EXAMS Flashcards

(448 cards)

1
Q

Why didn’t early hunter gatherers have a large presence of dental caries?

A

Due to the fact that hunter gatherers did not have a source of simple carbohydrates. This means that cariogenic bacteria were unable to develop, as cariogenic bacteria feast on simple carbohydrates.

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2
Q

What are the steps to radio-graph assessment?

A
  1. Exposure
  2. Detector orientation
  3. Horizontal detector positioning
  4. Vertical detector positioning
  5. Horizontal beam angulation
  6. Vertical beam angulation
  7. Central beam position
  8. Colimator rotation
  9. Sharpness
  10. Overall diagnostic value
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3
Q

What are the steps to gingival assessment?

A

C - colour
C - contour
C - consistency
T - texture
E - exudate

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4
Q

What are the steps to ILA?

A
  1. Patient
  2. CC
  3. MHx
  4. SHx
  5. DHx
  6. Exam
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5
Q

What is TRIM?

A

TRIM is an acronomy for:
Timing
Relevance
Involvment
Method

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6
Q

What is differential diagnosis?

A

It is a process where a physician is able to assign probability of one illness in comparison to others accounting for patients sympotms.

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7
Q

What is a white spot lesion?

A

A white spot lesion is an incipient caries lesion, it has a dull opaque chalky appearance and occurs due to demineralisation of enamel caused by cariogenic bacteria

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8
Q

What is the pathogenesis of caries?

A
  1. Cariogenic bacteria requires simple sugars for anaerobic respiration
  2. Glucose is processed through glycolysis in the cariogenic bacteria
  3. Glucose is converted into 2 pyruvate
  4. In order to than convert NADH electron carrier into NAD+, pyruvate is converted into lactic acid
  5. Lactic acid accumulates in the cariogenic bacteria and is released into the oral environemnt
  6. Lactic acid has pH of about 2.35 which is slower than the critical pH of hydroxyapatite which means Lactic acids is able to cause dissociation of hydroxyal groups in hydroxyapatite which leads to demineralisation of the enamel
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9
Q

How can we remineralise a tooth?

A

In presence of Calcium, Phopshate and/or Fluoride in the biofilm or in salivary pool, if pH of above 4.5 is restored the tooth would be immediatley remineralised

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10
Q

Why is fluoride so effective?

A
  1. It is able to stop cariogenic bacteria metabolism
  2. Drive remin
  3. Create fluoride salivary pool
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11
Q

Why are incipient carious lesion look so much opaque?

A

Due to increased porosity. Increased posicity of enamel traps water which has a different refractive index which makes it look more dull

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12
Q

Why is calcium still needed for fluoride incorpiration?

A

Fluoroapatite still needs calcium and phosphate

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13
Q

How would you describe WSL

A

L - location
C - colour
T - texture
C - contour

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14
Q

How is calculus formed?

A
  1. Acid attack occurs
  2. Statherin releases Ca
  3. Excess calcium is able to percipitate on the biofilm as it can be used as an epitatic agent
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15
Q

What are the steps of rubber dam critique?

A
  1. Dam preperation (hole positionin, punching)
  2. Clamp selection (choice, gingival trauma, retention)
  3. Clamp placement (gingival trauma)
  4. Dam placement (alignment of dam)
  5. Frame placement (positioning of frame)
  6. Dam finish (isolation of appropriate teeht, moistture control)
  7. Dam removal
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16
Q

What are the major salivary glands?

A

Parotid (serous), Submandibular (mixed) sublingual (mixed).

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17
Q

Where are the Von Ebners glands located?

A

Circumvallate papillae and they are serous.

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18
Q

What are the functions of the salivary proteins and dissolved materials?

A

1.Acid neutralisation

2.Promotion of remineralisation

3.Creation of pellicle

4.Antibacterial properties

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19
Q

What type of buffer does stimulated saliva?

A

Bicarbonate

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20
Q

What type of buffer is in unstimulated saliva?

A

Phosphate

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21
Q

In what conditions can enamel remineralise?

A

In super saturated conditions of the close system

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22
Q

What is the sialo-microbial-dental complex?

A

They are interaction between saliva, biofilm and tooth.

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23
Q

What can change the balance of the oral environment?

A

1.More refined, softer foods

2.Refined CHO

3.Increase in fermentation

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24
Q

Why is erosion so effective?

A

Because it occurs in an open system, where acid is able to remove the minerals used for remineralisation entirely

