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Disease and Defense > Test 2 (week 1) > Flashcards

Test 2 (week 1) Flashcards

1
Q

A bacterium that stains blue would suggest which type of bacteria?

A

gram positive

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2
Q

Which bacteria (gram +/-) have outer membranes that covers the cell wall (two layers)?

A

gram negative bacteria

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3
Q

What is the name of this cell shape?

A

coccus

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4
Q

What is the name of this cell shape?

A

Bacillus

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5
Q

What is the name for this type of cell organization?

A

strepto-

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6
Q

What is the name for this type of cell organization?

A

staphylo-

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7
Q

What’s a common way to distinguish between staphylococcus and streptococcus?

A

A catalase test. If it is a staphylococcus, the addition of hydrogen peroxide will result in formation of bubbles because of the presence of catalase. Catalase is not found in streptococcus.

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8
Q
  • Multimeric toxins that form pores
  • Punch hole in host cell membrane
A

•Cytolysins/hemolysins

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9
Q

What are the two functional components of AB exotoxins?

A

•Two functional components:

–A: toxic component
–B: binding component
•Highly specific with respect to cellular target

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10
Q

What is the most common mechansism of toxicity of the A portion of the AB exotoxin?

A

•Most common mechanism:
–ADP-ribosylation of host proteins

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11
Q

–Integral component of the cell envelope
–Released only when the cell dies

A

endotoxin (LPS)

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12
Q

In which bacterial cell type do you see endotoxin (LPS)?

A

gram negative only

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13
Q

encodes all essential genes

A

chromosome

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14
Q

do not encode essential genes

A

plasmids

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15
Q

replicate independently

A

plasmids

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16
Q

enzymes that regulate the overwinding or underwinding of DNA

A

topoisomerase

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17
Q

Two plasmids can co-exist in the same cell only if replication control systems are ______.

A

different

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18
Q

Describe virulent bacteriophages.

A

–Take over host machinery to replicate themselves
- Always kills the host cell

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19
Q

Describe temperate bacteriophages.

A

–Has the ability to incorporate itself into host chromosome and live happily ever after……

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20
Q

a bacteriophage (often shortened to “phage”) genome inserted and integrated into the circular bacterial DNA chromosome or existing as an extrachromosomal plasmid

A

prophage

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21
Q

•genetic elements that reside in, and move between, DNA molecules

A

transposable elements

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22
Q

What are two components shared by all transposable elements?

A

–Inverted repeats at each end (ATCG……………GCTA)
–Proteins required for transposition

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23
Q

What’s the equation for Fick’s Law?

A

Fick’s Law predicts the rate of movement of molecules across a barrier (i.e., the amount of drug crossing the membrane per unit time). The rate depends upon:

  1. Concentration gradient (Co – Ci)
  2. Permeability coefficient, governed by lipid solubility, ionization
  3. Thickness of the biological membrane
  4. Area of the absorbing surface
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24
Q

Lipid solubility of a drug is inversely proportional to ____.

A

charge

–Only unionized drugs cross membranes by lipid diffusion.

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25
Q

glomerular filtration rate

A

130 ml/min

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26
Q

active tubular secretion rate:

A

•650 ml / min

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27
Q

only unbound drugs can be filtered in ____ .

A

glomerular filtration

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28
Q

Protein bound drug can be secreted in _____ .

A

active tubular secretion

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29
Q

What increases elimination of bases?

A

•acidification increases elimination of bases

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30
Q

What increases elimination of acids?

A

•alkalization increases elimination of acids

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31
Q

uptake of “free” DNA from dead cells

A

transformation

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32
Q

phage mediated transfer of bacterial DNA

A

transduction

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33
Q

plasmid mediated transfer of DNA

A

conjugation

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34
Q

Plasmids are said to be self-transmissable when they contain what?

A

•all tra genes (Effective Contact + Mobilization)

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35
Q

Plasmids are said to be mobilizable when they have what?

A

some tra genes (mobiliztion only)

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36
Q

Plasmids are said to be non-mobilizable when they contain what?

A

no tra genes (just a plain ‘ol plasmid)

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37
Q

Only enzymes in the _____ are inducible by drugs.

A

smooth ER

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38
Q

the fraction of a dose absorbed intact into the body

A

bioavailability (F)

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39
Q

the frequency of administering a maintenance dose

A

dosing interval (tau)

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40
Q

the rate of IV infusion used to achieve a desired response

A

infusion rate

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41
Q

Penicillin is active only against _____.

