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BDS 2 > Body, Cells and Biochemistry > Flashcards

Body, Cells and Biochemistry Flashcards

1
Q

what is mucosa

A

the epithelium and underlying connective tissue - lamina propria

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2
Q

what are the percentage consituents of blood

A

55% plasma
45% RBC
<1% buffy coat - WBC and platelets

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3
Q

what is the buffy coat of vlood

A

<1% of blood containing WBC and platelets

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4
Q

how much blodo does an adult have

A

~5L

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5
Q

how do we find haemocrit value

A

percentage of RBC e.g. 45% of RBC = 0.45 haemocrit

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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

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7
Q

what is the main function of plasma

A

provide fluidity of blood and dissolve constituents

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8
Q

what cells do all blood cells come from

A

pluripotent hematapoetic stem cells

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9
Q

what cells produce platelets

A

megakaryocyte produce thrombocytes

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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
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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

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12
Q

are pluripotent or multipotent stem cells more limited in their differentiation

A

multipotent

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13
Q

what does a blood smear test test when someones ill

A

RBC:WBC to see inflammatory resposne

in health 1000:1

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14
Q

what is the structure of RBC

A

biconcave disc with no nucleus or mitochondria packed with haemoglobin

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15
Q

what is the implication of RBC not having nuclei

A
  • cannot repair DNA

- more space for haemoglobin

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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

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17
Q

what hormone increases haematopoiesis and what secretes it

A

erythropoietin EPO produced by kidneys due to cellular hypoxia (lack of oxygen)

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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

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19
Q

what is thrombopoietin and why is it produced

A

hormone that increases thrombocytes (platelets) released by kidneys and liver
stimulate thomrbopoesis

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20
Q

what receptor detects low oxygen in the kidney

A

Hif

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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

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22
Q

what causes anaemia

A

chronic deficiency in B6, B9 (folate), B12 and iron

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23
Q

what are signs of anaemia

A 
fatigue
dizziness
lack of energy
out of breath
tacchycardia
pale nail beds 
pale conjunctiva
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24
Q

what can cause increased Haemacrit

A

Dehydration

HPO increase due to reduced oxygen due to environment, smoking, altitude, Polycythaemia cancer of kidney

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25
Q

how do platelets work

A

circulate in resting state
stick to damaged vessel wall
become activated and sticky and release mediators
cause aggregation of more plateletes

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26
Q

what is normal platelet level

A

140-400 x 10^9 / L

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27
Q

what level of platelets in blood lead to increased risk of bleeding and spontaneous bleeding/bruising

A

80 x 10^9 / L

20 x 10^9 / L

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28
Q

what happens if platelet production is too high

A 
increased thrombosis in arteries
increased blood pressure
blood clots
strokes
heart fialure
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29
Q

what is albumin, function and production site

A

protein in blood plasma controlling blood volume and osmosis

produced in the liver

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30
Q

What does the plasma carry

A

plasma proteins such as albumin to control blood volume
blood clotting factors
immunoglobulins IG
hormones

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31
Q

what are clotting factors

A

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

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32
Q

what is the ABO system and what are the 4 classifications, which is recessive and dominant?

A 
way of classifying the blood cell identifying glycoproteins 
A
B
AB
O

A and B are dominant, O is recessive

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33
Q

what is the universal donor and recipient ABO blood type

A 
donor = O
recipient = AB
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34
Q

if we are blood type A what antibodies do we make

A

anti - B antibodies

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35
Q

what is the most important of the 50 proteins of rhesus blood type

A

D dominant

d recessive

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36
Q

what percent of population are rhesus negative

A

15

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37
Q

when is rhesus blood type most important

A

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

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38
Q

if someone is AB negative what can we tell about their blood tpye

A

AB in ABO

d negative in rhesus

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39
Q

what can go wrong during transfusion

A

ABO incompatability
fluid overload
iron overload in heart

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40
Q

when do we give blood transfusions

A

high blood loss

severe symptomatic anaemia

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41
Q

What do neutrophils looks like

A

Tri-nucleated

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42
Q

How does high pH act against microbes

A 
Damages bacterial cytoplasmic membranes
Denatures proteins
Damages DNA 
Inactivates bacterial enzymes
Bacterial replication is associated with loss of genes and lethal mutations
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43
Q

How does high pH act against microbes?

A 
Damages bacterial cytoplasmic membranes
Denatures proteins
Damages DNA 
Inactivates bacterial enzymes
Bacterial replication is associated with loss of genes and lethal mutations
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44
Q

what is inflammation and what are the 4 signs of this

A 
bodies reaction to infection
red
hot
swollen
painful
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45
Q

what is acute inflammation

A

initial inflammatory reaction to stimulus with quick onset and short lived

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46
Q

give some examples of acute inflammation in the oral cavity

A

acute pulpitis

abscess

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47
Q

what 2 events is acute inflammation separated into?

