Body, Cells and Biochemistry Flashcards
1
Q
what is mucosa
A
the epithelium and underlying connective tissue - lamina propria
2
Q
what are the percentage consituents of blood
A
55% plasma
45% RBC
<1% buffy coat - WBC and platelets
3
Q
what is the buffy coat of vlood
A
<1% of blood containing WBC and platelets
4
Q
how much blodo does an adult have
A
~5L
5
Q
how do we find haemocrit value
A
percentage of RBC e.g. 45% of RBC = 0.45 haemocrit
6
Q
what does high haemocrit usually mean and what can it lead to
A
dehydration (less plasma) and therefore can lead to stroke
thrombosis
7
Q
what is the main function of plasma
A
provide fluidity of blood and dissolve constituents
8
Q
what cells do all blood cells come from
A
pluripotent hematapoetic stem cells
9
Q
what cells produce platelets
A
megakaryocyte produce thrombocytes
10
Q
what two cells do pluripotent haematopoetic stem cells form and what do they then differentiate into
A
common myeloid progenitor cells:
- RBC
- megakaryocyte
- myeoblast that form neutrophils and macrophages
common lymphoid progenitor cells:
- T killer cells
- T cells
- B cells
- PLasma Cells
11
Q
where does haematopoiesis occur in adults and children and what cells are blood cells derived from
A
in the bone marrow of all children bones
in bone marrow of all axial bones and proximal ends of long bones for adults
(liver and spleen if in need of RBC or malignant tumour in bone marrow)
pluripotent haematopoetic stem cell
12
Q
are pluripotent or multipotent stem cells more limited in their differentiation
A
multipotent
13
Q
what does a blood smear test test when someones ill
A
RBC:WBC to see inflammatory resposne
in health 1000:1
14
Q
what is the structure of RBC
A
biconcave disc with no nucleus or mitochondria packed with haemoglobin
15
Q
what is the implication of RBC not having nuclei
A
- cannot repair DNA
- more space for haemoglobin
16
Q
when can the liver and spleen be the site of haematopoesis
A
if high demand for haemaglobin e.g. anaemia
malignant tumour in bone marrow
17
Q
what hormone increases haematopoiesis and what secretes it
A
erythropoietin EPO produced by kidneys due to cellular hypoxia (lack of oxygen)
18
Q
when is EPO abused and what can be consequences of this. when is it used clinically.
A
EPO = erythropoietin
used by cheating athletes to increase RBC count can lead to heart failure
used clinically with anaemia
19
Q
what is thrombopoietin and why is it produced
A
hormone that increases thrombocytes (platelets) released by kidneys and liver
stimulate thomrbopoesis
20
Q
what receptor detects low oxygen in the kidney
A
Hif
21
Q
what is the structure of Hb
A
2 alpha protein chains and 2 beta protein chains
quaternary protein folding of different protein chains
haem groups (Fe2+) in each chain to bind to oxygen
22
Q
what causes anaemia
A
chronic deficiency in B6, B9 (folate), B12 and iron
23
Q
what are signs of anaemia
A
fatigue dizziness lack of energy out of breath tacchycardia pale nail beds pale conjunctiva
24
Q
what can cause increased Haemacrit
A
Dehydration
HPO increase due to reduced oxygen due to environment, smoking, altitude, Polycythaemia cancer of kidney
25
how do platelets work
circulate in resting state
stick to damaged vessel wall
become activated and sticky and release mediators
cause aggregation of more plateletes
26
what is normal platelet level
140-400 x 10^9 / L
27
what level of platelets in blood lead to increased risk of bleeding and spontaneous bleeding/bruising
80 x 10^9 / L
| 20 x 10^9 / L
28
what happens if platelet production is too high
```
increased thrombosis in arteries
increased blood pressure
blood clots
strokes
heart fialure
```
29
what is albumin, function and production site
protein in blood plasma controlling blood volume and osmosis
| produced in the liver
30
What does the plasma carry
plasma proteins such as albumin to control blood volume
blood clotting factors
immunoglobulins IG
hormones
31
what are clotting factors
a group of proteins that circulate in blood plasma in their inactive state
when activated cause clotting
soluble fibrinogen (inactive clotting factor I) converts to insoluble fibrin
32
what is the ABO system and what are the 4 classifications, which is recessive and dominant?
```
way of classifying the blood cell identifying glycoproteins
A
B
AB
O
```
A and B are dominant, O is recessive
33
what is the universal donor and recipient ABO blood type
```
donor = O
recipient = AB
```
34
if we are blood type A what antibodies do we make
anti - B antibodies
35
what is the most important of the 50 proteins of rhesus blood type
D dominant
| d recessive
36
what percent of population are rhesus negative
15
37
when is rhesus blood type most important
in 2nd pregnancy
if female is d negative
male is D positive
baby will likely have D positive
mother produces anti D antibodies when bloods mix at birth
in second pregnancy, anti-D antibodies will attack baby causing death
38
if someone is AB negative what can we tell about their blood tpye
AB in ABO
| d negative in rhesus
39
what can go wrong during transfusion
ABO incompatability
fluid overload
iron overload in heart
40
when do we give blood transfusions
high blood loss
| severe symptomatic anaemia
41
What do neutrophils looks like
Tri-nucleated
42
How does high pH act against microbes
```
Damages bacterial cytoplasmic membranes
Denatures proteins
Damages DNA
Inactivates bacterial enzymes
Bacterial replication is associated with loss of genes and lethal mutations
```
43
How does high pH act against microbes?
```
Damages bacterial cytoplasmic membranes
Denatures proteins
Damages DNA
Inactivates bacterial enzymes
Bacterial replication is associated with loss of genes and lethal mutations
```
44
what is inflammation and what are the 4 signs of this
```
bodies reaction to infection
red
hot
swollen
painful
```
45
what is acute inflammation
initial inflammatory reaction to stimulus with quick onset and short lived
46
give some examples of acute inflammation in the oral cavity
acute pulpitis
| abscess
47
what 2 events is acute inflammation separated into?
