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Pharmacology N2100 > Unit 14 - Infection > Flashcards

Unit 14 - Infection Flashcards

1
Q

Name 3 nonspecific body defenses

A
  • physical barriers (skin & mucous membranes)
  • cellular barriers (phagocytes)
  • process barriers (*inflammation & fever)
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2
Q

Name 2 specific body defenses

A
  • humoral immune response (B-cells & antibodies)

- cell-mediated immune response (T-cells & cytokines)

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3
Q

describe the assessment of a pt with a local infection

A

redness, swelling, pain (tenderness), warm to touch, drainage/pus, loss of function

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4
Q

describe the assessment of a pt. with a systemic infection

A

malaise, aching, elevated temperature, elevated WBC, elevated sedimentation rate

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5
Q

3 ways bacteria can be differentiated/types:

A
  • staining of the cell wall (gram + = thick walls) (gram - = thin walls)
  • use of oxygen (aerobic, anaeroobic)
  • basic shape (bacilli-rod, cocci-sphere, spirilla-spiral)
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6
Q

superinfections related to certain antibiotics may occur as often as ____ of the time, but most often is never related back to the ______ _______

A

30%, offending antibiotic

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7
Q

T/F: antibiotics cause more superinfection that others

A

T

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8
Q

superinfection frequently occurs when the ______ ______ are suppressed and supplanted by ______ _______

A

normal flora, (primarily gram positive anaerobes), pathogenic flora

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9
Q

superinfection potential is related to two primary features of an antibiotic:

A
  • does active antibiotic get to the site of the normal flora (the GI tract is of primary concern)
  • when the antibiotic gets to the site of the normal flora (ex. GI tract) does it have antimicrobial activity against the normal flora
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10
Q

T/F: inflammation & infection are the same

A

F! you ca have inflammation without infection, however cannot have infection without inflammation

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11
Q

how normal flora help bacterial infections

A

because there are so many, they crowd out the more harmful bacteria/yeast/microogranisms preventing them from spreading

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12
Q

T/F: normal flora can cause infection

A

T, if they are introduced into another part of the body where they don’t belong

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13
Q

MRSA

A

methicillin resistant staphylococcus aureus

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14
Q

VRE

A

vancomycin enterococcus faecium

  • scary because vancomycin is a last resort drug
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15
Q

What are Pseudomonoas Aeruginosa & Klebsiella Pneumonia associated with

A

pnemonia

  • Pseudomonoas Aeruginosa: seen in burn units
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16
Q

nosocomial

A

HAIs (Healthcare Associated Infections)

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17
Q

what is generally the key to breaking chain of infection

A

prevention

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18
Q

an infection on top of another infection

A

superinfection

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19
Q

what is antibiotic-induced diarrhea

A

a marker of disruption of the normal flora & superinfection potential

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20
Q

common sites on body for superinfections

A
  • GI
  • intestines
  • bladders
  • vagina
  • lungs
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21
Q

culture & sensitivity test

A
  1. identify microorganism
  2. identify sensitivity to antibiotic (what will kill it)

(ex. culture: grow out bacteria that is there so we can identify)
(ex. sensitivity: drop different chemicals on different parts of bacteria & see what kills it)

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22
Q

how do bacteria become resistant

A

accidental mutation

  1. create enzymes that destroy drug
  2. find a way that drug cannot penetrate cell
  3. create pumps that will pump antibiotic out of cell
  4. can create an alteration at drug site of action
  5. create alternative metabolic pathways
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23
Q

4 ways we can increase effectiveness of antibiotics and decrease infections

A
  • prevent infection (making sure we’re using proper techniques)
  • preventing transmission
  • diagnosing & treating infections appropriately
  • using antimicrobials wisely
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24
Q

5 mechanisms of actions of antibiotics

A
  1. Cell wall synthesis inhibitors
  2. DNA synthesis inhibitors
  3. Antimetabolites
  4. Protein synthesis inhibitors
  5. RNA synthesis inhibitors
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25
Q

bacteriocidal vs. bacteriostatis

A

bacteriocidal: kill bacteria (cell wall synthesis inhibitors)
bacteriostatic: slow growth of bacteria (the rest of types of bacteria)
* you should