A

vascular

cellular

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48
Q

what cells produce histamine and what causes this response

A

mast cells and basophil

trauma, complement, cytokines

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49
Q

what occurs in the 1st stage of acute inflammation

A

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
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50
Q

what chemicals cause dilation of blood vessels in acute inflammation

A

nitric oxide
histamine - mast cells
serotonin - platelets
prostoglandins

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51
Q

what is vascular stasis

A

slowing down of blood flow due to decreased pressure

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52
Q

what sign of inflammation is caused by increased vascular permeability and why

A

swelling
endothelial cells separate allowing oedema to leak into tissues
builds up tissue pressure = swelling

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53
Q

what is oedema and what does it contain

A 
excess of fluid in the tissue full of proteins
WBC 
complement 
antibodies
clotting factors
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54
Q

what chemicals cause vascular permeability

A

histamine - mast cells

C3a, C5a- complement factor

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55
Q

what is the most important step in the complement cascade

A

c3 –. c3a and c3b

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56
Q

how do complement factors C3a, C5a and C3b cause inflammation (6)

A
  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
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57
Q

what is MAC

A

membrane attack complex
complement factors 5-9 form transmembrane channels
allows fluid to enter cells and cause lysis

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58
Q

what does thrombin do?

A

changes soluble fibrinogen to non-soluble fibrin which causes clotting

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59
Q

when does the second stage of acute inflammation occur

A

2-3 hours after infection - cellular response

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60
Q

when do neutrophils and macrophages arrive at a acute inflammation sites

A 
neutrophils = 2-3 hours
macrophages = 20 hours
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61
Q

what is C3b function

A

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

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62
Q

explain the cellular innate response of acute inflammation

A
  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
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63
Q

what is the function of oedema (2)

A

supply tissue with inflammatory cells

dilute bacteria and toxins

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64
Q

what is margination and what inflammatory mechanisms aid this

A

where neutrophils are pushed up against the endothelial walls
aided by vascular stasis due to vasodilation caused by
histamine, nitric oxide, seretonin, prostoglandins

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65
Q

what is pavementation

A

neutrophils attach via their CD15 glycoprotein to
E-selectins on endothelial cells and roll
heptahelical receptors on neutrophils attach to endothelial cell firmly attaching

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66
Q

what is extravasation and what inflammatory mechanisms aid this

A

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

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67
Q

what cells can undertake phagocytosis

A

neutrophils, macrophages

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68
Q

when are cytokines released

A

when phagocytosis occurs and any time where inflammation needs to be activated

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69
Q

what is degranulation and what cells do this

A

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

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70
Q

what are NETs

A

neutrophil extracellular traps
membrane of neutrophil perforates and released DNA (apoptosis)
DNA creates meshwork which traps and destroys pathogens with proteases

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71
Q

what causes pain in acute inflammation (2)

A

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

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72
Q

what is bradykinin

A

inflammatory mediator that is involved in triggering pain receptors to tell the body to rest this part of the body

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73
Q

what are the three outcomes of acute inflammation

A

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

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74
Q

which tissues are likely to scarr

A

brain, heart, skin

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75
Q

what are the difference in cells in acute and chronic inflammation

A

acute - neutrophils, macrophages

chronic - lymphocytes, plasma cells, macrophages

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76
Q

what is chronic inflammation

A

continued and prolonger inflammation
cycle of repair and destruction
only cellular stage

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77
Q

how many stages are involved with chronic inflammation

A

1 - cellular

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78
Q

what can cause chronic inflammation

A

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

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79
Q

what are features of chronic inflammation

A

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

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80
Q

what is granulation tissue made up of

A

collagen (from fibroblasts) inflammatory cells and vascular tissue (endothelial cells)

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81
Q

what is angiogenesis

A

formation of new blood vessels - chronic inflammation

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82
Q

what are macrophages derived from and what initiates this differantiation

A

large inflammatory cells that engulf anything with foreign antigen
monocytes in blood
initiated by T cells

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83
Q

what are the 3 functions of macrophages M1

A

M1 activated M1 macrophage
phagocytosis
antigen presentation for humoral response
production of cytokines/chemokines

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84
Q

what is the function of cytokines

A

attract inflammatory cells up their gradient

regulate inflammatory mechanisms e.g. cause endothelial cells to present E-selectin for pavementation

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85
Q

what is the function of M2 macrophages

A

release growth factors for endothelial cells and fibroblasts for granulation tissue healing

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86
Q

how does antigen presentation lead to plasma cell production

A

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

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87
Q

what are eosophils

A

similar to neutrophils
pink cytoplasm with multinucleate
specific proteins for destroying parasites

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88
Q

if we had a paracytic infection, which inflammatory cell would be high? how can we tell

A

eosinophil

histologiy ; multinucleate cell with pink cytoplasm

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89
Q

when is TNF alpha important

A

causes endothelial cells to present E-selectin which aids Pavementation of neutrophils for cellular response of acute inflammation

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90
Q

why will tissue damage occur in inflammation

A

proteases released by neutrophils e.g. mmp8
cytotoxic T cells
RANKL bone loss
PGE 2 bone loss -fibroblasts

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91
Q

what stimulates granulation tissue formation and what cells release this

A

growth factors released from M2 macrophages to stimulate fibroblast and endothelial growth

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92
Q

histologically, how can we see scarring

A

high fibroblasts and collagen (pink)

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93
Q

in reaction to chronic inflammation we get a focal granuloma forming, what is its structure

A

centre with lots of macrophages and giant cells (large multinucleated fused macrophages)
rim of leukocytes

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94
Q

what is likely to happen to the centre of very large granulomatous inflammation

A

necrosis

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95
Q

what is H&E stain

A

haematoxylin - stains neuclei/DNA blue/purple

eosin - stains ECM/proteins red

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96
Q

how can we tell apart mature and woven bone histologically

A 
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
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97
Q

what is haemostasis

A

stopping of blood flow - blood clotting

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98
Q

what is blood coagulation

A

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

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99
Q

what is the structurer and function of platelets

A

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

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100
Q

what are the two coagulation pathways and what common end result do they have

A

intrinsic pathway
extrinsic pathway
final common pathway –> fibrinogen to fibrin

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101
Q

what differentiates the two coagulation pathways

A

the coagulation factors/proteins that trigger them

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102
Q

how is extrinsic pathway measured and what is its triggering protein/factor

A 
Prothrombin time / international normalised ratio
subendothelial collagen (tissue factor) - extrinsic to the vessel
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103
Q

how is the intrinsic coagulation pathway measured and what protein/factor triggers this

A

activated partial thromboplastin time.

