Exam Qs Flashcards
(133 cards)
1
Q
3 main routes of metastatic cancer spread
A
lymphatic
haematogenous
transcoelomic
2
Q
eg of cancer spreading and where it metastasises to
A
colon cancer can metastasise to liver-colon
3
Q
name 2 classifications of cancer and their subgroups
A
clinical: benign or malignant
histological: epithelial or mesenchyme
4
Q
5 features of a benign tumour
A
- growth is slow
- growth in non-invasive
- benign tumours do not spread
- tumour margins are not well defined
- they do not recur when removed
5
Q
5 features of a malignant tumour
A
- growth is rapid
- growth is invasive & destroys tissue
- tumour spreads
- recurrence after excision is very common
- tumour margins are well defined
6
Q
name 2 benign tumours and their tissue of origin
A
1.lipoma - fat tissue
2. chondroma - cartilage
7
Q
name 2 malignant tumours and their tissue of origin
A
- carcinoma - epithelial cells
- lymphoma - blood forming cell
8
Q
what are demographic factors and name some
A
characteristics of a population expressed statistically e.g. gender, age, postcode, employment status, religion, birth rate, death rate
9
Q
name 5 types of questionnaires
A
- open
- closed
- scales (likert scales)
- yes / no
- rhetoric
10
Q
what are the 5 stages of feeding
A
- ingestion
- stage 1 transport
- mechanical processing
- stage 2 transport
- swallowing pharyngeal phase
11
Q
describe ingestion
A
movement of food from external to internal environment
12
Q
describe stage 1 transport
A
food gathered on tongue tip and moved to level of posterior teeth
13
Q
describe mechanical processing
A
solid foods are broken down and mixed with saliva before swallowing
moist solid foods e.g. fruit has to have fluid removed before transport and swallowing
food is chewed with premolars & molars and soft foods are squashed against hard palate
14
Q
describe stage 2 transport
A
bolus moved posteriorly by ‘squeeze back’
solid foods moved through fauces to pharyngeal surface of tongue
‘seal’ holds liquids at pillars of fauces
15
Q
describe the swallowing pharyngeal phase
A
involuntary movements push bolus through pharynx into oesophagus
epiglottis seals off larynx preventing food entering the respiratory tract
UOS relaxes to allow bolus into oesophagus and then contracts to counteract backflow
16
Q
why does ditching occur in amalgam restorations
A
material is repeatedly stressed for long periods of time at low level stresses below the elastic limit
it may flow resulting in permanent deformation
amalgam sits proud of surface due to flow and is vulnerable to fracture
17
Q
what can we do in cavity prep to prevent amalgam ditching
A
remove all caries
correct acid etch & bond
use a lining material
lining material will help spread force down long axis of the tooth, instead of placing stress on interface between tooth & restoration
this will reduce stress on amalgam therefore reducing creep and therefore ditching
18
Q
4 factors contributing to formation of secondary caries underneath an amalgam restoration
A
- microleakage due to no chemical bond between restoration & tooth
- fracture of enamel at margins causing ditching compromised any seal that was present at restoration / tooth interface
- poor oral hygiene will prevent removal of cariogenic plaque and allow proliferations around margins
- if no lining material underneath amalgam the dentine has no protection from bacteria & endotoxins
19
Q
5 risk factors for a high caries incidence
A
- poor OH regime over time (brushing & flossing)
- susceptible tooth surface i.e. tight contacts, receded gingiva
- diet - high in sugars/fermentable carbohydrates forming cariogenic plaque & frequency of intake
- presence of cariogenic bacteria - strep mutans / lactobacilli
- xerostomia - drugs, disease, diet
20
Q
how is cystic fibrosis passed down
A
inherited disorders
21
Q
explain the genetics of cystic fibrosis
A
CFTR gene - chromosome 7
recessive gene so both parents must have the gene
22
Q
how to treat cystic fibrosis
A
physio
medication
exercise
transplantation
23
Q
how does cystic fibrosis affect the body (4)
A
- inherited defect in cell Cl- channels
- produces excess sticky mucus
- lungs are congested
- pancreas: malabsorption of nutrients
24
Q
how to test for cystic fibrosis
A
- perinatal testing; all children now screened at birth
- sweat test; measures salt content of sweat which is higher in CF patients
25
eg adv & disadv of IV medication
e.g. - midazolam
adv - rapid, immediate onset of drug, avoids FPM so nearly 100% bioavailability, continuous, closely monitored administration
disadv - required IV access which is painful & can be difficult to obtain, increased infection risk
26
eg, adv & disadv of subcutaneous medication
e.g. - insulin, heparin
adv - avoids FPM so higher bioavailability in body, constant, slow & prolonged absorption by fatty tissue
disadv - needle breaks protective barrier against infection
27
eg adv & disadv of IM medication
e.g. - glucagon, adrenaline
adv - rapid onset, shorter duration, muscle can absorb liquid better than subcutaneous layer
