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Dentistry BDS 2 Sem 1 > Exam questions > Flashcards

Exam questions Flashcards

1
Q

What are ILA steps?

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

What are steps to gingival assessment?

A

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

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3
Q

What are the steps to radiograph assessment?

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

How would you assess the teeth on the radiograph?

A
  1. Identify teeth present, unerupted/missing, not imagted and restorations
  2. Identify abnormalities that are present
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5
Q

What framework would you use to assess a lesion?

A

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

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6
Q

Describe the process of odontogenesis

A

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

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7
Q

What are the stages of amelogenesis?

A

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

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8
Q

What is hypoplasia?

A

It is the reduction in the amount of enamel matrix produced - presents as pitting, may caause sensitivity

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9
Q

What is hypomineralisation?

A

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

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10
Q

What is hypocalcification?

A

It is insufficient inorganic material deposition during maturative stage - teeth adopt chalky, yellow appearance, highly vulnerable to staining and tooth wear

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11
Q

What are 3 types of amelogenesis imperfecta?

A
  1. Hypoplasia
  2. Hypomineralisation
  3. Hypocalcification
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12
Q

How would you identify gingivitis?

A

1.Localised - 10% - 30% BOP
2.Generalised - >30% BOP
No pain or no clinical attachment loss

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13
Q

How would you identify periodontitis?

A

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

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14
Q

What is the aetiology of periodontitis

A
  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
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15
Q

Give example of two local and two systemic factor for gingivitis and periodontitis.

A

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

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16
Q

What are some of the treatment for perio?

A

Debridment.

Remember that long axis to the tooth should be parallel to the terminal shank

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17
Q

Describe the problem with syncope of a patient with type I diabetes?

A

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.

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18
Q

What to do if a patient faint due to hypoglycemic syncope?

A
  1. Stop treatment
  2. Lay patient in supine position
  3. Provide refined carbohydrates
  4. Monitor and supervise - get help if needed
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19
Q

What are the affects of aging on endocrine function?

A

Reduction in:

  1. Oestrogen
  2. Growth hormone
  3. Aldosterone
  4. Melatonin
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20
Q

What happens when oestrogen production decreases?

A

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
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21
Q

What happens when growth hormone production decreases?

A
  1. Reduced muscle mass
  2. Increased adiposity
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22
Q

What happens when aldosterone production decreases?

A

Reduce secretion leads to hyponatremia or hyperkaleamia

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23
Q

What happens when melatonin production decreases?

A

Reduced secretion which causes advanced sleep phase syndrome

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24
Q

What is the difference between gram positive and gram negative bacteria in terms of the peptidoglycam layer?

A

Gram negative bacteria have a peptidoglycan layer is protected by an outer membrane unlike gram positive bacteria.

Which mean that antibacterials that target the peptidoglycan layer are more effective on gram positive bacteria than gram negative.

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25
Q

What are the steps to occlusal analysis?

A
  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 relationship
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26
Q

What is the pattern for erosion for intrinsic acids?

A

Palatal of maxillary posteriors and anteriors as the tongue covers the lower teeth relatively well

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27
Q

What is the pattern of erosion for extrinsic acids?

A

Mostly lower posteriors

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28
Q

What is the 4A’s framework?

A

Ask, assess, acknowledge and address that can be used to adress a patient with dental anxiety

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29
Q

What is TRIM?

A

T- time
R- relevance
I- involvment
M- method

It is a key for a succseful treatment plan

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30
Q

What is ALARA?

A

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
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31
Q

What happens to unpolarised resin?

A

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.

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32
Q

What are the steps to bonding resin to enamel?

A
  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
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33
Q

What are the steps to bonding to dentine?

A

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

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34
Q

How do GIC bond?

A

They bond chemically throguh ion exchange and can exchange ions with tooth and oral environment.

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35
Q

What are the steps of placing resin of top of GIC base?

A
  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
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36
Q

What is a closed sandwich technique?

