Unit 14 - Infection Flashcards
1
Q
Name 3 nonspecific body defenses
A
- physical barriers (skin & mucous membranes)
- cellular barriers (phagocytes)
- process barriers (*inflammation & fever)
2
Q
Name 2 specific body defenses
A
- humoral immune response (B-cells & antibodies)
- cell-mediated immune response (T-cells & cytokines)
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
4
Q
describe the assessment of a pt. with a systemic infection
A
malaise, aching, elevated temperature, elevated WBC, elevated sedimentation rate
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)
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
7
Q
T/F: antibiotics cause more superinfection that others
A
T
8
Q
superinfection frequently occurs when the ______ ______ are suppressed and supplanted by ______ _______
A
normal flora, (primarily gram positive anaerobes), pathogenic flora
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
10
Q
T/F: inflammation & infection are the same
A
F! you ca have inflammation without infection, however cannot have infection without inflammation
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
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
13
Q
MRSA
A
methicillin resistant staphylococcus aureus
14
Q
VRE
A
vancomycin enterococcus faecium
- scary because vancomycin is a last resort drug
15
Q
What are Pseudomonoas Aeruginosa & Klebsiella Pneumonia associated with
A
pnemonia
- Pseudomonoas Aeruginosa: seen in burn units
16
Q
nosocomial
A
HAIs (Healthcare Associated Infections)
17
Q
what is generally the key to breaking chain of infection
A
prevention
18
Q
an infection on top of another infection
A
superinfection
19
Q
what is antibiotic-induced diarrhea
A
a marker of disruption of the normal flora & superinfection potential
20
Q
common sites on body for superinfections
A
- GI
- intestines
- bladders
- vagina
- lungs
21
Q
culture & sensitivity test
A
- identify microorganism
- 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)
22
Q
how do bacteria become resistant
A
accidental mutation
- create enzymes that destroy drug
- find a way that drug cannot penetrate cell
- create pumps that will pump antibiotic out of cell
- can create an alteration at drug site of action
- create alternative metabolic pathways
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
24
Q
5 mechanisms of actions of antibiotics
A
- Cell wall synthesis inhibitors
- DNA synthesis inhibitors
- Antimetabolites
- Protein synthesis inhibitors
- RNA synthesis inhibitors
25
bacteriocidal vs. bacteriostatis
bacteriocidal: kill bacteria (cell wall synthesis inhibitors)
bacteriostatic: slow growth of bacteria (the rest of types of bacteria)
* you should
26
Can you use bacteriocidal & bacteriostatic antibiotics together
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
27
difference between bacteria & human cells
bacteria cells have cell walls & human cells don't, so we don't destroy human cells when using antibiotics and reduce adverse effects
28
do antibiotics work better on gram positive or negative
gram positive: thick cell wall = more chances for antibiotic to cause problem in cell wall = more effective
29
how do these antibiotics work
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
30
what is the beta lactam ring
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
31
T/F: beta lactam rings can be destroyed by bacteria
T, bacteria can create betalactamasys
32
4 antibiotics that have beta lactam ring
- penicillin: penicillin, ampicillin
- cephalosporin: cefazolin
- carbapenems: impenem-cilastatin
- misc: vancomycin
33
natural penicillin
penicillin
34
prototype for borad spectrum penicillin
ampicillin
35
extended spectrum (broad spectrum & kantipseudomonal)
Piperacillin
36
effective for penicillin resistant varieties of bacteria (antistapholococcal)
Oxacillin
37
is Oxacillin effective against MRSA
No
38
are penicillins more effective against gram positive or negative
positive
39
what kind of spectrum do penicillins generally have
narrow
40
T/F: penicillins are generally widely spread to all body tissues
T, excluding CSF
41
what excretes penicillin
rapidly excreted by kidneys
| very distinct smell in urine
42
do these penicillins have short or long half-lifes and how does this affect their drug schedule
short half-life, so they tend to need to be given more frequently
43
#1 adverse effect of penicillins
allergic reactions due to the chemical structure = body identifies it as foreign substance