vascular
| cellular
48
what cells produce histamine and what causes this response
mast cells and basophil
| trauma, complement, cytokines
49
what occurs in the 1st stage of acute inflammation
vascular events
1. arterioles vasoconstrict to prevent bleeding
2. Arterolar, capillary and venule and dilation affected area red and warm to get more blood = histamine, serotonin and nitric oxide
3. increased vascular permeability
4. vascular stasis
50
what chemicals cause dilation of blood vessels in acute inflammation
nitric oxide
histamine - mast cells
serotonin - platelets
prostoglandins
51
what is vascular stasis
slowing down of blood flow due to decreased pressure
52
what sign of inflammation is caused by increased vascular permeability and why
swelling
endothelial cells separate allowing oedema to leak into tissues
builds up tissue pressure = swelling
53
what is oedema and what does it contain
```
excess of fluid in the tissue full of proteins
WBC
complement
antibodies
clotting factors
```
54
what chemicals cause vascular permeability
histamine - mast cells
| C3a, C5a- complement factor
55
what is the most important step in the complement cascade
c3 --. c3a and c3b
56
how do complement factors C3a, C5a and C3b cause inflammation (6)
1. Dilation and increased vascular permeability (C3a)
2. Stimulate histamine release (C3a and C5a) --> dilation and permeability
3. Promote formation of leukotrienes (attracts neutrophils) and prostaglandins
(vasodilation)
4. Attract phagocytes (C3a and C5a)
5. Opsonization: C3b can also bind to pathogens and phagocytes have a C3b receptor
with which to bind to this
6. MAC - membrane attack complex C5-C9 form transmembrane channels disrupting
the phospholipid bilayer and osmosis of the cell
57
what is MAC
membrane attack complex
complement factors 5-9 form transmembrane channels
allows fluid to enter cells and cause lysis
58
what does thrombin do?
changes soluble fibrinogen to non-soluble fibrin which causes clotting
59
when does the second stage of acute inflammation occur
2-3 hours after infection - cellular response
60
when do neutrophils and macrophages arrive at a acute inflammation sites
```
neutrophils = 2-3 hours
macrophages = 20 hours
```
61
what is C3b function
attaches to bacterial cell surface and acts as an opsin (marks bacteria for phagocytosis)
phagocytes have C3b receptors on their surface so attach to this and therefor the bacteria
62
explain the cellular innate response of acute inflammation
1. phagocyte engulfs bacteria and released TNFalpha and IL-1
2. Margination due to vascular stasis - cells push against endothelial walls
3. TNF alpha and IL-1 triggers surface cells to present E-selectin (endothelial cells) or P-
selectin (platelets) on their outer surface
4. Pavementation - neutrophils' CD15 receptor binds to selectin proteins and roll along
surface until they stop and attach via heptahelical receptor
5. neutrophils enter through permeable endothelial cells by extravasation/emigration
and then move up the chemokine gradient
63
what is the function of oedema (2)
supply tissue with inflammatory cells
| dilute bacteria and toxins
64
what is margination and what inflammatory mechanisms aid this
where neutrophils are pushed up against the endothelial walls
aided by vascular stasis due to vasodilation caused by
histamine, nitric oxide, seretonin, prostoglandins
65
what is pavementation
neutrophils attach via their CD15 glycoprotein to
E-selectins on endothelial cells and roll
heptahelical receptors on neutrophils attach to endothelial cell firmly attaching
66
what is extravasation and what inflammatory mechanisms aid this
where neutrophils move through the endothelial cells into inflamed tissue from vascular vessels
aided by increased permeability caused by histamine, C3a and C5a
aided by chemokine concentration gradient secreted by leukocytes
67
what cells can undertake phagocytosis
neutrophils, macrophages
68
when are cytokines released
when phagocytosis occurs and any time where inflammation needs to be activated
69
what is degranulation and what cells do this
Degranulation is the immediate response of tissue mast cells and neutrophils to wounding, releasing preformed mediators into the local connective tissue which results in the recruitment of cellular and soluble effectors e.g. defensins, lactoferrin
70
what are NETs
neutrophil extracellular traps
membrane of neutrophil perforates and released DNA (apoptosis)
DNA creates meshwork which traps and destroys pathogens with proteases
71
what causes pain in acute inflammation (2)
increased pressure due to release of oedema (caused by tissue permeability histamine C3a and C5a)
release of inflammatory mediators that trigger pain receptors to rest the body e.g. prostaglandins and bradykinin
72
what is bradykinin
inflammatory mediator that is involved in triggering pain receptors to tell the body to rest this part of the body
73
what are the three outcomes of acute inflammation
complete resolution - inflammatory stimulus is removed
healing by sclerosis - scarring with granulation tissue more collagen + fibroblasts
chronic inflammation in failure to remove stimulus or balance of bacteria wins
74
which tissues are likely to scarr
brain, heart, skin
75
what are the difference in cells in acute and chronic inflammation
acute - neutrophils, macrophages
| chronic - lymphocytes, plasma cells, macrophages
76
what is chronic inflammation
continued and prolonger inflammation
cycle of repair and destruction
only cellular stage
77
how many stages are involved with chronic inflammation
1 - cellular
78
what can cause chronic inflammation
foreign bodies e.g. grit
non-vital tooth causing chronic inflammation in periapex
prolonged, failed resolution of acute inflammation
low grade stimulus
lack of blood supply
prolonged exposure to toxins
79
what are features of chronic inflammation
minimal vascular changes
presence of chronic cels e.g. plasma, lymphocytes
angiogenesis - formation of new blood vessels
attempts at repair with granulation tissue - collagen, fibroblasts, vascular tissue
80
what is granulation tissue made up of
collagen (from fibroblasts) inflammatory cells and vascular tissue (endothelial cells)
81
what is angiogenesis
formation of new blood vessels - chronic inflammation
82
what are macrophages derived from and what initiates this differantiation
large inflammatory cells that engulf anything with foreign antigen
monocytes in blood
initiated by T cells
83
what are the 3 functions of macrophages M1
M1 activated M1 macrophage
phagocytosis
antigen presentation for humoral response
production of cytokines/chemokines
84
what is the function of cytokines
attract inflammatory cells up their gradient
| regulate inflammatory mechanisms e.g. cause endothelial cells to present E-selectin for pavementation
85
what is the function of M2 macrophages
release growth factors for endothelial cells and fibroblasts for granulation tissue healing
86
how does antigen presentation lead to plasma cell production
specific T cells attach to the antigens presented
These T cells then move into lymphoid tissue to find and activate specific B cell
with antibodies to that antigen
factors and regulators lead to proliferation of the B cell into plasma cells that can secrete antibodies for the antigen
87
what are eosophils
similar to neutrophils
pink cytoplasm with multinucleate
specific proteins for destroying parasites
88
if we had a paracytic infection, which inflammatory cell would be high? how can we tell
eosinophil
| histologiy ; multinucleate cell with pink cytoplasm
89
when is TNF alpha important
causes endothelial cells to present E-selectin which aids Pavementation of neutrophils for cellular response of acute inflammation
90
why will tissue damage occur in inflammation
proteases released by neutrophils e.g. mmp8
cytotoxic T cells
RANKL bone loss
PGE 2 bone loss -fibroblasts
91
what stimulates granulation tissue formation and what cells release this
growth factors released from M2 macrophages to stimulate fibroblast and endothelial growth
92
histologically, how can we see scarring
high fibroblasts and collagen (pink)
93
in reaction to chronic inflammation we get a focal granuloma forming, what is its structure
centre with lots of macrophages and giant cells (large multinucleated fused macrophages)
rim of leukocytes
94
what is likely to happen to the centre of very large granulomatous inflammation
necrosis
95
what is H&E stain
haematoxylin - stains neuclei/DNA blue/purple
| eosin - stains ECM/proteins red
96
how can we tell apart mature and woven bone histologically
```
woven has more osteoblasts
woven has more rigid edges
woven has fewer reversal lines
woven is less pink - less collagen
mature has more adipose tissue (marow)
mature has osteocytes embedded
```
97
what is haemostasis
stopping of blood flow - blood clotting
98
what is blood coagulation
where soluble factors (fibrinogen) get turned into non-soluble factors (fibrin) via the coagulation cascade with coagulation factors that form a protein net that platelets get caught in, accumulate and form a blood clot
99
what is the structurer and function of platelets
Platelets are packets of cytoplasm without nuclei.
