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BDS 2 exam FINAL FLASHCARDS > BAMS > Flashcards

BAMS Flashcards

1
Q

Acellular extrinsic fibres cementum characteristics (3 marks)

A
  • collagen fibres from PDL (SHARPEY’s FIBRES)
    -equivalent to primary acellular cementum
  • present on cervical 2/3 of roots
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2
Q

Why is perio treatment less successful in furcation and apical areas ?

A

Less sharpeys fibres

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3
Q

Why do we need a periodontium?

A

Transfer forces from teeth to Bone (cushion to prevent bone damage as bone softer than teeth)

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4
Q

What are the nutrients canals called which penetrate the alveolar bone ?

A

Volkmans canals

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5
Q

2 classes of nerves in PDL

A

Mechanoreceptors and nociceptors

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6
Q

What is this called?

A

Gnarled Enamel

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7
Q

What is amelogenesis imperfecta?

A

No breakdown of amelogenins: disorder of tooth development. Causes teeth to be unusually small, discoloured, pitted or grooved. RAPID wear and breakage. GENETIC

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8
Q

What happens to the composition of enamel after restoration?

A

Changes- loses water and organic matrix

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9
Q

What are the 2 main marks on the enamel which the lines are pointing at ?

A

Enamel Spindles

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10
Q

What is this?

A

Enamel tuft

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11
Q

Difference between enamel lamella and tufts

A

Lamella extends all the way into rods unlike tufts

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12
Q

What are enamel spindles ?

A

formed when odontoblast processes extend across the DEJ and are trapped in the enamel when ameloblasts begin secreting enamel matrix

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13
Q

What is the box highlighting ?

A

Perikymata

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14
Q

What are perikymata?

A

Incremental growth lines that appear on the tooth surface

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15
Q

What causes cross striations in enamel ?

A

DAILY GROWTH: see long parallel rods, approx. 4um

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16
Q

proteins in the organic matrix of enamel?

A

amelogenins
enamelins
peptides
amino acids

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17
Q

Which has thinner enamel? permanent or deciduous

A

deciduous

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18
Q

Where is enamel most mineralised

A

SURFACE and its harder

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19
Q

What causes the brown transverse striae in enamel

A

weekly intervals of growth 25-35um apart

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20
Q

What is in dentine but not enamel

A

collagen

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21
Q

what other process can influence crystallite orientation?

A

tommes process

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22
Q

What ions can be substituted into HA

A

Fluoride
Mg2+
CO3(2-) - carbonate

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23
Q

When is carbonated apatite more common

A

when tooth erupting (as enamel matures carbonated apatite decreses)

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24
Q

What is meant by the neonatal line

A

particular band of incremental growth lines

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25
Q

How thick is enamel without any tooth wear

A

2mm

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26
Q

How do the brown striae of retzius run

A

thick brown lines that run obliquely from outer surface to the ADJ

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27
Q

Advantages of scalloping in ADJ

A

able to withstand high shearing forces

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28
Q

Why is prism orientation in regards to cavity rpeparations

A

want to be perpendicular to ADJ so no unsupported enamel

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29
Q

Why is it harder to bond to dentine closer to the pulp

A

less to bond to, there is more MOISTURE towards pulp as tubules closer together

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30
Q

Where is dentine formation

A

inside the tubules: intra-tubular dentine

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31
Q

What do A B and C represent

A

A= enamel
B= dead tracts of dentine
C= secondary dentine

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32
Q

Identify a-g

A

a= carious dentine
b= sclerotic dentine
c= dead tracts
d= secondary dentine
e- dentine
f= enamel
g= pulp

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33
Q

Where are dead tracts sealed any how does this occur

A

at the pulpal end- by deposition of tertiary dentine

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34
Q

How can the boundary between primary and secondary dentine be seen?

A

often hard but sometimes there is a change in orientation/direction of the dentinal tubules

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35
Q

When is primary dentine laid down?

