MFD Theme 3 Flashcards
(155 cards)
1
Q
what is antibiotic guardianship
A
supporting healthcare practitioners the need to give antimicrobials and when it is appropriate. If not bacterial induced drug will have no benefit.
2
Q
what are the 3 modes of action of antibiotics
A
bacteriostatic
bacteriocidal
bacteriolytic
3
Q
what is meant by bacteriostatic
A
holds bacterial cell in a steady state of growth, it does not stop/inhibit the- it stops them from increasing further
4
Q
what is meant by bacteriocidal
A
kills the bacteria (must kill 99%) total number of bacterial cells does not change, viable cells decrease
5
Q
what is meant by bacteriolytic
A
kills the bacteria and removes the remnants, decreases cell count and viable count
6
Q
what are common bacterial targets for antibiotics.
A
Cell membrane Cell wall Protein synthesis RNA polymerase DNA synthesis Folate metabolism
7
Q
what bacterial component do penicillins target
A
Cell wall
8
Q
what bacterial component do macrolides and tetracylines target
A
Protein synthesis
9
Q
what bacterial component do fluroquinolones target
A
DNA synthesis
10
Q
what bacterial component do Sulphonamides target
A
Folate metabolism
11
Q
why is the b-lactam ring in penicillins important
A
gives the penicillin the ability to interact with the cell wall
12
Q
what is the structure of a b-lactam
A
lactam with a heteroatomic ring structure, consisting of three carbon atoms and one nitrogen atom.
13
Q
what is a lactam
A
cyclic amide
14
Q
what are the types of penicillins
A
Benzylpenicillin
β-lactamase-resistant forms
Broad-spectrum penicillins
Extended-spectrum penicillins
Reversed-spectrum penicillins
15
Q
what are Benzylpenicillin
A
Original form
Not very active against gram negatives.
16
Q
when are important β-lactamase-resistant forms important and name an example
A
Flucloxacillin
important against B-lactamase producing bacteria
17
Q
what are Broad-spectrum penicillins effective against and name an example
A
More effective against gram-negative bacteria
amoxicillin
18
Q
what are Extended-spectrum penicillins effective against
A
Also effective against pseudomonads
19
Q
what are Reversed-spectrum penicillins- effective against and name an example
A
Greater activity against gram negatives than gram positives
Ticarcillin/Piperacilli
20
Q
what was the function of early penicillins and how effective were they effective
A
Early Penicillin’s destroyed by the acidic environment of the stomach
Acid labile
Oral route (Not very well absorbed)
Parenteral route
- Slow IV
- Preferably IM
- High availability
Narrow spectrum of activity
Gram-positives but only a few Gram-negatives
21
Q
what does the amino group of penicillin facilitate
A
• Amino group facilitates penetration of outer membrane (beta lactam) of Gram-negative bacteria
22
Q
what do penicillins to
A
Inhibit the enzyme (transpeptidases) which are responsible for reaction which establishes cross links in the peptidoglycan cell wall
The bacteria MUST be in a state of multiplication
23
Q
what is the structure of a bacterial cell wall
A
• Strength & organisation of cell dependent on complex polymer – Peptidoglycan straight chains cross-linked together
Each glycan chain has a side chain of amino acids with is linked to next chain by a pentaglycine cross-link -this is the site of attack of penicillin
24
Q
what are Cephalosporins
A
Bactericidal
Same mode of action as other beta-lactam antibiotics (such as penicillins)
but less susceptible to penicillinases
25
what are the b-lactam antiobiotics
Penicillins and Cephalosporins
26
outline absorption for penicillin
- Vary when given orally
| Delayed release preparations available (procaine and benzanthine)
27
outline Distribution for penicillin
- Widely distributed throughout the body although concentrations in tissues and body fluids vary.
- Do not normally enter CSF (except with meninges inflammation)
28
outline Metabolism for penicillin
Short half-lives (30-80 min)
29
outline Excretion for penicillin
Mainly through the kidney with 90% excreted by tubular secretion.
Clearance reduced in neonates.
Reduce excretion rate by use of probenecid, which inhibits tubular secretion.
30
what are the adverse reactions for penicillins
Hypersensitivity
- Seen with all penicillins
- Skin rashes, fever, anaphylactic shock (rare), serum sickness
- 10-15% will show repeat reaction
- Protein markers become antigenic so increased immune response by individual
GIT disturbance
-due to altered gut flora
Haemostatic effects
-Blood clotting
31
how do sulphonamides work
Selectively targets metabolic pathways; Folate biosynthesis.