disadv - neurovascular (nerve) damage, bleeding, painful & infection risk, dependent on blood flow: delayed absorption in shock
28
eg adv & disadv of transdermal medication
e.g. - isosorbide mononitrate
adv - avoids FPM so higher bioavailability in body, controlled & continuous release
disadv - skin is an effective barrier; only small molecule medications can work
29
why do we need a hybrid layer to bond to
carious dentine has a lower hardness and presence of mineral deposits in the tubules
this makes it difficult to produce the hybrid layer as there are denatured collagen fibres
without a sufficient hybrid layer in place, bond strength will be significantly weaker
30
how do we overcome the hybrid layer problem
RMGI - remineralisation through F- release
using self -etch technique to penetrate and incorporate smear layer
31
how to label micrograph of hybrid layer
hybrid layer can be seen overlying dentine
resin tags - resin that has permeated down tubules for micromechanical retention
32
outline creation of a hybrid layer
- hybrid layer consists of collagen network exposed by etching & embedding adhesive resin (resin tags) it is the interface between dentine & adhesive resin
- smear layer is first removed using a 37% phosphoric acid conditioner - top 10microM
- hydrophilic monomer (HEMA) penetrates the hydrophobic dentine surface (preferably primary, well structured dentine) and embeds the collagen fibres forming the hybrid layer
33
reasons why a bond to dentine might fail (4)
1. over etch - collagen fibres collapse therefore the resin cannot penetrate
2. over etch - too deep an etch and the primer cannot penetrate the full depth of the etch
3. too dry - dentine surface collapses
4. too wet - primer is diluted and strength is reduced
34
what the 3 stages in forming a clot
1. vasoconstriction
2. platelet plug & aggregation
3. conversion of fibrinogen to fibrin by thrombin
35
how does aspirin affect clotting
prevents formation of a platelet plug - inhibits platelets aggregation by altering balance between thromboxane A2 & prostacyclin
36
how does warfarin affect clotting
impacts conversion of fibrinogen to fibrin as it inhibits vitamin K dependent reactions of the coagulation cascade
37
how does heparin affect clotting
affects conversion of fibrinogen to fibrin as it is an indirect thrombin inhibitor. it binds antithrombin III & enhances natural anticoagulatory effect
38
aspirin & clopidogrel are often used in conjunction - why and what is their function
together they are effective anticoagulants; reducing risk of blood clotting so reducing risk of heart attack or stroke in the at risk population.
aspirin - inhibits platelet aggregation by altering prostacyclin / thromboxane A2 balance
clopidogrel - inhibits ADP induced platelet aggregation
39
explain genetics behind von willebrand's disease
autosomal dominant inheritance so one parent has the recessive gene
40
how does von willebrand's disease affect haemorrhage
reduced factor XIII level
vWF binds to this to prevent rapid breakdown in blood
reduced platelet aggregation as a result of deficient factor XIII
41
example of an antiplatelet and how it works
aspirin - enhances bleeding by inhibition of platelet aggregation altering balance between thromboxane A2 & prostacyclin; irreversible for the life of the platelet (7-10 days)
42
example of an anti-coagulant and how it works
warfarin - inhibits vitamin K dependent reactions of coagulation cascade
43
what constitutes hypertension
>140/90mmHg
120/80mmHg is considered normal
44
what is bioavailability
fraction of an administered dose of unchanged drug that reaches systemic circulation and is available for clinical effect
45
what is first pass metabolism
concentration of drug is greatly reduced before it reaches the systemic circulation
fraction of a drug lost during process of absorption in the gut and metabolism in the liver
46
2 disadvantages of oral route of medication
1. FPM effect reduces amount of drug passed to systemic circulation
2. risk of drug causing gastric irritation & ulceration e.g. NSAIDs
47
describe flowable composite (5)
lower filler content so less viscous than conventional composite
used for filling pit / fissure system, small fractures & as a luting agent
higher polymerisation shrinkage
lower fracture strength
place with fibre ribbons
48
describe wettability of flowable composite
adhesion requires an intimate contact between the adhesive material and substrate
to obtain maximum contact area between liquid adhesive and solid surface the substrate must show evidence of high wettability with regard to that liquid (hydrophilicity or dentine & material)
using acid etch technique
opportunity for excellent bond between composite & enamel
49
describe the light curing of flowable composite
extended working time
less finishing / waste / porosity
50
reasons against using flowable composite (4)
- reduced mechanical properties
- lower availability of shades
- more difficult to sculpt due to decreased viscosity