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25
What is the diffenrence between intrinsic/extrinsic acids and plaque acid?
Plaque acid is less strong than intrinsic/extrinsic acids, thus take longer to effect enamel
26
Summarise the factors that show that the patient is not at risk of caries.
1.High biodiversity in the biofilm 2.Low amount of acidogenic & aciduric bacteria 3.High numbers of Alkali producing bacteria 4.High resting pH of biofilm
27
What is the main driver of caries?
Lifestyle changes
28
What is the mode of action of APF?
It is able to use it's acidity to dissolve hydroxyapatite and use calcium for creation of fluorapatite – this is great for xerostomic conditions.
29
What is the mode of action of CPP-ACP?
Calcium is intact with a CPP and is able to penetrate deep into the caries lesion and release calcium for remin due to acidity produced by cariogenic bacteria
30
What are the three steps to re-establish a healthy oral health environment?
1.Change the ecology of the biofilm 2.Improve the saliva 3.Remove cause and re-establish new biofilm
31
Who is involved in treatment planning?
Patient and dentist work collectively to develop a plan that satisfies the patient's needs.
32
What do we need to explain to a patient?
1.Their oral health status 2.Waht will happen if nothing is done 3.Treatment options 4.What patient is required to do 5.IF they want to proceed
33
What info do we need for treatment planning?
Full examination, with all histories and potential extra test like bitewing radiographs
34
What are the basic principles of Soft tissue health & preventative treatment?
Focus on hygiene instructions and removal of plaque and stains. Could potentially make a diet diary
35
Why is GV not as advantageous?
Because it requires a removal of a large amount of healthy structure thus it is not ideal for a long term prognosis of the tooth.
36
What is the significance of MI philosophy that relates to the histology of the tooth?
MI philosophy indicates that maximum amount of tooth structure and affected dentine can remain intact IF infected dentine is removed and affected dentine is sealed.
37
What is Site 1?
Pits, fissures and enamel defects on occlusal surfaces of posterior teeth and cingulum and other smooth surfaces of the interiors
38
What is Site 2?
Approximal surfaces in relation to areas in contact with adjacent teeth
39
What is Site 3?
The cervical one-third of the crown, or following gingival recession, the exposed root
40
What are the desired properties of resin composites ?
1.Aesthetics 2.Handling properties 3.Biocompatibility 4.Protect tooth bioactive 5.Function 6.Longevity 7.Radiopacity
41
Where would we use resin composites?
1.Aesthetics 2.Toothstructure to bond 3.Strengthen tooth structure 4.Blood and moisture can be controlled 5.Where occlusal loads are not sever
42
What is the basic composition of composites?
Synthetic Organic resin (which is a viscous liquid) that is bonded to inorganic filler particles with a silane coupling agent made to set or light cured.
43
What particles may give resin radiopacity?
Barium or Strontium
44
What are the steps to bonding resin to enamel?
1.Prophylaxis 2.Acid treatment – for microporosities – increase of surface area for interlocking in the area and create a macromechenical bond – increase of surface area by 2000 times 3.Wash and dry – stop the demin process and remove moisture 4.Fluid (unfiled) resin – flow into microporosities to create resin tags – chemical bonding 5.Unfilled resin polymerised 6.Composite resin placed 7.Polymerised
45
What are the steps to bonding to dentine?
Etching – this will expose collagen – may cause pulpal fluid to flow up which can compromise the bond – etch for a little less Use a primer – wet or dry – dry: collagen is collapsed which rehydrated – wet: small amount of water remains – creation of hybrid zone Unfilled resin Polymerise Filled resin Polymerise
46
How do GIC bond?
They bond chemically throguh ion exchange and can exchange ions with tooth and oral environment.
47
How does acid-base reaction occurs in GIC?
1.Polyacid attacks glass particles – calcium, strontium and fluoride are released 2.Precipitation of salts occurs = gelatation and gathering occurs 3.Maturation phase = acid/base reaction continues for a few days
48
Why do we need to protect the GIC during the maturation phase?
GIC are vulnerable to take-up of extra water or water loss. This may create a loss in physical properties. This can be avoided by layering of unfilled resin of G-coat over the top.
49
What are the steps in applying GIC?
1.Clean the surfaces with pumice and water – for better ion exchange 2.Use Polyacrylic acid – depending on % - to remove the smear layer and exposure the clean tooth surface for ionic exchange 3.Wash it off – stop the reaction 4.Dry but do not desiccate – stop flow of dentinal fluid 5.Place GIC 6.Protect in the moisture sensitive phase
50
How does amalgam set?
When certain alloys are processed like silver or tin, they can harden when mixed with liquid mercury
51
What are the steps of amalgam placing?
1.Remove caries or remove failed amalgam 2.Consider depth of cavity – at least 2 mm into dentine 3.Remove unsupported enamel 4.Retention - macromechanical retention 5.Liner/base 6.Pack amalgam using a plugger – permite ect amalgam used in sim 7.Burnish 8.Carve using cuspal inclines 9.Articulating paper and adjustment 10.Polish 24 hours later
52
What are some of the techniques for caries diagnosis?
1.Visual Examination – clean, dry, illuminate well and use the tip of the explorer 2.Radiographs - just remember of superimposition, it is probably bigger than it is on radiographs 3.DIAGNOdent - measuring reflected light – little to no florescence in clean, healthy teeth
53
What are some of causes of damage to the dentine and pulp?
1.Caries - through bacterial acids, toxins and enzymes 2.Micro-leakage – due to unsealed margins – could cause sensitivity and recurrent caries – seal so bacteria can go into a dormant state 3.Mechanical damage – fracture, cavity preparation, cracked cusps, dehydration 4.Thermal damage – during cavity preparation friction, polishing, absence of insulation (base & liner) 5.Chemical damage – Hema & Tegma & other acids
54
What type of questions can we ask the patient about their pain?
1.Location 2.Commencement of pain 3.Character of pain 4.Frequency 5.Duration 6.Time 7.Precipitation factors 8.Other complains
55
Explain hydrodynamic theory.
Dentinal tubules contain an extension of the odontoblasts (odontoblastic process) in the part of the tubule that is proximal to the pulp. Around the odontoblastic process, coiled are small nerve extensions. The rest of the space inside a dentinal tubule is filled by dentinal fluid. If the fluid is disturbed through heat, cold, dehydration and even touch and pressure, it causes the fluid to move which activates the pulpal nociceptros around the odontoblastic processes this cause an action potential and signals for pain.
56
Why don't we advocate to polish the amalgam restoration less than 24 hours after placement?
Because amalgam would not reach it's set, meaning it may chip away and create ecological niches for bacteria to thrive.
57
Is caries a one way street?
NOPE. Even if we have early demin, we can actually remineralise the enamel by changing conditions in the oral cavity to supersaturated condition! We can do it all the way upto cavitation!
58
When can we remineralise the enamel?
1.When the demin is exclusive to the enamel 2.When there is affected dentine but no infected dentine
59
How do we assess the fractures?
1.Tissue exposed – enamel only, enamel and dentine or exposed pulp 2.Surfaces involved 3.Check occlusion
60
What is a bevel?
It is a process of cutting the enamel, at 45%, to increase the surface area of enamel for bonding. This could be created with high speed diamond burs.. Make sure that the transition is smooth. Pls do both palatal and labial.
61
What is the pattern of erosion relating to intrinsic sources?
1.Upper posteriors are affected first 2.Diffuses and affects the upper anterior next
62
What is the pattern of erosion relating to extrinsic sources?
1.Occlusal of lower affected first 2.Palatal of upper anterior
63
How would you assess the teeth on the radiograph?
1.Identify teeth present, unerupted/missing, not imagted and restorations 2.Identify abnormalities that are present
64
How would you identify gingivitis?
1.Localised - 10% - 30% BOP 2.Generalised - >30% BOP No pain or no clinical attachment loss
65
How would you identify periodontitis?
Proximal clinical attachment loss of equal or above 2 teeth, non-adjacent OR Buccal/oral clinical attachment loss of 3mm with 3mm pocketing at 2 teeth or more
66
What are the steps to occlusal analysis?
1.Teeth present/missing 2.Morphology of teeth 3.Wear - mild, moderate, sever 4.Crowding,spacingrotations 5.Axail inclanations 6.Shape of dental arch 7.Cruve of spee and wilsons curve 8.Angle molar classification/canine classification 9.Overbite (%) / overjet (mm) 10.Mediolateral
67
What is the 4A's framework?
Ask, assess, acknowledge and address that can be used to adress a patient with dental anxiety
68
What is ALARA?
It stand for as low as reasonably possible - which is a concept used in radiography in order to reduce radiation exposure for both the operator and patient. 1.Keep your distance 2.Shield 3.Do not take unnecessary radiographs
69
What is the significance of dental pelicle?
It is able to provide some protection to the enamel. It also allows for binding of bacteria to the surface of the tooth
70
What is the needle stick inury protocol in dental emergencies?
1. Stop 2. Place needle/sharp aside 3. Take off gloves 4. Wash hands with soap and water 5. Dry and cover with non-stick dressing 6. Apply pressure if bleeding 7. Let tutor know 8. Contact SADS registered nurse for risk assessment 9. Write up incident report - SLS
71
What is stage 1 periodontitis?
1.1-2mm attachment loss 2.Coronal third bone loss 3.No tooth loss 4.Maximum probing depth of below 4mm 5.Mostly horizontal bone loss 6.Extent variable
72
What is stage 2 periodontitis?
1.3-4mm attachment loss 2.Coronal third bone loss 3.No tooth loss 4.Maximum probing depth of below 5mm 5.Mostly horizontal bone loss 6.Extent variable
73
What is stage 3 periodontitis?
1.5mm or more attachment loss 2.Bone loss extending to middle or apical third of the root 3.Tooth loss due to periodontitis of 4 or less teeth 4.Probing depth of 6 mm or more 5.Vertical bone loss of 3 mm or more 6.Class II or III furcation 7.Moderate ridge defect
74
What is stage 4 periodontitis?
1.5mm or more attachment loss 2.Bone loss extending to middle or apical third of the root 3.Tooth loss due to periodontitis of 5 or more 4.Probing depth of 6 mm or more 5.Vertical bone loss of 3 mm or more 6.Class II or III furcation 7.Moderate ridge defect 8.Mastication disfunction
75
What is Grade A periodontitis?
When there are no evidence of loss over 5 years
76
What is Grade B periodontitis?
When there is a below 2 mm loss over 5 years.
77
What is Grade C periodontitis?
When there is an above 2mm loss over 5 years
78