A

When GIC if covered around with another material

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37
Q

What is an open sandwich technique?

A

When GIC is exposed outside the tooth – to the oral environment

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38
Q

What are the steps in applying GIC?

A
  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
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39
Q

Why do amalgam may need liners & base?

A

Due to their thermal properties

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40
Q

What are the steps of amalgam placing?

A
  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
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41
Q

What are the steps of resin based fissure sealant placement?

A
  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
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42
Q

What are the steps of GIC/RMGIC based fissure sealant placement?

A
  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
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43
Q

What theory are we using to describe dentine hyper sensitivity?

A

Hydrodynamic theory

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44
Q

Explain hydrodynamic theory.

A

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.

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45
Q

What is reversible pulpitis?

A

It is a reversible irritation of the pulp

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46
Q

What is irreversible pulpitis?

A

It is an irreversible irritation of the pulp

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47
Q

What is pulpal necrosis?

A

It is when pulp is non-vital

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48
Q

What are some of the materials are used in pulp protection?

A
  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
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49
Q

What are the steps of placing the liner in a relatively small cavity? Why so?

A
  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

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50
Q

What are the steps of placing a base in a relatively large cavity? Why so?

A
  1. Prepare cavity
  2. Condition the cavity
  3. Place a Fuji II material – larger amount for a larger cavity needed – advantage of being light curable
  4. Open enamel margins
  5. Etch
  6. Wash dry
  7. Use unfilled resin
  8. Cure
  9. Use filled resin
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51
Q

What is indirect pulp capping?

A

It is when a patient has a deep carious lesion with NO SIGNS OR SYMPTOMS OF IRREVERSIBLE PULPITIS.

Removal of all infected dentine is likely to result in pulp exposure.

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52
Q

What is direct pulp capping?

A

Pulp exposed but there are also no signs or symptoms of irreversible pulpitis

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53
Q

What are the steps for the current method of indirect pulp capping?

A
  1. Remove caries
  2. Place GIC/RMGIC to ARREST caries
  3. Leave or restore in the same appointment
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54
Q

What are the steps to direct pulp capping?

A
  1. Stop bleeding – sterile cotton pallet
  2. Apply CaOH on top of the exposure – causes sterile necrosis – creates calcific bridge
  3. GIC/RMGIC
  4. Restore
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55
Q

Name 3 components of saliva that have anti-bacterial properties.

A
  1. Non-immunological defences
  2. Physico-chemical barriers
  3. Immunological barriers
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56
Q

What role does lactoferrin play in reducing bacterial growth?

A

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.

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57
Q

What role do salivary mucins play in reducing numbers of oral bacteria?

A

Mucins are able to agglutinate microbe and aid their removal

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58
Q

What anti-bacterial enzyme is found in high concentration on tears and saliva? What is it’s mechanism of action against bacteria?

A

Lysozyme. It is able to hydrolyse peptidoglycans which are present on bacterial cells walls. It than triggers autolysins which cause bacterial degradation.

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59
Q

What are histatins and how do they interfere with the growth of oral bacteria?

A

Histatins are small peptides which are secreted by submandibular and parotid glands. They are able to interfere with membrane integrity of the bacterial membrane.

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60
Q

What are defensins?

A

Defensins are small antimicrobial peptides that are present in the granules of phagocytic cells thus are able to kill bacteria there

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61
Q

How does the flow rate of saliva vary during 24hr cycle?

A

The rate of saliva production is relatively high during the day and decreases significantly during the night time

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62
Q

Explain acidophilic

A

Bacteria who are able to survive and reproduce in acid

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63
Q

Explain aciduric.

A

Bacteria that are able to produce acid

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64
Q

Name 3 host defences that influence oral microbial growth.

A
  1. Physical defence – self cleansing, mechanical movement, flow and shedding
  2. Lysosymes
  3. PMNs
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65
Q

Name 3 Gram negative bacteria which are thought to lay a significant role in periodontal disease.