- discolouration over time
51
will use of 1 6mm increment of flowable suffice
no - takes 20 seconds to cure 2mm
larger than 2mm increments will result in an under polymerised base
52
describe polymerisation shrinkage
dependent on filler particle volume
affects bond to tooth - stresses develop at hard tissue (high configuration factor is a problem)
potential for cuspal fracture & microleakage
hinders good marginal adaptation
53
what are the 10 SICPs
1. patient placement / assessment for infection risk
2. hand hygiene
3. respiratory & cough hygiene
4. PPE
5. safe management of care environment
6. safe management of care equipment
7. safe management of linen
8. safe management of blood and body fluid spillages
9. safe disposal of waste (inc sharps)
10. occupational safety: prevention of exposure (inc sharps injuries)
54
what are the 6 links in the chain of infection
1. infectious agent
2. reservoir
3. portal of exit
4. mode of transmission
5. portal of entry
6. susceptible host
55
what are the 7 modes of transmission
direct // indirect // inhalation // ingestion // inoculation // intercourse // mother to infant
56
what are the 5 moments for hand hygiene
1. before touching a ptx
2. before a clean/aseptic procedure
3. after bodily fluid exposure risk
4. after touching ptx
5. after touching ptx surroundings
57
difference in social & hygienic hand hygiene
social - washing with an alcohol based gel when hands are not visibly soiled
hygienic - washing with an antimicrobial soap or washing with hot water and soap and then an alcohol based gel
58
when is it not appropriate to use an alcohol based gel to wash your hands
- hands are visibly soiled
- C. difficile
- if patient has GI infection
59
risk of infection following a sharps injury
hep B = 1/3
hep C = 1/30
HIV = 1/300
60
describe placement & disposal of sharps boxes
should be placed out of reach of children and close enough to operator for easy reach when disposing of sharps
taken for incineration when 3/4s full
61
what should you do in the event of a sharps injury
stop what you're doing, run injury under warm water and squeeze area to encourage bleeding. wash with soap and water thoroughly but do not scrub and cover with waterproof dressing. complete DATIX and report to occupational health
62
3 methods of sterilisation
cleaning
disinfection
sterilisation
63
4 categories of risk, e.g. of each & decontamination required of each
minimal risk - objects at a distance from ptx and unlikely to cause harm e.g. keyboard - cleaning & drying
low risk - objects in contact with intact skin e.g. dental chair - cleaning & drying
intermediate risk - objects in contact with intact membranes e.g. impression trays - disinfection
high risk - objects contact mucous membranes, blood and body fluids e.g. XLA forceps - sterilise
64
how do you manage a blood spillage
wear PPE & contain with paper towels
assemble spillage kit
sprinkle chlorine releasing granules (sodium dichloroiso-cyanurate & sodium hypochlorite) 10,000ppm over spillage and leave for 5 mins
clean affected area with paper towels and dispose of as clinical waste
wash with water & detergent then dry
make sure sharps / single use items are disposed
hand hygiene
65
give 2 egs of chlorine releasing agents
sodium hypochlorite &
sodium dichloro-iso-cyanurate 10,000ppm for 5 mins
66
give advantages of Hall technique
- allows pre formed metal crown to be placed over carious primary molars
- non invasive & quick
- requires no LA and no tooth prep
- requires ptx compliance & trust in operator ability
67
instruments required for hall crown
mirror, straight probe, excavator, flat plastic, cotton wool, gauze for airway, elastoplast to secure crown, band forming pliers (convex-concave)
68
what teeth are suitable for a hall crown
primary molars i.e. Es & Ds
69
how to choose correct SS crown
- choose smallest crown that will cover all cusps & partially seat crown until it engages all contact points
- adjustments may have to be made using adam's pliers
- where distal marginal ridge of D is missing & E has drifted mesially, use separators
- if unsuitable, remove crown using excavator before cement sets
70
indications for hall technique
no radiographical sign of pulpal involvement i.e. asymptomatic tooth
sufficient amount of sound tooth tissue
71
what is RAS / RAAS
RAS - renin angiotensin system or RAAS renin angiotensin aldosterone system is a hormone system that regulates blood pressure and water balance
72
describe RAS
- when blood volume is low, juxtaglomerular cells in kidney secrete renin
- renin converts angiotensin from liver to angiotensin I
- angiotensin I -> angiotensin II by enzyme angiotensin converting enzyme ACE resulting in increased blood pressure
- angiotensin II also stimulates secretion of hormone aldosterone from adrenal cortex
- aldosterone causes tubules of kidneys to increase reabsorption of sodium & water into the blood
- this increases the volume of fluid in the body which also increases BP
73
what are the components of stainless steel