How to do treatment planning?
1. Differential diagnosis presentation 2. Consent for further tests 3. Further investigation and tests pefromance 4. Presentation of treatment with products and justification and potential timeline 5. Recall to check the results of the treatment
79
How do we manage a patient with dental anxiety?
1.Recognise and acknowledge your patient's anxiety/fear 2.Invite your patient to talk about their anxiety/fear e.i. anything in particular that concerns them 3.Offer some piratical suggestions - try to work with a patient to accommodate for their needs.
80
How to deal with a dissatisfied patient?
1.Acknowledge the distress and the person's experience 2.Say wha has been, or will be, done to investigate the complaint 3.State wat has been done could be done to address the concerns 4.Mention any changes or action taken
81
What is acute pain?
Occurs at tissue damage before treatment. There is an emidiate onset which creates psychological response. It goes with resolution unlike chronic pain.
82
Why do we experience pain?
1.Warning about something 2.Reminding - for example healing promotion
83
Why does swearing increase pain tolerance?
Swearing can cause sympathetic response e.g. arousal - stressed induced analgesia due to increased fight or flight
84
Why does saying "Ow" increase pain tolerance?
There is a theory that motor activation has a modulatory effect in addition to arousal
85
Why do athletes continue playing even after receiving an injury?
The potential explanation is induced analgesia from stress
86
What is the clinical significance of anxiety for LA anaesthetic?
There are studies that show that local anaesthetic is more likely to fail in patient with high dental fear
87
How do we approach pain?
Using biophsycosocial model
88
What are two types of local anaesthetic?
1. Amino esther - broken down by enzymes 2. Amide type - metabolised in the liver
89
What is the mechanism of action of anaesthetics?
The molecules bind to amino acids on amino acids, and simply blocking the channel. This does not allow for depolarisation thus stop the propagation of action potential.
90
What is the main problem that LA needs to overcome prior to blocking the sodium ion channel?
To get through the phospho-lipid bi-layer of the cell membrane
91
How do we modify local anathetic to overcome the phospho-lipid bilayer?
We design it to be amphiphatic
92
What does the pKa in local anaesthetic represent?
It represent the balance between charged and uncharged molecles of the solution. I.E. at pKa 7.6 there is equal number of molecules, thus at pH 7.6 there will be am equal number of molecules
93
What is the importance of RN in local anaesthetic?
The uncharged RN molecules, represent the number of molecules that can pass through the phospho-lipid bi-layer as they are water soluble. Turns to RNH+ which actually bind to sodium channel.
94
Why is the pH of injecting site important?
The pH at the injecting site may alter the numbers of RN making it unable to diffuse into the cells.
95
What happens when the pKa of LA is high?
This can decrease the number of RNs at the injection site thus will prolong the onset of the anaesthetic.
96
What is the objective of vasoconstrictors in LA?
1.Decrease blood flow 2.Slow absorption of LA into blood stream 3.Maintain higher local concentrations of LA 4.Longer duration of LA action 5.Reduced bleeding
97
What are the most common local anaesthetics and their vasoconstrictors?
1. 2% Lignocaine (Xylocaine) with 1:80000 adrenaline 2. 3% Prilocaine (Citanest) with 0.03 iu/ml octapressin 3. 3% Mepivacaine (Scandonest Plain) - no vasocontrictor 4. 4% Articaine (Articadent) with 1:100000 adrenaline
98
What is the standard local anaesthetic equipment?
1. Aspirating and non-aspirating syringes 2. Short (25mm) and long (40mm) needles 3. 25, 27 (the usual size, and 30 gauge needles 4. Glass cartridges
99
What are 3 commonly used LA techniques?
1. Topical 2.Block 3.Infiltration
100
What are the landmarks that help to locate teh site of IAN?
1.Level - coronoid notch, 1cm above lower occlusal plane, midway between arches with mouth wide open, buccal pad 2.Angle - opposite premolars 3.Entry point - pterygotemporal depression
101
When was there a dramatic increase of dental caries?
Around industrial revolution due to production of sucrose
102
What is the main active pathogen in caries?
Acid produced by bacteria
102
What is the main active pathogen in caries?
Acid produced by bacteria
103
What are the 4 Koch's Postulates
1. The microbe should be found in all cases of the disease 2. The microbe can be grown on artificial medium 3. A pure culture of the organism should produce the disease in a susceptible animal 4. A high antibody titre to the microbe should be detected during the infection - may provide protection from subsequent re-infection
104
What are modified Koch's postulates for biofilm induced diseases?
1. The microbe should be present n sufficient numbers to initiate the disease 2. The microbe should generate increased levels of specific antibodies 3. The microbe should possess relevant virulence factors 4. The microbe should cause disease in an appropriate animal model 5. Elimination of the microbe should result in clinical improvement
105
What is the non-specific plaque hypothesis?
1890 hypothesis by Prof. Miller that said that non-specific bacteria and plaque on teeth as awhole is the reason for occurance of dental carries
106
What is the specific organism that causes dental caries?
Streptococcus mutans
107
What is a specific plaque hypothesis?
1960s hypothesis by Prof. Keys, which states that dental caries relates to prevalence for Streptococcus mutans and diet
108
What is the ecological plaque hypothesis?
Disease results from shifts in the balance of the resident plaque microflora. Sugar = increased in pH = increase in acidoduric Streptococcus mutans
109
What is the association between Mutans Streptococci and fissure caries?
Around 71% of fissure caries have a high number of Mutans streptococci
110
What is S. sanguinis?
It is a group of bacteria that is able to increase the pH of the nvironment. It is has an inverse relationship to Mutans streptococci
111
What bacteria is more commonly found in caries on rough surfaces?
Lactobacilli
112
What happens to the levels of Streptococcus Mutans when a subsurface lesion forms?
They dicrease with the depth of the lesion
113
What is a pathogen?
The ability of an organism to cause infectious disease
114
What are the 4 main abilities of pathogenesis?
1.Attache to host 2.Entry into host 3.Colonisation and growth within the host 4.Ability to avoid host defenses
115
What are opportunistic pathogens?
They cause disease in compromised individuals
116
What are pathobionts?
They are bacteria that can become pathogenic if environment changes
117
What is virulence of an organism?
It is the pathogens abilityt o cause disease
118
What are the two main benefits from causing cell damage for a pathogen?
1.Release of nutrients 2.Allow spreading to the next host, by inducing coughing or diarrhoea
119
What is an example of receptor adhesin binding in the mouth?
When bacteria attaches to the pellicle in order to create biofilm. Bacteria has a receptor and pellicle has an adhesin
120
What is a non-specific invasion?
Breaks in skin
121
What is a specific invasion?
Type III secretion
122
What are some of the evasion mechanism available to pathogens?
1. Trace element shortage. Pathogen remove iron from iron binding proteins found, in transferrin and lactoferrin which creates competition for resources 2. Bacteria sense cell density and express virulence genes only when their numbers reach a certain quorum (quorum sensing)
123
What are gingipans?
They are enzymes that are produced by P. Gingivalis. They produce many virulence factors. Gingipains are aggresive endopeptidases (protein distruction)
124
What are the two cells of adaptive immunity only?
T and B cells
125
Can you tell the differences between CD4+ and CD8+ T cells?
Nope, that is why we have the CD system
126
How does innate immunity recognise pathogens?
Through INNATE-PAMPS which are structure that are common to all bacteria but are not present on host cells
127
How does adaptive immunity recognise pathogens?
Through use of different types of marking using immunoglubulins or cytokines
128
What happens when there is no discrimination between self and non-self?
This leads to autoimmunity
129
What are the two modes of adaptive immunity?
1.Humoral immunity - using immunoglobulins 2. Cell mediated - using different T cells
130
Where are White Blood Cells originate from?
Bone marrow, B cells stay in bone marrow or spleen. T cells go to the thymus
131
What is the difference between the structure of the receptors on B and T cells?
T cells have a straight, alfa+beta chain receptor. B cells have an immunoglobulin as a receptor
132
Where usually do mature B and T lymphocytes reside?
T lymphocytes reside in blood and lymph. B lymphocytes just in blood
133
What is the purpose of the TCR receptor?
It is the major receptor on T cells that use used to recognise antigens. It is one of the most important receptors in adaptive immunity and without it the entire adaptive immune system would not be able to function.
134
What is the function of each MHC class of receptors?
MHC class I used used for activation of CD8+ cytotoxic pathway. MHC class II used for activation of helper CD4+ pathway
135
What is the acronym that can be used to remember all the immunoglobulin classes?
MADE in Germany
136
What is the most common immunoglobulin found in saliva
IgA
137
What are some of the functions of immunoglobulins?
1.Neutralisaiton 2.Opsonisation - labeling 3.Cross linking and immobilisation
138
What is interesting about GIC restorations and Mutans Streptococci?
GIC main contain protective components that lower the number of Mutans Streptococci than with amalgam
139
What bacteria is the main cause of root caries?
It is actually belived that root caries have a polymicrobial aetiology, meaning it is usually not just one type of bacteria
140
What are the 5 Pathogenic Determinants pf Cariogenic Bacteria?
1. Sugar transport - high and low affinity transport systems 2. Acid production for proliferation 3.Aciduricity - ability to survive in acidic environments 4.EPS production - contributions to plaque matrix 5.IPS production - allows for production of acit when sugar is not available
141
What are the three sugar transport systems available for S. Mutans?
1.Sucrose-PTS 2.Trehalose-PTS 3.Multi Sugar TS
142
In the EPS metabolism by S. Mutans, what is the function of a Mutan?
It aids in attachment to the biofilm structure to the tooth
143
What is the of glucosyltransferase?
They are extracellular enzymes that have a glucan-binding domain that aids in adherence
144
Why is sucrose so cariogenic?
Because it allows for the binding mechanism relating to GTFs to start unlike glucose
145
Explain ecological plaque hypothesis?
1.Increase sucrose consumption 2.Resulting in increasingly acidic environment 3.This favours acidoduric bacteria 4.This drive demineralisation
146
