PIA Final questions Flashcards
(308 cards)
1
Q
What are the symptoms and what is the physiological mechanisms of Vasovagal syncope?
A
Sympyoms: Light-headedness, narrowed vision, nausea.
Physiological mechanisms:
1. Sudden decrease in blood pressure due to stress
2. Decreased blood perfusion to the brain
3. Results in brain shut down due to low levels of oxyegn in the brain
2
Q
What are the symptoms and what is the physiological mechanisms of Postural hypotension?
A
Symptoms: Light-headedness/dizziness, blured vision, weakness, nausea
Physiological mechanisms:
1. Prolonged periods of being in supine position
2. Blood pools in veins of legs
3. There is a decrease in venous return
4. Decreases venous return reduces the cardiac output
5. Decrease in cardiac output results in decrease blood pressure, because blood pressure equals to the product of cardiac output and systemic vascular resistance
6. When patient rises to a sitting position and standing position, the reduced blood pressure causes a deficit of oxygen travelling to the brain
7. Brain has an absolute need for oxygen, thus when there is a deficit, it shuts down
3
Q
What are the symptoms and what is the physiological mechanisms of Changes in BGL?
A
Symptoms: Constant hunger, nausea, blurred vision, confusion
Physiological mechanisms (possible mechanism):
1. High blood glucose levels
2. Polyuria
3. Dehydration
4. Impared cognitive functions
5. Decrease in blood volume, decrease in systemic peripheral resistance, resulting in decreased blood pressure because blood pressure equals to the product of cardiac output and total peripheral resistance
6. Syncope due to brain shutting down due to low oxygen perfusion
4
Q
What are the symptoms and what is the physiological mechanisms of hyperventilation syncope?
A
Symptoms: Weakness, confusion, dizziness, shortness of breath
Physiological mechanisms:
1. Ventilation exceeds body’s metabolic needs for CO2 removal
2. Partial pressure of CO2 in blood decreases
3. Blood pH increases due to respiratory alkalosis
4. Hypocapnia
5. Cerebral vasoconstriction
6. Lowered cerebral perfusion
7. Syncope due to reduced cerebral perfusion
5
Q
What are the procedures in SADS to deal with a syncope?
A
- Stop dental treatment
- Implements DRSABCD:
Danger
Response
Send for help
Airway
Normal Breathing
CPR
Defibrilaetor - Call your tutor
- After incident, require dental record documentation including completing SLS incident report & debriefing with tutor
6
Q
What to do in SADS if a patient shows symptoms of syncope?
A
- Stop dental treatment
- Elevate patient’s legs to achieve a position where their head is lower than the heart. If patient is in dental chair, tilt the chair back to a horizontal angulation
- Allow patient to recover slowly
- Measure patient’s blood pressure & heart rate
7
Q
What is the difference between type I and Type II diabetes?
A
Type I - a lifelong autoimmune disease
Type II - a diseases that results from lifestyle choices mostly due to insulin resistance of body cells
8
Q
What are systemic manifestations of diabetes?
A
- Micro & Macro vascular damage
- Retinopathy
- pEripheral Vascular Disease
- Cardiac Disorders
- Kidney Problems
- Nerve Damage
9
Q
What are oral manifestation of diabetes?
A
- Caries risk & Periodontal disease
- Xerostomia
- Slow healing ability
- Susceptibility to developing oral mucosal disease
- Taste disturbance
- 2-way interaction of oral infections & increased BGL
10
Q
What are the steps to radio-graph assessment?
A
- Exposure
- Detector orientation
- Horizontal detector positioning
- Vertical detector positioning
- Horizontal beam angulation
- Vertical beam angulation
- Central beam position
- Colimator rotation
- Sharpness
- Overall diagnostic value
11
Q
What are the steps to gingival assessment?
A
C - colour
C - contour
C - consistency
T - texture
E - exudate
12
Q
What are the steps to ILA?
A
- Patient
- CC
- MHx
- SHx
- DHx
- Exam
13
Q
What is TRIM?