A
  1. P.Gingivalis
  2. P. Intermidia
  3. T. Forsythia
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66
Q

Name 3 functions of gingipans.

A
  1. Adherence to and colonisation of epithelial cells
  2. Disruption and manipulation of the inflammatory response
  3. Degradation of host proteins and tissues
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67
Q

What is the main nutritional source in healthy periodontium?

A

Gingival crevicular fluid

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68
Q

Is there an identified pathogen that causes gingivitis?

A

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.

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69
Q

What role does GCF play in gingivitis?

A

It is able to remove tissue breakdown products, introduce inflammatory mediators and antibodies

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70
Q

How do we approach treatment planning?

A
  1. Diagnosis presentation
  2. Consent
  3. Further investigation and tests
  4. Recall to check the results of the treatment
71
Q

What is a phenotype?

A

It is our genotype + environment

72
Q

What is the main difference between somatic cells and gametes?

A

Somatic cells have a diploid number of chromosomes. Gametes have a haploid number of chromosomes

73
Q

What is dominance/recessiveness?

A

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.

74
Q

What is the law of segregation?

A

The two alleles for a heritable character segregate during gamete formation and end up in different gametes

75
Q

What is the law of independent assortment?

A

Each pair alleles segregates independently of each other pair of alleles during gamete formation

76
Q

What are the phases of mitotic divisions?

A

Growth 1 phase

S phase – genetical replication phase

Growth 2 pahse

Mitotic phase – PMAT

Cytokinesis

77
Q

What are the 2 types of alterations?

A
  1. Somatic – only affects the host.
  2. Germline - may affect the offspring.
78
Q

Where does the exchange of genetic material occur during synapsis?

A

It occurs on non-sister chromatids.

79
Q

What are the genetic and phenotypic outcomes from single gene segregation in pure breeding parents?

A

The potential traits of the offspring can be predicted.

80
Q

What are homeobox genes?

A

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.

81
Q

What are transcription factors?

A

They are molecules that upregulate or downregulate the activity of certain genes

82
Q

What are morphogen gradients?

A

They are positional cues for cells during development; this establishes cell signalling networks to control gene expression

83
Q

How many homeobox clusters are there?

A

4 – C-7,-17,-12 and -2.

84
Q

What is a Hardy-Weinberg equilibrium law?

A

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.

85
Q

What are the necessary conditions for Hardy-Weinberg equilibrium?

A
  1. No new mutations
  2. No migration in or out of the population
  3. No selection
  4. Random mating
  5. Very large population
86
Q

How do we calculate genotype frequency?

A

Collect all frequency of 2 genes occuring (i.e. 2xWW, 3xWw and 1xww) and devide by the total number of samples

87
Q

How do we calculate the phenotype frequency?

A

We calculate all appearances and devide by the total number (i.e 10xwhitw 20x purple = 10/30 and 20/30)

88
Q

How do we calculate the alele frequency of aleles?

A

add the frequency of all aleles and devide by the total number (i.e. 10xW 15xw)

89
Q
A
90
Q

What are the main features of randomised control trials?

A
  1. High level of evidence
  2. Eandom assignment
  3. Groups are exchangeable
91
Q

What are the different types of RCTs?

A
  1. Parallel-arm RCTs
  2. Cross-over RCTs
  3. N-of-1 ‘single patient’ RCT
92
Q

What is the structure of the parallel-arm RCTs?

A
  1. Selection
  2. Randomisation
  3. Treatment and control group establishment and intervention
  4. Follow up measures
  5. Analysis
93
Q

What is the structure of the Cross-over RCTs?

A
  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
94
Q

What is the structure of the N-of-1 ‘single patients RCTs?

A
  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
95
Q

What is the design of a cohort study?

A
  1. Time baseline
  2. Time goes on
  3. We observe
  4. Analysis
  5. Outcome
96
Q

How does a cross sectional study work?