First protein is phospholipid and factor XIII which is released when endothelial cells burst due to trauma.

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104
Q

if we take someone’s blood to check their clotting speed, what must we do until we want to test the blood and why

A

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)

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105
Q

explain the prothrombin time test

A

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

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106
Q

what factors does prothrombin time test, test?

A

extrinsic and common pathway
I , II, VII, X
I = fibrinogen
II = thrombin

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107
Q

what is INR

A

international ratio
ratio of patients PT: average PT
tests extrinsic and final common pathway

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108
Q

if a patients INR is 2 what does this mean? does it mean it takes twice as long to clot? why?

A

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

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109
Q

when doing extractions on a patient, what must their INR be

A

international ratio
pt PT : avg PT
under 4 in the last 72 hours

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110
Q

what factors of coagulation does warfarin inhibit

A

II, VII, IX and X
II and X common
VII extrinisic

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111
Q

what is APTT

A

activated partial thromboplastin time
test intrinsic coagulation and final common pathway
add calcium, silicon and phospholipid to test tube and measure speed of coagulation

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112
Q

how does APTT work

A

activated partial thromboplastin time
phospholipids activate intrinsic pathway and calcium catalyses common final pathway
factors I, II, V, VIII, IX, X, XI, & XII measured

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113
Q

why is calcium important for coagulation

A

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

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114
Q

why is citrate added to a blood test to prevent clotting

A

citrate inactivates calcium which prevents activation of factor VII
stops conversion of prothrombin to thrombin
stops conversion of fibrinogen to fibrin

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115
Q

what factors are involved in the extrinsic, intrinsic and common pathway and which factors does warfarin affect

A

common - I, II, X, XIII
extrinisic - VII
intirnisc - VIII, IX, XI, XII
warfarin inhibits - II, VII, IX, X

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116
Q

what is haemophilia

A

deficiencies in coagulation factors affecting the intrinsic pathway
haemophilia A: factor VIII
haemaphilia B: factor IX

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117
Q

how do we do a haemophilia test and explain how this works (what is a differential diagnosis)

A

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

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118
Q

what is VWBF

A

von Willebrand factor
tightly bound with factor VIII in complex for platelet adhesion
affects intrinsic pathway because of factor VIII

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119
Q

what is von Willebrand disorder

A 
deficiency of VWBF
allows breakdown of factor VIII
decreased intrinsic pathway
increased APTT
decreases platelet function
increases bleeding time
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120
Q

what are the classifications of bleeding disorders

A

congenital

acquired

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121
Q

what are 2 congenital bleeding disorders

A

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

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122
Q

what are the vitamin K dependant coagulation factors? why is this relevant to pharmacology where are they all made?

A

II, VII, IX, X
warfarin prevents cycle of vitamin K
warfarin inhibits these factors
made in liver

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123
Q

why is the liver important for bleeding disorders and what can cause liver to not function correctly

A

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)

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124
Q

why does a heavy drinker bleed more?

A

alcoholism damages the liver
worsened liver function
less coagulation factors produced

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125
Q

pt is on kidney dialysis, why can we not take teeth out

A

on anticoagulants whilst on dialysis

this increased bleed time

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126
Q

if a kidney problem (acquired), how does this affect bleeding time

A

kidney function is related to platelet formation and calcium levels (used in extrinsic and common pathway for catalysing)
bleed more
increased PT and APTT

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127
Q

what is COX 1,2,3

A

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
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128
Q

what is thromboxane A-2

A

inflammatory factor that leads to platelet coagulation

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129
Q

what are prostaglandins

A

inflammatory proteins that cause pain

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130
Q

what is arachidonic acid

A

inflammatory marker that causes release of :
1. prostaglandins for pain
2. thromboxane A2 for platelet aggregation
with the enzyme OCX

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131
Q

what is bleeding time measured by

A

platelet function

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132
Q

what is the difference between platelet function and coagulation cascade

A

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.

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133
Q

what are the two stages of haemostasis

A

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

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134
Q

how does VWBD, haemophilia, warfarin and aspirin affect bleedig time, APTT and PT

A

VWBD: APTT, BT

haemophilia: APTT
warfarin: PT and APTT
aspirin: BT

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135
Q

what affects (6) do prostaglandins have and their implications

A

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

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136
Q

what is pyrexia and what causes it

A

high temperature

inflammatory markers allowing COX-2 to convert arachidonic to prostaglandins which increase temperature

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137
Q

in terms of healing, what is resolution

A

return to normal, no differences

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138
Q

in terms of healing, what is regeneration

A

lost tissue replaced with the same type of tissue

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139
Q

in terms of healing, what is repair

A

tissue lost replaced with fibrous scar tissue

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140
Q

what is the difference between regeneration and repair

A 
regeneration = lost tissue replaced with the same type of tissue
repair = lost tissue replaced by scar tissue
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141
Q

what are the three cell types regarding if they regenerate or repair (divisions)