A
TRIM is an acronomy for:
Timing
Relevance
Involvment
Method
14
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.
15
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
16
Q
What is the pathogenesis of caries?
A
- Cariogenic bacteria requires simple sugars for anaerobic respiration
- Glucose is processed through glycolysis in the cariogenic bacteria
- Glucose is converted into 2 pyruvate
- In order to than convert NADH electron carrier into NAD+, pyruvate is converted into lactic acid
- Lactic acid accumulates in the cariogenic bacteria and is released into the oral environemnt
- 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
17
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
18
Q
Why is fluoride so effective?
A
- It is able to stop cariogenic bacteria metabolism
- Drive remin
- Create fluoride salivary pool
19
Q
Why is calcium still needed for fluoride incorpiration?
A
Fluoroapatite still needs calcium and phosphate
20
Q
How would you describe WSL
A
L - location
C - colour
T - texture
C - contour
21
Q
What are the major salivary glands?
A
Parotid (serous), Submandibular (mixed) sublingual (mixed).
22
Q
Where are the Von Ebners glands located?
A
Circumvallate papillae and they are serous.
23
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
24
Q
What type of buffer does stimulated saliva?
A
Bicarbonate
25
What type of buffer is in unstimulated saliva?
Phosphate
26
What is the sialo-microbial-dental complex?
They are interaction between saliva, biofilm and tooth.
27
What can change the balance of the oral environment?
1.More refined, softer foods
2.Refined CHO
3.Increase in fermentation
28
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
29
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
30
How do GIC bond?
They bond chemically throguh ion exchange and can exchange ions with tooth and oral environment.
31
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.
32
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
33
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
34
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
35
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
36
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
37
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.
38
How do we assess the fractures?
1.Tissue exposed – enamel only, enamel and dentine or exposed pulp
2.Surfaces involved
3.Check occlusion
39
What is the pattern of erosion relating to intrinsic sources?
1.Upper posteriors are affected first
2.Diffuses and affects the upper anterior next
40
What is the pattern of erosion relating to extrinsic sources?
1.Occlusal of lower affected first
2.Palatal of upper anterior
41
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
42
How would you identify gingivitis?
1.Localised - 10% - 30% BOP
2.Generalised - >30% BOP
No pain or no clinical attachment loss
43
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
44
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
45
What is the 4A's framework?
Ask, assess, acknowledge and address that can be used to adress a patient with dental anxiety
46
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
47
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
48
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
49
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
50
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
51
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
52
What is Grade A periodontitis?
When there are no evidence of loss over 5 years
53
What is Grade B periodontitis?
When there is a below 2 mm loss over 5 years.
54
What is Grade C periodontitis?
When there is an above 2mm loss over 5 years
55
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.
56
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
57
What are two types of local anaesthetic?
1. Amino esther - broken down by enzymes
2. Amide type - metabolised in the liver
58
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.
59
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
60
How do we modify local anathetic to overcome the phospho-lipid bilayer?
We design it to be amphiphatic
61
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
62
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.
63
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.
64
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.
65
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
66
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
67
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
68
What are 3 commonly used LA techniques?
1. Topical
2.Block
3.Infiltration
69
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
70
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
71
What is the association between Mutans Streptococci and fissure caries?
Around 71% of fissure caries have a high number of Mutans streptococci
72
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
73
What bacteria is more commonly found in caries on rough surfaces?
Lactobacilli
74
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
75
What is virulence of an organism?
It is the pathogens abilityt o cause disease
76
What are gingipans?
They are enzymes that are produced by P. Gingivalis. They produce many virulence factors. Gingipains are aggresive endopeptidases (protein distruction)
77
How does adaptive immunity recognise pathogens?
Through use of different types of marking using immunoglubulins or cytokines
78
Where are White Blood Cells originate from?
Bone marrow, B cells stay in bone marrow or spleen. T cells go to the thymus
79
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.
80
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
81
What is the acronym that can be used to remember all the immunoglobulin classes?
MADE in Germany
82
What is the most common immunoglobulin found in saliva
IgA
83
What are some of the functions of immunoglobulins?