* Acts as a false substrate, looks exactly like pABA
* Bind to enzymes and act as a stereochemical inhibitor those enzymes.
* Trimethoprim does the same
* Prevents the conversion of tetrahydrofolate into DNA
32
what enzymes in folate synthesis do sulphonamides inhibit
dihydropteroate synthetase
dihydrofolate reductase
33
Why is sulphonamide selective meaning our DNA is not affected?
Humans can transport folic acid from diet into cells
Bacteria don’t have this mechanism- folic acid cannot enter cell so MUST be made within the cell itself
The drug will have equal effect but it will only be toxic to bacterial cell
34
outline absorption for sulphonamides
80-100% of drug given orally is absorbed from stomach and intestines.
35
outline Distribution for sulphonamides
Widely distributed including the CNS
36
outline Metabolism for sulphonamides
Metabolism occurs in liver by n-acetylation.
37
outline Excretion for sulphonamides
In urine ~ 30 mins.
38
Adverse reactions
Problem
Photosensitivity
Stevens-Johnson syndrome (<1% frequency).
Hemopoietic disturbances- impact on no of RBC and WBC
39
what are fluoroquinolones
Broad spectrum
Effective against Gram-positives & Gram-negatives
Discovered during search for antimalarial drugs
40
what to fluoroquinolones target
Target DNA replication via Type II topoisomerases:
DNA-gyrase
DNA topoisomerase IV
41
what is the function of DNA gyrase
Regulates amount of supercoiling
Facilitates movement of transcription and replication complexes through DNA helix
Removes knots
Helps fold DNA
42
what is the function ofDNA topoisomerase IV
Homologue of gyrase
| Unlinks daughter DNA replicons
43
in which bacteria do quinolones inhibit dna gyrase
gram negatives
44
in which bacteria do quinolones inhibit topoisomerase IV
gram positives
45
outline absorption of quinolones
Oral admin most effective
46
outline distribution of quinolones
Very well absorbed in upper GI tract.
47
outline metabolism of quinolones
Potent inhibitor of CYP1A2
48
outline excretion of quinolones
Mainly excreted in tubular secretion
49
what are the adverse reactions of quinolones
Hypersensitivity and GIT disturbance
50
what is the bacterial targets for macrolides
ribosomes & protein synthesis
| at the level of the 50S ribosome
51
what is the mechanism by which macrolides block protein synthesis
block translocation
Incoming tRNA comes to increase amino acid chain
binds to site near RNA exit tunnel
causes peptidyl-transferase RNA drop-off
no peptide chain development
specificity to the 50S unit rather than eukaryotic unit
52
outline absorption of macrolides
Oral admin requires protected tablets to avoid inactivation by gastric juice
53
outline distribution of macrolides
Diffuses readily into most tissues but does not cross BBB. Crosses placenta.
54
outline metabolism of macrolides
Metabolised by demethylation (CYP3A4). Can therefore potentiate the effects of other drugs
55
outline excretion of macrolides
Excreted in the bile.
56
what are the adverse reactions of macrolides
Cholestatic hepatitis may occur after prolonged use of erythromycin estolate
GIT disturbances seen at large doses
Transitory auditory impairment- partial deafness. If you take it away the hearing comes back.
Hypersensitivity reactions
57
what is the target for tetracyclines
bacterial ribosomes & protein synthesis at the level of 30S
58
what is the difference between the mechanism of action for macrolides and tetracyclines
both target protein synthesis but macrolides at the level of the 50S ribosome and tetracyclines at 30S
59
what is the mechanism of action for tetracylines
Stops tRNA from binding the ribosome in the first place
interrupts elongation phase of synthesis
several binding sites on 30S RNA subunit
sterically inhibits transfer RNA binding
- unbinds
- rebinds
- futile loop
60
outline absorption for tetracyclines
Absorption greater in fasting state and inhibited by concurrent ingestion of dairy products metal ions and certain antacids
61
outline distribution for tetracyclines
Widely distributed entering most tissues
62
outline metabolism for tetracyclines
Excreted both via the bile and in kidneys by glomerular filtration
63
outline excretion for tetracyclines
Relatively long half lives (6-18 hours due to enterohepatic recirculation)
64
What is antibiotic resistance?