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How would you assess the teeth on the radiograph?
1. Identify teeth present, unerupted/missing, not imagted and restorations 2. Identify abnormalities that are present
170
Describe the process of odontogenesis
Odontogenesis - formation of tooth germ from primary epithelial band and dental lamina Bud stage: Formation of epithelial bud surrounded by condensing ectomesenchyme Cap stage: Formation of enamel organ and initiasl differentiation of enamel cell types. Dental sac and papilla form and begin genesis of dentine and PDL/cementum respectively. Bell stage: Occlusal shape is now formed IEE cells, all cells of the enamel organ are now differentiated, communication with epithelial band is severed and tooth germ is embedded in ectomesenchyme
171
What are the stages of amelogenesis?
Morphogenic: IEE cells gain polarity Histodifferential: IEE cells differentiate into preaameloblasts - stimulate odontoblasts from DP cells - differentiate into ameloblasts Initial secretory: formation of initial layer of aprismatic enamel on dentine Secretory: Formation of Tome's processes, secrertion of enamel matrix. Proximal end of Tome's process forms interod enamel, distal portion forms rod enamel. Protective: Ameloblasts lay dormant, 50% of the initial population has now apoptosed
172
What is hypoplasia?
It is the reduction in the amount of enamel matrix produced - presents as pitting, may caause sensitivity
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What is hypomineralisation?
It is the inability for sufficient organic material to be removed during maturation stage of amelogenesis - presents as variation in colour from white-yellow-brown, teeth are highly vulnerable to staining and tooth wear
174
What is hypocalcification?
It is insufficient inorganic material deposition during maturative stage - teeth adopt chalky, yellow appearance, highly vulnerable to staining and tooth wear
175
What are 3 types of amelogenesis imperfecta?
1. Hypoplasia 2. Hypomineralisation 3. Hypocalcification
176
How would you identify gingivitis?
1.Localised - 10% - 30% BOP 2.Generalised - \>30% BOP No pain or no clinical attachment loss
177
How would you identify periodontitis?
Proximal clinical attachment loss of equal or above 2 teeth, non-adjacent OR Buccal/oral clinical attachment loss of 3mm with 3mm pocketing at 2 teeth or more
178
What is the aetiology of periodontitis
1. Bacterial build in biofilm - dominance of gram negative and opportunistic bacteria 2. Gram negative bacteria release LPS 3. This triggers an inflammatory response 4. Influx of neutrophils (due to release of IL-8 by epithelial tissue) to form palisade 5. Release of pro-inflamatory cytokines and enzyme - chemotaxic agents for leukocytes & marcophages 6. Need for creation of space for cells - break down of collagen fibres and lateral prolifiration + apical migration of the junction epithelium - creation of the pseudo pocket due to oedema 7. End result - damage to collagen but no damage to periodontal attachmnet
179
Give example of two local and two systemic factor for gingivitis and periodontitis.
Local: calculus and over hangs - more sites for harbouring of bacteria, xerostomia - reduciton in anti-microbial effect of saliva Systemic: Smoking - reduction in blood flow and immune function - more periodontopathogens arise,; Diabetes - increased formation of Advanced Glyation End Products - increased osteo clast function and oxidative stress - increased tissue destruction
180
What are some of the treatment for perio?
Debridment. Remember that long axis to the tooth should be parallel to the terminal shank
181
Describe the problem with syncope of a patient with type I diabetes?
Syncope can occur in patient when insulin administration is mistimed. Brain has an absolute need for oxygen, glucose and neural signalling. If a patient has type I diabetes and they miss their breakfast and take their medication, it can lead to hypoglycemia because the residue glucose will be taken up from the blood. Because brain requires a constant supply of glucose and is unable to do so in this situation, it shuts down.
182
What to do if a patient faint due to hypoglycemic syncope?
1. Stop treatment 2. Lay patient in supine position 3. Provide refined carbohydrates 4. Monitor and supervise - get help if needed
183
What are the affects of aging on endocrine function?
Reduction in: 1. Oestrogen 2. Growth hormone 3. Aldosterone 4. Melatonin
184
What happens when oestrogen production decreases?
Decreased production occurs upon completion of menstruation, leading to two distinct outcomes for 2 systems. For bone: 1. Reduced apoptosis of osteoclasts 2. Decreased IGF-1 formation leading to decreased formation of osteoblasts 3. Reduced osteoprotegerin formation For vasculature: 1. Reduced formation of coagulation factors 2. Reduced function of platelets
185
What happens when growth hormone production decreases?
1. Reduced muscle mass 2. Increased adiposity
186
What happens when aldosterone production decreases?
Reduce secretion leads to hyponatremia or hyperkaleamia
187
What happens when melatonin production decreases?
Reduced secretion which causes advanced sleep phase syndrome
188
What is the pattern for erosion for intrinsic acids?
Palatal of maxillary posteriors and anteriors as the tongue covers the lower teeth relatively well
189
What is the pattern of erosion for extrinsic acids?
Mostly lower posteriors
190
What is the 4A's framework?
Ask, assess, acknowledge and address that can be used to adress a patient with dental anxiety
191
What is ALARA?
It stand for as low as reasonably possible - which is a concept used in radiography in order to reduce radiation exposure for both the operator and patient. 1. Keep your distance 2. Shield 3. Do not take unnecessary radiographs
192
What happens to unpolarised resin?
It may damage the pulp because it is toxic thus it needs to be polymerised. Becomes a problem in wet environment or when placed in large increment.
193
What are the steps to bonding resin to enamel?
1. Prophylaxis 2. Acid treatment – for microporosities – increase of surface area for interlocking in the area and create a macromechenical bond – increase of surface area by 2000 times 3. Wash and dry – stop the demin process and remove moisture 4. Fluid (unfiled) resin – flow into microporosities to create resin tags – chemical bonding 5. Unfilled resin polymerised 6. Composite resin placed 7. Polymerised
194
What are the steps to bonding to dentine?
Etching – this will expose collagen – may cause pulpal fluid to flow up which can compromise the bond – etch for a little less Use a primer – wet or dry – dry: collagen is collapsed which rehydrated – wet: small amount of water remains – creation of hybrid zone Unfilled resin Polymerise Filled resin Polymerise
195
How do GIC bond?
They bond chemically throguh ion exchange and can exchange ions with tooth and oral environment.
196
What are the steps of placing resin of top of GIC base?
1. Cute the GIC and create space for resin 2. Etch 3. Put unfilled resin on the GIC and etch enamel – GIC has irregular shape = micro-mechanical bonding 4. Cure 5. Place resin 6. Cure
197
What is a closed sandwich technique?
When GIC if covered around with another material
198
What is an open sandwich technique?
When GIC is exposed outside the tooth – to the oral environment
199
What are the steps in applying GIC?
1. Clean the surfaces with pumice and water – for better ion exchange 2. Use Polyacrylic acid – depending on % - to remove the smear layer and exposure the clean tooth surface for ionic exchange 3. Wash it off – stop the reaction 4. Dry but do not desiccate – stop flow of dentinal fluid 5. Place GIC 6. Protect in the moisture sensitive phase
200
Why do amalgam may need liners & base?
Due to their thermal properties
201
What are the steps of amalgam placing?
1. Remove caries or remove failed amalgam 2. Consider depth of cavity – at least 2 mm into dentine 3. Remove unsupported enamel 4. Retention - macromechanical retention 5. Liner/base 6. Pack amalgam using a plugger – permite ect amalgam used in sim 7. Burnish 8. Carve using cuspal inclines 9. Articulating paper and adjustment 10. Polish 24 hours later
202
What are the steps of resin based fissure sealant placement?
1. Clean surface – remove debris 2. Etch (orthophosphoric acid 37%) 3. Wash - stop reaction 4. Dry well – frosty appearance 5. Flow in fissure – no bubbles 6. Light cure it 7. Check occlusion
203
What are the steps of GIC/RMGIC based fissure sealant placement?
1. Clean surface – pumice 2. Condition with polyacrylic acid 3. Wash 4. Dry - leave moist 5. Place in fissure 6. Apply protective coat 7. Cure 8. Check occlusion
204
What theory are we using to describe dentine hyper sensitivity?
Hydrodynamic theory
205
Explain hydrodynamic theory.
Dentinal tubules contain an extension of the odontoblasts (odontoblastic process) in the part of the tubule that is proximal to the pulp. Around the odontoblastic process, coiled are small nerve extensions. The rest of the space inside a dentinal tubule is filled by dentinal fluid. If the fluid is disturbed through heat, cold, dehydration and even touch and pressure, it causes the fluid to move which activates the pulpal nociceptros around the odontoblastic processes this cause an action potential and signals for pain.
206
What are some of the materials are used in pulp protection?
1. Varnishes - copalite – used to block dentine tubules – bad longevity 2. Liners - cover the dentine – placed under restorations – used for shallow cavity – CaOH cement (Life) - very alkaline - GIC line bond LC 3. Bases - similar to liners but are thicker – use as dentine replacement – ZnPO4 cement is an example – Zinc Oxide-Eugenol is another example – GIC like the Fuji series
207
What are the steps of placing the liner in a relatively small cavity? Why so?
1. Prepare cavity 2. Condition the cavity 3. Mix Fuji Bond LC 1:1 4. Apply 5. Cure 6. Etch the enamel 7. Wash dry 8. Use unfilled resin 9. Cure 10. Add filled resin This will make sure that RMGIC is able to release fluoride and create a chemical bond with resin
208
Name 3 components of saliva that have anti-bacterial properties.
1. Non-immunological defences 2. Physico-chemical barriers 3. Immunological barriers
209
What role does lactoferrin play in reducing bacterial growth?
Lactoferrin is an iron binding found on mucosal surfaces. Lactoferrin is able to deprive microbes of essential iron by binding iron in saliva, lowering the ability to aquire oxygen. Lactoferrin also enhances lysozyme action.
210
What role do salivary mucins play in reducing numbers of oral bacteria?
Mucins are able to agglutinate microbe and aid their removal
211
What anti-bacterial enzyme is found in high concentration on tears and saliva? What is it's mechanism of action against bacteria?
Lysozyme. It is able to hydrolyse peptidoglycans which are present on bacterial cells walls. It than triggers autolysins which cause bacterial degradation.
212
What are histatins and how do they interfere with the growth of oral bacteria?