A

growing cells (this is why it would be antagonistic to couple penicillin with a bacteriostatic)

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42
Q

What is the most common form of bacterial aquired resistance?

A

efflux pump (pump out the antibiotics)

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43
Q

amount of antibiotic required to inhibit growth

A

minimum inhibitory concentration (MIC)

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44
Q
  • Amount required to kill 99.9% of viable bacteria
  • Does not apply to bacteriostatic drugs
A

minimum bactericidal concentration

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45
Q

What do breakpoints depend on?

A

only the antibiotic itself

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46
Q

Describe the mechanism of action of Daptomycin (Cubicin) and what it is used to treat.

A

•Active against Gram-positive
bacteria (including MRSA)

  • Binds to cytoplasmic membrane resulting in depolarization
  • Disrupts cellular functions resulting in death (bactericidal)
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47
Q

What is a common characteristic of all beta-lactams?

A

–4-membered beta-lactam ring

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48
Q

What is the mechanism of action of beta lactams?

A

–Inhibit transglycosylation and transpeptidation reactions
•Impairs wall remodeling: disrupts cell division
•Induces autolysins: causes cell lysis

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49
Q

List some examples of beta-lactams.

A

penicillins, cephalosporins, carbapenems, monobactems

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50
Q

Describe the method of beta lactam resistance.

A

–Production of beta-lactamase (penicillinase)
•Degrades 4-membered beta-lactam ring
•Generally plasmid-encoded

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51
Q

what is the name of the relatively broad spectrum 5th generation cephalosporin used to treat MRSA?

A

ceftaroline

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52
Q

What is the mechanism of action of glycopeptides?

A

–Bind irreversibly to terminal alanines in pentapeptide chain required for cross-linking
•Inhibit translocation/transpeptidation reactions

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53
Q

Describe the aquired bacterial resistance to glycopeptide.

A

–Substitution of terminal D-alanine with D-lactate (no longer a terminal alanine for the glycopeptide to bind to)

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54
Q

What is a common glycopeptide?

A

vancomycin

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55
Q

Describe the mechanism of action of tetracyclines.

A

–Reversible binding of 30S subunit
—Prevents formation of 30S initiation complex

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56
Q

What is the bacterial resistance see with tetracyclines?

A

efflux pumps

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57
Q

Where do aminoglycosides have their effect on the bacteria?

A

30S ribosome

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58
Q

Describe the method of bacterial resistance to aminoglycosides.

A

they modify the antibiotics through acetylation, adenlyation, or phosphorylation

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59
Q

Describe the mechanism of action of Chloramphenicol.

A

targets the 50s ribosomal subunit and prevents elongation of the peptide chain

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60
Q

Describe the method of bacterial resistance to Chloramphenicol.

A

modification of the antibiotic

61
Q

What are the MLS antibiotics and what is their mechanism of action?

A

macrolides, lincosamide, streptogramin
•All bind the 50S subunit of the intact ribosome and inhibit translocation (movement of RNA along ribosome)

62
Q

What are some examples of macrolides?

A

•Erythromycin, azithromycin, clarithromycin

63
Q

What is an example of a lincosamide?

A

Clindamycin

64
Q

Describe the method of bacterial resistance for MLS antibiotics.

A

•Modification of 50S subunit target (unlike aminoglycosides and chloramphenicol, which is modification of the antibiotic)

By altering the target of the antibiotic, they reduce its affinity and capability to bind

65
Q

Describe the mechanism of action of Oxazolidinones (linezolid).

A

–Bacteriostatic
•Inhibits formation of 1st peptide bond (inhibits formation of initiation complex between tRNA, mRNA and ribosome)
•Binds 50S ribosomal subunit and inhibits formation of 70S initiation complex

66
Q

Pnemonic to remember sites of action for antibiotics

A

Buy AT 30, CELLS at 50.

A= aminoglycosides

T= tetracycline

C= chloramphenical (or clindamycin)

E= erythromycin

L= lincomycin (or clindamycin)

L= linezolid

S= Streptogramins (Synercid)

67
Q

What is the cornerstone drug for TB?

A

rifampin

68
Q

What is the mechansim of action of rifampin?

A

•Rifampin binds beta subunit of DNA-dependent RNA polymerase
–Prevents binding to promoter
–Does not impair mammalian RNA polymerase

69
Q

What is the mechanism of action of sulfonamides?