Full of thromboxane.
when bursts acts as a platelet aggregator that attracts other platelets to the site.
for blood coagulation
100
what are the two coagulation pathways and what common end result do they have
intrinsic pathway
extrinsic pathway
final common pathway --> fibrinogen to fibrin
101
what differentiates the two coagulation pathways
the coagulation factors/proteins that trigger them
102
how is extrinsic pathway measured and what is its triggering protein/factor
```
Prothrombin time / international normalised ratio
subendothelial collagen (tissue factor) - extrinsic to the vessel
```
103
how is the intrinsic coagulation pathway measured and what protein/factor triggers this
activated partial thromboplastin time.
| First protein is phospholipid and factor XIII which is released when endothelial cells burst due to trauma.
104
if we take someone's blood to check their clotting speed, what must we do until we want to test the blood and why
if left it will clot quickly
we must arrest clotting factor VII (activated by calcium) by adding citrate - stops both intrinsic and extrinsic pathway
when we want to test, add excess calcium to override citrate
(if extrinsic we have to add tissue factor)
105
explain the prothrombin time test
used to measure the extrinsic and final common pathway of coagulation
add calcium and tissue factor to blood test to initiate extrinsic and common final pathway
time how long it takes to clot blood
106
what factors does prothrombin time test, test?
extrinsic and common pathway
I , II, VII, X
I = fibrinogen
II = thrombin
107
what is INR
international ratio
ratio of patients PT: average PT
tests extrinsic and final common pathway
108
if a patients INR is 2 what does this mean? does it mean it takes twice as long to clot? why?
it means they take much longer to clot than average patient
no because:
-under lab conditions so patient factors will alter clotting time
-only tests extrinsic factor, not intrinsic
109
when doing extractions on a patient, what must their INR be
international ratio
pt PT : avg PT
under 4 in the last 72 hours
110
what factors of coagulation does warfarin inhibit
II, VII, IX and X
II and X common
VII extrinisic
111
what is APTT
activated partial thromboplastin time
test intrinsic coagulation and final common pathway
add calcium, silicon and phospholipid to test tube and measure speed of coagulation
112
how does APTT work
activated partial thromboplastin time
phospholipids activate intrinsic pathway and calcium catalyses common final pathway
factors I, II, V, VIII, IX, X, XI, & XII measured
113
why is calcium important for coagulation
calcium catalyses the conversion of prothrombin to thrombin and fibrinogen to fibrin in common pathway
calcium also converts factor VII into its active state in the extrinsic pathway
114
why is citrate added to a blood test to prevent clotting
citrate inactivates calcium which prevents activation of factor VII
stops conversion of prothrombin to thrombin
stops conversion of fibrinogen to fibrin
115
what factors are involved in the extrinsic, intrinsic and common pathway and which factors does warfarin affect
common - I, II, X, XIII
extrinisic - VII
intirnisc - VIII, IX, XI, XII
warfarin inhibits - II, VII, IX, X
116
what is haemophilia
deficiencies in coagulation factors affecting the intrinsic pathway
haemophilia A: factor VIII
haemaphilia B: factor IX
117
how do we do a haemophilia test and explain how this works (what is a differential diagnosis)
haemophilia is reduced action of the intrinsic pathway
do a PT prothrombin time test and APTT activated partial thrombinogen time test
if PT is normal (extrinsic pathway) but APTT is raised (intrinsic) this shows untreated haemophilia
could also be VWBF disorder as this affects VIII in intrinsic pathway
118
what is VWBF
von Willebrand factor
tightly bound with factor VIII in complex for platelet adhesion
affects intrinsic pathway because of factor VIII
119
what is von Willebrand disorder
```
deficiency of VWBF
allows breakdown of factor VIII
decreased intrinsic pathway
increased APTT
decreases platelet function
increases bleeding time
```
120
what are the classifications of bleeding disorders
congenital
| acquired
121
what are 2 congenital bleeding disorders
VWBF disorder lack of von Willebrand factor therefore lack of factor VIII - intrinsic
haemophilia; lack of factor VIII (A) or IX (B) both involved in intrinsic pathway
APTT increased
122
what are the vitamin K dependant coagulation factors? why is this relevant to pharmacology where are they all made?
II, VII, IX, X
warfarin prevents cycle of vitamin K
warfarin inhibits these factors
made in liver
123
why is the liver important for bleeding disorders and what can cause liver to not function correctly
liver produces all vitamin K dependant factors
liver produces most coagulation factors
paracetamol overdose or liver disease increases bleeding
increased PT shows liver disease (due to factor VII deficiency produced in liver - extrinsic factor)
124
why does a heavy drinker bleed more?
alcoholism damages the liver
worsened liver function
less coagulation factors produced
125
pt is on kidney dialysis, why can we not take teeth out
on anticoagulants whilst on dialysis
| this increased bleed time
126
if a kidney problem (acquired), how does this affect bleeding time
kidney function is related to platelet formation and calcium levels (used in extrinsic and common pathway for catalysing)
bleed more
increased PT and APTT
127
what is COX 1,2,3
inflammatory factors of the inflammatory cascade which lead to the release of
1. Thromboxane A2 - TXA2 which leads to platelet aggregation
2. Prostaglandins which lead to pain and gastric regulation
128
what is thromboxane A-2
inflammatory factor that leads to platelet coagulation
129
what are prostaglandins
inflammatory proteins that cause pain
130
what is arachidonic acid
inflammatory marker that causes release of :
1. prostaglandins for pain
2. thromboxane A2 for platelet aggregation
with the enzyme OCX
131
what is bleeding time measured by
platelet function
132
what is the difference between platelet function and coagulation cascade
Platelet plug stops the bleeding and is not dependent on the coagulation cascade l.