The ability of a microbe to resist the effects of medication that could previously have been used to eradicate the microbe
65
how does antibiotic resistance occur
1. some bacterial cells in the human body are drug resistant
2. Antibiotics kill bacteria but resistant strains remain
3. antibiotics resistant bacteria multiply
4. antibiotic resistance spreads
66
what is intrinsic resistance
an innate property of the bacterium seen in all strains
E.g.:
- resistance of Gram-negative bacteria to many b-lactams, b-lactam doesn’t reach the target. More effective in gram positive cell walls.
- resistance of Gram-negatives to vancomycin (too large to cross the cell membrane).
67
what is Acquired resistance
drug resistance is selected by antibiotic use
e. g.:
- penicillin resistance in Staphylococcus aureus.
- Develop by gaining genes or horizontal gene transfer
68
what is cross resistance and when does it occur
resistance to one antibiotic leads to resistance to another
- Often in the same class of antibiotics
- Occurs as a result of acquired resistance
69
what is multi-resistance
resistance to several antibiotics via independent mechanisms.
70
what are fusobacterium spp. intrinsically resistant to and why
vanomycin
- glycopeptides (large molecule) generally don't cross the gram negative outer membrane of fusobacterium
Neomycin
-Anaerobic bacteria lack electron transport chain and do not take up the drug.
71
what acquired resistance is there of staph aureus
MRSA: Methicillin resistant S. aureus
VISA: Vancomycin insensitive S. aureus
CA-MRSA: Community acquired MRSA
VRSA: Vancomycin resistant S. aureus
72
how does acquired resistance occur
Vertical GT- genes passed from mother cell to daughter cell. Through generations. Can lead to selection in population when exposed to a drug
```
Horizontal GT (Transformation
Transduction Conjugation) - Transferred from cell to cell, not from generation to generation.
```
Mutation
73
how does a mutation lead to acquired resistance
Chromosomal mutation resulting in a genetically-altered bacterial population. If there is a selection pressure for this then the chromosomal mutation is selected forward in the population
Alteration of DNA within cell
Evolutionary advantage
74
what are the mechanisms of horizontal gene transfer
transformation
transduction
conjugation
75
how does transformation take place
DNA taken up into the bacterial cell from the environment. In the case of a biofilm the DNA can be released in the biofilm ECM and uptaken by other cells. The DNA may encode genes that allow them to survive in environment.
DNA taken up encodes new genes and may include genes to confer antibiotic resistance
76
how does transduction take place
DNA transmitted via viruses
Certain viruses able to infect bacteria- bacteriophage infect bacterial cells
DNA picked up by viruses and passed from one bacterial cell to another
If infection not associated with phage lysis then the dna can spread from cell to cell. Or via transposons – ‘jumping genes’.
77
how does conjugation take place
occurs via pili
A donor cell containing a conjugative plasmid and a recipient cell which does not
Only donor cells have pili- donor cells form contact with a recipient cell
Cells are drawn together for the transfer of DNA
Plasmids are small rings of DNA
Resistance genes often on plasmids
Plasmids able to be transmitted between bacteria
78
what are the 3 main mechanisms bacteria use to become resistant to antibiotics
Modification of antibiotic / inactivating the antibiotic
Modification of target
Sequestering the antibiotic from its target – if its collected up and prevented drug from reaching target
79
what could bacterial resistance involve
Reduced uptake into the cell
Removal of the antibiotic from the cell
Production of enzymes to degrade / inactivate antibiotics
Structural alteration to drug target
80
what is the mode of action of amoxicillin
b-lactam antibiotic
bacteriocidal
inhibits synthesis of bacterial peptidoglycan cell wall by inhibition of transpeptidases which enable peptide bond formation
81
what are b-lactamases and how do they work
modified penicillin binding proteins produced by bacteria that provide multiresistance to b-lactam antibiotics.
they bind to the b-lactam ring of the antibiotic and hydrolyse it
82
what are some b-lactamases inhibited by
clavulanic acid
83
what is augmentin (co-amoxiclav) and how does it work
amoxicillin + clavulanic acid - used in more severe dental infections seen in hospital -
Inhibits b-lactamases therefore penicillin resistant infections are now penicillin susceptible
84
outline how NDM-1 is involved in antimicrobial resistance through horizontal gene transfer
Carbapenems are potent b-lactams
NDM-1 breaks down the carbapenem ring.