Histatins are small peptides which are secreted by submandibular and parotid glands. They are able to interfere with membrane integrity of the bacterial membrane.
213
What are defensins?
Defensins are small antimicrobial peptides that are present in the granules of phagocytic cells thus are able to kill bacteria there
214
How does the flow rate of saliva vary during 24hr cycle?
The rate of saliva production is relatively high during the day and decreases significantly during the night time
215
Name 3 Gram negative bacteria which are thought to lay a significant role in periodontal disease.
1. P.Gingivalis 2. P. Intermidia 3. T. Forsythia
216
Name 3 functions of gingipans.
1. Adherence to and colonisation of epithelial cells 2. Disruption and manipulation of the inflammatory response 3. Degradation of host proteins and tissues
217
What is the main nutritional source in healthy periodontium?
Gingival crevicular fluid
218
Is there an identified pathogen that causes gingivitis?
No. Gingivitis is a result of bacterial accumulation which could be the same type of bacteria or transition of bacteria from gram positive to gram negative.
219
What role does GCF play in gingivitis?
It is able to remove tissue breakdown products, introduce inflammatory mediators and antibodies
220
How do we approach treatment planning?
1. Diagnosis presentation 2. Consent 3. Further investigation and tests 4. Recall to check the results of the treatment
221
What is a phenotype?
It is our genotype + environment
222
What is the main difference between somatic cells and gametes?
Somatic cells have a diploid number of chromosomes. Gametes have a haploid number of chromosomes
223
What is dominance/recessiveness?
Differences in the DNA code between alleles at the same locus may give rise to dominance or recessivness which couple with sex linkage, may give rise to simple modes of inheritance.
224
What is the law of segregation?
The two alleles for a heritable character segregate during gamete formation and end up in different gametes
225
What is the law of independent assortment?
Each pair alleles segregates independently of each other pair of alleles during gamete formation
226
What are the phases of mitotic divisions?
Growth 1 phase S phase – genetical replication phase Growth 2 pahse Mitotic phase – PMAT Cytokinesis
227
What are the 2 types of alterations?
1. Somatic – only affects the host. 2. Germline - may affect the offspring.
228
Where does the exchange of genetic material occur during synapsis?
It occurs on non-sister chromatids.
229
What are the genetic and phenotypic outcomes from single gene segregation in pure breeding parents?
The potential traits of the offspring can be predicted.
230
What are homeobox genes?
They are genes that regulate the development of structure in the embryo. They perform they are functions on and off and are unequally distributed throughout the embryo in terms of effect.
231
What are transcription factors?
They are molecules that upregulate or downregulate the activity of certain genes
232
What are morphogen gradients?
They are positional cues for cells during development; this establishes cell signalling networks to control gene expression
233
How many homeobox clusters are there?
4 – C-7,-17,-12 and -2.
234
What is a Hardy-Weinberg equilibrium law?
It is a law that is used to calculate allele frequencies in non-evolving populations, with assumption that shuffling of alleles has no effect on the overall gene pool. Deviations from this law result in evolution. Due to limitations above this law cannot be used in natural populations but it help us to understand how the evolution occurs.
235
What are the necessary conditions for Hardy-Weinberg equilibrium?
1. No new mutations 2. No migration in or out of the population 3. No selection 4. Random mating 5. Very large population
236
How do we calculate genotype frequency?
Collect all frequency of 2 genes occuring (i.e. 2xWW, 3xWw and 1xww) and devide by the total number of samples
237
How do we calculate the phenotype frequency?
We calculate all appearances and devide by the total number (i.e 10xwhitw 20x purple = 10/30 and 20/30)
238
How do we calculate the alele frequency of aleles?
add the frequency of all aleles and devide by the total number (i.e. 10xW 15xw)
239
What are the main features of randomised control trials?
1. High level of evidence 2. Eandom assignment 3. Groups are exchangeable
240
What are the different types of RCTs?
1. Parallel-arm RCTs 2. Cross-over RCTs 3. N-of-1 'single patient' RCT
241
What is the structure of the parallel-arm RCTs?
1. Selection 2. Randomisation 3. Treatment and control group establishment and intervention 4. Follow up measures 5. Analysis
242
What is the structure of the Cross-over RCTs?
1. Selection 2. Randomisation 3. Treatment and control group and intervention 4. Washout period 5. Swap of control and treatment groups for second intervention 6. Outcomes of interventions 7. Analysis
243
What is the structure of the N-of-1 'single patients RCTs?
1. One patient is selected 2. They go through periods of treatment and non-treatments – the pattern is also random 3. Outcomes of interventions are recorded 4. Data is analysed
244
What is the design of a cohort study?
1. Time baseline 2. Time goes on 3. We observe 4. Analysis 5. Outcome
245
How does a cross sectional study work?
1. Select a group 2. See if they were exposed or not 3. Analyse 4. Outcomes
246
Why do we do a cross-sectional study?
Have a snapshot and see the prevalence of health problems in a population
247
What is a perspective study?
The study is conducted before data is gathered.
248
What is a retrospective study?
The study is conducted after the data is made available.
249
Why do we sample?
Reduce costs and it is more efficient
250
What are some of the sampling methods?
1. Simple random sample – equal chance being selected 2. Stratified random sample – equal participation of sexes, races and other parameters 3. Systematic - non-random – a set process e.g. every tenth person 4. Clustered - geographic areas are selected, after the clusters of multiple people are selected 5. Convenience sampling – just recruit people where we actively recruit people with needed traits
251
What is the main objective of case control study?
It is causal interference. What can we do to reduce the problem.
252
What is the main objective of ecological study?
It is casual interference. What can we do to reduce the problem.
253
What is the design of a case control study?
It starts with a known outcome that is classified as a "case". Non-cases are treated as a control group.
254
What is the design of a case control study?
1. A group of people with a known disease are classified as cases 2. A group of people who are known not to have a disease are used as controls 3. Both groups are sampled and separated into exposed and none exposed 4. We get 4 groups thus 4 data steams 5. Odds are calculated
255
What are ecological studies?
Ecological studies are epidemiological evaluations in which the unit of analysis is populations, or groups of people, rather than individuals. Example: Is the prevalence of dental caries lower in fluoridated areas?
256
What is a systematic error?
It relates to the way we conduct studies. It cannot be reduced by increasing sample size.
257
What is a systematic review?
They are a way of reviewing all the data and results from studies about a specific question in a standardized systematic way
258
What is empathy?
It is the ability to understand and share other people's emotions.
259
What does fluoride do to bacteria?
It can cause cytoplasmic acidification thus unabling functions of certain enzymes.
260
Why is the pKa of weak acids is important?
The protons in weak acids want to stay together, that is why they dissociate partially in water
261
When do cleft lip and palate occur?
Lip - 4-7 weeks Palate - 6-9 weeks
262
What is a typical structure of a local anaesthetic solution?
1. An aromatic portion that provides lipid solubility 2. An intermediate chain with either an ester or amide linkage 3. A terminal amide that provides water solubility
263
In what form does LA exist in the solution?
1. Unchanged lipid soluble molecules that are referred to as the base - more of it exist the better LA works - it can defuse through the cell membrane 2. Positively charged molecules RNH+ - this is the molecules that is able to inhibit the work of the Sodium channels in neurons which disables the propagation of action potential - it can not defuse through the cell membrane
264
What is the relationship between pH and Rn and RNH+?
1.When pH is low, there is a large number of RNH+ as RN is converted into RNH+ 2. IF pH is high, there is a large number of RN
265
How much of myelinated fibre needs to be covered by anaesthesia in order to anaesthetised the nerve?
8-10 mm
266
What are two main objective of LA?
1. The LA must diffuse through the nerve sheath 2. The LA must bind at receptor sites in the nerve membrane
267
What determines the number of basic and cationic forms of LA?
1. The pKa of the solution 2. The pH of the LA solution 3. The pH of the site of injection
268
What does methylparaben do in LA solution?
Acts as an anti-bacterial preservative but has the potential to cause allergy
269
What does bisulphite do in LA solution?
Acts as an anti-oxidant for the vasoconstrictor and also tends to lower the pH of the LA solution. May cause allergy problems
270
What does sodium chloride do in LA solution?
Makes the solution isotonic
271
What does sodium hydroxide do in LA solution?
Added to some LAs to adjust the pH
272
What does distilled water do in LA solution?
Used to dilute the solution and increase its volume
273
What does vasoconstriction do for LA solution?
1. Increased rate of absorption into the blood stream 2. Decreased duration of action and effectiveness 3. Increased bleeding at the site of injection, and 4. Possible overdose reactions due to high blood levels
274
What are the 3 essential components of local anaesthetic equipment?
1. Syringe 2. Needles 3. Cartridge
275
What are two common needles in SA dental clinics
1.Short, 25 mm length, 27 gauge 2.Long, 40 mm length, 27 gauge
276
What are 5 common anaesthetics in SA dental?
1. Lidocaine hydrochloride - Lignospan 2. Prilocaine hydrochloride - Citanest 3. Mepivacaine hydrchloride - Scandanest 4. Articane hydrochloride - Septanest 5. Bupivacaine hydrochloride - Marcaine
277
What type of topical anaesthetic is used in SA dental?
Benzocaine, 15-30 seconds applied to the area of anaesthetic
278
What are two main technique in LA?
1. Supraperiosteal infiltration - diffusion through cortical bone 2. Nerve block - depositing solution to a nerve trunk
279
What are types of infiltration can be administered?
Labial, buccal or palatal
280
What types blocks are available for the maxilla?
1. Maxillary - blockes whole of maxillary nerve 2. Tuberosity - blocks posterior superior alveolar nerves 3. Infraorbital - blocks anterior superior alveolar nerves 4. Nasopalatine - anaesthetises palate back to canines 5. Greter palatine - anaesthetises palate as far forward as canines
281
What are the steps of labial or buccal infiltrations?
