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MFD Theme 3 Flashcards

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.

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2
Q

what are the 3 modes of action of antibiotics

A

bacteriostatic
bacteriocidal
bacteriolytic

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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

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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

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5
Q

what is meant by bacteriolytic

A

kills the bacteria and removes the remnants, decreases cell count and viable count

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6
Q

what are common bacterial targets for antibiotics.

A 
Cell membrane 
Cell wall 
Protein synthesis 
RNA polymerase
DNA synthesis 
Folate metabolism
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7
Q

what bacterial component do penicillins target

A

Cell wall

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8
Q

what bacterial component do macrolides and tetracylines target

A

Protein synthesis

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9
Q

what bacterial component do fluroquinolones target

A

DNA synthesis

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10
Q

what bacterial component do Sulphonamides target

A

Folate metabolism

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11
Q

why is the b-lactam ring in penicillins important

A

gives the penicillin the ability to interact with the cell wall

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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.

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13
Q

what is a lactam

A

cyclic amide

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14
Q

what are the types of penicillins

A

Benzylpenicillin

β-lactamase-resistant forms

Broad-spectrum penicillins

Extended-spectrum penicillins

Reversed-spectrum penicillins

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15
Q

what are Benzylpenicillin

A

Original form

Not very active against gram negatives.

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16
Q

when are important β-lactamase-resistant forms important and name an example

A

Flucloxacillin

important against B-lactamase producing bacteria

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17
Q

what are Broad-spectrum penicillins effective against and name an example

A

More effective against gram-negative bacteria

amoxicillin

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18
Q

what are Extended-spectrum penicillins effective against

A

Also effective against pseudomonads

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19
Q

what are Reversed-spectrum penicillins- effective against and name an example

A

Greater activity against gram negatives than gram positives

Ticarcillin/Piperacilli

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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

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21
Q

what does the amino group of penicillin facilitate

A

• Amino group facilitates penetration of outer membrane (beta lactam) of Gram-negative bacteria

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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

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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

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24
Q

what are Cephalosporins

A

Bactericidal

Same mode of action as other beta-lactam antibiotics (such as penicillins)

but less susceptible to penicillinases

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25
Q

what are the b-lactam antiobiotics

A

Penicillins and Cephalosporins

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26
Q

outline absorption for penicillin

A
  • Vary when given orally

Delayed release preparations available (procaine and benzanthine)

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27
Q

outline Distribution for penicillin

A
  • Widely distributed throughout the body although concentrations in tissues and body fluids vary.
  • Do not normally enter CSF (except with meninges inflammation)
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28
Q

outline Metabolism for penicillin

A

Short half-lives (30-80 min)

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29
Q

outline Excretion for penicillin

A

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.

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30
Q

what are the adverse reactions for penicillins

A

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

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31
Q

how do sulphonamides work

A

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
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32
Q

what enzymes in folate synthesis do sulphonamides inhibit

A

dihydropteroate synthetase

dihydrofolate reductase

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33
Q

Why is sulphonamide selective meaning our DNA is not affected?

A

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

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34
Q

outline absorption for sulphonamides

A

80-100% of drug given orally is absorbed from stomach and intestines.

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35
Q

outline Distribution for sulphonamides

A

Widely distributed including the CNS

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36
Q

outline Metabolism for sulphonamides

A

Metabolism occurs in liver by n-acetylation.

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37
Q

outline Excretion for sulphonamides

A

In urine ~ 30 mins.

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38
Q

Adverse reactions

A

Problem

Photosensitivity

Stevens-Johnson syndrome (<1% frequency).
Hemopoietic disturbances- impact on no of RBC and WBC

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39
Q

what are fluoroquinolones

A

Broad spectrum

Effective against Gram-positives & Gram-negatives

Discovered during search for antimalarial drugs

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40
Q

what to fluoroquinolones target

A

Target DNA replication via Type II topoisomerases:

DNA-gyrase
DNA topoisomerase IV

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41
Q

what is the function of DNA gyrase

A

Regulates amount of supercoiling

Facilitates movement of transcription and replication complexes through DNA helix

Removes knots

Helps fold DNA

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42
Q

what is the function ofDNA topoisomerase IV

A

Homologue of gyrase

Unlinks daughter DNA replicons

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43
Q

in which bacteria do quinolones inhibit dna gyrase

A

gram negatives

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44
Q

in which bacteria do quinolones inhibit topoisomerase IV

A

gram positives

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45
Q

outline absorption of quinolones

A

Oral admin most effective

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46
Q

outline distribution of quinolones

A

Very well absorbed in upper GI tract.