The gene encoding NDM-1 is present on a plasmid 9- (Can be transferred between bacteria, including E.coli, Klebsiella and others.)
85
what are mechanisms for reduced antibiotic concentration at the target
Reduced drug concentration in the periplasm or cytoplasm: reduced import and increased export
Reduced import (porin-deficient mutants) is common in labs, but not clinically
Increased export can be due to:
- antibiotic-specific pumps (e.g. TetA for tetracycline)
- multidrug efflux pumps
86
what are the Oral Biofilm Antibiotic Resistance Mechanisms
Modification of the antibiotic
-Reaction with the extracellular matrix
Modification of the target
-Slow growth rate
Reduced intracellular concentration
- Exclusion by the matrix
- Up-regulation of efflux pumps (can pump drug out)
87
how is there increased antibiotic resistance in biofilm
slow penetration- antibiotic may fail to penetrate beyond the surface layers of biofilm
- antibiotic can be de-activated before it can diffuse through e.g. B-lactamase
resistant phenotype- some bacteria may differentiate into a protected phenotypic state
- persisters
altered microenvironment- in zones of nutrient depletion or waste product accumulation (red), antibiotic action may be antagonised
-microscale gradients can antagonise the antibiotics (e.g. O2, pH)
88
what are Factors Contributing to the Emergence and Spread of Antibiotic Resistance
Excessive and prolonged use of antibiotics.
Over-the-counter availability of antibiotics in many countries.
Prolonged survival and treatment of patients with chronic diseases.
Antibiotics in animal feeds.
International travel and migration of populations.
Including ‘medical tourism’.
International distribution of fresh produce
89
Why have dentists over-prescribed antibiotics? what are the Common errors
Unnecessary use of antibiotic
Inappropriate choice of antibiotic
Incorrect dosage
Incorrect length of prescription
Failure to check medical history- allergies etc
“Many practitioners prescribed antibiotics inappropriately with inconsistent frequency and dose, and for prolonged periods"
90
outline the Treatment of bacterial dental infections
* Local measures
* Drain pus if present
* Tooth extraction
* Access and drain through root canals
* Soft tissue pus drain by incision
* Debride infected periodontal pockets
* Irrigate / debride infected operculum
91
Which guidance should be followed to prescribe antibiotics ?
* BNF
* SDCEP Drug Prescribing in Dentistry
* FGDP (UK) Antimicrobial Prescribing for GDPs
* BSP Young Practitioner’s Guide
92
how can over prescribing be avoided
* Follow up-to-date prescribing guidance
* Prioritise local measures
* Ensure suitable length to appointments
* Informed consent for treatment – options, risks, benefits
* Communication regarding risks of over- prescribing
93
outline Responsible Prescribing
* Prescribing should be justified
* Follow current prescribing guidance
* Communication with patient regarding prescription
* Prescribing audits completed
* Prescribing monitored
94
how can there be an increase of public awareness of antimicrobial resistance
* Toolkit to support antimicrobial stewardship
* Ongoing training of staff and CPD
* Communication with patients
* Patient education
* Information for patients and posters for dental practice waiting rooms
95
what are the standard precautions in dentistry
```
hand hygiene
PPE
sharps safety
sterilisation/disinfection
surgery design
dental unit waterlines
waste management
vaccines/screening
```
96
what are the target precautions in infection control
patient specific
outbreak scenario
procedure specific
agent specific
97
what are some Infectious Agents
Blood borne viruses: HBV, HCV, HIV
Respiratory viruses: Common colds (rhinovirus) to influenza A
Bacteria: Mycobacterium tuberculosis, MRSA, pseudomonads, Legionella pneumophila
Prions
HIV and hepatitis easily killed by hepatitis
98
what are the routes of transmission
- Patient --> patient
- Patient --> dentist
- Dentist--> patient
99
what is nosocomial transmission
Originating or taking place in a hospital, acquired in a hospital, especially in reference to an infection.
Secondary to the original cause for treatment
100
what is iatrogenic transmission
Due to the action of a physician or a therapy
101
what is idiopathic transmission
Of unknown cause.