1. Position the patient 2. Pull lip or cheek firmly out 3. Define the fornix 4. Wipe if necessary, then apply small amount of typical 5. Insert needle, bevel towards bone, in the fornix 6. Keep close to bone without touching, insert 2-3 mm, parallel to long axis of tooth 7. Inject slowly (1-2ml depending on the procedure)
282
What are the steps to a palatal infiltration?
1. Define point of entry 2. Apply topical 3. Insert needle, approximately at right angles to the palate, at junction of alveolar process and horizontal plate 4. Advance needle gently 2-3 mm 5. Inject slowly approx. 0.5 ml
283
Where is the location of injection for the maxillary block?
1. Buccally beyond third molar 2. Through greater palatine foramen
284
What are the advantages of palatal block?
Wide area of LA, including maxillary sinus
285
What some of the technique for anaesthesia of the mandible?
1. Infiltration that is only possible in incisor region 2.Inferior alveolar nerve block
286
How to locate the place for IANB?
1. Level - palpate the coronoid notch, find the deepest point 2. Entry point - locate pterygotemporal depression. It is between the pterygomandibular fold medially and the ramus of the mandible laterally 3. Angle - the angle of insertion is along a line drawn from the opposite lower second premolar to the pterygotemporal depression
287
What is the location of the inferior alveolar nerves?
It is close to the ramus between the ramus and sphenomandibular ligament that runs from the spine of the spenoid to the lingula
288
What is the location of lingual nerve?
It is medial and anteriorly to the inferior alveolar nerve and in close proximity to the lateral surface of medial pterygoid muscle.
289
What are steps to IANB?
1. Position patient in chair 2. Palpate the right ramus with the left index finger and define the coronoid notch 3. Slide finger medially so that the ball of the finger lies in the retromolar area between the external and internal oblique ridges 4. Hold syringe in right hand, with the barrel parallel to the occlusal plane. Insert the needle halfway between the fingertip and PMF, with the barrel over premolars on the left hand side 5. Advance the needle with minimum force until it touches bone 6. Withdraw slightly, aspirate, inject 1-2 ml 7. Move barrel towrds midline, withdraw half the amount of insertion, inject for lingual nerve about 0.5 ml 8. Complete withdrawal
290
How to perform anaesthesia of buccal nerve?
1. Inject just medial to anterior border of mandible, distal buccal to the last molar tooth around the level of the lower occlusal plane 2. Hold the syringe parallel with the occlusal plane on the same side 3. Advance the neddle until the needles gently touches the mucp[eriosteum/bone, then slightly withdraw and then inject
291
What are the steps for a mental block?
1. Hold lip between finger and thumb and pull anteriorly and downwards 2. Insert needle just lateral to the fornix, distal to second premolar 3. Direct the needle medially, anteriorly and inward into the canal. Inject slowly
292
What nerve innovate the upper molars?
The posterior superior alveolar nerve
293
What nerve innovates the upper premolars?
The middle superior alveolar nerve
294
What nerve innovates the anterior upper teeth?
The anterior superior alveolar nerve
295
What is the procedure in emergencies?
DRSABCD: Danger Response Send help Airway Breathing Circulation Defibrillation
296
During odontogenic infection, what is the path of least resistance in the mandible?
1. If above the mylohyoid line, the infection would progress lingually, eroding the lingual cortical plate and entering the sublingual space. This will elevate the tongue and create diffuculties with breathing 2. If below the mylohyoid line, the infection would progress down into the submandibular space. This may causes swelling near the angle of the ,and able to potentially causing trismus and therefore diffuculties chewing..
297
How does an odotontic infection spread if it is not treated
298
How does an odotontic infection spread if it is not treated?
1. Caries reach the root 2. Pulpal progression 3. Root progression 4. Progression to the apex 5. Progression into other tissues and cavities
299
What is the usual cause of infection in the sub mandibular region?
Usually the source is second and third molar because their roots are entirely below the attachment of mylohyoid muscle. The infection starts in the periodontal pocket and spreads to the musculature of the floor of the mouth. Infection pierces through the lingual cortical plate of the mandible. The infection moves lingually rather than buccally, as the lingual aspect of the tooth socket is thinner and provides the path of least resistance. The infection than moves into sublingual space.
300
How can commensal members of the oral microbiome become pathogenic when they inhabit environments that are no their primary ecological niche?
Oral commensal flora includes opportunistic bacteria, which can cause disease in compromised situations. For bacteria to become pathogenic they must: 1.Avoid host defences - both specific and non-specific 2.Adhere to host surfaces 3.Gain entry to the pulp and periapical soft tissues 4.Gain adequate nutrients in the new environment
301
What are the most frequently isolated bacteria in pulpal disease?
1. Gram positive streptococci 2. Peptostreptococci 3. Staphylococcus aureu
302
What are common routes of pulpal entry for bacteria?
1. Exposed dentinal tubules 2. Cavitated carious lesions 3. Micro leakage of restoration 4. Injury
303
What is the function of odontoblasts during the defence of pulp against bacterial infections?
1.Express Pattern Recognising receptos 2.Secrete antibacterial products 3.Release cytokines for chemo attraction of defence molecules
304
What is the process of tertiarry dentine formation?
When odontoblasts receive signal about presence of bacteria near the pulp they are able to react by up regulating the production of reactive dentine (tertiary dentine) which creates a barrier between the pulp and the bacteria. If odontoblasts die, pulp is able to create reperative dentine. The main cells in deploying reparative dentine are the pulp fibroblasts or stem cells.
305
What is the function of neurovascular network in protection of pulp during bacterial infection?
Secretion of neuropeptides causing vasodilation, vascular permeability increased, and promotion of immune cells. This also promotes tertiary dentine formation
306
What are some of the way to treat an odontogenic infection?
Reffere to V3 of therapeutic guidlines
307
What type of tissue is labial mucosa?
Non-keratinised stratified squamous epithelium. Labial mucosa has many elastic finred for flexibility and blood supply.
308
What type of tissues are in the vermillion zone?
Thin orthokeratinised stratified squamous epithelium followed by a lamina propria.
309
What is the main arterial supply to the lips?
It is predominantly supplied by external carotid artery, specifically via the facial artery.
310
What is the main venous drainage from the lips?
Through superior and inferior labial veins into the facial vein into external jugular and into subclavian vein
311
What is the main nerve supply to the lips?
The supply to the muscles is via the facial nerve and sensory via trigeminal nerve
312
What mechanism does the cell regulate for prior to S phase?
1.Cell size 2. DNA damage
313
What mechanism does the cell regulate for prior to M phase?
1. DNA damage 2. DNA replication completeness
314
What mechanism does the cell regulate for prior to end of mitosis?
Chromosomes attachment to spindle
315
What are some external factors that regulate the cell cycle?
1. Physical signals - contact inhibition - when cell inhibit replication when they come in contact 2. Chemical signals - availability of growth factors or other hormones
316
What are some internal factors that regulate cell cycle?
1. Cyclins 2. Cyclin-dependent kinases
317
What are some common risk factors for oral cancer?
1. Tobacco use 2. Excessive sun exposure to the lips 3. Heavy alcohol use 4. HPV 5. Immune deficiencies
318
Why does tobacco increase the likely hood of cancer?
1. Epigenetic alteration of oral epithelial cells can cause abnormal expression of genes such as GLUT-1 transportes and diwn expression of p53 anti-tumor gene 2. Inhibits systemic immune functions of the host, causing defects in CD4+ and CD3+ T cell activity 3. Oxidative stress on tissues
319
Why does excessive sun exposure to the lips increases the likely hood of developing cancer?
1. UV rediation is carcinogenic 2. Causes excess bond to form between DNA, this lead to mutations in cells
320
Why does heavy alcohol use increas the probability of developing cancer?
The mechanism by which alcohol consumption causes cancer are not fully understood but maybe oxidative damage
321
Why does heavy alcohol use increase the probability of developing cancer?
The mechanism by which alcohol consumption causes cancer are not fully understood but maybe oxidative damage
322
Why does HPV increases the probability of developing cancer?
HPV affects the gene p16, which regulates the cell cycle - causes it to be overexpressed
323
Why do immune deficiencies increase the probability of developing cancer?
Depressed immune function means that immune surveillance amd recognition of cancer cells is also depressed. This decreases the likely hood that early malignant cells are recognised and terminated by white blood cells
324
What is an effective communication and Patient managment plan for treatment with LA?
1. Information gathering 2. Diagnosis explanation 3. Informed consent 4. Post op instructions
325
What is an effective way to manage an individual with dental anxiety?
1. Acknowledge the fear, show empathy 2. FInd out what is the pt particularly feel fearful about 3. Familiarized with the procedure as the operator and show confidence 4. Familiarise patient with the procedure in order to minimise surprise and pain 5. Positive encourgment during the procedure 6. Using topical gel to minimise the paint at injection site 7. Use method of distractions
326
What are the four main anatomical sites to consider when trying to administer IANB?
1. Pterygotemporal depression 2. Pterygomandibular fold 3. Lingula 4. Coronoid notch
327
What is the rationale for direct IANB?
1. Anaesthesia is supplied to the gingiva, mucoperiosteum, lower lip and mandibular teeth 2. Useful for procedures such as root canals, extraction of teeth and periodontal treatment
328
What are some common anatomical deviations and common reasons for failure of IANB?
1. Accessory innervation from other nerves, such as nerve to mylohyoid nerve 2. Long buccal nerve is unable to be anaesthetised 3. Type 4 bifid mandibular canal, an anatomical variation causing difficulty for IANB to effecgtively anaesthetise as there are two mandibular foramina where IAN enters at the same time 4. Mandibular prognathism where the lingula is located higher, making a larger height difference between the lingula and coronoid notch
329
What are some common complications with IANB?