The coagulation cascade stabilizes the platelet plug so it won't affect bleeding time.
133
what are the two stages of haemostasis
Primary haemostasis – the formation of a platelet plug (affecting bleeding time)
Secondary haemostasis – the activation of the clotting cascade which results in despoliation of fibrin to strengthen the platelet plug
134
how does VWBD, haemophilia, warfarin and aspirin affect bleedig time, APTT and PT
VWBD: APTT, BT
haemophilia: APTT
warfarin: PT and APTT
aspirin: BT
135
what affects (6) do prostaglandins have and their implications
directly act on pain receptors to cause pain (analgesics)
reduce gastric acidity - gastric ulcers if inhibited - protection of GI tract
increase vascular permeability allowing cellular acute inflammation
increase temperature pyrexia (fever)
regulation of sleep clock
contraction of smooth muscle
136
what is pyrexia and what causes it
high temperature
| inflammatory markers allowing COX-2 to convert arachidonic to prostaglandins which increase temperature
137
in terms of healing, what is resolution
return to normal, no differences
138
in terms of healing, what is regeneration
lost tissue replaced with the same type of tissue
139
in terms of healing, what is repair
tissue lost replaced with fibrous scar tissue
140
what is the difference between regeneration and repair
```
regeneration = lost tissue replaced with the same type of tissue
repair = lost tissue replaced by scar tissue
```
141
what are the three cell types regarding if they regenerate or repair (divisions)
```
labile = constantly dividing = liver = regeneration
stable = infrequently divide, can get larger = repair
permanent = never divide = repair
```
142
what three factors mainly affect ability to repair or regenerate
cell type - labile, stable, permanent
complexity of tissue
amount of tissue lost
143
explain repair of tissues breifly
repair is the replacement of lost tissue with scar tissue
granulation tissue (fibroblasts and endothelial cells) migrates into affected area
loose connective granulation tissue secretes collagen
becomes fibrous collagen scar tissue
144
what cells are involved in granulation tissue that has formed in an area for repair
neutrophils on surface
macrophages
endothelial cells
fibroblasts
145
what forms over a damaged area where epithelium has been broken
```
slough
mostly fibrin (clotting factor) and white
```
146
describe the general structure of the skin
three layers split into:
1. epidermis = epithelial waterproof covering - keratinized squamous stratified
2. dermis = connective tissue with collagen and fibroblasts, glands, nerves, blood supply
3. hypodermis = adipose tissue, fat cells
147
what are the layers of granulation tissue
top layer full of neutrophils for protection - slough
middle layer is immature granulation tissue
bottom is mature granulation tissue - more collagen
148
what are the 4 stages of wound healing
haemostasis
inflammation
proliferation
remodelling
149
describe haemostasis for wound
1st phase
vasoconstriction 5-10 minutes
immediate vessel rupture and release of tissue factor
initiates the intrinsic cascade for coagulation
ECM exposure leads to platelet thrombosis
vasodilation
150
describe inflammation phase of wound healing
1-3- days after injury
extravasation of neutrophils and monocyte --> macrophage
phagocytosis of foreign bodies, production of cytokines and growth factors
151
what do platelets release to cause proliferation of wound healing tissue (2)
PDGF attracts fibroblasts
| TGF-beta for fibroblast --> myofibroblast
152
what is PDGF
chemokine released by platelets when activated at wound site
| attract fibroblast for proliferation and granulation tissue formation
153
describe the structure of fibroblasts and myofibroblasts
fibroblasts are regular, smooth, small with large nuclei
| myofibroblasts are irregular undulating surface with multiple projections
154
what leads to myofibroblast formation
TGF-beta released by macrophages/platelets to convert fibroblasts to myofibroblasts
155
explain the 3rd phase of wound healing
1. haemostasis 2. inflammation 3. rpoliferation 4. remodelling
proliferation
angiogenesis (formation of new vessels)
TNF-beta causes fibroblasts --> myofibroblasts
secretion of ECM proteins e.g. collagen III
keratinocyte help reformation of epithelium
156
what collagen is laid down firstly
collagen III
157
explain remodelling phase of wound healing (3)
bone remodelled if involved
ECM is remodelled - collagen III converted to collagen I stronger
cells and capillaries reduced (less red)
cross linkage of collagen I (vitamin C dependant)
158
how is collagen remodelled
collagen III converted to collagen I
| corsslinkage increased strength - dependant on vitamin C
159
what is the general structure of collagen I in ECM
2 alpha-1 chains and 1 alpha-2 chain coiled around each other (fibrils)
many crosslinked fibrils form collagen fibres
160
how does age affect wound healing
affects time it takes, but quality is the same
161
what local factors affect wound healing
```
stimulus
movement around tissue
protection from more damage
infection
poor blood supply
```
162
what systemic factors effect wound healing
bleeding disorders e.g. haemophilia
nutrition - protein and vitamin C and zinc
diabetes or other diseases
collagen disorders e.g. EDS
drugs especially steroids (anti-inflammatory)
163
why is collagen V important
helps fibrillation (strengthening) of collagen I and II
164
what growth factors are secreted when a wound is healing (3)
broken endothelial cells and platelets
platelet derived growth factor (PDGF)
epidermal growth factor (EGF)
keratinocyte growth factor (KGF)
165
what controls the growth of new tissue in wound healing (2)
```
contact inhibition (or lack of - initiates growth)
growth factors PDGF, KGF, EGF, TNF-beta
```
166
where do new proliferating cells come from during wound healing
basal layer - where stem cells are
167
what growth factors stimulate proliferation of fibroblasts
TGF-alpha
FGF
PDGF
from macrophages, platelets and damaged endothelial walls
168
what stimulates and controls angiogenesis
macrophages release angiogenic factors in response to low oxygen
FGF stimulate fibroblast proliferation for endothelial cells
stimulates budding off of main vessels
anti-angiogenic factors control
169
what do fibroblasts secrete
all ECM protein and contents
collagen III
glycosaminoglycans and proteoglycans filling proteins
170
what is the difference between healing and cancer
cancer is unregulated, uncontrolled and involves irreversible steps
171
what type of scars are more likely to occur on black skin
hypertrophic scars (raised )
172
what is a keloid scar
large brown lump
173
what is a contracture
where a wound has entered muscle or tendon and during healing, scar tissue has shortened the muscle or tendon/
174
what causes keloid scarring
thick bundles of collagen, with high levels of type III
abnormal corsslinkage and high turnover
altered cytokine levels
175
if we remove a keloid scar, what is likely to happen
re-occurance
176
what is a neuroma
scar nerve tissue
a large bundle of nerve tissue that forms on nerve healing