1.Neutralisaiton
2.Opsonisation - labeling
3.Cross linking and immobilisation
84
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
85
What are the three sugar transport systems available for S. Mutans?
1.Sucrose-PTS
2.Trehalose-PTS
3.Multi Sugar TS
86
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
87
Why is sucrose so cariogenic?
Because it allows for the binding mechanism relating to GTFs to start unlike glucose
88
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111
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
112
What is hypoplasia?
It is the reduction in the amount of enamel matrix produced - presents as pitting, may caause sensitivity
113
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
114
What is hypocalcification?
It is insufficient inorganic material deposition during maturative stage - teeth adopt chalky, yellow appearance, highly vulnerable to staining and tooth wear
115
What are 3 types of amelogenesis imperfecta?
1. Hypoplasia
2. Hypomineralisation
3. Hypocalcification
116
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
117
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
118
What are some of the treatment for perio?
Debridment.
Remember that long axis to the tooth should be parallel to the terminal shank
119
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.
120
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
121
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
122
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
123
What is a closed sandwich technique?
When GIC if covered around with another material
124
What is an open sandwich technique?
When GIC is exposed outside the tooth – to the oral environment
125
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
126
Why do amalgam may need liners & base?
Due to their thermal properties
127
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
128
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
129
Name 3 components of saliva that have anti-bacterial properties.
1. Non-immunological defences
2. Physico-chemical barriers
3. Immunological barriers
130
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.
131
What role do salivary mucins play in reducing numbers of oral bacteria?
Mucins are able to agglutinate microbe and aid their removal
132
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.
133
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.
134
What are defensins?
Defensins are small antimicrobial peptides that are present in the granules of phagocytic cells thus are able to kill bacteria there
135
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
136
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
137
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
138
What is the main nutritional source in healthy periodontium?
Gingival crevicular fluid
139
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.
140
What role does GCF play in gingivitis?
It is able to remove tissue breakdown products, introduce inflammatory mediators and antibodies
141
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
142
What is a phenotype?
It is our genotype + environment
143
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
144
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.
145
What is the law of segregation?
The two alleles for a heritable character segregate during gamete formation and end up in different gametes
146
What is the law of independent assortment?
Each pair alleles segregates independently of each other pair of alleles during gamete formation
147
What are the phases of mitotic divisions?
Growth 1 phase
S phase – genetical replication phase
Growth 2 pahse
Mitotic phase – PMAT
Cytokinesis
148
What are the 2 types of alterations?
1. Somatic – only affects the host.
2. Germline - may affect the offspring.
149
How many homeobox clusters are there?
4 – C-7,-17,-12 and -2.
150
What are the main features of randomised control trials?
1. High level of evidence
2. Eandom assignment
3. Groups are exchangeable
151
What are the different types of RCTs?
1. Parallel-arm RCTs
2. Cross-over RCTs
3. N-of-1 'single patient' RCT
152
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
153
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
154
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
155
What is the design of a cohort study?
1. Time baseline
2. Time goes on
3. We observe
4. Analysis
5. Outcome
156
How does a cross sectional study work?
1. Select a group
2. See if they were exposed or not
3. Analyse
4. Outcomes
157
Why do we do a cross-sectional study?
Have a snapshot and see the prevalence of health problems in a population
158
What is a perspective study?
The study is conducted before data is gathered.
159
What is a retrospective study?
The study is conducted after the data is made available.
160
Why do we sample?
Reduce costs and it is more efficient
161
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
162
What is the main objective of case control study?
It is causal interference. What can we do to reduce the problem.
163
What is the main objective of ecological study?
It is casual interference. What can we do to reduce the problem.
164
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.
165
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
166
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?
167
What is a systematic error?
It relates to the way we conduct studies. It cannot be reduced by increasing sample size.
168
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
169
What is empathy?
It is the ability to understand and share other people's emotions.
170
When do cleft lip and palate occur?
Lip - 4-7 weeks
Palate - 6-9 weeks
171
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
172
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
173
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
174
How much of myelinated fibre needs to be covered by anaesthesia in order to anaesthetised the nerve?