A

laid down while the tooth is forming: it is completed when the root apex is fully formed

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36
Q

When is secondary dentine laid down?

A

during the life of th tooth: after the tooth if fully formed

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37
Q

dentinal tubules permeability; where are they most permeable and how if this overcome

A

most permeable in deeper areas: deeper the cavity the larger need for cavity lining

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38
Q

Difference between reactionary dentine and reparative dentine

A

reactionary: laid down by primary odontoblasts
reparative: recruited stem cells

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39
Q

Which has a slower rate of formation: secondary dentine or priamary dentine

A

secondary dentine

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40
Q

is pre-dentine mineralised?

A

NO

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41
Q

What appearance does the odontoblast layer have at the dentine pulp interface?

A

pseudo-stratified appearance

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42
Q

Name of dark red blobs in predentine and what don they represent

A

CALCOSPHERITES- centres of mineralisation (calcification)

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43
Q

structures in the inner part of dentine

A

an odontoblast process
unmyelinated nerve terminal 9especially in dentine under cusps)

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44
Q

structures in outer part of dentine

A

no vital cells

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45
Q

Extracellular components of the pulp

A

fibres- collagen and oxytalan
matrix - proteoglycans, chondroitin SO4, dermatin SO4

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46
Q

5 functions of the pulp ( DDDNN)

A

nutritive (blood vessels)
dentine growth
dentine repair (tertiary)
defence (immune cells and lymphatics)
neural (sensory pain response)

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47
Q

what causes bruxism

A

attrition

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48
Q

what causes abfraction

A

occlusal overload leading to fractures and cervical lesions

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49
Q

what does bad diet cause in relation to tooth wear

A

erosion

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50
Q

what separates pulp and tubular space

A

odontoblast layer

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51
Q

role of the odontoblast layer

A

permeability barrier - regulates movement of material between pulp and tubular ecf

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52
Q

what is raschow’s plexus

A

branches of alveolar nerve which fan out in sub-odontoblastic layer in pulp

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53
Q

branches of alveolar nerve which fan out in sub-odontoblastic layer in pulp?

A

raschow’s plexus

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54
Q

what os the spread of dentine innervation

A

40% under cusps
15% coronal dentine
4% root dentine
few axons enter tubules; most end in pulp-predentine region

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55
Q

What causes outward dentinal fluid flow?

A

cooling
drying
evaporation
hypertonic solutions
decreased hydrostatic pressure

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56
Q

what can cause inward dentinal flow?

A

increased hydrostatic pressure (syringe)

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57
Q

most common way for a restoration to cause dental pain

A

HIGH fillings

distortion onto dentine and created movement in dentinal fluid flow

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58
Q

what fibres are activated by hydro-dynamic stimuli applied to dentine

A

A beta
A delta

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59
Q

What activates c fibres

A

stimuli directly

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60
Q

5 branches of the maxillary artery

A

deep auricular artery
anterior tympanic artery
medial meningeal artery
accessory meningeal artery
inferior alveolar artery

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61
Q

Immediate dentine pulp response to injury

A

nociceptor activation- PAIN

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62
Q

What is pulpitis

A

toothache
acute inflammation in pulp is similar to other tissues except pulp cannot swell as it is confined in pulp chamber

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63
Q

Action of LA (simple)

A

La act on nerve ion channels to block propagation - stop signal passing to nerve

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64
Q

most commonly prescribed antiviral drug in dentistry

A

aciclovir

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65
Q

what can increase incidence of oral fungal infections

A

inhaler
dentures
orthodontics

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66
Q

what are corticosteroids

A

reduce the inflammation process

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67
Q

what are NSAIDs

A

reduce inflammatory mediators

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68
Q

which NSAID is often prescribed for wisdom tooth pain

A

Diclofenac

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69
Q

why might someone not be able to have aspirin

A

if they have a kidney issue

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70
Q

ASPIRIN: first order or zero order

A

1st order : rapid absorption from GIT

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71
Q

action of aspirin

A

inhibits COX1 - REDUCED PRODUCTION OF INFLAMMATORY MEDIATORS AND REDUCED SYNTHESIS OF PROSTAGLANDINS

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72
Q

side effects of NSAID

A

gastric irritation (erosions, ulcerations)
inhibition of platelet function (enhanced bleeding)
bronchospasm (make asthma worse)
allergic reaction
drug interaction- WARFARIN

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73
Q

is diclofenac more potent or less potent than ibuprofen?

