Lecture 1- Exam 1 Flashcards
(126 cards)
1
Q
Normal Flora of the mouth: (5)
A
- viridans group streptococci
- other strep species
- lactobacillus
- actinomyces species
- prevotella species
2
Q
Most of the normal flora of the mouth are considered:
A
Commensal organisms
(they live in mouth, help the mouth, the mouth doesn’t mind them)
3
Q
Of the following normal flora of the mouth, which are gram positive? Gram negative?
- viridans group streptococci
- other strep species
- lactobacillus
- actinomyces species
- prevotella species
A
Gram Postitive:
-viridans group strep
-other strep species
-lactobacillus
-actinomyces species
Gram Negative:
-prevotella species
4
Q
The main gram negative species of bacteria we see in the mouth is:
A
prevotella species
5
Q
What differentiates gram positive from gram negative bacteria?
A
Cell wall
6
Q
-bulk of oral bacteria
-primarily cocci or irregular shaped (plemorphic)
-oxygen tolerance varies from facultative anaerobes to strict anaerobes
-cell wall has thick peptidoglycan layer
A
Gram positive oral bateria
7
Q
-facultative anaerobes
-periodontal pockets
-dental plaques
-carious teeth
-gram positive organism
A
actinomyces
8
Q
-facultative anaerobe
-produces lactic acid
-role in dentin caries rather than enamel caries
-gram positive organism
A
lactobacillus
9
Q
-facultative anaerobe
-cocci
-produce lactic acid
-some implicated in caries
-gram positive organism
A
streptococcus
10
Q
Why do we have more drugs available to gram positive bacteria?
A
Our target site, the cell wall is more readily available to attack
11
Q
If oxygen is present this bacteria will readily utilize it, however is oxygen is not available they will still find the means to survive:
A
facultative anaerobes
12
Q
Main strep species associated with caries:
A
strep mutans
13
Q
What allows strep mutans to cause dental caries?
A
Acidogenic bacteria (acid producing) and aciduric (acid tolerant)
14
Q
The “bad” strep species of the oral cavity:
The “good” strep species of the oral cavity:
A
bad: strep mutans
good: strep mitis, strep sanguinis
15
Q
-acidogenic
-aciduric
-highly associated with caries
-notorious for dentin lesions
A
Strep mutans
16
Q
-first oral organisms detected in infants (primary colonizers)
-commensals
-peroxigenic (produce hydrogen peroxide)
A
Strep mitis
Strep sanguinis
17
Q
Why are S. mitis and S. sanguinis considered “good” bacteria for the mouth?
A
They are peroxogenic meaning they produce hydrogen peroxide- this inhibits the growth of S. mutans and P. gingivalis and other oral pathogens
18
Q
Gram ____ bacteria have a higher resistance to antibiotics
A
negative
19
Q
Many gram negative bacteria are found in the mouth but are especially established in:
A
subgingival plaque
20
Q
Describe the oxygen requirements for gram negative oral bacteria:
A
range of oxygen tolerance but most are strict or facultative anaerobes
21
Q
Describe the cell wall of gram negative oral bacteria:
A
-thin peptidoglycan layer
-contains beta-lactimase
-LPS/endotoxin
22
Q
T/F: We see more of a systemic effect with gram negative bacteria in the mouth
A
True- due to LPS/endotoxin
23
Q
List the gram negative bacteria found in the oral cavity:
A
- porphyromonas
- prevotella
- fusobacterium
- actinobacillus/aggregatibacter
- treponema
- neisseria
- veillonella
24
Q
Gram negative bacteria that are periodontal pathogens:
A
- P. gingivalis (major)
- P. intermedia
- F. nucleatum
25
Gram negative bacteria of the oral cavity associated with aggressive periodontitis:
A. actinomycetemcomitans
26
Gram negative bacteria that plays an important role in acute periodontal conditions (ANUG):
Treponema
27
T/F: PCNS and amoxicillins are good drugs to use for initial gram positive infections
True
28
Why are PCNS and amoxicillins less effective on gram negative bacteria?