A

•Competitive inhibitor of DHPS
•Bacteriostatic
–Partial shutdown of Tetrahydrofolate synthesis

70
Q

What is the mechanism of action of trimthoprim?

A

•Competitive inhibitor of DHFR
•Bacteriostatic
–Partial shutdown of Tetrahydrofolate synthesis

71
Q

Why do you always use Sulfonamides and Trimethoprim together?

A

because together they completely shut down tetrahydrofolate synthesis

72
Q

<!--StartFragment-->

Mechanism of Action of beta-Lactams<!--EndFragment-->

A

•Bind to Penicillin Binding Proteins (PBPs)
–Inhibit transpeptidase reaction and inhibitors of autolytic enzymes

73
Q

<!--StartFragment-->

What class of bacteria are susceptible to beta lactams? <!--EndFragment-->

A

primarily gram + bacteria

74
Q

What is the drug of choice for susceptible strains of Staphylococcus aureus?

A

nafcillin

•“think Staph? . . . think naf?”

75
Q

Name two common aminopenicillins.

A
  • Ampicillin (prototype)
  • Amoxicillin (prototype)
76
Q

What’s the perk of aminopenicillins over natural penicillins?

A

•Spectrum of Activity
–broader spectrum than natural pens
–spectrum includes that of natural pens
–plus other respiratory tract pathogens:
•Strep. pneumoniae (many strains)
•H. influenzae (many strains)

77
Q

<!--StartFragment-->

What is the drug of choice for uncomplicated gram(+) UTI?
<!--EndFragment-->

A

aminopenicillins (ampicillin or amoxicillin)

UNLESS THEY ARE HYPERSENSITIVE TO BETA LACTAMS

78
Q

What is the most active of Antipseudomonal penicillins against Pseudomonas?

A

piperacillin

79
Q

What are some adverse effects of penicillins?

A

•Hypersensitivity (up to 10% of patients)

–rash:
•Mild - maculopapular, urticarial rash
•Severe - Stevens-Johnson syndrome

–fever, serum sickness
–anaphylaxis

80
Q

Although cephalosporins are members of the beta lactam family, what are some pharmacokinetic differences they have in comparison to penicillins?

A

–many cephalosporins have longer t ½
–some cephalosporins are metabolized by the liver by deacetylation

81
Q

What is the drug of choice for gonorrhea?

A

ceftriaxone (third generation cephalosporin)

82
Q

What is an unusual adverse effect of cephalosporins?

A

–Disulfiram(drug given to alcoholics)-like reaction► buildup of acetaldehyde that makes you feel like crap

83
Q

What are the adverse reactions of carbapenems?

A

•Adverse reactions
–seizures if not dosed for CrCl
–30% chance of cross reaction if pt has type I reaction to penicillin

84
Q

Carbapenems have a mechanism of action similar to ____.

A

Penicillins. They treat a broade spectrum though.

85
Q

What is the spectrum of activity for monobactams?

A
  • Gram(-) aerobic bacilli: many members of the family Enterobacteriacea
  • Most Gram(+) organisms and anaerobes are resistant
86
Q

What is the mechanism of action of glycopeptide?

A

•Mechanism of Action:
–bind with high affinity to d-alanyl-d-alanine residues of peptidoglycan precursors
–inhibits release of d-alanine and thus transpeptidase reaction
–Cell lysis and death (-cidal)

87
Q

What is the spectrum of activity for glycopeptides?

A

•Spectrum of Activity:
–Gram(+) cocci: Staph and Strep

88
Q

What is the drug of choice for MRSA?

A

glycopeptides

89
Q

What are some adverse effects of glycopeptides?

A

•Adverse Effects:
–Hypersensitivities
Rapid IV injection (histamine release = flushing, or red man syndrome)

—ototoxicity

—nephrotoxicity

90
Q

What is the most commonly used glycopeptide?

A

<!--StartFragment-->

Vancomycin<!--EndFragment-->

91
Q

Why are drugs which bind with weak forces more selective?

A

–Drugs which bind with weak forces are more selective b/c weak forces require very close fit of drug to receptor

92
Q

The magnitude of a response to a drug is proportional to what?

A

•The magnitude of response is proportional to the number of receptors occupied.

93
Q

In a dose response curve, what does Kd represent?

A

it is the dose at which you reach half the maximum effect

94
Q

Which axis of a dose response curve is potency measured on?

A

X axis

95
Q

What axis of a dose response curve is efficacy measured on?

A

y axis

96
Q

How do you measure therapeutic index (measure of drug safety)?