A
  1. Select a group
  2. See if they were exposed or not
  3. Analyse
  4. Outcomes
97
Q

Why do we do a cross-sectional study?

A

Have a snapshot and see the prevalence of health problems in a population

98
Q

What is a perspective study?

A

The study is conducted before data is gathered.

99
Q

What is a retrospective study?

A

The study is conducted after the data is made available.

100
Q

Why do we sample?

A

Reduce costs and it is more efficient

101
Q

What are some of the sampling methods?

A
  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
102
Q

What is the main objective of case control study?

A

It is causal interference. What can we do to reduce the problem.

103
Q

What is the main objective of ecological study?

A

It is casual interference. What can we do to reduce the problem.

104
Q

What is the design of a case control study?

A

It starts with a known outcome that is classified as a “case”. Non-cases are treated as a control group.

105
Q

What is the design of a case control study?

A
  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
106
Q

What are ecological studies?

A

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?

107
Q

What is a random error?

A

It is an error that occurs because the estimates we produce are based on samples and samples may not accurately reflect what is really going on in the population at large. This can be reduced by increasing the sample size.

108
Q

What is a systematic error?

A

It relates to the way we conduct studies. It cannot be reduced by increasing sample size.

109
Q

What is a systematic review?

A

They are a way of reviewing all the data and results from studies about a specific question in a standardized systematic way

110
Q

What is empathy?

A

It is the ability to understand and share other people’s emotions.

111
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.

112
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

113
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
114
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

115
Q

What is the significance of dental pelicle?

A

It is able to provide some protection to the enamel. It also allows for binding of bacteria to the surface of the tooth

116
Q

What is the significance of biofilm in demineralisation?

A

Biofilm and calculus are able to create a more closed system where buffering agents from saliva are unable to penetrate, this may cause more demineralisation as lactic acid produced by carcinogenic bacteria is not buffered

117
Q

Why is brushing so good for caries prevention?

A

Brushing:

  1. removes biofilm
  2. introduces more fluoride for remin
118
Q

Why is fluoride so effective?

A
  1. It is able to stop cariogenic bacteria metabolism
  2. Drive remin
  3. Create fluoride salivary pool
119
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

120
Q

Why is calcium still needed for fluoride incorpiration?

A

Fluoroapatite still needs calcium and phosphate

121
Q

What would be your recommendation for an individual 1.5-6 years old for brushing?

A
  1. Low fluoride tooth paste to minimise fluorosis
  2. peasize
  3. Supervised
  4. Spit not rinse
122
Q

What would your recommendation for an individual 6+ years old?

A
  1. Standard dose fluoride
  2. Peasize
  3. Spit not rinse
  4. Supervise if needed
123
Q

What are the steps to rubber dam application?

A
  1. Tooth assessment and tooth prep
  2. Clamp selection and preparation
  3. Dam preperation
  4. Clamp placement
  5. Clamp and dam placement
  6. Anchorage
  7. Dam Frame
  8. Inversion
  9. Finishing
  10. Removal
124
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
125
Q

What are the 6 steps of orhostatic hypotension?

A
  1. Blood is evenly distrivuted through the body when lying flat
  2. On standing blood pools in the legs due to contraction of skeletal muscles and squeezing of veins
  3. Pooling blood cuases reduction in venous return, this causes the reduction in cardiac output, reducing blood pressure
  4. The body is unable to appropritley regulate it due to multiple factors
  5. Reduced pressure to the brain causes the brain to shut down due to lack of oxygen
  6. Person falls
126
Q

What causes the redness in inflamation?

A

It is caused by increased blood flow tp the area - which increases the number of red blood cells - red blood cells are red because of albumin

127
Q

What causes swelling in inflamation?

A

It is caused by increased leakage of protein rich fluid om the tissue are due to increased capillary permeability as a result of vasodialation.

128
Q

What causes heat in inflamation?

