BAMS Flashcards
(232 cards)
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
2
Q
Why is perio treatment less successful in furcation and apical areas ?
A
Less sharpeys fibres
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)
4
Q
What are the nutrients canals called which penetrate the alveolar bone ?
A
Volkmans canals
5
Q
2 classes of nerves in PDL
A
Mechanoreceptors and nociceptors
6
Q
What is this called?
A
Gnarled Enamel
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
8
Q
What happens to the composition of enamel after restoration?
A
Changes- loses water and organic matrix
9
Q
What are the 2 main marks on the enamel which the lines are pointing at ?
A
Enamel Spindles
10
Q
What is this?
A
Enamel tuft
11
Q
Difference between enamel lamella and tufts
A
Lamella extends all the way into rods unlike tufts
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
13
Q
What is the box highlighting ?
A
Perikymata
14
Q
What are perikymata?
A
Incremental growth lines that appear on the tooth surface
15
Q
What causes cross striations in enamel ?
A
DAILY GROWTH: see long parallel rods, approx. 4um
16
Q
proteins in the organic matrix of enamel?
A
amelogenins
enamelins
peptides
amino acids
17
Q
Which has thinner enamel? permanent or deciduous
A
deciduous
18
Q
Where is enamel most mineralised
A
SURFACE and its harder
19
Q
What causes the brown transverse striae in enamel
A
weekly intervals of growth 25-35um apart
20
Q
What is in dentine but not enamel
A
collagen
21
Q
what other process can influence crystallite orientation?
A
tommes process
22
Q
What ions can be substituted into HA
A
Fluoride
Mg2+
CO3(2-) - carbonate
23
Q
When is carbonated apatite more common
A
when tooth erupting (as enamel matures carbonated apatite decreses)
24
Q
What is meant by the neonatal line
A
particular band of incremental growth lines
25
How thick is enamel without any tooth wear
2mm
26
How do the brown striae of retzius run
thick brown lines that run obliquely from outer surface to the ADJ
27
Advantages of scalloping in ADJ
able to withstand high shearing forces
28
Why is prism orientation in regards to cavity rpeparations
want to be perpendicular to ADJ so no unsupported enamel
29
Why is it harder to bond to dentine closer to the pulp
less to bond to, there is more MOISTURE towards pulp as tubules closer together
30
Where is dentine formation
inside the tubules: intra-tubular dentine
31
What do A B and C represent
A= enamel
B= dead tracts of dentine
C= secondary dentine
32
Identify a-g
a= carious dentine
b= sclerotic dentine
c= dead tracts
d= secondary dentine
e- dentine
f= enamel
g= pulp
33
Where are dead tracts sealed any how does this occur
at the pulpal end- by deposition of tertiary dentine
34
How can the boundary between primary and secondary dentine be seen?
often hard but sometimes there is a change in orientation/direction of the dentinal tubules
35
When is primary dentine laid down?
laid down while the tooth is forming: it is completed when the root apex is fully formed
36
When is secondary dentine laid down?
during the life of th tooth: after the tooth if fully formed
37
dentinal tubules permeability; where are they most permeable and how if this overcome
most permeable in deeper areas: deeper the cavity the larger need for cavity lining
38
Difference between reactionary dentine and reparative dentine
reactionary: laid down by primary odontoblasts
reparative: recruited stem cells
39
Which has a slower rate of formation: secondary dentine or priamary dentine
secondary dentine
40
is pre-dentine mineralised?