Because the beta-lactimase produced by many of these bacteria
29
Drug that ARRESTS the growth of organism:
Bacteriostatic
30
What must be present in order for a bacteriostatic drug to be effective?
Must have active immune system
31
Drug that KILLS the organism:
Bactericidal
32
What type of patients would you AVOID using a bacteriostatic drug on?
patients without an immune system (neutropenic, meningitis, endocarditis for example)
33
T/F: Static drugs are dependent on the host immune system to actively arrest bacterial growth
True
34
Type of drugs more commonly used when patients have poor immune system function:
Bactericidal
35
What are the two mechanisms of bactericidal drugs?
1. cell wall inhibitors
2. DNA inhibitors
36
List some examples of bactericidal drugs that are cell wall inhibitors:
1. beta lactams
2. PCNS
3. cephalosporins
37
List some examples of bactericidal drugs that are DNA inhibitors:
1. fluoroquinolones
2. metronidazoles
38
How do bacteristatic drugs work?
Protein synthesis inhibitors
39
List some examples of bacteristatic agents that work via protein synthesis inhibitors:
1. macrolides
2. clindamycin
3. doxycycline
40
Drugs that work better, the higher the peak concentration gets above the minimum inhibitory concentration:
Concentration dependent
41
MIC:
minimum inhibitory concentration of a drug necessary to inhibit the growth of an organism
42
How do we typically dose concentration dependent drugs?
Give high dose with extended intervacls between doses
43
Concentration dependent drugs often have a ______ that is fairly long
PAE (post-antibiotic effect)
44
PAE:
Post-antibiotic effect
(bacterial suppression after antibiotic concentrations fall below MIC)
45
Type of drug that is dependent on the amount of time rather than concentration above the MIC:
Time-dependent
46
How do we dose time-dependent drugs:
Due to no PAE, we have to dose them more frequently throughout the day
(in order to keep the dose above the MIC)
47
Higher concentration ---> greater killing
Concentration dependent
48
Give some examples of concentration dependent drugs:
1. fluoroquinolones (dose one time daily)
2. metronidazole (dosed two times daily)
49
Concentrations need to be reinforced, leading to more dosing
More exposure ---> more killing
Time-dependent
50
Give some examples of time-dependent drugs:
1. Beta-lactams (no PAE)
2. Clindamycin (some PAE)
3. Azithromycin (some PAE)
4. Tetracyclines (some PAE)
51
Fill in the following information for Cephalexin:
1. Usual dosage range:
2. Professors recommended dosing
3. ____-dependent drug
4. categorized as a ______
5. half-life:
6. excretion:
1. 250-1000mg q6hrs or 500mg q12hrs
2. 500mg q6hrs
3. time dependent
4. Beta lactam
5. ~1hr
6. 80-100% as unchanged drug ni 6-8hrs
52
Patients who have a PCN allergy receive more:
-vancomycin
-clindamycin
-fluoroquinolones
53
What are two aspects that are "increased" due to PCN allergies?
1. increased cost of antibiotics
2. increased length hospitalization
54
When someone has a PCN allergy and other drugs are prescribed in place of PCN, we see increased drug resistant organisms including:
-69% increased risk of MRSA infections
-30.1% more VRE infections
-26% increased risk of C. Diff
55
Looking at statistics ____ in 10 patients report a PCN allergy
1 in 10
56
What percent of patients do NOT have. PCN allergy?