A 
labile = constantly dividing = liver = regeneration
stable = infrequently divide, can get larger = repair
permanent = never divide = repair
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142
Q

what three factors mainly affect ability to repair or regenerate

A

cell type - labile, stable, permanent
complexity of tissue
amount of tissue lost

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143
Q

explain repair of tissues breifly

A

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

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144
Q

what cells are involved in granulation tissue that has formed in an area for repair

A

neutrophils on surface
macrophages
endothelial cells
fibroblasts

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145
Q

what forms over a damaged area where epithelium has been broken

A 
slough
mostly fibrin (clotting factor) and white
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146
Q

describe the general structure of the skin

A

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
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147
Q

what are the layers of granulation tissue

A

top layer full of neutrophils for protection - slough
middle layer is immature granulation tissue
bottom is mature granulation tissue - more collagen

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148
Q

what are the 4 stages of wound healing

A

haemostasis
inflammation
proliferation
remodelling

149
Q

describe haemostasis for wound

A

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
Q

describe inflammation phase of wound healing

A

1-3- days after injury
extravasation of neutrophils and monocyte –> macrophage
phagocytosis of foreign bodies, production of cytokines and growth factors

151
Q

what do platelets release to cause proliferation of wound healing tissue (2)

A

PDGF attracts fibroblasts

TGF-beta for fibroblast –> myofibroblast

152
Q

what is PDGF

A

chemokine released by platelets when activated at wound site

attract fibroblast for proliferation and granulation tissue formation

153
Q

describe the structure of fibroblasts and myofibroblasts

A

fibroblasts are regular, smooth, small with large nuclei

myofibroblasts are irregular undulating surface with multiple projections

154
Q

what leads to myofibroblast formation

A

TGF-beta released by macrophages/platelets to convert fibroblasts to myofibroblasts

155
Q

explain the 3rd phase of wound healing

A
  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
Q

what collagen is laid down firstly

A

collagen III

157
Q

explain remodelling phase of wound healing (3)

A

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
Q

how is collagen remodelled

A

collagen III converted to collagen I

corsslinkage increased strength - dependant on vitamin C

159
Q

what is the general structure of collagen I in ECM

A

2 alpha-1 chains and 1 alpha-2 chain coiled around each other (fibrils)
many crosslinked fibrils form collagen fibres

160
Q

how does age affect wound healing

A

affects time it takes, but quality is the same

161
Q

what local factors affect wound healing

A 
stimulus
movement around tissue
protection from more damage
infection
poor blood supply
162
Q

what systemic factors effect wound healing

A

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
Q

why is collagen V important

A

helps fibrillation (strengthening) of collagen I and II

164
Q

what growth factors are secreted when a wound is healing (3)

A

broken endothelial cells and platelets
platelet derived growth factor (PDGF)
epidermal growth factor (EGF)
keratinocyte growth factor (KGF)

165
Q

what controls the growth of new tissue in wound healing (2)

A 
contact inhibition (or lack of - initiates growth)
growth factors PDGF, KGF, EGF, TNF-beta
166
Q

where do new proliferating cells come from during wound healing

A

basal layer - where stem cells are

167
Q

what growth factors stimulate proliferation of fibroblasts

A

TGF-alpha
FGF
PDGF
from macrophages, platelets and damaged endothelial walls

168
Q

what stimulates and controls angiogenesis

A

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
Q

what do fibroblasts secrete

A

all ECM protein and contents
collagen III
glycosaminoglycans and proteoglycans filling proteins

170
Q

what is the difference between healing and cancer

A

cancer is unregulated, uncontrolled and involves irreversible steps

171
Q

what type of scars are more likely to occur on black skin

A

hypertrophic scars (raised )

172
Q

what is a keloid scar

A

large brown lump

173
Q

what is a contracture

A

where a wound has entered muscle or tendon and during healing, scar tissue has shortened the muscle or tendon/

174
Q

what causes keloid scarring

A

thick bundles of collagen, with high levels of type III
abnormal corsslinkage and high turnover
altered cytokine levels

175
Q

if we remove a keloid scar, what is likely to happen

A

re-occurance

176
Q

what is a neuroma

A

scar nerve tissue
a large bundle of nerve tissue that forms on nerve healing
causes sudden pains, sharp, shooting

177
Q

who’s skin does not scar

A

foetus

178
Q

what is some non-scarring tissue

A

oral mucosa and foetal skin

179
Q

why will a wound not heal

A

chronic inflammation
decreased growth factors
increased proteases destroying ECM

180
Q

why does the oral mucosa not scar (3)

A

higher levels of growth factors and turnover
protective salivary layer
increased keratinocyte proliferation

181
Q

how do leeches help wound healing

A

suck blood bringing blood to infected area

inject saliva containing nitric oxide which causes vasodilation (acute inflammation)

182
Q

how can we aid wound healing

A 
dressings
antimicrobials
leeches/maggots
Vasoconstrictors or help haemastasis
Primary intention
183
Q

what is endocrine signalling

A

cell signalling from a distant cell

usually via hormone

184
Q

what is paracrine signalling

A

acing on immediate environment e.g. cytokines

185
Q

what is autocrine signalling

A

signal acts on the cell itself

186
Q

explain transduction of a ligand signal

A

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
Q

why do steroids and hormones have such a fast response

A

they are hydrophobic
can move through cell membrane and cause rapid response
don’t need to be transduced by receptor proteins