1. Pain during administration 2. Insufficient Anaesthesia 3. Iatrogenic and Self-Inflicted Damaged of Anaesthetised Tissues
330
What are some rare complications with IANB?
1. Needle Breakages 2. Skin paleness 3. Tissue Necrosis
331
What are causes for pain during administration during IANB?
1. Increased tissue pressure 2. Injection performed too quickly 3. Injecting too large a volume 4. Incorrect technique 5. pH/temp of anaesthetic
332
How to manage a patient with pain when administering IANB?
If the patient expresses one of the key signs/symptoms, pull the needle back slightly and if necessary to increase patient comfort, the direction of needle insertion should be altered before injecting the anaesthetic
333
What are causes for insufficient anaesthesia during IANB?
1. Incorrect technique 2. Incorrect site 3. Injection into an inflammed area
334
How to manage a patient with insufficient anaesthesia during IANB?
Carefully explain potential reasoning for insufficient anaesthesia and gain informed consent for examination and possibly a second dose
335
What are causes for Iatrogenic and Self-Inflicted Damage of Anaesthetised tissues during IANB?
1. Accidental damage due to numbness 2. Burn wounds caused by smoking or hot foods thay go unnoticed
336
How to manage a patient with Iatrogenic and Self-Inflicted Damage of anaesthetised tissues during IANB?
The companions of these patients should be warned of the possible injuries and should be told to keep watch on them for anaesthetic period. They should not allow them to smoke, eat or drink during this time.
337
What are reasons for failure of IANB besides anatomical variation?
Operator factors: Technical errors - poor technique Patient factors: 1. Pathological processes 2. Infection/inflammation 3. Psychological causes 4. Accessory innervation
338
What is anaesthesia?
It is the absence of all sensory modalities
339
What is paraesthesia?
An abnormal sensation (tingling) whether spontaneous or evoked
340
What is dysaesthesia?
An unpleasant abnormal sensation, wether spontaneous or evoked
341
What is hyperesthesia?
Increased sensitivity to stimulation, excluding special senses
342
What is trismus?
The restriction of range of motin of the jaws
343
What are some of steps for management of trismus?
1. Heat therapy 2. Analgesics 3. Muscle relaxants 4. Physiotherapy 5. No further dental treatment 6. Antibiotic therapy potentially 7. Reference to oral surgeon
344
What is rheumatic heart disease?
Rheumatic heart disease is a condition in whch rheumatic fever causes damage to the heart tissue or any of the valves
345
What is ineffective endocarditis?
It is when bacteria are able to infect heart tissue. This disease is strongly associated with rheumatic heart disease
346
What is rheumatic fever?
It is a multi system disease that results from mistreatment of Scarlet Fever, which is caused by Type A streptococcus bacteria
347
What is the concentration of fluoride in fluoridated water supply?
About 1 ppm
348
What type of bacterial growth inhibitor is chlorhexidine?
It is a broad spectrum mouth rinse. It has bacteriostatic levels and is able to stick around the mouth for around 5 hours. It blocks adherence and interferes with ATP'ase ion channels. IT DOES NOT UPSET THE NORMAL MICROBIAL ECOLOGY. DO NOT USE WITH FLUORIDE.
349
What is selective cytotoxicity?
It is a process in which there is preference to targeting bacteria without causing damage to host cells
350
What are antibiotics, chemotherapeutic substances and semisynthetic antibiotics?
Antibiotics - natural substances produced by certain groups of microorganisms Chemotherapeutic substances - they are chemically synthesised in a lab Semisynthetic antibiotics - hybdri compounds, chemically modified antibiotics
351
What are two types of action of antibiotics?
Cidal - killing the bacteria Static - gives immune system time to attack by stopping the bacteria from dividing
352
What are some of the desirable properties of a clinically useful antibiotic?
1. Non-toxic to host 2. Spectrum which does not include normal microflora 3. Bactericidal rather than bacteriostatic 4. Bacterial resistance not readily induced 5. Does not induce allergic reaction in host 6. Retains activity in body tissues and fluids 7. Soluble and stable in water 8. Inexpensive to produce
353
What does penicilin do?
Penicilin, is a b-lactama antiobiotic, which inhibits X-linking of peptide side chains by targeting the enzyme transpeptidase. Penicillin is a suicide inhibitor.
354
What are the major difference between different beta-lactams?
Standard stuff like spectrum of activity, toxicit, stability in body and so on.
355
What are some of the protein synthesis inhibiting anti-biotics?
Macrolides, aminoglycosides, lincomycin & clindamycin
356
What is an advantage and disadvantage of inhibitors of nucleic acid function?
Disadvantage: They are not selectivity toxic Advantage: Some of them can be used in cancer treatments
357
What are some examples of inhibitors of nucleic acid function?
Quinolones, rifampicin, 5-nitroimidazoles
358
What are cell membrane inhibitors?
They are antibiotics that disorganise structure or inhibit function of bacterial membranes
359
What are advantages of penicillin and ampicillin?
They are relativley broad, targeting both gram positive and gram negative bacteria. Even tho, these antibiotics could cross react with cephalosporins, but at a very low probability.
360
What is the advatage o flucloxacillin?
It maintaince slightly less of broad spectrum of work, but it is good for patient with B-lactam allergy
361
What is the advantage of cepjalosporins antibiotics?
They reduce activity of gram-positive bacteria and are good for treating multi-resistant organisms.
362
What are three main mechanisms of bacterial drug resistance?
1. Altered permeation/Efflux 2. Altered target site 3. Drug inactivation
363
What are the 10 steps to effective antibiotic use?
1. Is an antibiotic indicated on clinical grounds? 2. Have appropriate investigations been performed? 3. What organisms are most likely to cause this infection? 4. Which agent is best? 5. Is an antibiotic combination appropriate 6. Are any host factors relevant? 7. What is the best route of administration? 8. What is the appropriate dose? 9. Can therapy be modified when lab results are obtained? 10. What is the optimal duration of therapy?
364
What are some of the causes for cell injury?
1.Oxygen deprivation - hypoxia 2. Physical agents - mechanical trauma, temperature extremes, radiation 3. Chemical agents 4. Infectious agents 5. Immunological reaction - collateral damage, autoimmune reactions 6. Genetic changes - deficiency of functional proteins, susceptibility of cells 7. Nutritional imbalances
365
What are basic principals of cell injury?
1. Cell response depends on type, duration and intensity of injury 2. Consequences of injury depend on the type, state and adaptability of the cell 3. Cell injry has detrimental effects on several cellular/biochemical mechanisms
366
What are some of the mechanisms of cell injury?
1. Nitochondrial damage - decrease in ATP production 2. Entry of Ca2+ - loss of calcium homeostasis - activation of enzymes regulating apoptosis 3. Membrane damage - leading to loss of cellular components and increase in enzymatic digestion 4. Protein misfolding due to DNA damage
367
What are free radicals?
Free radicals are chemical species that have a single unpaired electron. They are highly reactive thus are damaging to the cells. One of the free radicals is oxygen
368
What are some of the pathological effects of free radicals?
1. Lipid perioxidation which damage the cell membrane 2. Protein modification - which causes breakdown and misfolding of proteins 3. DNA damage - leading to mutation
369
What are two main light microscopic changes are characteristic of reversible cell injury?
1. Hydropic change - cellular swelling, cells incapable of maintaining ionic and fluid homeostasis 2. Fatty change - hypoxic injury, metabolic injury and hepatocytes
370
What are two different processes of cell death?
1. Necrosis 2. Apoptosis
371
When does necrosis occur?
It occurs as a result of irreversible cell injury. It is unregulated form of cell death due to ischaemia, toxins, infections and trauma. Elicits a host reaction - inflammation.
372
What morhological changes occur in necrosis?
Denaturation of intracellular proteins and enzymatic digestion of irreversibly injured cell resulta in: Inability to maintain membrane integrity Elicit an inflammatory response Increased eosinophilia Nuclear changes
373
What are 3 different [patterns of tissue necrosis?
1. Coagulative necrosis 2. Liquefactive necrosis 3. Caseous necrosis
374
What happens during coagulative necrosis?
1. Preservation of tissue architecture 2. Eosinophilic, anucleate cells 3. Removal of necrotic cells by phagocytosis
375
What happens during liquafactive necrosis?
1. Enzymatic digestion of necrotic cells 2. Infections, production of pus
376
What happens during caseous necrosis?
1. Collection of fragmented necrotic cells 2. Granulomatous inflammation Usually hapens during tuberculosis
377
What is apoptosis?
It is programmed cell death. Activation of intracellular enzymes. Degradation of nuclear DNA and nuclear and cytoplasmic proteins.
378
What are some of physiological causes of apoptosis?
1. Embryogenesis 2. Involution of hormone-dependent tissues due to hormone withdrawal 3. Protection against autoimmune disease 4. Resolution of inflammatory and immune response
379
What are some of the morphological changes in apoptosis?
1. Cell shrinkage 2. Condensation of nuclear chromatin 3. Formation of membrane bound apototic bodies 4. Phagocytosis of apoptotic cells or apoptotic bodies 5. Absence of inflammation
380
What are the 5 changes in cell growth?
1. Hypertrophy - An increase in the size of particular tissue by increase in cell size. 2. Hyperplasia - An increase in the size of a particular tissue by increase in cell number. Is reversible. 3. Metaplasia - An acquired form of altered differentiation. Transformation of one mature differentiated cell type to another. Is riversible 4. Dysplasia - An increased cell growth with atypical morphology. May be reversible in early stages. 5. Neoplasia - Abnormal, uncoordinated and excessive cell growth
381
What are 4 different types of cell growth?
1. Multiplicated growth - increase in cell number 2. Auxetic growth - increase in cell size 3. Accretionary growth - increase in intercellular tissue compartment 4. Combined patterns of growth
382
What is important to remember with hypertrophy and hyperplasia?
Important to remember that following the removal of the stimulus causing the hypertrophy or hyperplasia, the tissue return to normal. Meaning, these conditions are reversible.
383
What is atrophy?
It is the decrease in size of an organ or cell. Could be physiological or pathological
384
Why is their inflammation?
It is a protective process that deals with infection and injuries but it does cause damage to surrounding tissues
385
What are 5 stages of respond to initial insult?
1. Initial insult 2. Inflammation 3. Tissue damage 4. Resolution 5. Repair
386