causes sudden pains, sharp, shooting
177
who's skin does not scar
foetus
178
what is some non-scarring tissue
oral mucosa and foetal skin
179
why will a wound not heal
chronic inflammation
decreased growth factors
increased proteases destroying ECM
180
why does the oral mucosa not scar (3)
higher levels of growth factors and turnover
protective salivary layer
increased keratinocyte proliferation
181
how do leeches help wound healing
suck blood bringing blood to infected area
| inject saliva containing nitric oxide which causes vasodilation (acute inflammation)
182
how can we aid wound healing
```
dressings
antimicrobials
leeches/maggots
Vasoconstrictors or help haemastasis
Primary intention
```
183
what is endocrine signalling
cell signalling from a distant cell
| usually via hormone
184
what is paracrine signalling
acing on immediate environment e.g. cytokines
185
what is autocrine signalling
signal acts on the cell itself
186
explain transduction of a ligand signal
ligand is very specifically shaped to receptor
when they fit together, changes in tertiary protein structure = activated
receptor protein leads to amplification of signal within cell
187
why do steroids and hormones have such a fast response
they are hydrophobic
can move through cell membrane and cause rapid response
don't need to be transduced by receptor proteins
188
what do scaffolding proteins do
regulate transduction of cell signals
189
Explain the structure and function of G-Coupled Heptahelical receptors
proteins that cross the membrane of the cell surface 7 times parrallel to eachother with G protein and GDP attached
when ligand binds to receptor, G protein is activated and GDP swaps for GTP
which initiated secondary messengers to cause transduction and amplification
when inactivated, GTP swaps for GDP
190
what do G-coupled receptors respond to
hormones e.g. testosterone, epinephrine
| senses e.g. light, smell
191
what proteins are swapped when G proteins are activated on heptahelical receptors
GDP inactive for GTP active
192
explain how tyrosine kinase receptors work
enzyme linked dimerization
ligand attaches and causes two dimers to come together
causing autophosphorylation (kinases) and becoming active- autocrine
proteins on inside of cell can now attach and amplify
193
explain how ligand ion channels work
ligand binds to receptor on ion channel
| ion channel opens allowing diffusion of charged particles
194
what does he suffix Mab mean
monoclonal antibody
195
what does the suffix Nib mean
chemical inhibitor
196
how much of our DNA is functioning and non-functioning
3% coding
| 80% non-functional with historic evidence
197
briefly explain how transcription
DNA telomerase unwinds the helix
DNA strands separated via DNA helicase breaking H bonds
transcription factor binds to promotor and enhancer region to recruit RNA polymerase
RNA polymerase attaches to promotor region and reads coding strand and transcribes DNA binding complimentary RNA nucelotides to form pre-mRNA
198
what is the 'trans' in transcription factor telling us
protein is made from a different gene of which it is working on
199
where do we find the 'tata' box
25-30 nucleotides up stream from he 5' end from coding DNA containing promotor reigon
200
are promotors and enhancers trans or cis acting and why
cis
| on the same gene to which they are regulating
201
explain splicing and what enzyme is involved in this
pre-mRNA is modified
removal of mutated genes and introns by splicesomes
leaving just coding exons
202
what is done to mRNA after splicing before translation and why
5' CAP is added - prevents degradation, initiates translation
3' Poly-A-Tail added - allows strain to exit nucleus and prevent degradation
203
what is the function of enhancers and where re they found
control efficiency and rate of transcription of genes
| found before promotor region of coding DNA
204
what is DNA fingerprinting and what gene is used
using small parts of non-coding DNA to identify a person
may be a random number of repeats of this gene
myoglobin gene changes in size and shape from person to person
205
how can genes be cut from DNA to do DNA fingerprinting
bacterial restriction enzymes
206
what is PCR
Polymerase chain reaction
| means of amplifying DNA to measure the transcription of a gene
207
what is Taq and why is it useful
Thermostable polymerase
| able to polymerase DNA in high temperatures where DNA remains uncoiled
208
explain steps of PCR test
heat sample at 94 degrees for 1 minute to break coil
add primers for section of DNA we are looking for with fluorescent tags
add thermostable polymerase to replicate primed DNA strand for 2 minutes
209
which gene can be studied to find high risk of periodontitis and why
IL-a1 interleukin alpha 1
inflammatory marker of periodontal tissue which has a VNTR variable number of tandem repeats
2 tandem repeats of intron 2 of IL-a1 are coincident with high risk periodontitis
210
how long is the intron 2 of IL-a1
86 base pairs long
211
what is VNTR and how many is a high risk of periodontitis in intron 2 of IL-a1
variable number of tandem repeats
| 2
212
how is intron 2 IL-a1 linked to periodontitis
if intron 2 has 2 tandem repeats of the 86 base pair sequence, this is related to periodontists
not causative as within intron so not coded
it will be related to other coding genes
213
what is a SNP
single nucleotide polymorphism
214
where do most SNPs occur
2 out of 3 occur in C and T
215
what percent of genetic variation is down to SNPs
SNP = single nucleotide polymorphism
| 90% of variation down to SNPs
216
what types of SNP can we have and what are their implications
SNP = single nucleotide polymorphism
synonymous SNP = change doesn't alter the gene expressed = no change
non-synonymous SNP = changes the gene expressed = mutation = changes function and maybe cancer
217
how do we get a DNA sample orally
bite cheeks to remove epithelial tissue and spit into tube
centrifuge to separate pellet (cells) and supernatant (saliva)
Pippette pellet out
Add isotonic saline solution to pellet and repeat centrifugation
218
what are the stages of the cell cycle
```
rest phase
interphase
prophase
metaphase
anaphase
telophase
```
219
what checkpoints during cell cycle are there and what occurs at each stage and why is this important
G1 - checking environment is right for growth, growth factors, nutritional stability, size of cell and space
G2 - checking DNA replication (s phase) has occurred proper ally
M - checking chromosomes have aligned properly
this ensures DNA and cell replication occurs properly reducing risk of uncontrolled cell division and cancer
220
why are cyclins important for cell cycle and what controls these
cell enzymes that control the activation of different stages of the cell cycle
controlled by cyclic dependant kinases
these are controlled by cyclic dependant kinase inhibitors
221
what 2 enzymes are released to initiate mitosis and anaphase and what controls these enyzmes
MPF and APC
mitosis promoting factor initiates mitosis controlled by G2 checkpoint
anaphase promoting complex initiates anaphase after M checkpoint