188
Q

what do scaffolding proteins do

A

regulate transduction of cell signals

189
Q

Explain the structure and function of G-Coupled Heptahelical receptors

A

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
Q

what do G-coupled receptors respond to

A

hormones e.g. testosterone, epinephrine

senses e.g. light, smell

191
Q

what proteins are swapped when G proteins are activated on heptahelical receptors

A

GDP inactive for GTP active

192
Q

explain how tyrosine kinase receptors work

A

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
Q

explain how ligand ion channels work

A

ligand binds to receptor on ion channel

ion channel opens allowing diffusion of charged particles

194
Q

what does he suffix Mab mean

A

monoclonal antibody

195
Q

what does the suffix Nib mean

A

chemical inhibitor

196
Q

how much of our DNA is functioning and non-functioning

A

3% coding

80% non-functional with historic evidence

197
Q

briefly explain how transcription

A

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
Q

what is the ‘trans’ in transcription factor telling us

A

protein is made from a different gene of which it is working on

199
Q

where do we find the ‘tata’ box

A

25-30 nucleotides up stream from he 5’ end from coding DNA containing promotor reigon

200
Q

are promotors and enhancers trans or cis acting and why

A

cis

on the same gene to which they are regulating

201
Q

explain splicing and what enzyme is involved in this

A

pre-mRNA is modified
removal of mutated genes and introns by splicesomes
leaving just coding exons

202
Q

what is done to mRNA after splicing before translation and why

A

5’ CAP is added - prevents degradation, initiates translation
3’ Poly-A-Tail added - allows strain to exit nucleus and prevent degradation

203
Q

what is the function of enhancers and where re they found

A

control efficiency and rate of transcription of genes

found before promotor region of coding DNA

204
Q

what is DNA fingerprinting and what gene is used

A

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
Q

how can genes be cut from DNA to do DNA fingerprinting

A

bacterial restriction enzymes

206
Q

what is PCR

A

Polymerase chain reaction

means of amplifying DNA to measure the transcription of a gene

207
Q

what is Taq and why is it useful

A

Thermostable polymerase

able to polymerase DNA in high temperatures where DNA remains uncoiled

208
Q

explain steps of PCR test

A

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
Q

which gene can be studied to find high risk of periodontitis and why

A

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
Q

how long is the intron 2 of IL-a1

A

86 base pairs long

211
Q

what is VNTR and how many is a high risk of periodontitis in intron 2 of IL-a1

A

variable number of tandem repeats

2

212
Q

how is intron 2 IL-a1 linked to periodontitis

A

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
Q

what is a SNP

A

single nucleotide polymorphism

214
Q

where do most SNPs occur

A

2 out of 3 occur in C and T

215
Q

what percent of genetic variation is down to SNPs

A

SNP = single nucleotide polymorphism

90% of variation down to SNPs

216
Q

what types of SNP can we have and what are their implications

A

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
Q

how do we get a DNA sample orally

A

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
Q

what are the stages of the cell cycle

A 
rest phase
interphase
prophase
metaphase
anaphase
telophase
219
Q

what checkpoints during cell cycle are there and what occurs at each stage and why is this important

A

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
Q

why are cyclins important for cell cycle and what controls these

A

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
Q

what 2 enzymes are released to initiate mitosis and anaphase and what controls these enyzmes

A

MPF and APC
mitosis promoting factor initiates mitosis controlled by G2 checkpoint
anaphase promoting complex initiates anaphase after M checkpoint

222
Q

what must happen before APC is released

A

M checkpoint checks metaphase alignment of chromosomes

then APC anaphase promoting complex can be released to initiate anaphase

223
Q

what must happen before MPF is released

A

G2 checkpoint ensuring S phase is complete and DNA replicated properly with good DNA integrity

224
Q

what state are most cells in

A

G0 phase of quiescent phase

not replicating, undergoing normal cellular function

225
Q

which cells will never enter cell cycle again

A

terminally differentiated cells/Senescent

e.g. cells in skin

226
Q

what is a tumour suppressor gene and how does it function

A

detects damaged DNA

intitates DNA repair, apoptosis or arrests cell cycle

227
Q

what is a common tumour suppressor gene and why is it relevant

A

p53
p53 is mutated in 50% of cancers
leading to fualty DNA going into the cell cycle and replicating this DNA

228
Q

when is apoptosis necessary (4)

A

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
Q

how is apoptosis initiated

A

removal of positive growth factors

addition of negative factors

230
Q

what is the main effector for apoptosis na dhow do they work

A

caspase cascade
made of proteolytic enzymes that break down cell into smaller fragments for phagocytosis
amplify apoptotic signal throughout cell

231
Q

what are the two pathways for apoptosis

A

intrinsic and extrinsic

232
Q

briefly explain the intrinsic pathway of apoptosis

A

mitochondrial membrane disrupted
cytochrome C released into cytoplasm
bins to Apaf-1 initiating caspase cascade of proteolytic enzymes

233
Q

briefly explain extrinsic pathway of apoptosis

A

external signals form cytotoxic cells
bind to ‘death’ receptors
causing caspase cascade of proteolytic enzymes