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26
Q

Can you use bacteriocidal & bacteriostatic antibiotics together

A

No, because bacteriocidal are depending on the fact that bacteria is dividing & proliferating quickly & if we give an antibiotic that slows that growth, then we are preventing the bacteriocidal from working properly/efficiently

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27
Q

difference between bacteria & human cells

A

bacteria cells have cell walls & human cells don’t, so we don’t destroy human cells when using antibiotics and reduce adverse effects

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28
Q

do antibiotics work better on gram positive or negative

A

gram positive: thick cell wall = more chances for antibiotic to cause problem in cell wall = more effective

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29
Q

how do these antibiotics work

A

by binding to outside of the wall, don’t have to get inside bacteria cell to work = disrupts outside cell wall

*work by beta lactum ring

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30
Q

what is the beta lactam ring

A

the chemical part of the antibiotic that is responsible for killing the bacteria, the part that binds with bacteria cell wall and disrupts it enough to kill it

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31
Q

T/F: beta lactam rings can be destroyed by bacteria

A

T, bacteria can create betalactamasys

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32
Q

4 antibiotics that have beta lactam ring

A
  • penicillin: penicillin, ampicillin
  • cephalosporin: cefazolin
  • carbapenems: impenem-cilastatin
  • misc: vancomycin
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33
Q

natural penicillin

A

penicillin

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34
Q

prototype for borad spectrum penicillin

A

ampicillin

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35
Q

extended spectrum (broad spectrum & kantipseudomonal)

A

Piperacillin

36
Q

effective for penicillin resistant varieties of bacteria (antistapholococcal)

A

Oxacillin

37
Q

is Oxacillin effective against MRSA

A

No

38
Q

are penicillins more effective against gram positive or negative

A

positive

39
Q

what kind of spectrum do penicillins generally have

A

narrow

40
Q

T/F: penicillins are generally widely spread to all body tissues

A

T, excluding CSF

41
Q

what excretes penicillin

A

rapidly excreted by kidneys

very distinct smell in urine

42
Q

do these penicillins have short or long half-lifes and how does this affect their drug schedule

A

short half-life, so they tend to need to be given more frequently

43
Q

1 adverse effect of penicillins

A

allergic reactions due to the chemical structure = body identifies it as foreign substance

44
Q

narrow vs. broad spectrum

A

fancy word for saying whether an antibiotic will kill a lot of a few things

narrow: very specific in the kinds of bacteria it will kill
broad: it kills lots of different kinds of bacteria (whether its different shape, uses oxygen or not, or gram +/-) = likely to kill our normal flora

45
Q

which is more likely to kill normal flora, broad or narrow spectrum bacteria

A

broad

46
Q

largest class of antibiotics

A

cephalosporins

47
Q

what do cephalosporins treat

A

mostly gram -

48
Q

T/F: cephalosporins are bacteriocidal

A

T

49
Q

T/F: cephalosporins have beta lactam rings

A

T

50
Q

T/F: cephalosporins & penicillins are similar in their mechanism of actions, side effects, & nursing considerations

A

T

51
Q

Difference between cephalosporins & Penicillins

A

Cephalosporins are also used for gram -

52
Q

_____ of people that have allergy to penicillin also have a cross allergy to cephalosporin

A

5-10%

53
Q

Describe 1st generation of Cephalosporins

A
  • contain a beta-lactam ring
  • most affective against gram +
  • only moderate activity against gram -
  • do not cross BBB (doesn’t enter CSF)
54
Q

Describe 2nd generation of Cephalosporins

A
  • broader spectrum against gram - than 1st gen
  • more potent and less sensitive to beta lactamase
  • unable to enter CSF
  • largely been replaced by 3rd generation
55
Q

Describe 3rd generation of Cephalosporins

A
  • broader spectrum against gram - than 2nd gen
  • longer duration of action
  • resistant to beta lactamase
  • able to enter CSF to treat CNS infections
56
Q

Describe 4th generation of Cephalosporins

A
  • more effective against organisms that have developed resistance to earlier cephalosporins
  • able to enter CSF in high concentrations to treat CNS infections
57
Q