A

•=LD50/ED50
** To remember which one goes on top, remember that the end values are always greater than 1

97
Q

Describe competitive antagonism.

A
  • Can be surmounted by increasing the dose of the agonist.
  • shifts ED50 to the right (decreases potency)
  • No change in maximal response (efficacy)
98
Q

Describe non-competitive antagonism.

A
  • can not be overcome or surmounted by increasing dose
  • no shift of ED50
  • decrease in maximal response (decreased efficacy)
99
Q

What happens in drug tolerance?

A

•Occurs with chronic administration of drug, resulting in:

  1. A decrease in the effect of a given dose.
  2. An increase in the dose required to produce a given effect.
100
Q

What is dispositional tolerance and what are some mechanisms by which it occurs?

A

•A reduction in drug effect as a result of a lowered drug concentration at the receptor
•Mechanisms
–changes in absorption, distribution, or excretion
–change in rate and extent of metabolism (aka, metabolic tol.)

101
Q

What is pharmacodynamic tolerance and what is the mechansim by which it takes place?

A

•a reduction in drug effect without a change in drug concentration
•mechanisms
–a reduction in number of receptors (down regulation)
–a change in drug-receptor coupling
–change in effector components distal to receptor

102
Q

What is behavioral tolerance?

A
  • Occurs with drugs that act on CNS
  • It is a learned ability to compensate for the effects of the drug
  • Example—an alcoholic learns to walk a straight line when intoxicated
103
Q

What is cross tolerance?

A

•Development of tolerance to one drug after repeated administration of a second drug

104
Q

What is cross dependence?

A
  • Cross-dependence occurs when a second drug substitutes for the primary drug of abuse in an dependent person.
  • Similar to cross-tolerance, except here the drugs substitute with each other to maintain dependence.
  • Example: Methadone is used to block withdrawal symptoms and signs and alleviate cravings for heroin in heroin addicts.
105
Q

What is the mechanism of action of aminoglycosides?

A

–bind to 30S ribosomal subunit
–interfere with initiation of protein synthesis
–block further translation of mRNA to protein

106
Q

What is the medicine combo used to combat susceptible strains of streptococci?

A

–aminoglycosides with b-lactam or vancomycin for susceptible strains of Streptococci (Enterococci)

107
Q

Aminoglycosides are active against which kind of bacteria?

A

–gram(-) aerobic bacilli

108
Q

Aminoglycosides are synergistic with _____.

A

Beta lactams

109
Q

What is the drug of choice for VRE (vancomycin resistant enterococcus)?

A

comination of beta lactam and aminoglycosides

110
Q

What are the toxicities of aminoglycosides?

A

nephrotoxicity and ototoxicity

111
Q

Why are aminoglycosides toxic on the kidneys and inner ear?

A

in these tissues, the half life of the drugs can be from 30-700 hour range

112
Q

What is the 1st choice aminoglycoside?

A

gentamicin

113
Q

What is a major side effect tetracyclines?

A

superinfection with pseudomembranous colitis

114
Q

What is the DOC for chlamydia?

A

doxycycline

115
Q

What is the DOC for<!--StartFragment-->Rickettsiae (Rocky Mt. Spotted fever)?<!--EndFragment-->

A

doxycycline

116
Q

What is the mechanism of action of macrolides?

A

•Mechanism of Action
–reversibly bind to the 50S ribosomal subunit
•at or near the clindamycin and chloramphenicol site
MLSb site

117
Q

What is the spectrum of activity for macrolides?

A

•Spectrum of Activity
–most effective for aerobic gram(+) cocci and bacilli

–some gram (-) bacilli

118
Q

What is the unique activity of macrolides?

A

•Unique activity
–Show efficacy below lab MIC
–Penetrate mammalian cells
–Taken up extensively by phagocytes
•Phagocytes localize at site of infection
–Boom!

119
Q

What is one of the more adverse effects of macrolides?

A

•prolonged QTc interval
–Can cause arrhythmias

120
Q

What are the prototype macrolides?

A

•erythromycin, clarithromycin, azithromycin

121
Q

What is the mechanism of action of<!--StartFragment--> Lincomycins/Lincosamides?<!--EndFragment-->

A

Mechanism of action: reversibly binds to 50s Ribosome <!--EndFragment-->

122
Q

<!--StartFragment-->

What is the spectrum of activity for Lincomycins/Lincosamides<!--EndFragment-->?

A

gram (+) cocci and aneorobes

123
Q

What is the most severe adverse effect of lincomycins/lincosamides?