222
what must happen before APC is released
M checkpoint checks metaphase alignment of chromosomes
| then APC anaphase promoting complex can be released to initiate anaphase
223
what must happen before MPF is released
G2 checkpoint ensuring S phase is complete and DNA replicated properly with good DNA integrity
224
what state are most cells in
G0 phase of quiescent phase
| not replicating, undergoing normal cellular function
225
which cells will never enter cell cycle again
terminally differentiated cells/Senescent
| e.g. cells in skin
226
what is a tumour suppressor gene and how does it function
detects damaged DNA
| intitates DNA repair, apoptosis or arrests cell cycle
227
what is a common tumour suppressor gene and why is it relevant
p53
p53 is mutated in 50% of cancers
leading to fualty DNA going into the cell cycle and replicating this DNA
228
when is apoptosis necessary (4)
in growth of fingers/extremities where invagination's are needed
bone remodelling
inflammatory cells so inflammation is not constant
remove damaged cells or damaged DNA
229
how is apoptosis initiated
removal of positive growth factors
| addition of negative factors
230
what is the main effector for apoptosis na dhow do they work
caspase cascade
made of proteolytic enzymes that break down cell into smaller fragments for phagocytosis
amplify apoptotic signal throughout cell
231
what are the two pathways for apoptosis
intrinsic and extrinsic
232
briefly explain the intrinsic pathway of apoptosis
mitochondrial membrane disrupted
cytochrome C released into cytoplasm
bins to Apaf-1 initiating caspase cascade of proteolytic enzymes
233
briefly explain extrinsic pathway of apoptosis
external signals form cytotoxic cells
bind to 'death' receptors
causing caspase cascade of proteolytic enzymes
234
how does BCL-2 effect the body and where is it relevent
BCL-2 prevents binding of
cytochrome-C from mitochondria in intrinsic apoptosis pathway
to Apaf-1 in cytoplasm
preventing caspase cascade therefor stopping apoptosis
occurs in lots of cancers
235
what enzyme prevents binding of cytochrome C to apaf-1 and when does this occur
BCL-2 in cancer
236
what is a common death deceptor
Fas-L
237
compare apoptosis and necrosis
necrosis uncontrolled, non-energy dependant, inflammatory, swells cell, leads to scarring
apoptosis is controlled, energy dependant, non-inflammatory, shrinks cells, no scarring
238
what protein mutations can cause cancer due to failed apoptosis
p53 controlls apoptosis of damaged DNa cells
Apaf-1 (intrinsic binding to cytochrome C)
Cytochrome C (intrinsic binding to Apaf-1)
FasL (extrinsic death receptor)
presence of BCL-2 prevents binding of cytochrome C to apaf-1
239
how do apoptotic bodies show histologically
very pink
| membrane bound vesicles show very pink high in protein
240
how does apoptosis occur
signalled
cell broken down into smaller vesicles
macrophages phagocytose
capsase cascade
241
why is apoptosis important for dentistry
```
tooth growth invaginations
craniofacial clefts
bone remodelling
wound healing
inflammation removal of inflammatory cells
```
242
what is an epigenetic trait and what affects these traits
stably heritable phenotype resulting from changes in a chromosome without alterations in the DNA sequence
methylation, non-coding DNA (microDNA), nucleosome location, histone modification
243
what can affect epidemiology
methylation, non-coding DNA (microDNA), nucleosome location, histone modification
244
how can the environment affect our DNA
carcinogens can cause mutations
| some environmental factors can alter methylation causing a change in how genes are expressed (epidemiology)
245
what is epigenetics
study of how DNA is read and expressed, not involved with mutations
246
what is an epigenetic factor
something that affects how DNA is expressed
247
what is the most common trans epigenetic factor
transcription factor produced by the cell it is signalling: self-sustaining
248
is methylation and histone change a cis or trans epidemiological factor
cis
| DNA is modified physically
249
what is the difference between a cis and trans epidemiological factor
cis = affects the physical DNA
| trans - released and acts on the DNA e.g. transcription factor
250
what does methylation of DNA generally cause and what type of effect is this
prevents binding of proteins like transcription factors to genes, reducing production of certain proteins
interferes with transcription
this is an epidemiological affect
251
what does methylation of DNA generally cause and what type of effect is this
prevents binding of proteins like transcription factors to genes, reducing production of certain proteins
interferes with transcription
this is an epidemiological affect
252
how can epigenetic affects lead to cancer
no mutations
changes in methylation
reduced methylation leads to inappropriate activation of genes
over expression and overgrowth or uncontrolled growth = neoplasm
253
what is an isoform
two very similar proteins with the same coding DNA but different exons/introns removed
254
what are the 3 steps to PCR polymerase chain reaction
denaturation at 94 degrees
annealation at 54 degrees
extension extension ay 72 degrees
255
explain denaturation during PCR
DNA is denatured at 94 degrees for 1 minute to unravel the helix and break H bonds between nucleotides
256
what happens in the annealing process of PCR
magnesium, Taq Polymerase and forward/reverse primers are added at 54 degrees for 45 seconds to copy specific genes
257
what happens in the extension process of PCR
dNTRs are added (artificial DNA nucleotides ATCG) to attach to complimentary copied DNA for 2 minutes at 72 degrees
258
what is needed as a catalyst for Taq thermostable polymerase from thermus aquaticus
magnesium and heat
259
how do we amplify DNA
PCR denature - denaturation at 94 degrees for 1 minute
polymerase to copy the wanted gene DNA - annuleation at 54 degrees for 45 seconds
extension at 72 dgerees for 2 minutes - additon of dNTPs
repeat
260
what is an oncogene
gene/protein with the potential to cause cancer
261
how much calcium do we have in our body and where is it found
1kg in body
99% in bone
1% = 10g calcium elsewhere mainly in blood
very little in cells
262
explain where calcium is important in the body
forms hydroxyapatite which is the main mineral in tooth enamel
very important for bone formation
needed for coagulation cascade converting fibrinogen --> fibrin, prothrombin to thrombin and Factor VIIa to VII
needed for myosin activation for muscle contraction
263
after calcium triggers myosin to contract, what then happens to the calcium
actively transported back into sarcoplasmic reticulum
264
compare transcellular and paracellular absorption
transcellular is between cells through tight junctions - passive
paracellular is through the cl via receptors and channels e.i. active transport, diffusion through membranes
265
which glands are responsible for calcium storage in the bones
thyroid and parathyroid
266
which vitamin is needed for increased uptake of calcium
activated Vitamin D
267
how does vitamin D aid calcium absorption