A

Heat is caused by increased blood flow to the area - this increase in heat increases the metabolic rate of cells

129
Q

What is the needle stick inury protocol in dental emergencies?

A
  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
130
Q

What is the mode of action of CPP-ACP

A
  1. Casein phospho peptides can stanilise amorphouc calcium pjopshate as casei proteins can bind calcium and phosphate and release these mineralisations during acid attacks
  2. Product can penetrate down the laminar pores of enamel and remin the depth of the lesion
  3. Caclcium based products can also result in a release of calcium & phosphate which is required for remin
131
Q

What is the mode of action of acidulate phosphate fluoride?

A
  1. It contains a small amount of acid which triggers demin
  2. The demineralised Ca2+ from the tooth can be used to form fluroapetite
  3. Better for xerostomia as it uses calcium from the tooth
132
Q

What does PICO stand for?

A

Patient

Intervention

Comparison

Outcome

133
Q

What is the action of the masseter muscles?

A

Elevate the mandible

134
Q

What is the action of the temporalis?

A
  1. Elevate the mandible
  2. Retrude mandible
135
Q

What is the action of the medial pterygoid muscles?

A
  1. Elevate the mandible
  2. Retrude the mandible
136
Q

What is the action of the lateral pterygoid muscle?

A

Depression of the mandible

137
Q

What does informed consent include?

A
  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
138
Q

What is origin and insertion of masseter muscles?

A

Origin: Zygomatic arch

Insertion: Mandible angle and mandible ramus

139
Q

What is the origin and insertion of the temporalis muscles?

A

Origin: Temporal fossa

Insertion: Mandible coronoid process

140
Q

What is the origin and insertion of medial pterygoid muscles?

A

Origin: Maxillary tuberosity

Insertion: Medial surface of mandible angle

141
Q

What is the origin and insertion of the lateral pterygoid muscles?

A

Origin: Infratemporl crest of greater wing of sphenoid bone

Insertion: Pterygoid fovea on Mandible condyle anterior neck

142
Q

What is stage 1 periodontitis?

A
  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
143
Q

What is stage 2 periodontitis?

A
  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
144
Q

What is stage 3 periodontitis?

A
  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
145
Q

What is stage 4 periodontitis?

A
  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
146
Q

What is Grade A periodontitis?

A

When there are no evidence of loss over 5 years

147
Q

What is Grade B periodontitis?

A

When there is a below 2 mm loss over 5 years.

148
Q

What is Grade C periodontitis

A

When there is an above 2mm loss over 5 years

149
Q

What is cleft lip?

A
  1. It is a congenital defect
  2. Due to failur of primary palate to form
  3. Primary palate forms as the maxillary processes fuse with merded medial nasak processes
  4. Etiology is multifunctional
150
Q

What is a cleft palate?

A
  1. It is a congenital defect
  2. Due to failure of the secondary palate to form
  3. The secondary palate forms as the lateral palatine shelves fuse together, with nasal suptum, and with the median palatine shelf
  4. Etiology is multifactorial
151
Q

Which gene can be responsible for cleft lip and palate?

A

HYAL2 - a gene that is used to break down hyluronic acid.

If the gene is unavailable, the thick covering or merging stuftures is not broken down meaning there could be no fusion.

152
Q

What mutation can cause amelogenesis imperfecta?

A

AMELX, ENAM and MMP20 are genes that encode for proteins that are used in amelogenesis. Failure to synthesis those proteins could cause amelogenesis.

153
Q

What are the 4 steps of buccal stage?

A
  1. Compression of the bolus against hard palate
  2. Retraction of the tongue forces bolus into the oropharynx
  3. Elevation of the soft palate seals off the oropharynx
  4. Once bolus enters the oropharynx, reflex response are initiated and the bolus is moved towards the stomach
154
Q

What are the 4 steps of pharyngeal stage?