8-10 mm
175
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
176
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
177
What does methylparaben do in LA solution?
Acts as an anti-bacterial preservative but has the
potential to cause allergy
178
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
179
What does sodium chloride do in LA solution?
Makes the solution isotonic
180
What does sodium hydroxide do in LA solution?
Added to some LAs to adjust the pH
181
What does distilled water do in LA solution?
Used to dilute the solution and increase its volume
182
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
183
What are the 3 essential components of local anaesthetic equipment?
1. Syringe
2. Needles
3. Cartridge
184
What are two common needles in SA dental clinics
1.Short, 25 mm length, 27 gauge
2.Long, 40 mm length, 27 gauge
185
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
186
What type of topical anaesthetic is used in SA dental?
Benzocaine, 15-30 seconds applied to the area of anaesthetic
187
What are two main technique in LA?
1. Supraperiosteal infiltration - diffusion through cortical bone
2. Nerve block - depositing solution to a nerve trunk
188
What are types of infiltration can be administered?
Labial, buccal or palatal
189
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
190
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)
191
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
192
Where is the location of injection for the maxillary block?
1. Buccally beyond third molar
2. Through greater palatine foramen
193
What are the advantages of palatal block?
Wide area of LA, including maxillary sinus
194
What some of the technique for anaesthesia of the mandible?
1. Infiltration that is only possible in incisor region
2.Inferior alveolar nerve block
195
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
196
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
197
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.
198
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
199
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
200
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
201
What nerve innovate the upper molars?
The posterior superior alveolar nerve
202
What nerve innovates the upper premolars?
The middle superior alveolar nerve
203
What nerve innovates the anterior upper teeth?
The anterior superior alveolar nerve
204
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..
205
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
206
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.
207
What are the most frequently isolated bacteria in pulpal disease?
1. Gram positive streptococci
2. Peptostreptococci
3. Staphylococcus aureu
208
What are common routes of pulpal entry for bacteria?
1. Exposed dentinal tubules
2. Cavitated carious lesions
3. Micro leakage of restoration
4. Injury
209
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
210
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.
211
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
212
What type of tissue is labial mucosa?
Non-keratinised stratified squamous epithelium. Labial mucosa has many elastic finred for flexibility and blood supply.
213
What is the main arterial supply to the lips?
It is predominantly supplied by external carotid artery, specifically via the facial artery.
214
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
215
What is the main nerve supply to the lips?
The supply to the muscles is via the facial nerve and sensory via trigeminal nerve
216
What mechanism does the cell regulate for prior to S phase?
1.Cell size
2. DNA damage
217
What mechanism does the cell regulate for prior to M phase?
1. DNA damage
2. DNA replication completeness
218
What mechanism does the cell regulate for prior to end of mitosis?
Chromosomes attachment to spindle
219
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
220
What are some internal factors that regulate cell cycle?
1. Cyclins
2. Cyclin-dependent kinases
221
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
222
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
223
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
224
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
225
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
226
Why does HPV increases the probability of developing cancer?
HPV affects the gene p16, which regulates the cell cycle - causes it to be overexpressed
227
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
228
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
229
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
230
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
231
What is anaesthesia?
It is the absence of all sensory modalities
232
What is paraesthesia?
An abnormal sensation (tingling) whether spontaneous or evoked
233
What is dysaesthesia?
An unpleasant abnormal sensation, wether spontaneous or evoked
234
What is hyperesthesia?
Increased sensitivity to stimulation, excluding special senses
235
What is trismus?
The restriction of range of motin of the jaws
236
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
237
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
238
What is ineffective endocarditis?
It is when bacteria are able to infect heart tissue. This disease is strongly associated with rheumatic heart disease
239
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
240
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.
241
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.
242
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.
243
What are three main mechanisms of bacterial drug resistance?
1. Altered permeation/Efflux
2. Altered target site
3. Drug inactivation
244
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
245
What are two different processes of cell death?