NO
41
What appearance does the odontoblast layer have at the dentine pulp interface?
pseudo-stratified appearance
42
Name of dark red blobs in predentine and what don they represent
CALCOSPHERITES- centres of mineralisation (calcification)
43
structures in the inner part of dentine
an odontoblast process
unmyelinated nerve terminal 9especially in dentine under cusps)
44
structures in outer part of dentine
no vital cells
45
Extracellular components of the pulp
fibres- collagen and oxytalan
matrix - proteoglycans, chondroitin SO4, dermatin SO4
46
5 functions of the pulp ( DDDNN)
nutritive (blood vessels)
dentine growth
dentine repair (tertiary)
defence (immune cells and lymphatics)
neural (sensory pain response)
47
what causes bruxism
attrition
48
what causes abfraction
occlusal overload leading to fractures and cervical lesions
49
what does bad diet cause in relation to tooth wear
erosion
50
what separates pulp and tubular space
odontoblast layer
51
role of the odontoblast layer
permeability barrier - regulates movement of material between pulp and tubular ecf
52
what is raschow's plexus
branches of alveolar nerve which fan out in sub-odontoblastic layer in pulp
53
branches of alveolar nerve which fan out in sub-odontoblastic layer in pulp?
raschow's plexus
54
what os the spread of dentine innervation
40% under cusps
15% coronal dentine
4% root dentine
few axons enter tubules; most end in pulp-predentine region
55
What causes outward dentinal fluid flow?
cooling
drying
evaporation
hypertonic solutions
decreased hydrostatic pressure
56
what can cause inward dentinal flow?
increased hydrostatic pressure (syringe)
57
most common way for a restoration to cause dental pain
HIGH fillings
distortion onto dentine and created movement in dentinal fluid flow
58
what fibres are activated by hydro-dynamic stimuli applied to dentine
A beta
A delta
59
What activates c fibres
stimuli directly
60
5 branches of the maxillary artery
deep auricular artery
anterior tympanic artery
medial meningeal artery
accessory meningeal artery
inferior alveolar artery
61
Immediate dentine pulp response to injury
nociceptor activation- PAIN
62
What is pulpitis
toothache
acute inflammation in pulp is similar to other tissues except pulp cannot swell as it is confined in pulp chamber
63
Action of LA (simple)
La act on nerve ion channels to block propagation - stop signal passing to nerve
64
most commonly prescribed antiviral drug in dentistry
aciclovir
65
what can increase incidence of oral fungal infections
inhaler
dentures
orthodontics
66
what are corticosteroids
reduce the inflammation process
67
what are NSAIDs
reduce inflammatory mediators
68
which NSAID is often prescribed for wisdom tooth pain
Diclofenac
69
why might someone not be able to have aspirin
if they have a kidney issue
70
ASPIRIN: first order or zero order
1st order : rapid absorption from GIT
71
action of aspirin
inhibits COX1 - REDUCED PRODUCTION OF INFLAMMATORY MEDIATORS AND REDUCED SYNTHESIS OF PROSTAGLANDINS
72
side effects of NSAID
gastric irritation (erosions, ulcerations)
inhibition of platelet function (enhanced bleeding)
bronchospasm (make asthma worse)
allergic reaction
drug interaction- WARFARIN
73
is diclofenac more potent or less potent than ibuprofen?