What are macroscopic features of acute inflammation?
1. Redness 2. Heat 3. Swelling 4. Pain 5. Loss of function
387
What changes in vessel calibre occur during inflammation?
1. Increased vascular permeability - formation of fluid exudate 2. Movement of neutrophils into the extravascular space - formation of cellular exudate 3. Arteriolar vasoconstriction 4. Capillary dilatation 5. Arteriolar dilatationn 6. FLuid exudation into extravascular space
388
What are some of the benefits of acute inflammation?
1. Dilution of toxins 2. Entry of antibodies 3. Transport of drugs 4. Fibrin formation 5. Delivery of nutrients and oxygen 6. Stimulation of the immune response
389
What are some of the harmful effects of acute inflammation?
1. Destruction of normal tissues 2. Swelling 3. Inappropriate inflammatory response
390
What is the sequelae of acute inflammation?
1. Resolution 2. Suppuration 3. Repair and organisation 4. Fibrosis 5. Chronic inflammation
391
What is a collection of pus called?
An abscess
392
What are granulomas?
A granuloma is a collection of macrophages and or their derivatives. Basically it is a small area of inflamation
393
How does pulpal tissue respond to an insult?
1. Inflammation 2. Reparative dentine formation 3. Fibrosis and reduced cellularity 4. Granulation tissue formation
394
Why does pulpal tissue die?
1. Limited capacity for drainage 2. Limited access for repair 3. Limited space for swelling 4. Concentrated stimulus 5. Limitations of material to treat
395
When does perioapical abcess occur?
It occurs due to untreated pulpal necrosis and acute inflammation in periapical tissues.
396
What can happen when periapical abcess is not treated?
It can turn into periapical granuloma. Due to granulation process a granuloma could form.
397
What is regeneration?
It is the replacemenet of dead or injured cells and tissues by cells and tissues of the indentical type.
398
What is repair?
It is replacement of dead/injured cells by "repair" tissue which is usualy fibrous connective tissue - scar tissue
399
What are to basic patterns of wound healing?
Primary intention - the wound is closed up for example using sutures - results in decreased area of repair Secondary intention - the wound is left open - results in increased area of repair
400
What is angiogenesis?
Increase in blood vessels. Process by which new blood vessels grow into damaged, ischaemic or necrotic tissues. Activated by vascualr endothelial growth factor (VEGF). Released by hypoxic cells and macrophages
401
What are some of the factors that influence healing?
1. Nutrition 2. Infection 3. Metabolic disorders other
402
How does healing of bone occur?
Through secondary intention plus bone regeneration. It is dependent on the site of fracture, normal vs pathologic bone and type of fracture.
403
What is a dry socket?
It is a condition where the site of extraction did not create an adequate blood clot and there is exposed bone. Could lead to necrosis of lamina dura and bone.
404
What is traumatic neuroma?
It is a bundle or nodule of thick neural tissues that forms after injury to a nerve.
405
What is neoplasia?
Literally means "new growth". A neoplasm is a lesion that arises from genetic a mutations in cells. Abnormal growth of cells.
406
What is a basic make up of neoplastic lesions?
Neoplastic cells or tumour parenchyma and tumour stroma
407
What influences the growth and spread of tumour cells?
It is influenced by the stromal components
408
What is the difference between bening tumours and malignant tumours?
Benign tumour have no potential for metastasis. Malignant tumours have potential for metastisis
409
What is carcinogenesis?
It is process of transformation of a normal cell to a neoplastic cell by causing permanent genetic alterations.
410
What is viral carcinogenesis?
It is the integration of viral genome into host DNA or viral proteinsthat lead to interference. One of these coudl be HPV wich cuases cervical carcinoma
411
What are some of physical agents that could cause carcinoma?
Ionisng radiation UV radiation
412
What si the relationship between dysplasia and epithelial atypia and carcinoma?
Many carcinomas are thought to arise as a result of progression and invasion of pre-existing epithelial dysplasia. Dysplasia could be a pre-neoplastic lesion. When dysplastic changes are maked and involve the entire thickness of the epithelium the lesion is referred to as carcinoma in situ which is a pre-invasive stage of cancer.
413
What is epithelial atypia?
It is changes in a normal epithelial lining. Such could be architectural changes such as drop shaped rete pegs, loss of polarity of basal cells. Superficial mitoses. Irregular epithelial sratification and so on
414
What are some cytological changes during epithelial atypia?
Nuclear pleomorphism, abnormal variation in nuclear size, abnormal variation in nuclear shape, cellular pleomorphism, abnormal variation in cell size.
415
How do we collectively refer to signs of epithelial atypia?
Epithelial dysplasia
416
What are oncogenes?
They encode proteins that promote normal cell growth and proliferation. Genetic alterations can alter the transcription of oncogenes or the behaviour of their products. Abnormal expression of oncogenes drive normal cells towards the neoplastic state
417
What are clinical effects of benign neoplasma?
1. Pressure on adjacent tissues 2. Obstruction to the the flow of fluid 3. Production of a hormone 4. Transformation into a malignant neoplasm 5. Anxiety
418
What are clinical effects of malignant neoplasms?
1. Pressure on and destruction of adjacent tissue 2. Formation of secondary tumours 3. Blood loss from ulcerated surfaces 4. Obstruction of flow 5. Production of a hormone 6. Paraneoplastic effects causing weight loss and debility 7. Anxiety and pain
419
What is a squamous cell carcinoma?
It is the most common primary malignant neoplasm of the oral cavity. It arises from the oral mucosal epithelium. Clinical features Age: any age Sex: More males than females Hugh risk sites: lower lip, anterior floor of mouth, lateral border of tongue and other Early clinical features: fixed white patch, exophytic papillary or wart-like lesion, speckled leukoplakia Early lesions are usually painless while symptoms of late lesions may include: pain, parathesia, loss of function, enlarged lymph nodes, radiographic changes
420
What is differentiation?
The degree to which the tumour tissue resembles the tissue of origin. Well differentiated - resemble mature cells. Poorly differentiated - slight resemblance to mature cells.
421
What is anaplasia?
Refers to a lack of differentiation of tumour cells, however often equated with poor differentiation at a tissue level.
422
What are the 5 grades of histological tumour differentiation?
Carcinoma in situ - Pre-invasive scc Grade 1 - well differentiated scc Grade 2 - moderately differentiated scc Grade 3 - poorly differentiated scc Grade 4 - anaplastic scc
423
What is the universal staging system for cancers?
T = size of primary tumour N = condition of regional lymph nodes M = presence/absence of distant metastases
424
What are some subdivision of T in the TNM staging system?
T1 = primary <2 2cm diameter T2 = primary 2-4 cm diameter T3 = primary > 4 cm diameter T4 = primary > 4 cm diamtere and invading local structures
425
What are some subdivision of N in the TNM staging system?
N0 = No nodes clinically N1 = Palpable nodes N2 = Contralateral or bilateral nodes N3 = Fixed palpable nodes
426
What are some subdivisions of M in the TNM staging system?
M0 = No distant metastasis M1 = Evidence of distant metastasis
427
What are the stages of cancer?
Stage 1: T1 N0 M0 Stage 2: T2 N0 M0 Stage 3: T3 N0 M0; Any T with N1 Stage 4: Any T with N2 or N3; Any T, Any N with M1
428
What is immune tolerance?
It is the ability to recognise self from nonself, thus immune cells do not attack body's own cells or commensal organisms
429
What are two types of tolerance?
1. Central tolerance - negative selection and elimination of autoreactive T cells - usually within thymus and bone marrow 2. Peripheral tolerance - limited selection, deletion or tolerise - in the paripheral after exiting centra organs
430
What are major mechanisms of T cell tolerance?
1. Apoptosis - induced by pro-apoptotic proteins 2. Clonal anergy - long-lived functional unresponsiveness 3. Suppression - use of T cells to supress immune function in order to reduce autoimmunity
431
What does the loss of immune tolerance can lead to?
Loss of immune tolerance lead to autoimmunity like Type I diabetes or Multiple sclerosis
432
What is the etiologu of any autoimmune disease?
Unknown. Cqauses are heterogeneous & multifunctional
433
What is hypersensitivity?
Immune responses can cause tissue injury and disease known as hypersensitivity disease. It is an excessive or inappropriate immune responsee. Mostly harmless. Can lead to host tissue damage
434
What are the 4 types of hypersensitivity reactions?
Type I - Immediate hypersensitivity Type II - Bound antigen Type III - Immune complex Type IV - delayed hypersensitivity
435
What is a mnemonic that could be used to hypersensetivities?
ACID Type I - Allergic Type II - Cytotoxic Type III - Immune complex deposition Type IV - Delayed
436
How to administer an epipen?
BLUE TO THE SKY ORANGE TO THE THIGH. Remove the blue cap, put orange to the thigh, hard squeeze and hold for 10 seconds.
437
What are some of the latex products in the dental clinic?
Gloves, rubber dam, gutta percha, impression material, bite blocks and more
438
What are the three reactions to latex?
1. Irritative dermatitis - non-immunological reaction 2. Hypersensitivity type I - immunological 3. Hypersensitivity type IV - immunological
439
What does immunodeficiency lead to?
Any type of immunodeficiency leads to the individual being immunocompromised
440
What are the two types of immunodeficiency?
1. Primary immunodeficiency - when you are born with it 2. Secondary immunodeficiency - mostly acquired
441
What is one of the most common causes of immunodeficiency?
Malnutrition
442
What are three common immune cell defects?
1. T cell defects - leading to fungi, viruses and parasites 2. B cell defects - hypogammaglobulinemia 3. Phagocyte defects
443
What are some oral complications with T cell defects?
Due to lowered immune function, many opportunistic batcteria are able to thrive in an oral environment. MHC receptors on CD4+ are unable to perform their function, thus opportunistic pathogens are able to trhive like Herpes simplex viruses.
444
What is important to consider when treating a patient who is immunocompromised?
Aggresive preventive care. Patient with immunodeficiency are extremely vulnerable to a range of oral opportunistic bacteria.
445
What is a virus and what is a virion?
Virus - the tiny infectious particle. Virion - an entire mature virus particle
446
What is the function of viruses?
1. Virus inserts its genome into its host 2. Takes over the host's functions
447
How are viruses divided into groups or families?
1. Nucleic acid types & structure 2. Replication strategy 3. Capsid morphology 4. Presence or absence of lipid envelope