modifies tight junctions to allow more transcellular diffusion
upregulates active transport paracellular movement of calcium
268
how do we get vitamin D
pro-vitamin D is abundant in the body as a derivative of cholesterol
sunlight can convert this to active vitamin D
hydroxylation can also occur in the kidney and lver
269
what is the precursor for vitamin D and how do we ge tthis
pro-Vitamin D
| derivative of cholesterol
270
which hormone mainly controls calcium homeostasis and where is it made
parathyroid hormone
| chief cells of the parathyroid gland
271
explain the relationship between parathyroid hormone and calcium
calcium inhibits PTH
| if calcium is low, PTH is active and this activates osteoclasts for bone resorption to release calcium
272
what is the name for break down of bone
osteocytic osteolysis
273
explain thyroids role in calcium regulation
thyroid gland released calcitonin - derivative of vitamin D
| inhibits Ca2+ absorption and inhibits bone resoprtion - acting against PTH
274
what are the two main hormones involved in calcium regulation and what secretes them
PTH parathyroid hormone secreted by chief cells of PT - activates osteoclasts to increase calcium
calcitonin secreted by parafollicular cells of thyroid - decreased bone resorption to decrease calcium levels
275
what is osteogrens affect on bone and vitamin D
inhibit bone resorption osteoclasts
| promotes vitamin D activity = more calcium
276
how do osteocytes act on bone formation
secrete FGF23 fibroblast growth factor 23
| inhibits bone formation
277
how could we artificially implant a tooth germ
collect epithelial tissue (enamel organ) and mesenchymal tissue (dental papilla)
culture for a few days until a combined germ forms
implant into jaw
278
where can we find tooth germ stem cells for tooth growth
baby teeth and wisdom teeth germs
279
what process can locate genes on DNA
CRISPR
279
what process can locate genes on DNA
CRISPR
280
what is SHED and what is it involved in
stem cells from human exfoliated dentition
| using stem cells from teeth for regenerative procedures
281
what 3 components are needed for tooth regeneration
scaffold including collagen and proteins
cells including stem cells, germ cells
signals to induce growth like HEX genes and TGF
282
at what platelete count do we have spontaneous bleeding
<20 x 10^9 /l
283
at what platelet count do we class as safe to do any surgery other than neurosurgery
>80 x10^9/l
284
what is thrombocytopenia
reduced platelet count
285
what is thrombocytosis
increased platelet count
286
how do we diagnose a bleeding disorder
bleeding history:
- past surgery
- past extractions
- bleed when teeth exfoliate?
- long, spontaneous bruising?
- nose bleeds? (epistaxis)
examination:
- any bruising (ecchymoses)
- BP
- purpura (purple coloured spots in mouth)
- menstrual bleeding for more than 7 days
- sings of liver disease
- spleenomegaly (large spleen)
```
investigation:
-PT, APTT, BT
-platelet count
-VWF count
-
```
287
what is epistaxis
nose bleed
288
what is the name for a nose bleed
epistaxis
289
what would small purple dots on the inside of mouth or on the skin be called
purpura
290
what is the proper name for a bruise
ecchymoses
291
what is menorrhagia
menstrual bleeding for over 7 days
292
what blood test investigations can we do into haemotosis
Full blood count to check RBC and platelet number
Coagulation tests : PT, APTT, fibrinogen
Bleeding time
WVDF count
293
how do we treat haemophilia
type A: give lifelong doses IV of factor VIII
type B: give lifelong doses IV of factor IX
or given SC every 2 weeks instead of daily IV
294
how do we treat thrombocytopenia
platelet transfusion
295
how is haemophilia passed down
on X chromosome - dominant
| only affects men
296
if a pt has mild haemophilia and we want to do a minor dental surgery, what can we give them
Desmopressin DDAVP - released factor VIII from endothelial cells
297
why can desmopressin not be used for haemophilia B
releases factor VIII from endothelial cells
| haemophilia B is a deficiency in factor IX, so factor VII will not help
298
what risks come with haemophilia factor concentrate
infection due to high amounts of blood donors
| prior to 1985 viral deactivation did not happen so possible HIV infection
299
what is the most common inherited bleeding disorder and how does it act
Von Willenbrans Factor Disease in 3 severities
1:1000
acts on reduced platelet number and reduces factor VIII in coagulation cascade
300
would a coagulation or platelet disease affect the oral cavity more
platelet diseases affect oral cavity more than coagulation disordeers
301
name 3 platelet diseases
Glazmanns disease
Storage pool disease
VWBD
302
what is a thrombosis
coagulation within a vessel
303
compare arterial and venous thrombosis
Arterial:
- caused by platelets and high blood pressure
- risk factors: high atherosclerotic plaque, obesity, smoking, high LDL
- lead to myocardinal infarction and stroke
- treat with antiplatelets
Venous:
-causes by high fibrin and low blood pressure
-risk factors: pregnancy, surgery, imobility, congenital, obesity, cancer, serious illness combined contraceptive pill
-leads to deep vein thrombosis
-
304
explain primary haemostasis
endothelial breakage caused vasoconstriction and platelets become activated
with help of VWBF, platelets adhere to exposed collagen causing platelet to change shape
release cytokines like prothrombin 2, serotonin, platelet activating factor causing
recruitment of more platelets
305
what do platelets do when attached to exposed collagen
change shape and come more sticky and pointy for aggregation
release mediators like PAF (platelet activation factor), Tromboxane2, serotonin for
platelet recruitment
306
what chemicals do platelets release when attached to exposed collagen
thromboxane 2
serotonin
platelet activating factor
307
what is thrombophilia
where blood clots too easily causing thrombosis - venous or arterial
308
what are 5 inherited thrombophilia
```
Antithrombin deficiency 1 in 3,000
Protein C deficiency 1 in 300
Protein S deficiency 1 in 300
Factor V Leiden 1 in 20
Prothrombin G20210A 1 in 75
```
309
what causes thrombocytopenia
deficiency leading to less production of platelet
increased consumption of platelets - immune thrombocytopenia
Hyperplenism
310
what causes failure to produce plateletes
B12 or folate deficiency
bone marrow metastasis or infiltration
radiation therapy
311
when does immune thrombocytopenia occur
acute infection with children - lack of platelets
| chronic inflammation in adults
312
what are the results of thrombocytopenia
reduced haemostasis
| huge internal bleeds
313
what is the function of the spleen
remove old platelets from blood
| act as storage holding 1/3 of bodies platelets
314
how do we diagnose immune thrombocytopenia
identify thrombocytopenia - reduced platelet count
exclusion of other causes e.g inherited
bone marrow examination
315
why does splenomegaly cause thrombocytopenia and how do we treat this
larger spleen holds more of the bodies platelets meaning less in circulation
Splenectomy
316