more potent= more side effects= more effective
74
drugs used to reduce anxiety
benzodiazepines
DIAZEPAM/ MIDAZOLAM
75
definition of a drug
external substance that acts on living tissue to produce a measurable change in the function of that tissue
76
difference between hormone messages and neural messages
hormone: general info to all tissues
neural: targeted information for specific tissues
77
What is given to a hypothyroidism patient and what does it do
thyroxine tablet
replaces missing T3 and T4
78
what is adrenaline
beta agonist - speeds up heart rate
AUTONOMIC
79
example of b blocker and what is does
atenolol
slows heart rate - blocks adrenaline receptor so stopping action
REDUCES arrythmias and lowers BP
80
How do receptors work for drugs
couples to ion channels - channel opens
- coupled to G -proteins - change conformation to trigger cascade
- coupled to gene transcription
81
occupancy
the fraction of bound receptors
82
affinity
how avidly the drug brind to its receptor
83
efficacy
maximum response achievable and capacity for sufficient effect or beneficial change
84
pharmacokinetics
what the body does to a drug
85
pharmacodynamics
how the drug effects the organism
86
4 phases of drug from intake
absorption
clinical effect
metabolism
excretion
87
4 things that modify bioavailability
dosage form
destruction in the gut
poor absorption
first pass metabolism
88
phase 1 drug elimination reaction
oxidation, reduction and hydrolysis
little changes to molecule, no longer bind to receptor, inactivate it
89
phase 2 drug elimination reaction
conjugation for excretion
glucuronidation, sulphation, methylation, acetylation and glutathione
90
5 methods of drug excretion
renal - urine
liver - bile
lungs - exhale gas
sweat
saliva
91
how can renal excretion be modified
change urine pH - make more alkaline can get rid of excess acidic drug
92
single compartment model
drug behaved as if it is evenly distributed throughout the body
93
two compartment model
drug behaved as if it is in equilibrium with different tissues in the body -blood flow dependant
94
what method of administeration is best for mophine
transdermal patch- want a lot of pain relief for prolonged time
95
phase 1 in inactivation and excretion
adds or takes away sections so cannot bind to receptor (in liver)
96
phase 2 in drug inactivation and excretion
conjugate with other molecules so it can be removed by kidney and gut
97
leading causes in dentinal hypersensitivity
tooth wear- attrition abrasion and erosion
gingival recession
98
prevalence of dentine hypersensitivity
1 in 3
99
how many dentinal tubules are in a mm squared of dentine
approx. 32000
100
2 treatment methods for dentine hypersensitivity
tubule occlusion
potassium salts (potassium nitrate)
101
What is used for tubule occlusion
novamin and stannous fluoride
102
what is it in toothpaste that some people can react to?
sodium lorosulphate (SLS)
103
what is virulence
ability of the microbe to cause damage
104
what is dose
the number of microbe entering the body
105
6 steps in chain of infection
infectious agent
reservoir
portal of exit
means of transmission
portal of entry
susceptible host
106
2 virulence factors and examples
endotoxins - lipopolysaccharide , p. gingivalis and e.coli
exotoxins- p. gingivalis, s. aureus enterotoxin
107
exotoxins: GN/GP and how are they released
Gram positive
active process
108
endotoxins: GN/GP and how are they released
Gram negative
from cell walls
109
term used for human pathogens that come from animals
zoonoses
110
what is a fomite
contaminated object or surface
111
why is it important to have standard infection control procedures?
asymptomatic carriers
112
2 types of mode of escape
natural - cough or sneeze
artificial - blood donation or dental handpiece aerosols
113
How are biological agents classified
COSHH
114
4 bases COSHH uses to classify human pathogens
ability to cause infection
severity of the disease it may result in
vaccine and treatment availability
risk of population spread
115
R0<1
infection will die out in the long run
116
R0
the number os cases one case generates on average over the course of its infectious period
117
R0> 1
infection will spread in a population
118
what type of virus if influenza
RNA virus with segmented genome
119
how many types of influenza
3
ABC
120
Which types of influenza cause major outbreaks
A
B
121
symptoms of mild uncomplpicated influenza
fever
cough
headaches
fatigue
122
symptoms of severe complicated influenza
bacterial pneumonia, ear and sinus infections
worsening of chronic medical conditions
123
how long is someone infectious with influenza
3-5 days
124
droplets
large particles from respiratory tract approx > 10nm
125
aerols
small particles from respiratory tract
approx <10nm
126
what is primary prevention of cardiovascular disease
stop the risk which is going to give you the disease
127
what is secondary prevention of CV disease
once contracted how to stop it getting worse
128
3 tests for method of primary prevention of Cv disease
cholesterol
BP
diabetes (type 2)
129
How can someone present with CV disease ?