A

more potent= more side effects= more effective

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74
Q

drugs used to reduce anxiety

A

benzodiazepines
DIAZEPAM/ MIDAZOLAM

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75
Q

definition of a drug

A

external substance that acts on living tissue to produce a measurable change in the function of that tissue

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76
Q

difference between hormone messages and neural messages

A

hormone: general info to all tissues
neural: targeted information for specific tissues

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77
Q

What is given to a hypothyroidism patient and what does it do

A

thyroxine tablet
replaces missing T3 and T4

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78
Q

what is adrenaline

A

beta agonist - speeds up heart rate
AUTONOMIC

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79
Q

example of b blocker and what is does

A

atenolol
slows heart rate - blocks adrenaline receptor so stopping action
REDUCES arrythmias and lowers BP

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80
Q

How do receptors work for drugs

A

couples to ion channels - channel opens
- coupled to G -proteins - change conformation to trigger cascade
- coupled to gene transcription

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81
Q

occupancy

A

the fraction of bound receptors

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82
Q

affinity

A

how avidly the drug brind to its receptor

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83
Q

efficacy

A

maximum response achievable and capacity for sufficient effect or beneficial change

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84
Q

pharmacokinetics

A

what the body does to a drug

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85
Q

pharmacodynamics

A

how the drug effects the organism

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86
Q

4 phases of drug from intake

A

absorption
clinical effect
metabolism
excretion

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87
Q

4 things that modify bioavailability

A

dosage form
destruction in the gut
poor absorption
first pass metabolism

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88
Q

phase 1 drug elimination reaction

A

oxidation, reduction and hydrolysis
little changes to molecule, no longer bind to receptor, inactivate it

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89
Q

phase 2 drug elimination reaction

A

conjugation for excretion
glucuronidation, sulphation, methylation, acetylation and glutathione

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90
Q

5 methods of drug excretion

A

renal - urine
liver - bile
lungs - exhale gas
sweat
saliva

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91
Q

how can renal excretion be modified

A

change urine pH - make more alkaline can get rid of excess acidic drug

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92
Q

single compartment model

A

drug behaved as if it is evenly distributed throughout the body

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93
Q

two compartment model

A

drug behaved as if it is in equilibrium with different tissues in the body -blood flow dependant

94
Q

what method of administeration is best for mophine

A

transdermal patch- want a lot of pain relief for prolonged time

95
Q

phase 1 in inactivation and excretion

A

adds or takes away sections so cannot bind to receptor (in liver)

96
Q

phase 2 in drug inactivation and excretion

A

conjugate with other molecules so it can be removed by kidney and gut

97
Q

leading causes in dentinal hypersensitivity

A

tooth wear- attrition abrasion and erosion
gingival recession

98
Q

prevalence of dentine hypersensitivity

A

1 in 3

99
Q

how many dentinal tubules are in a mm squared of dentine

A

approx. 32000

100
Q

2 treatment methods for dentine hypersensitivity

A

tubule occlusion
potassium salts (potassium nitrate)

101
Q

What is used for tubule occlusion

A

novamin and stannous fluoride

102
Q

what is it in toothpaste that some people can react to?