A
  1. Tactile receptors on palatal arches & uvula are stimulated
  2. Pattern of muscle contraction in the pharyngeal muscles is triggered by th swallowing center in the medulla
  3. Elevation of the larynx & folding of the epiglottis results from contractions of the pharyngeal muscles
  4. Pharyngeal constrictors then force the bolus thru the pharynx, past closed glottis and into oesophagus
155
Q

What are the steps to maxillary development?

A
  1. Arise from first pharyngeal arch
  2. By end of week 4, maxillary prominance arises
  3. The center of ossification is between the intraorbital and anterior superior alveolar nerve - both paart of the trigeminal nerve
156
Q

When does development of teeth occur?

A

At six weeks in eutero

157
Q

WHat are the two starting components in tooth development?

A
  1. Primitive orl epithelium derived from ectoderm
  2. Ectomesenchyme derived from craniofacial neural crest cells
158
Q

How do oral epithelium and ectomesenchyme interact?

A

They interect recepricolly to regulate the formation, location and specialisation of teeth

159
Q

What are the initial stages of odontogenesis?

A
  1. Thickening of oral epithelium on both maxilla andmandible prominances
  2. Separation of oral epithelium to lingual and buccal lamina
  3. Cells in lingual lamina re signalled to proliferate &invaginate to positions of future teeth by signalling proteins - forming dental plaquoates
  4. Interaction between oral epithelium and ectomesenchyme cause cells proliferation and initiation of Bud, Cap and Bell stages
160
Q

What happens during bud stage?

A
  1. Dental plaqoues prolifirates
  2. It is conected to dental lamina
  3. It is surrounded by ectomesenchymal cells
  4. It is filled with low columnar and polygonal cells
161
Q

What happens during cap stage?

A
  1. Cell proliferate and create 3 distinct layers of epithelium - Stellate reticulum, outer enamel epithelium and inner enamel epithelium
  2. Stellate reticullum allows for accumulation of water making them star shapped
  3. Enamle knots are present - mostly for signalling for cusp formation
  4. Ectomesenchymal cells continue to prolifereate especially near the invagination
  5. Dental papilla is formed near the invegination
162
Q

What occurs during bell stage?

A
  1. Cervical loop is formed
  2. Stratum intermedium is formed
  3. Stellate reticulum collapses
163
Q

What happens during the histodifferentiation?

A

Dental papilla cells become ameloblasts and odontoblasts

164
Q

How does root formation occur?

A

Root formation occurs after the crown formati and is guided by the cervical loop cells

165
Q

What nerves supply which branchyal arches?

A

The facial (VII) nerve supplies the muscles derived from the first arch. The nerve of the third branchial arch is the glossopharyngeal (IX) nerve. Two branches of the vagus (X) nerve supply the remaining branchial arches. The superior laryngeal nerve innervates derivatives of the sixth branchial arch.

166
Q

What is a normal blood pressure in pregnant women?

A

Lower blood pressure occurs due to vasodilation of blood vessels. Vasodilation occurs due to increased volume of blood that is needed due for grwoth and development of the feuotus.

167
Q

Why do most fissure sealant fail?

A
  1. Placed in moist invironments
  2. Too much material - attrition force
168
Q

What is a purpose of empathy?

A

Empathy is important because it helps us understand how others are feeling so we can respond appropriately to the situation.

169
Q

Why do bacteria produce lactic acid?

A

It relates back to creating of ATP. Pyruvate, a product that is used to harvet electrons for the electron transport chain. The biproduct of harvesting electtrons is lactic acid

170
Q

What does fluoride do to bacteria?

A

It can cause cytoplasmic acidification thus unabling functions of certain enzymes.

171
Q

Why is the pKa of weak acids is important?

A

The protons in weak acids want to stay together, that is why they dissociate partially in water

172
Q

When do cleft lip and palate occur?

A

Lip - 4-7 weeks

Palate - 6-9 weeks

173
Q
A

Dentistry BDS 2 Sem 1 (15 decks)

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