angina
Mi
stroke
claudication
130
main anti platelet drug to prevent CV disease
ASPIRIN
131
how can total cholesterol be controlled
statin treatment
reduce cholesterol by 25 %
132
Types of drugs used in Cv disease to prevent further disease
anti platelet
lipid lowering
anti arrhythmics
anticoagulants
133
how does aspirin work
inhibits platelet aggregation
134
how much aspirin to prevent platelet function
75mg
135
what do anti platelet drugs do in preventing Cv
significantly reduce the chance of a heart attach or stroke - only at risk population
136
2 new antiplatelet drugs
prasugrel
ticagrelor
137
INR less than 2
risk of clot
138
INR more than 4
risk of bleed
139
example of direct thrombin inhibitor
dabigatran
140
benefit of DOAC
short half life
predictable bioavailability
usually postpone extraction until stopped short course
141
statin drug interaction
antifungals - fluconazole
142
B blockers role in Cv prevention
stop arrhythmias leading to cardiac arrest - blocks affect of adrenaline on heart
prevent increase in heart rate
143
side effect of diuretic
can lead to Na/K imbalance if not monitored carefully - DRY MOUTH IN ELDERLY
144
What do nitrates do
dilate veins - reduce preload to heart
reduce cardiac workload
dilate collateral coronary artery supply - reduce ANGINAL pain
145
purpose of long acting nitrate
prevention of angina pectoris
isosorbide mononitrate
146
side effect of nitrates
headache
147
how do calcium channel blockers help prevent CV
hypertension - reduce
relaxation and vasodilation of smooth muscle
148
dental side effect of calcium channel blocker
make gums bigger - gingival hyperplasia
149
ACE inhibitors. what do they do
inhibit conversion of angiotensin 1 to 2. angiotensin 2 in a. vasoconstrictor
150
main actions of ACE inhibitors
reduce blood pressure and reduce excess salt and water retention
151
side effect of ace inhibitor
couch
hypertension
angio oedema
152
example of ace inhibitor
ramapril
lisinopril
end in PRIL
153
where do coronary arteries come away from
aorta
154
3 main coronary arteries
right
left
circumflex
155
difference between classical and unstabe angina symptoms
‘classical’ angina gets worse with exercise
‘unstable’ angina has symptoms at rest with no biomarkers
156
function assesment of angina
isotope studies
157
how can you bypass blocked/narrowed vessels to treat angina?
CABG
coronary artery bypass grafting
158
What is PVD
angina of the tissues : usually lower limb
159
3 ways how can ischeamia lead to infarction?
atheroma in vessels
thombosis can enalarge rapidly to block vessel
plaque surface/platelets detach
160
how to prevent further myocardial infarction episode
risk factor management
aspirin
161
what is a brain infraction
stroke
162
how does a stroke occur
usually emobism from atheroma
occasionaly a cerebral bleed
rarely vessel thrombosis
163
signs and symptoms of Mi
pain nausea pale sweaty
"GOING TO DIE "
164
ECG for MI
St elevation
165
cardiac enzyme to investigate MI
troponin
166
medical management of MI
risk modification and aspirin
b blocker will reduce risk of abnormal heart rhythm
ace inhibitor - live longer
167
why do blood vessels need to be able to self -repair
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
5 blood constituents
cell component
plasma protein
lipids
nutrients
water
169
HCT
Haematocrit
ratio of the volume of red blood cells to the total volume of blood
170
polycythaemia
raised Hb above the reference range
171
leukaemia
neoplastic proliferation of white cells
172
lymphoma
neoplastic proliferation of white cells, usually a solid tumour
173
group a blood has
a antigens
b antibodies
174
group b blood has
b antigens
a antibodies
175
group AB blood has
A and B antigens
no antibodies
176
group 0 blood has
no antigens
A and B antibodies
177
what will happen if a patient is transfused incompatible blood
RBC lysis (burst)
fever jaundice death
178
vascular component of haemostatic disorder
retraction of the vessel (hole smaller)
179
cellular component of haemostatic disorders
platelets number and function
180
coagulation component of haemostatic disorder
adequate clotting
181
how can we asses platelet function
bleeding time
182
how many days to form new platelets
7-10 days
183
when are increased tendencies to form blood clots...