72% - Iron
18% - Chromium
8% - Nickel
1.7% - Titanium
0.3% - Carbon
74
type of stainless steel used in orthodontics
18/8 austenitic stainless steel alloy
75
chromium + stainless steel
enables corrosion resistance
lowers temperature at which martensite forms
76
nickel + stainless steel
causes critical temperature to be lowered (i.e. lowers temp at which austenitic structure breaks down on cooling)
improves corrosion resistance
increases strength
77
titanium + stainless steel
added to prevent precipitation of chromium carbides at grain boundaries when alloy is heated during welding or soldering as carbon combines with titanium in preference to chromium
78
work hardening
also known as cold working
is strengthening of a metal by plastic deformation which occurs because of dislocation movement
79
benefits of increased ductility & springiness in SS (4)
- SS used in long clasps to engage 0.75mm undercuts & used as wire in splint
- therefore must be flexible and have the ability to undergo prolonged periods of stress without subjecting to permanent deformation
- increased ductility would allow wires & clasps to bend without fracturing
- increased springiness allows SS to undergo large deflections without permanent deformation when it is regularly placed under stress
80
what teeth are normally affected by MIH
hypomineralisation of permanent molars and affected incisors
81
what questions would you ask parent of child with MIH
i) antenatal period - did you have any infections or illnesses during pregnancy e.g. hypocalcaemia, vit D deficiency or hypertension
ii) 2 q's about child birth - how was child delivered, was child delivered prematurely, were there any birth complications
iii) 2 q's about health of child from birth to 2yrs - has the child had chicken pox/rubella/measles/any other relevant childhood illness e.g. asthma, cardiac, epilepsy
82
why do we ask the q's we do to mothers who have children with MIH
MIH has a higher prevalence amongst children who had pre natal peri natal or post natal medical problems
mothers of MIH affected children experienced more disease throughout pregnancy
83
what will ptx with MIH complain of
appearance of teeth
sensitivity to hot & cold
84
would dentine be affected in MIH
dentine would not be affected by hypomineralisation; effect would be felt however - dentine would become hypersensitive as it has become exposed due to porous enamel, fluid flow within tubules (hydrodynamic theory) and pulpal inflammation may be present
85
outline formation of dentine
- dentinogenesis = first feature in crown stage of development
- must occur before formation of enamel
- odontoblasts differentiate from cells of dental papilla
- primary dentine formed before root formation and form outermost layer of mantle dentine and an inner layer of circumpulpal dentine
- secondary dentine forms after root formation and grows at a slower rate
- tertiary dentine forms in response to stimuli such as attrition or caries aka reparative dentine
86
outline formation of enamel
- amelogenesis during crown stage of tooth development after formation of dentine by ameloblasts
- secretory stage first & maturation stage occurs to complete enamel formation
87
hyper vs hypothyroidism
hyper - Grave's disease - increased metabolism
hypo - hashimoto's thyroiditis - decreased metabolism
88
hyper vs hypothyroidism TSH + T3
hyper - low TSH // high T3 = T3 build up
hypo - high TSH // low T3 = TSH build up
89
hyper vs hypothyroidism symptoms
hyper - hyperactive, heat intolerance, palpitations & weight loss
hypo - tiredness, cold intolerance, slow heart & weight gain
90
hyper vs hypothyroidism signs
hyper - goitre, AF (tachycardia), warm moist skin
hypo - goitre, depression, bradycardia, poor libido, constipation
91
hyper vs hypothyroidism treatment
hyper - beat blockers to reduce symptoms, antithyroid drugs i.e. carbizamole
hypo - thyroxine which shrinks goitre
92
hyper vs hypothyroidism test
hyper - test for free T3 & TSH - graves is an autoimmune disorder and oedema can be seen in the eye
hypo - test for free T4 & TSH - autoimmune destruction of the thyroid gland
93
hypothalamic pituitary axis HPA controls stress reaction
- direct influences and negative feedback control
- between hypothalamus (CRH) -> anterior pituitary (ACTH) -> adrenal glands (cortisol)
- cortex hormones - corticosteroids
- mineralocorticoids - aldosterone
- glucocorticoids - cortisol
- medulla - adrenaline
- insulin facilitates glucose uptake into cells, glucagon raises blood sugar, SS inhibits both
94
describe informed consent
- voluntary & continuing permission of an appropriately informed individual who has capacity to consent, sufficient knowledge of purpose, nature, likely effects & risks of treatment. must be aware of likelihood of success of procedure & any alternatives
should have
1. informed consent -enough info to make decision
2. voluntary - must make decision themselves
3. ability to make informed decision
capacity assumed in ptx over 16 unless reason to believe otherwise.