A

sodium lorosulphate (SLS)

103
Q

what is virulence

A

ability of the microbe to cause damage

104
Q

what is dose

A

the number of microbe entering the body

105
Q

6 steps in chain of infection

A

infectious agent
reservoir
portal of exit
means of transmission
portal of entry
susceptible host

106
Q

2 virulence factors and examples

A

endotoxins - lipopolysaccharide , p. gingivalis and e.coli
exotoxins- p. gingivalis, s. aureus enterotoxin

107
Q

exotoxins: GN/GP and how are they released

A

Gram positive
active process

108
Q

endotoxins: GN/GP and how are they released

A

Gram negative
from cell walls

109
Q

term used for human pathogens that come from animals

A

zoonoses

110
Q

what is a fomite

A

contaminated object or surface

111
Q

why is it important to have standard infection control procedures?

A

asymptomatic carriers

112
Q

2 types of mode of escape

A

natural - cough or sneeze
artificial - blood donation or dental handpiece aerosols

113
Q

How are biological agents classified

A

COSHH

114
Q

4 bases COSHH uses to classify human pathogens

A

ability to cause infection
severity of the disease it may result in
vaccine and treatment availability
risk of population spread

115
Q

R0<1

A

infection will die out in the long run

116
Q

R0

A

the number os cases one case generates on average over the course of its infectious period

117
Q

R0> 1

A

infection will spread in a population

118
Q

what type of virus if influenza

A

RNA virus with segmented genome

119
Q

how many types of influenza

A

3
ABC

120
Q

Which types of influenza cause major outbreaks

A

A
B

121
Q

symptoms of mild uncomplpicated influenza

A

fever
cough
headaches
fatigue

122
Q

symptoms of severe complicated influenza

A

bacterial pneumonia, ear and sinus infections

worsening of chronic medical conditions

123
Q

how long is someone infectious with influenza

A

3-5 days

124
Q

droplets

A

large particles from respiratory tract approx > 10nm

125
Q

aerols

A

small particles from respiratory tract
approx <10nm

126
Q

what is primary prevention of cardiovascular disease

A

stop the risk which is going to give you the disease

127
Q

what is secondary prevention of CV disease

A

once contracted how to stop it getting worse

128
Q

3 tests for method of primary prevention of Cv disease

A

cholesterol
BP
diabetes (type 2)

129
Q

How can someone present with CV disease ?

A

angina
Mi
stroke
claudication

130
Q

main anti platelet drug to prevent CV disease

A

ASPIRIN

131
Q

how can total cholesterol be controlled

A

statin treatment
reduce cholesterol by 25 %

132
Q

Types of drugs used in Cv disease to prevent further disease

A

anti platelet
lipid lowering
anti arrhythmics
anticoagulants

133
Q

how does aspirin work

A

inhibits platelet aggregation

134
Q

how much aspirin to prevent platelet function

A

75mg

135
Q

what do anti platelet drugs do in preventing Cv

A

significantly reduce the chance of a heart attach or stroke - only at risk population

136
Q

2 new antiplatelet drugs

A

prasugrel
ticagrelor

137
Q

INR less than 2

A

risk of clot

138
Q

INR more than 4

A

risk of bleed

139
Q

example of direct thrombin inhibitor

A

dabigatran

140
Q

benefit of DOAC

A

short half life
predictable bioavailability
usually postpone extraction until stopped short course

141
Q

statin drug interaction

A

antifungals - fluconazole

142
Q

B blockers role in Cv prevention

A

stop arrhythmias leading to cardiac arrest - blocks affect of adrenaline on heart
prevent increase in heart rate

143
Q

side effect of diuretic

A

can lead to Na/K imbalance if not monitored carefully - DRY MOUTH IN ELDERLY

144
Q

What do nitrates do

A

dilate veins - reduce preload to heart
reduce cardiac workload
dilate collateral coronary artery supply - reduce ANGINAL pain