99%
57
Less than 1 out of 1000 PCN allergies result in:
Anaphylaxis
58
Three characteristics of side effect:
1. predictable
2. dose-related
3. can affect anyone
59
Four characteristics of drug allergies:
1. unpredictable (hypersensitivity rxn)
2. not dose-related
3. cannot affect anyone
4. antibody or T-cell stimulation
60
Resemble allergic reactions but are not immune mediated:
Allergic-like or pseudo-allergic reaction
61
Give two examples of psuedo-allergic reactions:
1. vancomycin infusion reaction
2. morphine rash
62
Antibody responsible for anaphylaxis:
IgE
63
If a patients response to a drug is rash, when you give them that drug again, their response will be:
rash (not anaphylaxis)
64
T/F: There is no genetic component to allergies
True
65
Less than ___% of all reported PCN allergies result in anaphylaxus
1%
66
Rash characterized by skin breakdown or falling off:
SJS
67
What are some high risk signs of PCN allergy indicating likely an IgE or T cell response:
1. lip/facial swelling
2. breathing difficulty/wheezing
3. skin peeling
4. mouth blisters
5. drop in BP
68
T/F: Hives is a reason to avoid PCN
False
69
Most common cause of hives:
Viral infections
70
T/F: Common rash and itching likely do not represent true IgE allergy and therefore do NOT require avoidance of PCN
True
71
Helps to distinguish a side effect rash from an allergy rash:
Time of onset
72
T/F: if a rash appears within one hour of the initial dose of the drug it is much more likely for that to be a sign of a true allergic reaction
True
73
-delayed onset (6+ hrs after drug given)
-typically less pruritic
-lesions lasting >24hrs
-fine desquamation with resolution over days to weeks
Benign T-cell mediated (not a true allergic rxn)
74
-onset minutes to hours after drug given
-significant pruritus
-raised off the skin
-each lesion last <24hrs
-fades without scarring
IgE-mediated (true allergic rxn)
75
-onset days to weeks after drugs given
-mucosal and/or organ involvement
-blistering and/or desquamation
-usually requires hospitalization
Severe T-cell mediation or severe cutaneous
76
T/F: PCN true IgE rxn is rare
True
77
Are the following indicators a patient may truly have a PCN allergy?
-family history of PCN allergy
-GI symptoms
-headache
-yeast infection
No
78
Is there cross-sensitivity between PCN and Cephalosporin allergies
No
79
PCN and cephalosporins both contain:
Beta-lactam rings
80
T/F: the allergy to PCN is related to the beta-lactam ring
False
(the R side chain is associated with the allergic rxn)
81
Although there is little to no cross-sensitivity with PCN and cephalosporin rxns, the most common cephalosporin rxns when a patient is allergic to PCN occur with:
Cephalosporins that have a similar R-side chain to PCNs (first and second generation cephalosporins)
82
1. Do you need to avoid amoxicillin?
2. Can you use a cephalosporin?
-Drug: PCN
-Rxn: Rash
-Onset timing: Unsure
-How long ago: 20+ yrs
-Treatment: none
1. No
2. Yes
83
1. Do you need to avoid amoxicillin?
2. Can you use a cephalosporin?
-Drug: PCN
-Rxn: Unknown
-Onset timing: Unsure
-How long ago: 30+ yrs
-Treatment: none
1. No
2. Yes
84
1. Do you need to avoid amoxicillin?
2. Can you use a cephalosporin?
-Drug: amox
-Rxn: rash
-Onset timing: 2 days
-How long ago: 5 yrs
-Treatment: none
1. No
2. Yes
85
1. Do you need to avoid amoxicillin?
2. Can you use a cephalosporin?
-Drug: augmentin
-Rxn: rash + itching
-Onset timing: 4 days
-How long ago: 12 yrs
-Treatment: none
1. No
2. Yes
86
1. Do you need to avoid amoxicillin?
2. Can you use a cephalosporin?
-Drug: IV PCN
-Rxn: difficulty breathing
-Onset timing: hours
-How long ago: 50+ yrs
-Treatment: hospital
1. Yes
2. Yes (certain ones)
87
1. Do you need to avoid amoxicillin?
2. Can you use a cephalosporin?
-Drug: Ampcillin
-Rxn: Skin ulcerations
-Onset timing: 1-2 days
-How long ago: 15-20 yrs
-Treatment: hospital
1. yes
2. yes (certain ones)
88
The deadliest antibiotic you can prescribe:
Clindamycin
89
What is the main risk associated with the dangers of Clindamycin?
C. Difficile infection
90
Once C. Diff is contracted, 1 in 5 people will get it again.