44
narrow vs. broad spectrum
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
which is more likely to kill normal flora, broad or narrow spectrum bacteria
broad
46
largest class of antibiotics
cephalosporins
47
what do cephalosporins treat
mostly gram -
48
T/F: cephalosporins are bacteriocidal
T
49
T/F: cephalosporins have beta lactam rings
T
50
T/F: cephalosporins & penicillins are similar in their mechanism of actions, side effects, & nursing considerations
T
51
Difference between cephalosporins & Penicillins
Cephalosporins are also used for gram -
52
_____ of people that have allergy to penicillin also have a cross allergy to cephalosporin
5-10%
53
Describe 1st generation of Cephalosporins
- contain a beta-lactam ring
- most affective against gram +
- only moderate activity against gram -
- do not cross BBB (doesn't enter CSF)
54
Describe 2nd generation of Cephalosporins
- 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
Describe 3rd generation of Cephalosporins
- broader spectrum against gram - than 2nd gen
- longer duration of action
- resistant to beta lactamase
- able to enter CSF to treat CNS infections
56
Describe 4th generation of Cephalosporins
- more effective against organisms that have developed resistance to earlier cephalosporins
- able to enter CSF in high concentrations to treat CNS infections
57
Describe 5th generation of Cephalosporins
- broad spectrum c extended gram + effectiveness
- effective against MRSA
- still in development; first drug, ceftraline, approved 2010
58
"ceph" or "cepha"
cephalosporin
59
"penems"
carbapenems
60
Are carbapenems a type of bacteriocidal
yes
61
are carbapenems narrow or brad spectrum
broad (kills most gram +, _, & anaerobes)
62
What type of drugs are resistant to desctruction
Carbapenems
63
Why do we combine Cilistatin & Imipenem
So the Cilistatin can help prevent the Imipenem in the kidneys
64
steps to protein synthesis
mRNA: carrying message from DNA to ribosome
tRNA: attaches amino acids together from ribosome
Ribosome: site of protein synthesis
65
why don't antibiotics that affect protein synthesis affect human cells
most human ribosomes are not the same size as the bacteria ribosomes, so structurally they don't fit
66
how antibiotics that affect protein synthesis work
they bind to the ribosomes in bacterial cells & prevent the protein synthesis from happening (bacteria can't make protein in order to reproduce)
67
2 things macrolides are used for
- treatment of gram + in pt's allergic to penicillins
| - H. Pylori
68
mechanism of action of macrolides
inhibit bacterial protein synthesis by binding to 50S ribosome
69
are macrolides bacteriocidal or bacteriostatic
usually bacteriostatic, but can be bacteriocidal
70
mechanism of action of Fluoroquinolones
- prevent bacterial DNA from replicating
| - treat many gram + & _
71
Are Fluoroquinolones bacteriostatic or bacteriocidal
bacteriocidal
72
what are Fluoroquinolones used for
- drug of choice for UTIs
- travellers diarrhea
- respiratory, GI & Gu infections
73
do Fluoroquinolones affect human DNA
no
74
"floxacin"
Fluoroquinolones
75
1 weird side effect of Fluoroquinolones
cartilage problems: tendon rupture
| especially in kids who are developing cartilage & tendons, so can not be used < 18 yrs
76
mechanism of action of Sulfonamides & UTI meds
- 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
what are urinary antiseptics used for
- to treat UTI because of high concentrations in urinary tract due to renal excretion
- not effective for systemic infections
78
_____ 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
vaccines
79
what is active immunity
when the body creates an immune response to an antibody or its vaccine
80
what is passive immunity
when actual pre-formed antibodies are given to someone, without the person's own immune system creating them
81
4 types of vaccines
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
can you use attenuated vaccines in immunosuppressed pt's
no, because they actually could develop a case of the disease harmful enough to hurt
83
can you use MMR or Rubella immunizations in pregnant women
no
84
VAERS
vaccine adverse effect reporting system: any effects that require medical treatment
85
T/F: penicillins are very painful
T, especially IM
86
what's the main different between penicillin & ampicillin
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
"floxacin"
Fluoroquinolones