234
Q

how does BCL-2 effect the body and where is it relevent

A

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
Q

what enzyme prevents binding of cytochrome C to apaf-1 and when does this occur

A

BCL-2 in cancer

236
Q

what is a common death deceptor

A

Fas-L

237
Q

compare apoptosis and necrosis

A

necrosis uncontrolled, non-energy dependant, inflammatory, swells cell, leads to scarring
apoptosis is controlled, energy dependant, non-inflammatory, shrinks cells, no scarring

238
Q

what protein mutations can cause cancer due to failed apoptosis

A

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
Q

how do apoptotic bodies show histologically

A

very pink

membrane bound vesicles show very pink high in protein

240
Q

how does apoptosis occur

A

signalled
cell broken down into smaller vesicles
macrophages phagocytose
capsase cascade

241
Q

why is apoptosis important for dentistry

A 
tooth growth invaginations
craniofacial clefts
bone remodelling
wound healing 
inflammation removal of inflammatory cells
242
Q

what is an epigenetic trait and what affects these traits

A

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
Q

what can affect epidemiology

A

methylation, non-coding DNA (microDNA), nucleosome location, histone modification

244
Q

how can the environment affect our DNA

A

carcinogens can cause mutations

some environmental factors can alter methylation causing a change in how genes are expressed (epidemiology)

245
Q

what is epigenetics

A

study of how DNA is read and expressed, not involved with mutations

246
Q

what is an epigenetic factor

A

something that affects how DNA is expressed

247
Q

what is the most common trans epigenetic factor

A

transcription factor produced by the cell it is signalling: self-sustaining

248
Q

is methylation and histone change a cis or trans epidemiological factor

A

cis

DNA is modified physically

249
Q

what is the difference between a cis and trans epidemiological factor

A

cis = affects the physical DNA

trans - released and acts on the DNA e.g. transcription factor

250
Q

what does methylation of DNA generally cause and what type of effect is this

A

prevents binding of proteins like transcription factors to genes, reducing production of certain proteins
interferes with transcription
this is an epidemiological affect

251
Q

what does methylation of DNA generally cause and what type of effect is this

A

prevents binding of proteins like transcription factors to genes, reducing production of certain proteins
interferes with transcription
this is an epidemiological affect

252
Q

how can epigenetic affects lead to cancer

A

no mutations
changes in methylation
reduced methylation leads to inappropriate activation of genes
over expression and overgrowth or uncontrolled growth = neoplasm

253
Q

what is an isoform

A

two very similar proteins with the same coding DNA but different exons/introns removed

254
Q

what are the 3 steps to PCR polymerase chain reaction

A

denaturation at 94 degrees
annealation at 54 degrees
extension extension ay 72 degrees

255
Q

explain denaturation during PCR

A

DNA is denatured at 94 degrees for 1 minute to unravel the helix and break H bonds between nucleotides

256
Q

what happens in the annealing process of PCR

A

magnesium, Taq Polymerase and forward/reverse primers are added at 54 degrees for 45 seconds to copy specific genes

257
Q

what happens in the extension process of PCR

A

dNTRs are added (artificial DNA nucleotides ATCG) to attach to complimentary copied DNA for 2 minutes at 72 degrees

258
Q

what is needed as a catalyst for Taq thermostable polymerase from thermus aquaticus

A

magnesium and heat

259
Q

how do we amplify DNA

A

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
Q

what is an oncogene

A

gene/protein with the potential to cause cancer

261
Q

how much calcium do we have in our body and where is it found

A

1kg in body
99% in bone
1% = 10g calcium elsewhere mainly in blood
very little in cells

262
Q

explain where calcium is important in the body

A

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
Q

after calcium triggers myosin to contract, what then happens to the calcium

A

actively transported back into sarcoplasmic reticulum

264
Q

compare transcellular and paracellular absorption

A

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
Q

which glands are responsible for calcium storage in the bones

A

thyroid and parathyroid

266
Q

which vitamin is needed for increased uptake of calcium

A

activated Vitamin D

267
Q

how does vitamin D aid calcium absorption

A

modifies tight junctions to allow more transcellular diffusion
upregulates active transport paracellular movement of calcium

268
Q

how do we get vitamin D

A

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
Q

what is the precursor for vitamin D and how do we ge tthis

A

pro-Vitamin D

derivative of cholesterol

270
Q

which hormone mainly controls calcium homeostasis and where is it made

A

parathyroid hormone

chief cells of the parathyroid gland

271
Q

explain the relationship between parathyroid hormone and calcium

A

calcium inhibits PTH

if calcium is low, PTH is active and this activates osteoclasts for bone resorption to release calcium

272
Q

what is the name for break down of bone

A

osteocytic osteolysis

273
Q

explain thyroids role in calcium regulation

A

thyroid gland released calcitonin - derivative of vitamin D

inhibits Ca2+ absorption and inhibits bone resoprtion - acting against PTH

274
Q

what are the two main hormones involved in calcium regulation and what secretes them

A

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
Q

what is osteogrens affect on bone and vitamin D

A

inhibit bone resorption osteoclasts

promotes vitamin D activity = more calcium

276
Q

how do osteocytes act on bone formation

A

secrete FGF23 fibroblast growth factor 23

inhibits bone formation

277
Q

how could we artificially implant a tooth germ

A

collect epithelial tissue (enamel organ) and mesenchymal tissue (dental papilla)
culture for a few days until a combined germ forms
implant into jaw