One in three of patients with recurrent C. Diff:
Will die within 6 months
91
Most significant risk factor for C. Diff infection:
Antibiotic use
92
The highest risk for C. Diff is ____ after antibiotic exposure
first month
93
To reduce the risk of C. Diff, a dentist should prescribe _____ antibiotics as opposed to ____. As well as using is ____ duration
1; 2; shorter
94
Patients taking _____ are twice as likely to contract C. Diff due to antibiotic use
PPI
95
List the components to C. Diff prevention through antibiotics stewardship:
1. limit spectrum of antibiotic therapy
2. limit duration of antibiotic therapy
3. limit combination antibiotic therapy
96
You've given an antibiotic script to the patient with the following how can you help to prevent C. Diff:
-65yo+
-recent hospitalization or nursing home
-weak immune system (HIV/AIDS, CA, or on immunosuppressants)
-previous C. diff infection
-taking PPI
Prescribe probiotic
97
Beta lactam mechanism of action:
Binds and inhibits PCN binding protein (PBP)
98
Probiotics reccomended for adults and children on antibiotic treatment:
1. S. Boulardii
2. L. Acidophilus + L. Casei
3. L. Acidophilus + L. Delbrueckii + B. Bifidum
4. L. Acidophilus + L. Delbrueckii + B. Bifidum + S. Salivarius
99
Who might we suggest the use of probiotics to?
1. individuals 65+yo
2. recent hospitalization or nursing home
3. weak immune system
4. previous C. Diff infection
5. anyone taking PPI
100
____% of PCN allergie labels are acquired before the age of 3
75%
101
_____ are the best anti-infectives
Beta-lactams
(extremely powerful, extremely effecticve, extremely safe)
102
Beta-lactam mechanism of action:
Binds & inhinitis PCN binding protein (PBP)
103
Binds to PCN binding proteins (PBP); Blocks cell wall synthesis causing the walls to leak; Lowers cell death threshold:
beta-lactams
104
T/F: ALL beta-lactams are bactericidal
True
105
Most used and effective antibiotics with the least toxicity:
Beta-lactams
106
What accounts for the differences in beta-lactams (such as acid stability, absorption, spectrum, susceptibility to beta-lactamases):
Side chains
107
T/F: Beta-lactams cannot cross the placenta and are not distributed into breast milk
False- they can cross the placenta and are distributed into breast milk
108
Natural PCNs include:
1. PCN G
2. PCN VK
109
Natural PCNs mechanism of action is predominately active against:
Strep species
110
Natural PCNS are ineffective against:
Gram negative species
111
Extended spectrum PCNs are also referred to as:
Aminopenicillins
112
Aminopenicillins include:
1. Ampicillin
2. Amoxicillin
113
What is the benefit of the amino group on aminopenicillins:
They are able to penetrate the gram-negative cell wall
114
All PCNs (amino & natural) are inhibited by:
Beta-lactamases
115
Enzymes that break down beta-lactams:
Beta-lactamases
116
Resistance mechanisms utilized by bacteria to avoid antibiotics:
1. efflux pumps
2. beta-lactamases
3. RNA modification
117
What is the reason behind adding Clavulonate with Amoxicillin?
Clavulonate is a beta-lactamase inhibitor
(extends out the amoxicllins ability to tackle the gram negative bacteria)
118
Clavulonate + Amoxicillin =
Augmentin
119
What does Augmentin work against? (Clavulonate + Amoxicillin)
More gram negatives, anaerobes & Staph
120
If you have a dental infection with an abscess that has failed amoxicillin. what is a suitable option?
Augmentin
121
When an abscess is present in the mouth, we should start to think it is caused by:
When an abscess is present on the outside of the body, were should start to think it is caused by:
Gram negative anaerobes
MRSA
122
Group of antibiotics that have a beta-lactam ring as part of the structure:
B-lactams
123
Enzyme released by bacteria that disables the beta-lactam ring thus the antibiotic is ineffective:
B-lactamase
124
Compound added to a B-lactam antibiotic that disables the B-lactimase thus the antibiotic is effective again:
B-lactimase inhibitor
125
A major side effect with augmentin:
diarrhea
126