implied consent for minor procedures, expressed consent for major invasive procedure
oral & written consent are equally lawful if a record is kept
95
describe clinical negligence
- dentist owed a duty of care
- duty was breached i.e. dentist did not adopt that practise
- the course the dentist adopted is one which no dentist of ordinary skill would have taken if acting with ordinary care
- breach caused or contributed to harm
- damage was reasonably foreseeable and had negative consequences
96
steps to help avoid negligence (3)
1. document any steps taken, precaution when taking x rays e.g. working lengths
2. GDP judged by standards of other GDPs
3. risk of instrument failure is well known and so foreseeable so assessment should be conducted prior to using any equipment
97
key factors in ulcerative colitis
continuous disease
rectum always involved
anal fissures 25%
ileum involved 10%
mucosa granulomatous & ulcerated
vascular
serosa normal
diarrhoea, abdominal pain, PR bleeding
98
key factors in Crohn's disease
discontinuous
rectum involved 50% time
anal fissures 75% of time
ileum involved 30%
mucosa cobbled & fissures
non vascular - oedematous
serosa inflamed
orofacial granulomatosis
99
causes of Vit B12/folate deficiency
- lack of intrinsic factor which is needed to absorb B12
- autoimmune disease attacking gastric mucous membrane inhibiting IF release
- ptx may develop pernicious anaemia
- bowel problems / vegan diet
- alcoholic gastritis can cause blood loss in young
- reduced energy as B12 helps absorb folic acid facilitating release of energy
- MCV = macrocytic as large RBC caused by B12/folic acid deficiency
- beefy tongue
100
iron deficient anaemia causes
- heavy menstrual period / pregnancy
- bleeding into GIT caused by aspirin & NSAIDs
- poor absorption of Fe i.e. coeliac
- hookworm infection which lives off blood in GIT
- alcoholic gastritis causing blood loss in young
- MCV = microcytic - small RBC caused by Fe deficiency or thalassemia (genetic mutation of Hb chains)
- smooth tongue
101
how to tell from bloods if it is a bleeding disorder
decreased RCC
MCV normal
HCT normal
102
how to tell from blood tests if it is a deficiency
RCC normal
MCV - micro or macrocytic
HCT low
103
4 emergency drugs essential in a dental practice
GTN spray
adrenaline
salbutamol inhaler
oral glucose (hypoglycaemia) / glucagon
104
4 emergency pieces of equipment essential for every dental practice
oxygen mask & tubing
external defibrillator
blood glucose measurement device
pulse oximeter
105
where is LA deposited during an IAN block
it is deposited around the nerve trunk
106
when should you use an IAN
for lower second premolars and molars
107
what is the pterygomandibular raphe
ligamentous fibrous band attached to the hamulus of the medial pterygoid muscle and mylohyoid
108
where is the pterygomandibular raphe found
posteriorly to the last standing tooth and is recognised by palpating anterior notch with thumb
109
what structures enter the mandible at the mandibular foramen
inferior alveolar nerve and inferior alveolar artery
110
what is the lingula of the mandible
prominent bony ridge at the entrance to the mandibular canal that attaches the sphenomandibular ligament
111
why aspirate
to ensure needle is not lying in a blood vessel and ensures the LA solution is not delivered into the systemic circulation
112
when LA deposited in IAN the tip of the needle will lie in the pterygomandibular space - where is this
between the ramus of the mandible and medial pterygoid muscle
113
infiltration of gingiva during IAN
buccal gingiva - buccal nerve
lingual gingiva - lingual nerve branches off the IAN and supplies this are with sensory innervation so lingual nerve often anaesthetised when IAN block delivered
114
clinical signs IAN has worked
numbness of lower lip as mental nerve is branch of IAN that has been anaesthetised
115
after IAN if corner of ptx mouth starts to droop what has happened
facial palsy - needle has punctured the parotid gland and paralysed the facial nerve
116
immediate concern in facial palsy
protect eye - blink reflex has been disabled so eye patch must be worn. to test ask ptx to blink
117
describe procedures required to determine attachment loss at a particular site
- position of gingival margin relative to amelocemental junction (CJ) at 6 points around tooth recorded
- pocket depth recorded at these points
- loss of attachment calculated by adding gingival margin level to pocket depth
- pocket depth considered + if below gingival margin (recession) and considered - if it lies above gingival margin (inflammation)
118
tooth mobility grading
graded according to how much the tooth moves bucco-lingually in socket when a finger is placed on top of it
grade 1 - <1mm
grade 2 - 1-2mm
grade 3 - >2mm and/or rotation or depression
119
2 sites have the same loss of attachment but A has gingival overgrowth and B has gingival recession -which has the deeper pocket?