A

•superinfection: pseudomembranous colitis produced by Clostridium difficile (up to 10%)

124
Q

<!--StartFragment-->

What is the most prominent lincomycins/lincosamides?
<!--EndFragment-->

A

clindamycin

125
Q

What is the major side effect of chloramphenicol (why we don’t use it anymore)?

A

causes aplastic anemia like a crazy man and causes grey baby syndrome

126
Q

<!--StartFragment-->

What is the mechanism of action of Oxazolidinones (linezolid-prototype)?<!--EndFragment-->

A

–binds to 50S ribosomal subunit
•near Macrolide/Lincomycin/Streptogramin B site
–inhibits formation of the initiation complex
•ribosomal-mRNA-tRNA complex
–inhibits protein synthesis

127
Q

What is the spectrum of activity of<!--StartFragment--> Oxazolidinones (linezolid-prototype)?<!--EndFragment-->

A

Gram (+) organisms only
•gram(-) organisms have efflux pumps on the cell membrane that prevent oxazolidinone accumulation

128
Q

What is a major adverse drug interaction of<!--StartFragment--> Oxazolidinones (linezolid)?<!--EndFragment-->

A

Don’t work with MAO inhibitors
–in presence of MAOI, high concentrations of tyramine causes displacement and massive release of NE from nerve terminals
–Don’t serve red wine, cheese or smoked sausages in hospital

129
Q

Streptogramins

A

Bind to the 50S ribosome of bacteria
–net effect
•synergistic (dalfopristin/quinupristin) inhibition of protein synthesis
•early termination of peptide elongation

130
Q

What is the spectrum of activity of streptogramins?

A

gram(+) cocci

131
Q

What is a major adverse effect of streptogramins?

A

•Adverse Effects
–Potent inhibitor of CYP3A4 P450 enzyme
•Increase plasma levels of many drugs

132
Q

What is the mechanism of action of fluoroquinolones?

A

•Mechanism of Action
–DNA Gyrase (Topoisomerase II) inhibition
•DNA gyrase and DNA are trapped into a complex

133
Q

What is the spectrum of activity of fluoroquinolones?

A

work agains Gram (+) and (-) bacteria

134
Q

Which antibiotics can become inactivated by divalent cations?

A

fluoroquinolones and tetracyclines due to chelation of their rings

135
Q

Which antibiotic is particular good for a IV to PO switch?

A

fluoroquinolones

136
Q

What is the suffix for all fluoroquinolones?

A

-oxacin

137
Q

Fluoroquinolones are great for what?

A

respiratory tract infections

138
Q

what are the “respiratory quinolones”?

A

levoxicin and moxifloxicin

139
Q

What is a major adverse effect of fluoroquinolones?

A

•Adverse Effects
–Connective Tissue
•arthropathy, arthralgias
–especially in children
–risk of tendon rupture

140
Q

What are the first line drugs against TB?

A

rifamycins

141
Q

What is the mechanism of action for rifamycins?

A

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•Inhibit bacterial (but not human) DNA-dependent RNA polymerase.
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142
Q

What is one of the major side effects of rifamycin?

A

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•Drug interactions: MANY!! induces cytochromes P450 which metabolize and inactivate many drugs, including hormonal contraceptives, sulfonylureas, corticosteroids, clarithromycin, and most statins.
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143
Q

What is the spectrum of action of rifamycins?

A

•Broad-spectrum, bactericidal against intracellular, extracellular, and atypical mycobacteria

144
Q

What is the only bacteria that forms spores?

A

gram (+) rods

145
Q

What is an episome?

A

A plasmid converted into the chromosome.

146
Q

What creates an F’ plasmid?

A

F’ plasmids are formed when imprecise excisison leads to the incorporation of chromosomal DNA into the plasmid

147
Q

How does methicilin resistance (or more likely, oxacillin resistance) come about?

A

the bacteria acquire a unique gene (mecA) encoding a unique penicillin binding protein PBP2A–> this confers resistance to all beta lactam antibiotics

148
Q

What is the mechanism responsible for the intermediate level of resistnace in VISA (vancomycin intermediate s. aureus) or GISA (glycopeptide intermediate s. aureus)?

A

the production of an abnormally thick cell well with an overabundance of D-ala/D-ala termini. This results in the “absorption” of the drug at the surface of the cell wall and the failure to disrupt the remainder of the wall to an extent that is lethal.

149
Q
A

Disease and Defense (3 decks)

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