278
Q

where can we find tooth germ stem cells for tooth growth

A

baby teeth and wisdom teeth germs

279
Q

what process can locate genes on DNA

A

CRISPR

279
Q

what process can locate genes on DNA

A

CRISPR

280
Q

what is SHED and what is it involved in

A

stem cells from human exfoliated dentition

using stem cells from teeth for regenerative procedures

281
Q

what 3 components are needed for tooth regeneration

A

scaffold including collagen and proteins
cells including stem cells, germ cells
signals to induce growth like HEX genes and TGF

282
Q

at what platelete count do we have spontaneous bleeding

A

<20 x 10^9 /l

283
Q

at what platelet count do we class as safe to do any surgery other than neurosurgery

A

> 80 x10^9/l

284
Q

what is thrombocytopenia

A

reduced platelet count

285
Q

what is thrombocytosis

A

increased platelet count

286
Q

how do we diagnose a bleeding disorder

A

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
Q

what is epistaxis

A

nose bleed

288
Q

what is the name for a nose bleed

A

epistaxis

289
Q

what would small purple dots on the inside of mouth or on the skin be called

A

purpura

290
Q

what is the proper name for a bruise

A

ecchymoses

291
Q

what is menorrhagia

A

menstrual bleeding for over 7 days

292
Q

what blood test investigations can we do into haemotosis

A

Full blood count to check RBC and platelet number
Coagulation tests : PT, APTT, fibrinogen
Bleeding time
WVDF count

293
Q

how do we treat haemophilia

A

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
Q

how do we treat thrombocytopenia

A

platelet transfusion

295
Q

how is haemophilia passed down

A

on X chromosome - dominant

only affects men

296
Q

if a pt has mild haemophilia and we want to do a minor dental surgery, what can we give them

A

Desmopressin DDAVP - released factor VIII from endothelial cells

297
Q

why can desmopressin not be used for haemophilia B

A

releases factor VIII from endothelial cells

haemophilia B is a deficiency in factor IX, so factor VII will not help

298
Q

what risks come with haemophilia factor concentrate

A

infection due to high amounts of blood donors

prior to 1985 viral deactivation did not happen so possible HIV infection

299
Q

what is the most common inherited bleeding disorder and how does it act

A

Von Willenbrans Factor Disease in 3 severities
1:1000
acts on reduced platelet number and reduces factor VIII in coagulation cascade

300
Q

would a coagulation or platelet disease affect the oral cavity more

A

platelet diseases affect oral cavity more than coagulation disordeers

301
Q

name 3 platelet diseases

A

Glazmanns disease
Storage pool disease
VWBD

302
Q

what is a thrombosis

A

coagulation within a vessel

303
Q

compare arterial and venous thrombosis

A

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
Q

explain primary haemostasis

A

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
Q

what do platelets do when attached to exposed collagen

A

change shape and come more sticky and pointy for aggregation
release mediators like PAF (platelet activation factor), Tromboxane2, serotonin for
platelet recruitment

306
Q

what chemicals do platelets release when attached to exposed collagen

A

thromboxane 2
serotonin
platelet activating factor

307
Q

what is thrombophilia

A

where blood clots too easily causing thrombosis - venous or arterial

308
Q

what are 5 inherited thrombophilia

A 
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
Q

what causes thrombocytopenia

A

deficiency leading to less production of platelet
increased consumption of platelets - immune thrombocytopenia
Hyperplenism

310
Q

what causes failure to produce plateletes

A

B12 or folate deficiency
bone marrow metastasis or infiltration
radiation therapy

311
Q

when does immune thrombocytopenia occur

A

acute infection with children - lack of platelets

chronic inflammation in adults

312
Q

what are the results of thrombocytopenia

A

reduced haemostasis

huge internal bleeds

313
Q

what is the function of the spleen

A

remove old platelets from blood

act as storage holding 1/3 of bodies platelets

314
Q

how do we diagnose immune thrombocytopenia

A

identify thrombocytopenia - reduced platelet count
exclusion of other causes e.g inherited
bone marrow examination

315
Q

why does splenomegaly cause thrombocytopenia and how do we treat this

A

larger spleen holds more of the bodies platelets meaning less in circulation
Splenectomy

316
Q

what are some acquired platelet function abnormalities

A

liver and kidney disease
antiplatelet drugs
DIC

317
Q

how do we treat beading with renal disease

A

desmopressin DDAVP or dialysis

318
Q

what are 3 signs of liver disease

A

yellow skin
increased bleeding time
increased PT

319
Q

what are 3 causes of bleeding with liver disease

A

decreased production of vitamin K clotting factors II, VII, IX, X
hypersplenism
increased fibrinolysis

320
Q

when might we have vitamin K deficiency and how do we treat

A

at birth every baby given vitamin K

malabsorption - provide IV vitamin K

321
Q

what bleeding investigation finds vitamin K deficnecy

A

prolonged PT

322
Q

what is the risk of DVT

A

deep vein thrombosis poses risk of PE
pulmonary embolism
fractured part of clot travelling to lungs causing life threatening clots

323
Q

what is a pulmonary embolism and how do we prevent

A

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
Q

what is APLS

A

antiplatelet syndrome
autoimmune disorder attacking phospholipid membrane
increases incidence of blood clotting –> venous and arterial thrombosis