plane, inactive
184
visual sign of poor coagulation history
purpura
185
common condition with thrombophilia
DVT
186
porphyria
abnormality of haem metabolism
187
clinical effect of porphyria
photosensitive rash at any time
hypertension and tachycardia
188
RBC life span
120 days
189
how can reduced normal red cells lead to anaemia
190
normal marrow appearance
cellular
bone trabecular
191
what is iron stored in cell as
ferritin
192
what disease can reduce iron absorption and how does this occur
coeliac disease
lose villi on endothelial of small intestine
193
how can someone have iron loss: conditions (4)
= gastric erosions and ulcers
= IBD
=Bowel cancer
= haemorrhoids
194
folic acid sources
green leafy veg
195
why is folic acid important
needed for nerve maturation
196
oral sign of b12 deficiency
beefy tongue
197
oral sign of iron deficiency
smooth tongue
198
oral sign of haematinic deficiency
pale mucosa
199
anaemia signs
pale
tachycardia
200
anaemia symptoms
tired and weak
dizzy
dysnopea
201
what injection can be used for anaemia patients with production failure
erythropoietin injections can boost haemoglobin levels to normal
202
dental aspect: anaemia
- GA- o2 capacity
- deficiency states- FE usually , mucosal atrophy, candidiasis, recurrent oral ulceration
203
GA risk for anaemics
greater risk of hypoxia
204
2 types of bone
cortical - compact
cancellous - spongy
205
cortical is
dense outer plate 80-85% of skeleton
206
cancellous is
internal trabecular scaffolding 15-20% of skeleton
207
composition of bone by weight
60% inorganic HA
15% water
25% organic
208
what makes up 25% organic portion of bone
glycoproteins - osteo. -calcin -nectin. - pontin
proteoglycans , chondroitin SO4, heparan SO4
209
types of bone resorption you can get in the oral cavity
vertical and horizontal
vertical resorption of bone can maybe grow bone to have more attachment between bone and tooth
210
What makes up the extracellular matrix
Glycos-amino- glycans
fibres (collagen and elastin)
211
woven bone properties
rapidly laid down
irregular deposition of collagen
212
lamellar bone properties
laid down more slowly
well organised : collagen fibres laid down in parallel
213
what are lacunae
small canals
214
where do osteoblasts lie and where do they derive from
on surface of bone- mesenchymal stem cells
215
osteocytes are
become trapped in mineralised bone
216
How can bone remodelling be used to dentist advantage
orthodontic treatment
217
what is achondroplasia
genetic defect of cartilage growth
218
2 groups that blood stem cell differenciate into
myeloid
lymphoid
219
myeloproliferative disorders
thrombocythemia
220
what is leukaemia
group of cancers of the bone marrow which prevent normal manufacture of the blood and therefor result in anaemia, infection, thrombocytopenia (platelets)
221
pathogenesis of leukarmia and lymphoma
clonal proliferation
replacement of marrow
222
ways to clinically present with leukaemia or lymphoma
anaemia
neutropenia
thrombocytopenia
splenomegaly
bone pain
223
what 3 things does staging assess
number of nodes involved and site
where lumps are
how far down progression line
224
why is staging important
predicting prognosis and deciding treatment
225
stage 1 (leukaemia and lymphoma)
single lymph node region or single extralymphatic site
226
hodgkin lymphoma peak incidence age
15-40 (more males0
227
amyloidosis
antibodies in excess amount
228
Q
4 concepts to know about for the process of leukaemia and lymphoma treatment
induction
remission
maintenance and consolidation
relapse
229
induction ?
intense chemotherapy
230
remission
none left (no more acute issues)
231
maintenance and remission
haven't managed to remove all the cancer cells in first place
232
relapse
can have multiple relapses but then still improve