1. Necrosis
2. Apoptosis
246
What are 3 different [patterns of tissue necrosis?
1. Coagulative necrosis
2. Liquefactive necrosis
3. Caseous necrosis
247
What happens during liquafactive necrosis?
1. Enzymatic digestion of necrotic cells
2. Infections, production of pus
248
What happens during caseous necrosis?
1. Collection of fragmented necrotic cells
2. Granulomatous inflammation
Usually hapens during tuberculosis
249
What is apoptosis?
It is programmed cell death. Activation of intracellular enzymes. Degradation of nuclear DNA and nuclear and cytoplasmic proteins.
250
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
251
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
252
What are 5 stages of respond to initial insult?
1. Initial insult
2. Inflammation
3. Tissue damage
4. Resolution
5. Repair
253
What are macroscopic features of acute inflammation?
1. Redness
2. Heat
3. Swelling
4. Pain
5. Loss of function
254
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
255
What are granulomas?
A granuloma is a collection of macrophages and or their derivatives. Basically it is a small area of inflamation
256
How does pulpal tissue respond to an insult?
1. Inflammation
2. Reparative dentine formation
3. Fibrosis and reduced cellularity
4. Granulation tissue formation
257
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
258
When does perioapical abcess occur?
It occurs due to untreated pulpal necrosis and acute inflammation in periapical tissues.
259
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
260
What is neoplasia?
Literally means "new growth". A neoplasm is a lesion that arises from genetic a mutations in cells. Abnormal growth of cells.
261
What is a basic make up of neoplastic lesions?
Neoplastic cells or tumour parenchyma and tumour stroma
262
What is the difference between bening tumours and malignant tumours?
Benign tumour have no potential for metastasis.
Malignant tumours have potential for metastisis
263
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
264
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
265
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
266
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
267
What is anaplasia?
Refers to a lack of differentiation of tumour cells, however often equated with poor differentiation at a tissue level.
268
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
269
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
270
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
271
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
272
What are some subdivisions of M in the TNM staging system?
M0 = No distant metastasis
M1 = Evidence of distant metastasis
273
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
274
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
275
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
276
What does the loss of immune tolerance can lead to?
Loss of immune tolerance lead to autoimmunity like Type I diabetes or Multiple sclerosis
277
What is the etiologu of any autoimmune disease?
Unknown. Cqauses are heterogeneous & multifunctional
278
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
279
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
280
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.
281
When does Cleft lip and palate occur and why does it occur?
It occurs between 4-8 weeks in utero due to teratogenic agents emrbyos are exposed to.
Facial clefts - result from insufficient mesenchyme in the facial region. There are different types like unilateral,bilateral,median and oblique cleft lips.
Cleft lip - occurs when the medial nasal prominence and maxillary prominence are unable to fuse due to factors like the failure of a messenchymal tissue to breakdown
Cleft palate - occurs when the palatal shelves are unable to fuse together during the formation of secondary palate. Can occur in combination with cleft lip or by itself.
282
What happens during the oral/buccal phase?
Trituration of food involving mechanical breakdown + moistering to form a bolus. Tongue presses bolus against the soft palate, pushing it posteriorly through the fauces, into oropharynx
283
What happens during pharyngeal phase?
Bolus triggers receptors in medulla oblongata, causing the soft palate to elevate to seal nasopharynx and inhibit respiration. Relaxation of upper esohageal sphincter. Bolus enter esophagus.
284
What happens during esophageal phase?
Peristalsis wave is triggered. Pushing the bolus down the esophagus. Relaxation of lower esophageal sphincter to allow bolus entering into stomach.
285
What causes CLP?
Cleft lip and palate are caused by a combination of genes and other factors during pregnancy, such as consumption of alcohol, smoking, vitamin deficiency, and substance abuse. It may also be hereditary.
286
What happens during amelogenesis imperfecta?
Amelobalsts become switched off resulting in a decrease in secretion of enamel matrix. Mutations in amelogenin gene causes x-linked inheritance but mutations in the enamelin gene causes autosomal inherited forms.