site A
120
3 changes you would see in a full mouth pocket chart following non surgical treatment of ptx with chronic perio
- probing depth (pocket depth) would decrease
- increased attachment; formation of junctional epithelium
- stronger tissue; resistant to probing so there would be more blanching of gingival tissues
121
where is LA deposited during infiltration
deposited around terminal branches of nerves
122
name a topical anaesthetic
benzocaine
123
infiltration LA placement in relation to apex of premolar
over apex at mucobuccal fold
124
infiltration - what types of nerve fibres are anaesthetised
A-delta (cold) & C fibres (hot, thermo, noci), A-beta, A-alpha (motor-mechano)
125
what branch of trigeminal innervates the maxilla
maxillary branch, superior alveolar, PSA, MSA & ASA
126
name 3 types of LA
- lignocaine 2% HCl + 1:80,000 adrenaline
- prilocaine 4% HCl + felypressin
- articaine
127
adv of vasoconstrictor + egs
increases duration of action
most LA are vasodilators and increased blood flow will 'wash out' LA
egs are adrenaline and felypressin
128
stages of RPD design
1st clinical - exam, info gathering, history, primary imps
1st lab - pour & mount casts on articulator, special trays
prior to 2nd - survey casts, txp, RPD design
2nd clinical - definitive imps
2nd lab - pour definitive casts, occlusal rims
3rd clinical - jaw reg
3rd lab - tooth trial
4th clinical - tooth trial assessment
4th lab - CoCr base or finish acrylic denture present on master cast
5th clinical - CoCr assessment or delivery of acrylic
5th lab - tooth trial on CoCr
6th clinical - CoCr wax trial on teeth
6th lab - finish denture, present on master cast
7th clinical - delivery of CoCr
129
maxillary intraoral landmarks
incisive papilla, rugae, palatine torus, palatine raphe, palatine fovea, vibrating line, hamular notch, maxillary tuberosity, residual ridge, labial frenum, buccal frenum, zygomatic buttress, buccal sulcus, labial sulcus
130
mandibular intraoral landmarks
buccal shelf, pear shaped pad, retromolar pad lies behind, mylohyoid ridge, mandibular torus, lingual pouch, lingual sulcus, labial sulcus, buccal sulcus, lingual frenum, labial & buccal frenum
131
drawbacks of CoCr
low ductility - not a great ability to deform under stress and has a high YM so clasps are not flexible and can't fit an undercut >0.25mm
difficult to adjust once made as it work hardens rapidly so required precision casting when first made
aesthetics - denture can't be easily hidden
132
5 differences between CoCr & type IV gold alloy
- CoCr less dense; will be more defects but will be lighter
- CoCr higher hardness; harder to polish but effects will last
- CoCr lower ductility; cannot deform under stress
- CoCr has a higher modulus of elasticity YM
- CoCr has a higher shrinkage
133
describe the possible clinical & pathological sequence of leaving caries untreated in an adult tooth
- enamel: caries spread will start in enamel of pit & fissure system
- chronic reversible pulpitis: once caries spreads through enamel to reach ADJ it will progress rapidly along ADJ and spread through dentinal tubules; at this stage there is bacterial invasion & pulp becomes irritated
- chronic irreversible pulpitis: caries reaches pulp chamber of tooth, ptx experiences pain caused by hydrostatic pressure of dentinal fluid & inflammation of blood vessels within the pulp
pulp necrosis: infection spread to pulp chamber down root and irreversible damage is done, abscess may be seen as inflammation spreads to gingiva
- tx options are RCT or XLA