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47
Q

outline metabolism of quinolones

A

Potent inhibitor of CYP1A2

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48
Q

outline excretion of quinolones

A

Mainly excreted in tubular secretion

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49
Q

what are the adverse reactions of quinolones

A

Hypersensitivity and GIT disturbance

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50
Q

what is the bacterial targets for macrolides

A

ribosomes & protein synthesis

at the level of the 50S ribosome

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51
Q

what is the mechanism by which macrolides block protein synthesis

A

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

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52
Q

outline absorption of macrolides

A

Oral admin requires protected tablets to avoid inactivation by gastric juice

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53
Q

outline distribution of macrolides

A

Diffuses readily into most tissues but does not cross BBB. Crosses placenta.

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54
Q

outline metabolism of macrolides

A

Metabolised by demethylation (CYP3A4). Can therefore potentiate the effects of other drugs

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55
Q

outline excretion of macrolides

A

Excreted in the bile.

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56
Q

what are the adverse reactions of macrolides

A

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

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57
Q

what is the target for tetracyclines

A

bacterial ribosomes & protein synthesis at the level of 30S

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58
Q

what is the difference between the mechanism of action for macrolides and tetracyclines

A

both target protein synthesis but macrolides at the level of the 50S ribosome and tetracyclines at 30S

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59
Q

what is the mechanism of action for tetracylines

A

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
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60
Q

outline absorption for tetracyclines

A

Absorption greater in fasting state and inhibited by concurrent ingestion of dairy products metal ions and certain antacids

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61
Q

outline distribution for tetracyclines

A

Widely distributed entering most tissues

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62
Q

outline metabolism for tetracyclines

A

Excreted both via the bile and in kidneys by glomerular filtration

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63
Q

outline excretion for tetracyclines

A

Relatively long half lives (6-18 hours due to enterohepatic recirculation)

64
Q

What is antibiotic resistance?

A

The ability of a microbe to resist the effects of medication that could previously have been used to eradicate the microbe

65
Q

how does antibiotic resistance occur

A
  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
Q

what is intrinsic resistance

A

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
Q

what is Acquired resistance

A

drug resistance is selected by antibiotic use

e. g.:
- penicillin resistance in Staphylococcus aureus.
- Develop by gaining genes or horizontal gene transfer

68
Q

what is cross resistance and when does it occur

A

resistance to one antibiotic leads to resistance to another

  • Often in the same class of antibiotics
  • Occurs as a result of acquired resistance
69
Q

what is multi-resistance

A

resistance to several antibiotics via independent mechanisms.

70
Q

what are fusobacterium spp. intrinsically resistant to and why

A

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
Q

what acquired resistance is there of staph aureus

A

MRSA: Methicillin resistant S. aureus

VISA: Vancomycin insensitive S. aureus

CA-MRSA: Community acquired MRSA

VRSA: Vancomycin resistant S. aureus

72
Q

how does acquired resistance occur

A

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
Q

how does a mutation lead to acquired resistance

A

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
Q

what are the mechanisms of horizontal gene transfer

A

transformation
transduction
conjugation

75
Q

how does transformation take place

A

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
Q

how does transduction take place

A

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
Q

how does conjugation take place

A

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
Q

what are the 3 main mechanisms bacteria use to become resistant to antibiotics

A

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
Q

what could bacterial resistance involve

A

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
Q

what is the mode of action of amoxicillin

A

b-lactam antibiotic
bacteriocidal
inhibits synthesis of bacterial peptidoglycan cell wall by inhibition of transpeptidases which enable peptide bond formation