what are some acquired platelet function abnormalities
liver and kidney disease
antiplatelet drugs
DIC
317
how do we treat beading with renal disease
desmopressin DDAVP or dialysis
318
what are 3 signs of liver disease
yellow skin
increased bleeding time
increased PT
319
what are 3 causes of bleeding with liver disease
decreased production of vitamin K clotting factors II, VII, IX, X
hypersplenism
increased fibrinolysis
320
when might we have vitamin K deficiency and how do we treat
at birth every baby given vitamin K
| malabsorption - provide IV vitamin K
321
what bleeding investigation finds vitamin K deficnecy
prolonged PT
322
what is the risk of DVT
deep vein thrombosis poses risk of PE
pulmonary embolism
fractured part of clot travelling to lungs causing life threatening clots
323
what is a pulmonary embolism and how do we prevent
fractured part of a deep vein thrombosis into lungs causing life threatening clot
identify high risk of venous thrombosis e.g. pregnant, obese, no mobility
give anticoagulants e.g. edoxaban, herparin, warfarin
324
what is APLS
antiplatelet syndrome
autoimmune disorder attacking phospholipid membrane
increases incidence of blood clotting --> venous and arterial thrombosis
325
what classes as anaemia
haemaglobin levels:
<125g/l in men
<115g/l in women
326
how do we find the 'normal range' of a protein e.g. haemaglobin
find people +/- 2SD around the mean
327
what are symptoms of anaemia
```
shortness of breath
fatigue under exercise
angina
palpitations
Pallor
hypotension
heart failure
```
328
what are oral manifestations of anaemia
Glossitis (b12/folate)
Angular Stomatitis
Pallor
329
what is Pallor
being pale, eyes, conjunctiva, nail bed
330
how do we diagnose anaemia
full blood count (can affect WBC and platelet aswell as RBC)
| microscopic evaluation of size of RBC
331
what is MCV when diagnosing anaemia
mean cell volume
332
what classes as normal MCV
82-96fl
333
what is MCV measured in
fl
334
what are the three types of anaemia and how do we differentiate
microcytic anaemia = MCV < 82fl
normocytic anaemia = 82 < MCVfl < 96
macrocytic anaemia = MCV>96fl
335
what is the leading cause of microcytic anaemia and how does it present
iron deficiency (inherited red cell disorders thallasaemia, chronic disease)
small cells
MCV < 82fl
336
if iron deficiency has been excluded from diagnosis, what else can cause microcytic anaemia
inherited red blood cell thalassaemia
| chronic disease
337
what can cause macrocytic anaemia
B12 and folate deficiency
338
what can cause macrocytosis without anaemia
alcohol consumption
liver disease
hypothyroidism
339
what is macro/microcytosis
larger or smaller red blood cells
340
what are common causes of normocytic anaemia
acute bleed
haemolysis (congenitcal or aquired)
Aplastic anaemia
chronic disease
341
what type of anaemia do we get after an acute bleed
normocytic anaemia
342
what causes iron deficency and what does this cause
reduced intake (very rare due to fortified cereals)
increased requirement e..g growth, pregnancy, menstruation, malabsorption
increased loss of blood e..g menorrhagia (increased menstruation), GI bleeds or cancer below oesophagus
causes microcytic anaemia = angular stomatitis, koilonychia - bending nails
343
what is koilonychia
concave nail bed caused by iron deficency
344
how do we investigate iron deficency without a blood test
history
- any recent big bleeds
- change in stool consistency, colour
- abdominal pain
- heavy/frequent/long menstruation
examination:
- feel for lymph nodes for GI cancer
- rectal exam to find blood
- gastroscopy/colonoscopy to check for ulcer/bleed
345
how do we treat microcyitic anaemia
if iron deficient:
- ferrous sulphate 200mg daily (BSP says TDS but unnecessary)
- TREAT CAUSE FIRST must find cause, exclude cancer
346
for a macrocytic anaemia pt, what problems will there be with their full blood count and why
lacking RBC, WBC and platelets
caused by b12 and b9 deficiency
needed for haematopoiesis and DNA replication
reduction in ALL blood cells
347
how big is your b12 store and how long does it last
lasts 4 years
348
if we do not have intrinsic factor, what will the result be
chronic
after 4 years, B12 deficiency as IF is needed for absorption
B12 deficiency leads to macrocytic anaemia
349
what is Pernicious anaemia and what type is it
autoimmune disroder antibodies against binding
prevention of binding between Intrinisc factor (parietal cells) and b12
leads to b12 deficiency
leads to macrocytic anaemia
350
what is Pancytopenia
reduction in all blood cells : RBC, WBC and plateletes
| caused by b12/b9 deficency
351
what does chronic b12 deficiency lead to (3)
macrocytic anaemia
pancytopenia = reduced RBC, WBC and platelet
affects all body cells, especially neuropathy
glossitis and angular stomatitis
352
how do we diagnose pernicious anaemia
b12 levels
| intrinisc factor antibodies
353
when do we get b9 deficency
lack of diet - eating poorly without fresh fruit and veg
malasborption - coaeliac
increased requirment e.g. pregnancy, growth
some drugs
354
what is haemolytic anaemia and what 2 classifications does it have
red cells are broken down in circulation or spleen
or have odd shapes
can be inherited or acquired
355
what are some causes of inherited haemolytic anaemias
red cell membrane anaemia e..g spherocytosis
abnormal red cell metabolism
haemoglobin abniormalities e.g. sickle cell
356
what is the most common acquired haematolytic anaemia
alloimmune rhesus disease in new-born where antibodies are made against own blood type
357
what types of aquired haematolytic anaemia
fragmented red blood cell (mechically by fake valves, small blood clots)
autoimmune/alloimmune disorders e..g Rhesus disease
infection
358
what are some causes of fragmented RBC
artificial valves can block and force cells through tiny spaces, fragmenting
blood clots can fragment RBC
359
explain sickle cell anaemia
auatosomal recessive
heterozygous mutation leads to protection of malaria
RBC are sickle shaped carrying less Hb
chronic lifelong anaemia
360
what type of mutation causes sickle cell
single point mutation
361
when would we see erythroblasts and what are they
nucleated red cells
| if there is high amount of haemolysis and bone marrow stress - sickle cell or chronic anaemia
362
what is the function of albumins
hydrophobic molecules in blood to reduce water potential of blood to draw water out of cells to increased hydrostatic pressure
363
what receptors are responsible for 'burning' sensation
TRP
364
what is the function of basophils
secrete histamine + inflammation
365
briefly describe different WBCs
neutrophils - aid inflammation and phagocytosis
plasma cells = produce antibodies for neutralisation and opsonisation
Eosinophils = helpful in fighting off parapsychic infections
Basophils = release histamines for inflammation and allergic reactions
Macrophages = phagocytosis and antigen presentation + amplification
366
what bodily cells does adrenaline act on
beta 1 adrenal receptors
367
when is i
368
What is the name for too many and too few platelets
Thrombocytopenia - too few
| Thrombocythemia -too many