Enamel becomes hypoplastice, can result in decrease in the size of teeth as the enamel layer is very thin. Ridging may also be present as some ameloblasts secrete normal enamel matrix resulting in depressions within the enamel.
287
What is the action of captopril?
Captopril is an ACE inhibitor. As an ACE inhibitor, captopril interferes with RAAS, inhibiting conversion angiotensin I into angiotensin II, thus inhibiting action of angiotensin II and aldosterone. This lowers vasoconstriction, lowers sodium and water retention thus lowering the blood pressure.
288
What is the action of amlodipine?
Amlodipine is a calcium channel blocker. It minimizes calcium influx into cardiac & smooth muscle cells during depolarisation prevent contractile processes occuring. It promotes relaxation of vascular smooth muscle, decrease systemic vascular resistance. This lower BP.
289
How write periodontal diagnostic statement?
Gneralised biofilm-induced gingivitis on reduced periodontium for examples
290
Name the following
291
What are some of the Upstream factors?
Systemic racism
Political policy
Education system
292
What are some of the Middlestream factors?
Local economy
Education quality
Housing quality
293
What are some downstream factors?
Family socioeconomic status
Family stability
Food security
294
What is the difference between sign and symptom?
Symptom - are reported by the patients
Signs - are detected by the physician
295
What would your brushing instruction would be for a person between ages of 0-1.5
No fluoride
296
What would be your recommendation for an individual 1.5-6 years old for brushing?
1. Low fluoride tooth paste to minimise fluorosis
2. peasize
3. Supervised
4. Spit not rinse
297
What would your recommendation for an individual 6+ years old?
1. Standard dose fluoride
2. Peasize
3. Spit not rinse
4. Supervise if needed
298
What are the four classic biomedical principles?
1. Non-maleficence
2. Beneficence
3. Autonomy
4. Justice
299
What does informed consent include?
1. Alternatives and all options for treatment
2. Information surrouding the nature and what the treatment involves
3. Risks of treatment
4. Pros and Cons of treatment and No intervention
5. Cost of treatment
300
What does PICO stand for?
Patient
Intervention
Comparison
Outcome
301
Name the following
302
What are contra indications for use of lignospan special?
It should not be used with patients with epilepsy, bradycardia, sever shock or heart block
303
What are contra indications for use of Septanest?
It should not be used on patients with allergy to articane or epilepsy
304
What are contra indications for use of Scandanest?
No major contraindications, good for people with sulfite
305
What is the trigemanimal pathway for pain, temperature and crude touch?
1. Stimulus occurs
2. Action potential from a receptor in the tooth travels to the trigeminal ganglion
3. The action potential travels to PONS
4. The action potential switches the neurons at the spinal nucleus
5. Action potential travels again from the spinal nucleus to the midbrain and into the thamalamus
6. Last synapses occurs between the thamalus and post-cntral gyrus
306
What is the trigeminal pathway for fine touch and vibration?
1. Stimulus occurs
2. Action potential from a receptor in the tooth travels to the trigeminal ganglion
3. The action potential travels to PONS
4. At the chief nucleus there is a cross over into the pontine nucleus
5. Action potential travels again from the pontine nucleus to the midbrain and into the thamalamus
6. Last synapses occurs between the thamalus and post-central gyrus
307
What is the trigeminal pathway for propriception in muscle of mastication?
1.Stimulus occurs
2. The receptors in the muscles of mastication travels through the motor brunch of trigeminal ganglion, through the pons and into the mesencephalic nucleus in the midbrain
3. A cross over occurs in the mesenceohalic nucleus and action potential travels into the thalamus
4. A cross over occurs in the thalamus and travels into the post-ctrl gyrus
308
What is the trigeminal pathway for movement of muscle of mastication?
1. The action potential occurs in the pre-central gyrus
2. It travels through a upper motor neuron to the motor nucleus in the PONS
3. There is usually a cross over occuring here, meaning the signal of the right pre-central gyrus affect the the left muscle of mastication
4. From the motor nucleus, lower motor neuron propagates the action potential to the corresponding muscle mastication.