81
Q

what are b-lactamases and how do they work

A

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
Q

what are some b-lactamases inhibited by

A

clavulanic acid

83
Q

what is augmentin (co-amoxiclav) and how does it work

A

amoxicillin + clavulanic acid - used in more severe dental infections seen in hospital -

Inhibits b-lactamases therefore penicillin resistant infections are now penicillin susceptible

84
Q

outline how NDM-1 is involved in antimicrobial resistance through horizontal gene transfer

A

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
Q

what are mechanisms for reduced antibiotic concentration at the target

A

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
Q

what are the Oral Biofilm Antibiotic Resistance Mechanisms

A

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
Q

how is there increased antibiotic resistance in biofilm

A

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
Q

what are Factors Contributing to the Emergence and Spread of Antibiotic Resistance

A

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
Q

Why have dentists over-prescribed antibiotics? what are the Common errors

A

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
Q

outline the Treatment of bacterial dental infections

A
  • 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
Q

Which guidance should be followed to prescribe antibiotics ?

A
  • BNF
  • SDCEP Drug Prescribing in Dentistry
  • FGDP (UK) Antimicrobial Prescribing for GDPs
  • BSP Young Practitioner’s Guide
92
Q

how can over prescribing be avoided

A
  • 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
Q

outline Responsible Prescribing

A
  • Prescribing should be justified
  • Follow current prescribing guidance
  • Communication with patient regarding prescription
  • Prescribing audits completed
  • Prescribing monitored
94
Q

how can there be an increase of public awareness of antimicrobial resistance

A
  • 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
Q

what are the standard precautions in dentistry

A 
hand hygiene 
PPE 
sharps safety 
sterilisation/disinfection 
surgery design 
dental unit waterlines 
waste management 
vaccines/screening
96
Q

what are the target precautions in infection control

A

patient specific
outbreak scenario
procedure specific
agent specific

97
Q

what are some Infectious Agents

A

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
Q

what are the routes of transmission

A
  • Patient –> patient
  • Patient –> dentist
  • Dentist–> patient
99
Q

what is nosocomial transmission

A

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
Q

what is iatrogenic transmission

A

Due to the action of a physician or a therapy

101
Q

what is idiopathic transmission

A

Of unknown cause.

102
Q

what does transmission requires

A

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
Q

what are the Biggest source of infection

A

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
Q

what are other sources of infection

A

Environmental micro-organisms

  • environmental microbe: Salmonella spp, Shigella spp, Campylobacter spp
  • environmental mycobacteria: Clostridium spp

Normal commensal microflora
Staphylococci
-Staphylococcus epidermidis
-Staphylococcus aureus

105
Q

what are issues with sources of infection

A 
•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
Q

what are the vehicles to blood transmission

A

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
Q

what are Six routes of transmission

A 
•	In utero
•	Inhalation
•	Ingestion
•	Implantation
•	Inunction
Injection
108
Q

how can infection be transmitted by in utero

A

Placenta is a barrier for most microbes
oTreponema pallidum - syphilis
oCytomegalovirus
oRubella - German measles

Relevance to the clinic - low

109
Q

how can infection be transmitted by inhalation

A 
across moist surfaces
aerosols-  Aerosols are everywhere!
- Corynebacterium diphtheriae
- Streptococcus pyogenes
- Neisseria meningitidis
- Bordetella pertussis
- Streptococcus pneumoniae
- Mycobacterium tuberculosis
110
Q

how can infection be transmitted by ingestion

A

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
Q

how can infection be transmitted by Implantation

A

often via trauma to skin

  • Staphylococcus epidermidis and Staph. aureus
  • Clostridium tetani and Cl. Perfringens
  • Streptococcus pyogenes

Relevance to the clinic - high

112
Q

how can infection be transmitted by • Inunction

A

microbes driven into tissue by rubbing

  • Staphylococcus epidermidis and Staph. aureus
  • Neisseria gonorrhoeae

Relevance to the clinic – moderate/low

113
Q

how can infection be transmitted by injection

A

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
Q

How is there Transmission of infection by inhalation of serious pathogens:

A

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
Q

how is infection transmitted by ingestion, implantation and injection

A

Ingestion

  • Contaminated
  • ->Instruments
  • ->Clothing
  • ->surfaces

Implantation

  • Contaminated
  • ->instruments

Injection

  • contaminated instruments
  • injected material
  • ->needlestick
116
Q

what are Infection control procedures

A

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
Q

what is the difference between infection and sterilisation

A

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
Q

what are the general principles of sterilisation and disinfection (graphically)

A

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
Q

what does sterile mean

A

< 1 in 106 chance of a single viable organism being present

120
Q

what does the K constant determine

A

Constant determines the efficiency of killing

121
Q

what are the Methods for disinfection

A

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
Q

what is chemical disinfection affected by

A

o concentration
o temperature
o pH
o protein contamination

123
Q

what are the Methods for sterilisation

A

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
Q

what is autoclaving

A

High pressure saturated steam

121°C for 15 minutes

125
Q

what are Transmissable spongiform encephalopathies

A

Kuru

BSE (mad cow disease) & scrapie

Creutzfeldt-Jacob-Disease (CJD)

Prions

126
Q

what are prions and how are they transmitted

A 
misfolded proteins
no nucleic acid
capable of propogation
can not be cultured (yet)
extreme resistance to heat, radiation &amp;  disinfectants

transmitted through infected nervous tissue

127
Q

what are dentists advised to ensure to safeguard against Transmissible spongiform encephalopathies:

A

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
Q

what are Infection control procedures

A

•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
Q

why are Chemical Mouthrinses Necessary?

A
  • 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
Q

what are the arguments against chemical mouthrinses

A

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
Q

what are the antimicrobial chemicals used in the UK

A
  • Iodine- dressing to a socket after tooth extraction
  • Sanguinarine
  • Chlorhexidine
  • Hexetidine
  • Triclosan
  • Sodium Lauryl Sulphate
  • Thymol
  • Cetylpyridinium Chloride
132
Q

what are Phenolic mouthrinses

A
  • Listerine
  • Sainsbury’s Antiseptic Mouthwash with Fluoride
  • Sainsbury’s Oral Health Extra
  • Strength Antiseptic Mouthwash
  • Sotol Mouthwash Tablets
  • Boots Thymol Glycerin
133
Q

what is chlorohexidine, how is it used and what are the problems with it

A

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
Q

what is Triclosan

A

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
Q

how does Triclosan have antimicrobial activity

A

Targets lipid synthesis (enoyl reductase)

Inhibits glycolysis (lactate dehydrogenase/pyruvate kinase)

Inhibits H+-ATPase (cellular pH falls)

136
Q

what is Listerine

A

Blend of essential oils with antiseptic properties.

137
Q

what is risk

A

the probability an individual will develop a disease in a particular time period-usually expressed as a %

138
Q

what is a risk factor

A

a factor that increases the likelihood that an individual will develop the disease

139
Q

what are factors that contribute to risk

A

environmental, behavioral or biological factors

140
Q

what is a risk determinant

A

a risk factor that cannot be modified

e.g. race (not very useful in practice although is seen in literature), gender, genetic factors

141
Q

what is a risk marker associated with

A

disease risk but is not necessarily on the causal pathway.

142
Q

what is the strongest to weakest hierarchy of scientific evidence

A

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
Q

what is the strongest to weakest hierarchy of scientific evidence

A

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
Q

what are some of the risks for periodontitis

A
  • 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
Q

what are the risk factors for dental caries (outline the categories )

A

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
Q

what does the odds ratio (OR) represent

A

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
Q

what do the OR factors tell us

A

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
Q

when is OR useful

A

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
Q

how are biological assays used to asses the individual risk

A

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
Q

what are the characteristics of a good biological assay

A

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
Q

what is meant by sensitivity (and what is the eq for this)

A

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
Q

what is meant by specificity (and what is the eq for this)

A
  • 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
Q

what are some biological assays which can be used for assessing periodontal risk

A

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
Q

what does the BANA test measure

A

Measures proteolytic enzyme activity

Most activity in plaque is due to P. gingivalis, Treponema denticola, Tannerella forsythia in plaque sample

155
Q

what does Oral IQ™ 11 assess

A

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

Stage 2 (16 decks)

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