Describe 5th generation of Cephalosporins

A
  • broad spectrum c extended gram + effectiveness
  • effective against MRSA
  • still in development; first drug, ceftraline, approved 2010
58
Q

“ceph” or “cepha”

A

cephalosporin

59
Q

“penems”

A

carbapenems

60
Q

Are carbapenems a type of bacteriocidal

A

yes

61
Q

are carbapenems narrow or brad spectrum

A

broad (kills most gram +, _, & anaerobes)

62
Q

What type of drugs are resistant to desctruction

A

Carbapenems

63
Q

Why do we combine Cilistatin & Imipenem

A

So the Cilistatin can help prevent the Imipenem in the kidneys

64
Q

steps to protein synthesis

A

mRNA: carrying message from DNA to ribosome

tRNA: attaches amino acids together from ribosome

Ribosome: site of protein synthesis

65
Q

why don’t antibiotics that affect protein synthesis affect human cells

A

most human ribosomes are not the same size as the bacteria ribosomes, so structurally they don’t fit

66
Q

how antibiotics that affect protein synthesis work

A

they bind to the ribosomes in bacterial cells & prevent the protein synthesis from happening (bacteria can’t make protein in order to reproduce)

67
Q

2 things macrolides are used for

A
  • treatment of gram + in pt’s allergic to penicillins

- H. Pylori

68
Q

mechanism of action of macrolides

A

inhibit bacterial protein synthesis by binding to 50S ribosome

69
Q

are macrolides bacteriocidal or bacteriostatic

A

usually bacteriostatic, but can be bacteriocidal

70
Q

mechanism of action of Fluoroquinolones

A
  • prevent bacterial DNA from replicating

- treat many gram + & _

71
Q

Are Fluoroquinolones bacteriostatic or bacteriocidal

A

bacteriocidal

72
Q

what are Fluoroquinolones used for

A
  • drug of choice for UTIs
  • travellers diarrhea
  • respiratory, GI & Gu infections
73
Q

do Fluoroquinolones affect human DNA

A

no

74
Q

“floxacin”

A

Fluoroquinolones

75
Q

1 weird side effect of Fluoroquinolones

A

cartilage problems: tendon rupture

especially in kids who are developing cartilage & tendons, so can not be used < 18 yrs

76
Q

mechanism of action of Sulfonamides & UTI meds

A
  • bacteriostatic: slow bacterial growth by inhibiting folic acid production (don’t effect human cells because we don’t make folic acid)
  • broad: treat gram + & -
77
Q

what are urinary antiseptics used for

A
  • to treat UTI because of high concentrations in urinary tract due to renal excretion
  • not effective for systemic infections
78
Q

_____ are used to create an immune response in the body to be able to fight a true antigen when it is encountered in the future

A

vaccines

79
Q

what is active immunity

A

when the body creates an immune response to an antibody or its vaccine

80
Q

what is passive immunity

A

when actual pre-formed antibodies are given to someone, without the person’s own immune system creating them

81
Q

4 types of vaccines

A
  1. attenuated (live)
  2. inactivated (killed by heat or chemical) (safer than attenuated)
  3. toxoid (make it so that body doesn’t effect organism itself so much that it attacks the toxins that the microorganism is giving out)
  4. recombinant (lab generated proteins = body will recognize as foreign substance & create antibodies)
82
Q

can you use attenuated vaccines in immunosuppressed pt’s

A

no, because they actually could develop a case of the disease harmful enough to hurt

83
Q

can you use MMR or Rubella immunizations in pregnant women

A

no

84
Q

VAERS

A

vaccine adverse effect reporting system: any effects that require medical treatment

85
Q

T/F: penicillins are very painful

A

T, especially IM

86
Q

what’s the main different between penicillin & ampicillin

A

ampicillin is a little more broad spectrum = useful because it’s commonly used for infections that are not easily cultured (ex. sinus infections because you can’t get a swab of it to culture)

87
Q

“floxacin”

A

Fluoroquinolones

Pharmacology N2100 (26 decks)

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