325
Q

what classes as anaemia

A

haemaglobin levels:
<125g/l in men
<115g/l in women

326
Q

how do we find the ‘normal range’ of a protein e.g. haemaglobin

A

find people +/- 2SD around the mean

327
Q

what are symptoms of anaemia

A 
shortness of breath
fatigue under exercise
angina
palpitations
Pallor
hypotension
heart failure
328
Q

what are oral manifestations of anaemia

A

Glossitis (b12/folate)
Angular Stomatitis
Pallor

329
Q

what is Pallor

A

being pale, eyes, conjunctiva, nail bed

330
Q

how do we diagnose anaemia

A

full blood count (can affect WBC and platelet aswell as RBC)

microscopic evaluation of size of RBC

331
Q

what is MCV when diagnosing anaemia

A

mean cell volume

332
Q

what classes as normal MCV

A

82-96fl

333
Q

what is MCV measured in

A

fl

334
Q

what are the three types of anaemia and how do we differentiate

A

microcytic anaemia = MCV < 82fl
normocytic anaemia = 82 < MCVfl < 96
macrocytic anaemia = MCV>96fl

335
Q

what is the leading cause of microcytic anaemia and how does it present

A

iron deficiency (inherited red cell disorders thallasaemia, chronic disease)
small cells
MCV < 82fl

336
Q

if iron deficiency has been excluded from diagnosis, what else can cause microcytic anaemia

A

inherited red blood cell thalassaemia

chronic disease

337
Q

what can cause macrocytic anaemia

A

B12 and folate deficiency

338
Q

what can cause macrocytosis without anaemia

A

alcohol consumption
liver disease
hypothyroidism

339
Q

what is macro/microcytosis

A

larger or smaller red blood cells

340
Q

what are common causes of normocytic anaemia

A

acute bleed
haemolysis (congenitcal or aquired)
Aplastic anaemia
chronic disease

341
Q

what type of anaemia do we get after an acute bleed

A

normocytic anaemia

342
Q

what causes iron deficency and what does this cause

A

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
Q

what is koilonychia

A

concave nail bed caused by iron deficency

344
Q

how do we investigate iron deficency without a blood test

A

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
Q

how do we treat microcyitic anaemia

A

if iron deficient:

  • ferrous sulphate 200mg daily (BSP says TDS but unnecessary)
  • TREAT CAUSE FIRST must find cause, exclude cancer
346
Q

for a macrocytic anaemia pt, what problems will there be with their full blood count and why

A

lacking RBC, WBC and platelets
caused by b12 and b9 deficiency
needed for haematopoiesis and DNA replication
reduction in ALL blood cells

347
Q

how big is your b12 store and how long does it last

A

lasts 4 years

348
Q

if we do not have intrinsic factor, what will the result be

A

chronic
after 4 years, B12 deficiency as IF is needed for absorption
B12 deficiency leads to macrocytic anaemia

349
Q

what is Pernicious anaemia and what type is it

A

autoimmune disroder antibodies against binding
prevention of binding between Intrinisc factor (parietal cells) and b12
leads to b12 deficiency
leads to macrocytic anaemia

350
Q

what is Pancytopenia

A

reduction in all blood cells : RBC, WBC and plateletes

caused by b12/b9 deficency

351
Q

what does chronic b12 deficiency lead to (3)

A

macrocytic anaemia
pancytopenia = reduced RBC, WBC and platelet
affects all body cells, especially neuropathy
glossitis and angular stomatitis

352
Q

how do we diagnose pernicious anaemia

A

b12 levels

intrinisc factor antibodies

353
Q

when do we get b9 deficency

A

lack of diet - eating poorly without fresh fruit and veg
malasborption - coaeliac
increased requirment e.g. pregnancy, growth
some drugs

354
Q

what is haemolytic anaemia and what 2 classifications does it have

A

red cells are broken down in circulation or spleen
or have odd shapes

can be inherited or acquired

355
Q

what are some causes of inherited haemolytic anaemias

A

red cell membrane anaemia e..g spherocytosis
abnormal red cell metabolism
haemoglobin abniormalities e.g. sickle cell

356
Q

what is the most common acquired haematolytic anaemia

A

alloimmune rhesus disease in new-born where antibodies are made against own blood type

357
Q

what types of aquired haematolytic anaemia

A

fragmented red blood cell (mechically by fake valves, small blood clots)
autoimmune/alloimmune disorders e..g Rhesus disease
infection

358
Q

what are some causes of fragmented RBC

A

artificial valves can block and force cells through tiny spaces, fragmenting
blood clots can fragment RBC

359
Q

explain sickle cell anaemia

A

auatosomal recessive
heterozygous mutation leads to protection of malaria
RBC are sickle shaped carrying less Hb
chronic lifelong anaemia

360
Q

what type of mutation causes sickle cell

A

single point mutation

361
Q

when would we see erythroblasts and what are they

A

nucleated red cells

if there is high amount of haemolysis and bone marrow stress - sickle cell or chronic anaemia

362
Q

what is the function of albumins

A

hydrophobic molecules in blood to reduce water potential of blood to draw water out of cells to increased hydrostatic pressure

363
Q

what receptors are responsible for ‘burning’ sensation

A

TRP

364
Q

what is the function of basophils

A

secrete histamine + inflammation

365
Q

briefly describe different WBCs

A

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
Q

what bodily cells does adrenaline act on

A

beta 1 adrenal receptors

367
Q

when is i

A
368
Q

What is the name for too many and too few platelets

A

Thrombocytopenia - too few

Thrombocythemia -too many

BDS 2 (13 decks)

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