102
what does transmission requires
A source of infection
- index case (person to person)
- contamination
- Source- In a dental setting it’s a person or contaminated instrument
A vehicle
- blood
- saliva
- contaminated instruments
A route
- Six recognised routes
103
what are the Biggest source of infection
Overly infected
Incubating a disease
- prodomal stage of infection
- sometimes no signs of disease
- can be highly infectious
Healthy carriers
- convalescent carrier (past carriers, persistent resevoirs, diphtheria, sore throat, hepB)
- asymptomatic carriers- no past history, hep B
104
what are other sources of infection
Environmental micro-organisms
- environmental microbe: Salmonella spp, Shigella spp, Campylobacter spp
- environmental mycobacteria: Clostridium spp
Normal commensal microflora
Staphylococci
-Staphylococcus epidermidis
-Staphylococcus aureus
105
what are issues with sources of infection
```
•healthy vs compromised patient
•cutting tissue
•overt pathogens
- HIV
- Hep B
- Mycobacterium tuberculosis
•opportunistic pathogens
- almost anything
- does the patient need to be compromised?
```
106
what are the vehicles to blood transmission
Blood
- HIV
- Hep B
```
Saliva
- Glandular fever (infectious mononucleosis)
Epstein-Bar Virus
- Not HIV or Hep B
o unless blood is present
```
Direct contact (skin)
- Staphylococci
- non-commensal (environmental) contamination
Objects (fomites)
- Instruments
- clothing
107
what are Six routes of transmission
```
• In utero
• Inhalation
• Ingestion
• Implantation
• Inunction
Injection
```
108
how can infection be transmitted by in utero
Placenta is a barrier for most microbes
oTreponema pallidum - syphilis
oCytomegalovirus
oRubella - German measles
Relevance to the clinic - low
109
how can infection be transmitted by inhalation
```
across moist surfaces
aerosols- Aerosols are everywhere!
- Corynebacterium diphtheriae
- Streptococcus pyogenes
- Neisseria meningitidis
- Bordetella pertussis
- Streptococcus pneumoniae
- Mycobacterium tuberculosis
```
110
how can infection be transmitted by ingestion
usually food and drink but in the dental clinic it is objects introduced into the mouth
- Corynebacterium diphtheriae
- Streptococcus pyogenes
- Neisseria meningitidis
- Salmonella spp
- Mycobacterium tuberculosis
Relevance to the clinic - high
111
how can infection be transmitted by Implantation
often via trauma to skin
- Staphylococcus epidermidis and Staph. aureus
- Clostridium tetani and Cl. Perfringens
- Streptococcus pyogenes
Relevance to the clinic - high
112
how can infection be transmitted by • Inunction
microbes driven into tissue by rubbing
- Staphylococcus epidermidis and Staph. aureus
- Neisseria gonorrhoeae
Relevance to the clinic – moderate/low
113
how can infection be transmitted by injection
often by a biting insect
- Malaria (mosquitos)
- >Plasmodium
- Typhus (rat & mouse fleas)
- >Rickettsia
- Yellow fever virus (mosquitos)
- HIV
- Hepatitis
Relevance to the clinic – high
- needlestick
114
How is there Transmission of infection by inhalation of serious pathogens:
Pneumonic plague
- no insect vector required
- high mortality
- rapid onset
- Yersinia pestis
Tuberculosis
- once considered an occupational disease for dentists
- Mycobacterium tuberculosis
Influenza
- apparently associated with coughing but may require direct contact
- Viral
Legionnaires’ Disease
- associated with air-con and hot tubs
- Legionella pneumophila
Severe Acute Respiratory Syndrome (SARS)/Middle East Respiratory Syndrome (MERS)
- direct contact and aerosols
- A corona virus
115
how is infection transmitted by ingestion, implantation and injection
Ingestion
- Contaminated
- ->Instruments
- ->Clothing
- ->surfaces
Implantation
- Contaminated
- ->instruments
Injection
- contaminated instruments
- injected material
- ->needlestick
116
what are Infection control procedures
Check patient medical history
Physical barriers
Disinfection of surgery surfaces
- separation of areas
Clean & sterile instruments
- Sterilisation- killing everything alive on the instruments and those not alive to e.g. spores, viruses
- Single use disposable instruments/material
Safe waste disposal
Boost host defences
- behaviour change
- immunisation
Prions not susceptible
117
what is the difference between infection and sterilisation
sterilisation is “The inactivation or removal of all self- propagating biological entities.” - however doesnt include prions
