common macrolides?

A

erythromycin, azithromycin, and clarithromycin

215
Q

where do the macrolides bind and what is there MOA?

A

to the 50s; blocks peptidyl transferase and translocation

216
Q

are macrolides static or cidal?

A

static

217
Q

T/F: macrolides also have a plasmid mediated resistance method

A

treu

218
Q

what does the macrolide resistance plasmid carry?

A

gene for methylation of ribosome

219
Q

Macrolides have cross resistance with (blank)

A

lincomycin/clindamycin

220
Q

Besides being generally broad, define the spectrum of macrolides?

A

most active against aerobic, gram pos

221
Q

What is the clinical use of macrolides?

A

firstline for mycoplasma and Legionella, alternative for PCN if allergic

222
Q

(blank) inactivates macrolides, therefore oral dosing is givien as enteric-caoted or more-stable salts or esters

A

gastric acid

223
Q

Which macrolide is acid stable?

A

azithromycin

224
Q

What are the only areas where macrolides are not well distributed?

A

brain and CSF

225
Q

what is the primary mode of excretion of macrolides?

A

BILIARY WTF

226
Q

What are the side effects of macrolides? (think of mode of excretion)

A

hepatotoxicity
stimulates GI motility–i.e. GI upset
INHIBITOR OF CYP450; SIG. DRUG INTERACTIONS
CARDIAC ARRHYTHMIAS

227
Q

sulfonamides and trimethoprim both function in what pathway?

A

folic acid metabolism

228
Q

suflonamides block the synthesis of (blank)

A

dihydrofolic acid

229
Q

Trimethoprim blocks the synthesis of (blank)

A

T for Tetrahydrofolic acid

230
Q

THF is used in the synthesis of (blank)

A

DNA and RNA

231
Q

while sulfonamides block the synth of DHF, they are analogs to (blank)

A

PABA

232
Q

By what mechanism do sulfonamides block DHF synth?

A

competitive inhibitor

233
Q

are sulfonamides cidal or static?

A

static

234
Q

Plasmid resistance of sulfonamides mediates production of (blank) enzyme with decreased affinity for the drug

A

dihydropteroate synthetase

235
Q

Gram pos, gram neg, chlamydia, and NOCARDIA are in the spectrum of (blank)

A

sulfonamides

236
Q

T/F: you can use sulfonamides for UTIs

A

true

237
Q

T/F: sulfonamides have good GI absorption

A

true

238
Q

T/F: sulfonamides are excreted in feces

A

false; urine

239
Q

What is the common side effect to sulfonamides?

A

hypersensitivity reactions – rash and hivez

240
Q

Confluent dermatological necrosis is an emergency that is part of the (blank) syndrome in response to sulfonamides

A

Stevens-Johnson syndrome; shows with the confluent epidermal necrosis and immune reaction

241
Q

Hemolytic anemia, agranulocytosis, aplastic anemia, and other hematopoietic disorders are rare side effects associated with (blank)

A

sulfonamides

242
Q

T/F: trimethoprim is synergistic with sulfonamides

A

true

243
Q

cotrimoxazole (Bactrim and Septra) is a combo of what?

A

trimethoprim and sulfamethoxazole

244
Q

what is the drug of choice for Pneumocystis jirovecii??

A

trimethoprim

245
Q

what is a firstline for MRSA?

A

sulfamethoxazole/trimethoprim

246
Q

Impaired folate usage is a side effect of sulfa/trimeth?

A

trimeth

247
Q

What is the MOA of Isoniazid?

A

PRODRUG that is activated in the bacteria; inhibits synthesis of mycolic acids

248
Q

What is the very limited spectrum of Isoniazid?

A

only effective agains MYCOBACTERIA

249
Q

T/F: Resistance against Isoniazid is very common

A

true

250
Q

What is the mechanism of resistance against Isoniazid?

A

deletion of gene encoding the activating enzyme that takes it from prodrug to active drug

251
Q

What is the use of isoniazid?

A

TB tx

252
Q

What are the methods of administration of Isoniazid?

A

orally and IM

253
Q

Isoniazid will inhibit Cyp450 so you need to check for drug interactions and potential (blank) as a side effect

A

hepatitis

254
Q

What are the five general mechanisms of abx resistance?

A
  1. enzymatic inactivation of abx
  2. decreased permeability
  3. efflux of abx
  4. mod of molecular target
  5. failure to convert prodrug to active form
255
Q

What are the two ways that an abx is enzymatically modified so it doesn’t work?

A

it is either destroyed or modded so it fails to reach/bind its target

256
Q

What are the two locations for decreased permeability?

A

outer membrane permeability (gram neg) or inner (cytoplasmic) membrane permeability (gram neg or pos)

257
Q

What are some of the modifications to the molecular target of an abx to create resistance?

A
  1. altered binding site for abx
  2. protection of binding site
  3. overproduction of target (think vancomycin)
  4. binding up of abx
258
Q

Resistance to what types of abx is controlled by enzymatic alteration of the abx?

A

B-lactams and aminoglycosides

259
Q

Resistance to what types of abx is controlled by efflux of abx?

A

tetracylcine

260
Q

Resistance to what types of abx is controlled by altered abx binding site?

A

B-lactams, glycopeptides, quinolones, rifampin, macrolides, lincosamides, and sulfa/trimeth

261
Q

T/F: it is always best to choose the shortest effective abx regimen

A

true

262
Q

What factor should you consider when prescribing empirically?

A

local susceptibility trends

263
Q

What is an abx diffusion test?

A

Spread isolate on plate, drop on the abx discs, and measure the diameter of inhibition

264
Q

What does a diffusion test tell you?

A

estimates the minimum inhibitory concentration of an abx

265
Q

WHat are the disadvantages to a diffusion test?

A

non-quantitative interpretation
does not measure bacteriCIDAL activity
inappropriate for slow growers and slow diffusers

266
Q

In a dilution test, are you diluting solutions of bacteria or abx?

A

abx

267
Q

What are you able to calculate using a dilution test?

A

minimum bactericidal concentratoin–the least amount of abx needed to kill the bacteria

268
Q

Does a dilution or diffusion test determine bactericidal activity?

A

dilution test

269
Q

The (blank) test is influenced by growth rate while the (blank) is not

A

diffusion is, dilution is not

270
Q

Which bacterial assay provides quantitative results?

A

dilution testing

271
Q

Automated tests are mechanized (blank) tests

A

dilution

272
Q

in automated tests, bacterial growth is determined by (blank)

A

reduction in light transmittance or increase in scattering

273
Q

What is the advantage of automated tests?

A

better standardization, produces more info, and rapid results

Block 6 Week 4 Colt (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions