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Unit 2- Pharm > Red/Bolded Words/Review - Deck 1 > Flashcards

Red/Bolded Words/Review - Deck 1 Flashcards

1
Q

What is unique about chemotherapy?

A

Selectively toxic against infectious agent

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2
Q

Every time you prescribe, you are selecting for

A

resistance

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3
Q

Chemotherapy resistance can be

A

natural or acquired

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4
Q

Natural chemotherapy resistance means that:

Example?

A

the antiobiotic cannot get into inner membrane –>

enterococci - penicillins can weakly bind to penicillin-binding protein and aminoglycosides can get inside the cell

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5
Q

Bacteriostatic drugs work how?

A

They keep infectious agent from growing so host immune system can take care of infectious agent

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6
Q

Good example of drug synergy?

A

Penicillins and aminoglycosides

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7
Q

Transferring resistance

A

transduction

transformation

conjugation

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8
Q

How does conjugation work?

A

requires direct contact with pilus

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9
Q

How does transformation work?

A

incorporates free DNA information from environment

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10
Q

How does transduction work?

A

bacteriophages passes resistance from one bacteria to another

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11
Q

Bacteriostatic pharmacokinetic important property

A

Maintain blood level because they are static –> as soon as blood level drops below threshold, the growth of the bacteria will start again

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12
Q

Empirical therapy

A

Don’t know what is going on, use clinical judgment. If they need antibiotics, you may need to change antibiotic when you find out lab results.

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13
Q

If septic, what kind of empirical therapy is used?

A

Broad spectrum - parenteral

Carbapenims,
Cefapime, combine aminoglycoside (good G-) with parenteral G+ (like Pen G)

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14
Q

Cidal v static

A

Cidal = cell death

Static = growth inhibition

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15
Q

Immunocompromised patient should be on what kind of antibiotic?

A

Cidal

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16
Q

Concentration-dependent killing

Example?

A

high concentration to have effect

Aminoglycosides

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17
Q

Time-dependent killing

A

Must be in system for a certain amount of time to be effective

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18
Q

Minimum inhibitory concentrations

A

smallest concentration to keep cells from growing

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19
Q

Minimum bactericidal concentrations

A

smallest concentration to kill cells

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20
Q

Serial Dilution Susceptibility Test (MIC and MBC)

A

Bacteria is growing –> MIC occurs –> innoculate MIC cultures into antimicrobial-free media –> MBC occurs

MIC tells us when growth will be inhibited, but MBC tells us when cell death occurs

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21
Q

Post-antibiotic effect

Example

Why is this important/beneficial?

A

Persistent suppression of bacterial growth –> extension of antimicrobial effect even when concentration is below threshold but there is still inhibition of growth.

PAE –> less you have to dose –> less adverse side effects

Aminoglycosides

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22
Q

Synergism

What bacteria do we always treat with synergism?

A

Use multiple drugs together

Pseudomonas

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23
Q

Drug antagonism

A

Drugs do not work well together

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24
Q

Why do static and cidal drugs not work well together?

A

Static drug require cell growth and cidal drugs inhibit cell wall synthesis (cell growth)

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25
Q

Development of superinfections more common with what kind of spectrum of antibiotics?

Why?

Example

A

broad spectrum antibiotics

disturbance of flora

C. diff.

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26
Q

Overgrowth of C.Diff leads to

A

pseudomembranous colitis

also a superinfection

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27
Q

What are the beta-lactams (inhibitors of cell wall synthesis)?

A
  1. Penicillins
  2. Cephalosporins
  3. Carbapentims
  4. Monobactims
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28
Q

How do beta-lactams inhibit cell wall synthesis ?

A

Bind to penicillin-binding protein which affects cell wall which is integral to the integrity of cell –> cell blows up

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29
Q

Inhibitors of cell wall synthesis: static of cidal

A

Cidal

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30
Q

Entire penicillin group is susceptible to penicillinase BESIDES:

A

pencillinase-resistant penicillins

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31
Q

Penicillinase is only a problem for

A

penicillins (besides penicillinase resistant penicillins)

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32
Q

Difference between bacterial and mammalian cells is

A

rigid cell wall

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33
Q

Cell wall protects bacterial cells from

A

osmotic rupture

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34
Q

Structure conferring cell wall rigidity and resistance to osmotic lysis in both G+ and G- is

A

peptidoglycan

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35
Q

G+ peptidoglycan

A

only layered structure external to cell membrane and is thick

36
Q

G- has an outer membrane external to what?

A

very thin peptidoglycan layer

37
Q

What does transglycosylation do?

A

joins NAM and NAG

38
Q

What does transpeptidation do?

A

cross links pentapeptides

39
Q

Transglycosulation and transpeptidation are enzymatic actions performed by:

A

penicillin binding proteins

40
Q

If antibiotic targets penicillin binding proteins, what does/does not occur?

A

transglycosulation and transpeptidation

41
Q

Beta-lactams prevent

A

transpeptidation

42
Q

What do autolysins do to initiate cell death/lysis?

A

Autolysins are remodeling enzymes that cleave peptidoglycan bonds in normal course of cell growth. In presence of inhibitors of cell wall synthesis, autolysis proceeds without normal cell-wall repair –> lysis

43
Q

In order for autolysis to occur, what needs to be happening?

A

cell needs to be growing

44
Q

Natural Pencillins have the highest antibacterial activity against certain gram (___) bacterial including anaerobic/aerobic

A

G+, anaerobic

45
Q

Do natural penicillins have any G- coverage?

A

Some

46
Q

Natural penicillins are readily inactivated by

A

beta-lactamase (penicillinase)

47
Q

Natural penicillins have/do not have anti-pseudomonal actviity?

A

Do not have

48
Q

Penicillinase-Resistant Penicillins have increased/decreased activity against G+ bacteria compared to natural penicillins

A

lower activity

49
Q

Penicillinase resistance penicillins have increased/decreased G- coverage compared to natural penicillins?

A

increased

50
Q

Penicillinase-Resistant penicillins are the DOC for

A

penicillinase-producing S. aureus - MSSA

51
Q

What kind of metabolism and excretion do penicillinase-resistant penicillins have?

A

hepatic metabolism and renal excretion

52
Q

How does MRSA work?

A

MRSA produces alternate penicillin-binding protein which decreases affinity of beta-lactam antibiotics to PBPs

53
Q

ONLY beta-lactam that is used to treat MRSA?

A

ceftaroline

54
Q

Extended spectrum penicillins have increased/decreased G+ coverage compared to natural penicillins?

A

decreased

55
Q

Extended spectrum have increased G (__) coverage

A

G- coverage

56
Q

Do extended spectrum penicillins have antipseudomonal activity?

A

No

57
Q

DOC for lysteria?

A

ampicillin (oral)

58
Q

Is the ampicillin rash a sign of hypersensitivty?

A

No - does not preclude future use of penicillin

59
Q

Antipseudomonal penicillins have what kind of spectrum?

A

extended plus some enteric gram negative bacilli

60
Q

What are the two major uses of antipseudomonal penicillins?

A

P. aeruginosa and acinetobacter

61
Q

What do we use antipseudomonal penicillins in combo with? Why?

A

Aminoglycosides

prevent resistance

62
Q

3 Beta-lactamase inhibitors:

A

clavulanic acid, sulfactam, tazobactam

63
Q

What four penicillins are beta-lactamase given in conjunction with?

A

ampicillin, amoxicillin, ticarcillin, piperacillin

64
Q

Combination products are/are not effective agaisnt MRSA?

A

Are not - MRSA does not affect beta-lactamase - it affects PBP

65
Q

5 ways cell wall synthesis is inhibited?

A 
Transglycosylation
Transpeptidation
NAG reduction to NAM
Transport across inner membrane
Amino acid mimicry - pentapeptide chain
66
Q

Which of the natural penicillins (Pen G, Benzathine penicillin, procraine penicillin, or Pen V) are used only orally?

A

PEN V

67
Q

Gold standard for G+ infections?

A

Pen G

68
Q

Which natural penicillin would you use if you needed treatment to start immediately?

A

Pen G d/t parenteral administration

69
Q

Only group of penicillins that has anti-pseudomonal properties and is used to treat pseudomonas?

A

Anti-pseudomonal penicillins

70
Q

If you have a bacteria that produces penicillinase, what group is completely out?

A

Natural penicillins

71
Q

Which drug (ONLY ONE) in penicillinase resistant penicillins are give parenterally? Other two given orally

A

Naficillin

72
Q

Penicillinase resistant penicillins are DOC for

A

MSSA (produces penicillinase)

73
Q

How does MRSA occur?

A

MRSA produces alternate PBP which decreases affinity of beta-lactam antibiotics. Has nothing to do with beta-lactamase itself.

74
Q

Amoxicillin and Ampicillin are both adminstered

A

orally

75
Q

Ampicillin and amoxicillin can have inhibitor of beta-lactamase added to them.

Amoxicillin becomes what? And is it oral or parenteral?

Ampicillin becomes what? Oral or parenteral?

A

Augmentin - oral

Ampicillin - parenteral (hospital use)

76
Q

Ampicillin and amoxicillin both have lower ____ and higher ____ coverage than natural penicillins.

A

Lower G+ and higher G-

77
Q

____ rash: NOT a hypersensitivity reaction

A

Ampicillin

78
Q

Anti-pseudomonal penicillins are used with what?

A

aminoglycosides (beta lactamase inhibitors)

79
Q

Bacterial resistance: penicillins

inactivation of penicillin by:

A

bacterial beta-lactamase

80
Q

Bacterial resistance: penicillins

______ ______ of bacterial cell to penicillins (G-)

A

decreased permeability

81
Q

Bacterial resistance: penicillins

Alteration inf _____ which prevents penicillin from binding (MRSA)

A

PBPs

82
Q

Bacterial resistance: penicillins

____ enzymes not being activated thus forming tolerant organisms or non-growing persistent bacteria which are recalcitrant to antibiotics

A

activated

83
Q

Bacterial resistance: penicillins

No ____ ____

A

cell wall

84
Q

permeability is really only an issue for

A

gram negatives

85
Q

Toxicity to worry about with penicillins?

A

allergies

Unit 2- Pharm (9 decks)

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