disinfection is more vague: The reduction in viable organisms to the point where risk of infection is acceptable
118
what are the general principles of sterilisation and disinfection (graphically)
Efficiency is: N=k/CT
k depends on many things
- species of microbe present
- physiological state of the microbe
- presence of organic material (blood/saliva)
For a given value of C
- graph of Log10 count vs Time can predict when sterility is achieved
- Slope = Death Rate
- D = time to achieve 90% reduction in viable count
119
what does sterile mean
< 1 in 106 chance of a single viable organism being present
120
what does the K constant determine
Constant determines the efficiency of killing
121
what are the Methods for disinfection
Heat: boiling water- kills bacteria but not spores
Pasteurisation
- 2 types
- heat to 66oC/71oC
- kills Mycobacterium tuberculosis but not some bacteria (heat resistant) or spores
```
Chemical disinfection
- wide variety eg
o glutaraldehyde
o chlorine compounds
o phenolics
o alcohol
o chlorhexidine
```
122
what is chemical disinfection affected by
o concentration
o temperature
o pH
o protein contamination
123
what are the Methods for sterilisation
Dry heat
-oven
Moist heat
- Autoclave
- Tyndalisation
Radiation sterilisation
- cobalt 60 (60Co)
- specialised environment
- used mainly for disposables
- syringes, needles, catheters etc
- very effective but may damage article
Sterilising gases/chemicals
-eg sulphur dioxide, ethylene oxide
Filtration
- physical removal
- IV fluids
124
what is autoclaving
High pressure saturated steam
| 121°C for 15 minutes
125
what are Transmissable spongiform encephalopathies
Kuru
BSE (mad cow disease) & scrapie
Creutzfeldt-Jacob-Disease (CJD)
Prions
126
what are prions and how are they transmitted
```
misfolded proteins
no nucleic acid
capable of propogation
can not be cultured (yet)
extreme resistance to heat, radiation & disinfectants
```
transmitted through infected nervous tissue
127
what are dentists advised to ensure to safeguard against Transmissible spongiform encephalopathies:
Endodontic reamers and files are treated as single use,
The highest standards of decontamination are observed for all dental instruments,
Manufacturers’ decontamination instructions are followed for all instruments, and where instruments are difficult to clean, single use instruments should be used wherever possible.
High risk patients include symptomatic and asymptomatic (e.g. family history of disease).
128
what are Infection control procedures
•Check patient medical history
•Physical barriers
•Disinfection of surgery surfaces
-separation of areas
Clean & sterile instruments
- Single use disposable instruments/material
Safe waste disposal- Separation of clinical and domestic waste
Boost host defences
- behaviour change
- immunisation
Separation of clinical and domestic waste
- yellow bags
- black bags
sharps bins
Occupational health
HIV/HCV screening
Hep B
- Vaccination
- sero-conversion check
Stay up to date with:
- Diphtheria
- Tetanus
- Polio
- MMR
Recommended
- Annual flu vaccine
129
why are Chemical Mouthrinses Necessary?
* Plaque causes disease
* Plaque consists of microbes
* Oral microbes are very numerous
* Microbes multiply rapidly
* Eradication by mechanical means is probably impossible
* Use of chemical antimicrobials will reduce the oral load of microbes and alleviate disease
130
what are the arguments against chemical mouthrinses
Adverse effects on microbial ecology of the mouth
Lazy???- easier to mouthwash than to floss
Efficacy???
Other measures are more effective
Diet
Fluoride in toothpaste/drinking water
Good prophylaxis
131
what are the antimicrobial chemicals used in the UK
* Iodine- dressing to a socket after tooth extraction
* Sanguinarine
* Chlorhexidine
* Hexetidine
* Triclosan
* Sodium Lauryl Sulphate
* Thymol
* Cetylpyridinium Chloride
132
what are Phenolic mouthrinses
* Listerine
* Sainsbury’s Antiseptic Mouthwash with Fluoride
* Sainsbury’s Oral Health Extra
* Strength Antiseptic Mouthwash
* Sotol Mouthwash Tablets
* Boots Thymol Glycerin
133
what is chlorohexidine, how is it used and what are the problems with it
High substantivity* (up to 12 hours)- relates to the persistence of its antimicrobial activity of the surface.
2x daily rinse with 0.2% solution
•Plaque growth completely inhibited
•Gingivitis inhibited
•Efficacy confirmed by numerous studies
Problems:
•Tooth staining (iron salts)
•Taste
•Allergy
134
what is Triclosan
Polychlorophenoxyphenol.