145
Q

purpose of long acting nitrate

A

prevention of angina pectoris
isosorbide mononitrate

146
Q

side effect of nitrates

A

headache

147
Q

how do calcium channel blockers help prevent CV

A

hypertension - reduce
relaxation and vasodilation of smooth muscle

148
Q

dental side effect of calcium channel blocker

A

make gums bigger - gingival hyperplasia

149
Q

ACE inhibitors. what do they do

A

inhibit conversion of angiotensin 1 to 2. angiotensin 2 in a. vasoconstrictor

150
Q

main actions of ACE inhibitors

A

reduce blood pressure and reduce excess salt and water retention

151
Q

side effect of ace inhibitor

A

couch
hypertension
angio oedema

152
Q

example of ace inhibitor

A

ramapril
lisinopril
end in PRIL

153
Q

where do coronary arteries come away from

A

aorta

154
Q

3 main coronary arteries

A

right
left
circumflex

155
Q

difference between classical and unstabe angina symptoms

A

‘classical’ angina gets worse with exercise

‘unstable’ angina has symptoms at rest with no biomarkers

156
Q

function assesment of angina

A

isotope studies

157
Q

how can you bypass blocked/narrowed vessels to treat angina?

A

CABG
coronary artery bypass grafting

158
Q

What is PVD

A

angina of the tissues : usually lower limb

159
Q

3 ways how can ischeamia lead to infarction?

A

atheroma in vessels
thombosis can enalarge rapidly to block vessel
plaque surface/platelets detach

160
Q

how to prevent further myocardial infarction episode

A

risk factor management
aspirin

161
Q

what is a brain infraction

A

stroke

162
Q

how does a stroke occur

A

usually emobism from atheroma
occasionaly a cerebral bleed
rarely vessel thrombosis

163
Q

signs and symptoms of Mi

A

pain nausea pale sweaty
“GOING TO DIE “

164
Q

ECG for MI

A

St elevation

165
Q

cardiac enzyme to investigate MI

A

troponin

166
Q

medical management of MI

A

risk modification and aspirin
b blocker will reduce risk of abnormal heart rhythm
ace inhibitor - live longer

167
Q

why do blood vessels need to be able to self -repair

A

if vessel gets a hole in it needs to be able to repair itself so has no long lasting effect on platelets and coagulation

168
Q

5 blood constituents

A

cell component
plasma protein
lipids
nutrients
water

169
Q

HCT

A

Haematocrit
ratio of the volume of red blood cells to the total volume of blood

170
Q

polycythaemia

A

raised Hb above the reference range

171
Q

leukaemia

A

neoplastic proliferation of white cells

172
Q

lymphoma

A

neoplastic proliferation of white cells, usually a solid tumour

173
Q

group a blood has

A

a antigens
b antibodies

174
Q

group b blood has

A

b antigens
a antibodies

175
Q

group AB blood has

A

A and B antigens
no antibodies

176
Q

group 0 blood has

A

no antigens
A and B antibodies

177
Q

what will happen if a patient is transfused incompatible blood

A

RBC lysis (burst)
fever jaundice death

178
Q

vascular component of haemostatic disorder

A

retraction of the vessel (hole smaller)

179
Q

cellular component of haemostatic disorders

A

platelets number and function

180
Q

coagulation component of haemostatic disorder

A

adequate clotting

181
Q

how can we asses platelet function

A

bleeding time

182
Q

how many days to form new platelets

A

7-10 days

183
Q

when are increased tendencies to form blood clots…

A

plane, inactive

184
Q

visual sign of poor coagulation history

A

purpura

185
Q

common condition with thrombophilia

A

DVT

186
Q

porphyria

A

abnormality of haem metabolism

187
Q

clinical effect of porphyria

A

photosensitive rash at any time
hypertension and tachycardia

188
Q

RBC life span

A

120 days

189
Q

how can reduced normal red cells lead to anaemia

A
190
Q

normal marrow appearance

A

cellular
bone trabecular

191
Q

what is iron stored in cell as

A

ferritin

192
Q

what disease can reduce iron absorption and how does this occur

A

coeliac disease
lose villi on endothelial of small intestine

193
Q

how can someone have iron loss: conditions (4)