Plax (briefly) and other Colgate-
Palmolive products
Substantivity is low cf CHX (co-polymer added)
Lipid soluble (penetrates skin & mucosa)-
Antiphlogistic
Broad spectrum antimicrobial (multiple targets)- does have antimicrobial activity
Efficacy demonstrated against gingivitis
135
how does Triclosan have antimicrobial activity
Targets lipid synthesis (enoyl reductase)
Inhibits glycolysis (lactate dehydrogenase/pyruvate kinase)
Inhibits H+-ATPase (cellular pH falls)
136
what is Listerine
Blend of essential oils with antiseptic properties.
137
what is risk
the probability an individual will develop a disease in a particular time period-usually expressed as a %
138
what is a risk factor
a factor that increases the likelihood that an individual will develop the disease
139
what are factors that contribute to risk
environmental, behavioral or biological factors
140
what is a risk determinant
a risk factor that cannot be modified
| e.g. race (not very useful in practice although is seen in literature), gender, genetic factors
141
what is a risk marker associated with
disease risk but is not necessarily on the causal pathway.
142
what is the strongest to weakest hierarchy of scientific evidence
meta-analyses & systematic reviews
randomised controlled trials
cohort studies
case control studies
cross sectional studies
animal trials and in vitro studies
case reports, opinion papers and letters
143
what is the strongest to weakest hierarchy of scientific evidence
meta-analyses & systematic reviews
randomised controlled trials
cohort studies
case control studies
cross sectional studies
animal trials and in vitro studies
case reports, opinion papers and letters
144
what are some of the risks for periodontitis
* Age major risk factor e.g. cancers, autoimmune diseases
* Systemic disease
* Poor restorations
* Anticancer agents may remove saliva
* Composition of plaque- shift towards more pathogenic microflora, inflammation, caries
* Family/socio-economic status
145
what are the risk factors for dental caries (outline the categories )
factors that directly contribute to caries development- diet, tooth, time, bacteria in biofilm
oral environmental factors- fluoride, chewing gum, protein, saliva etc
personal factors- oral health literacy, knowledge, education, income, dental insurance coverage
146
what does the odds ratio (OR) represent
the odds that an outcome (e.g. oral health) will occur given a particular ‘exposure’ (e.g. potential risk factor), compared to the odds of the outcome occurring in the absence of that exposure.
147
what do the OR factors tell us
the higher the factor the bigger the risk
- OR=1 Exposure does not affect odds of outcome
- OR>1 Exposure associated with higher odds of outcome
- OR<1 Exposure associated with lower odds of outcome
148
when is OR useful
when confirming whether an ‘exposure’ is a risk factor for the outcome
when comparing the magnitude of different risk factors. Looking at the odds ratio.
149
how are biological assays used to asses the individual risk
Measure biological factors associated with disease risk, e.g. specific bacteria, host factors (e.g destructive enzymes)
Possible aid in assessment of current disease ‘activity’, prediction of future disease risk and treatment planning
150
what are the characteristics of a good biological assay
Validity
-The test measures what it is intended to measure
Reliability
-The test is consistent when used at different times/by different people
Clarity, simplicity and objectivity
-Measurement criteria should be simple and unambiguous
Quantifiability
-Measurements amenable to statistical analysis, usually better than traffic light system
Acceptability
-The test should not be painful or demeaning to the subject
High sensitivity and specificity
-Determines how good clinical test is
151
what is meant by sensitivity (and what is the eq for this)
does it pick up all the individuals that have the disease and distinguish them from patients who don’t
SENSITIVITY: a/(a+c) x 100
-the proportion of people who test positive and go on to develop disease
152
what is meant by specificity (and what is the eq for this)
* How specific is the test at distinguishing those who will get disease from those who remain healthy
* Ratio of the true negatives over all the negatives
SPECIFICITY: d/(b+d) x 100
-the proportion of people who have a negative test result and remain disease-free
153
what are some biological assays which can be used for assessing periodontal risk
medium- saliva, GCF, serum
markers- Markers of pathogenic bacterial load, Host response markers, Tissue breakdown products, Host enzymes, Inflammatory mediators, Genetic markers
The BANA test
154
what does the BANA test measure
Measures proteolytic enzyme activity
Most activity in plaque is due to P. gingivalis, Treponema denticola, Tannerella forsythia in plaque sample
155
what does Oral IQ™ 11 assess
Assesses identity and action of 11 bacteria associated with periodontitis
Not utilised in everyday practice
Tells the bacteria that are present, however it’s the host response that determines periodontal health, which this does not measure