A

= gastric erosions and ulcers
= IBD
=Bowel cancer
= haemorrhoids

194
Q

folic acid sources

A

green leafy veg

195
Q

why is folic acid important

A

needed for nerve maturation

196
Q

oral sign of b12 deficiency

A

beefy tongue

197
Q

oral sign of iron deficiency

A

smooth tongue

198
Q

oral sign of haematinic deficiency

A

pale mucosa

199
Q

anaemia signs

A

pale
tachycardia

200
Q

anaemia symptoms

A

tired and weak
dizzy
dysnopea

201
Q

what injection can be used for anaemia patients with production failure

A

erythropoietin injections can boost haemoglobin levels to normal

202
Q

dental aspect: anaemia

A
  • GA- o2 capacity
  • deficiency states- FE usually , mucosal atrophy, candidiasis, recurrent oral ulceration
203
Q

GA risk for anaemics

A

greater risk of hypoxia

204
Q

2 types of bone

A

cortical - compact
cancellous - spongy

205
Q

cortical is

A

dense outer plate 80-85% of skeleton

206
Q

cancellous is

A

internal trabecular scaffolding 15-20% of skeleton

207
Q

composition of bone by weight

A

60% inorganic HA
15% water
25% organic

208
Q

what makes up 25% organic portion of bone

A

glycoproteins - osteo. -calcin -nectin. - pontin
proteoglycans , chondroitin SO4, heparan SO4

209
Q

types of bone resorption you can get in the oral cavity

A

vertical and horizontal
vertical resorption of bone can maybe grow bone to have more attachment between bone and tooth

210
Q

What makes up the extracellular matrix

A

Glycos-amino- glycans
fibres (collagen and elastin)

211
Q

woven bone properties

A

rapidly laid down
irregular deposition of collagen

212
Q

lamellar bone properties

A

laid down more slowly
well organised : collagen fibres laid down in parallel

213
Q

what are lacunae

A

small canals

214
Q

where do osteoblasts lie and where do they derive from

A

on surface of bone- mesenchymal stem cells

215
Q

osteocytes are

A

become trapped in mineralised bone

216
Q

How can bone remodelling be used to dentist advantage

A

orthodontic treatment

217
Q

what is achondroplasia

A

genetic defect of cartilage growth

218
Q

2 groups that blood stem cell differenciate into

A

myeloid
lymphoid

219
Q

myeloproliferative disorders

A

thrombocythemia

220
Q

what is leukaemia

A

group of cancers of the bone marrow which prevent normal manufacture of the blood and therefor result in anaemia, infection, thrombocytopenia (platelets)

221
Q

pathogenesis of leukarmia and lymphoma

A

clonal proliferation
replacement of marrow

222
Q

ways to clinically present with leukaemia or lymphoma

A

anaemia
neutropenia
thrombocytopenia
splenomegaly
bone pain

223
Q

what 3 things does staging assess

A

number of nodes involved and site
where lumps are
how far down progression line

224
Q

why is staging important

A

predicting prognosis and deciding treatment

225
Q

stage 1 (leukaemia and lymphoma)

A

single lymph node region or single extralymphatic site

226
Q

hodgkin lymphoma peak incidence age

A

15-40 (more males0

227
Q

amyloidosis

A

antibodies in excess amount

228
Q

Q
4 concepts to know about for the process of leukaemia and lymphoma treatment

A

induction
remission
maintenance and consolidation
relapse

229
Q

induction ?

A

intense chemotherapy

230
Q

remission

A

none left (no more acute issues)

231
Q

maintenance and remission

A

haven’t managed to remove all the cancer cells in first place

232
Q

relapse

A

can have multiple relapses but then still improve

BDS 2 exam FINAL FLASHCARDS (1 decks)

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