Blood Flashcards
1
Q
what volume of blood is a human
A
5L
2
Q
is blood involved in paracrine signalling?
A
no
3
Q
what is the origin or all blood cells
A
multi potential haematopoetic stem cells
4
Q
what is the difference between myeloid and lymphoids
A
myeloid = all non-immune blood cells
lymphoid is all immune cells
5
Q
what is the ration between blood plasma and RBC
A
55% blood plasma - 45% RBC
6
Q
what does blood plasma contain
A
albumin, immunoglobulins and fibrinogen
7
Q
what is serum made up of
A
serum = plasma “-“ clotting factor
8
Q
what is special about AB blood type
A
they have no antibodies so can receive blood from all types
9
Q
what antibodies does A have and what can they receive to
A
has B antibodies and can receive A and O
10
Q
what is special about O blood type
A
universal donor of blood but can only receive o blood
11
Q
what happens when you give the wrong blood type to someone
A
acute haemolytic reaction - hypotension, kidney failure and bleeding
12
Q
what is haemogloburia
A
free haemoglobin excreted in the urine
13
Q
what happens to blood in leukaemia
A
decreased RBC and platelets - increase WBC - later on decrees WBC due to BM failure causing tiredness and bleeding
14
Q
what happens to blood in hodgkins lymphoma
A
there is the presence of reed-sternberg cells (giant cells)
15
Q
what happens when you have iron deficiency
A
main cause of anaemia which leads to microcytic anaemia (pale and small RBC)
16
Q
what causes large red blood cells (macrocytic anaemia)
A
vitamin B12/folate deficiency
17
Q
what is normocytic anaemia
A
normal blood loss (doesnt affect RBC)
18
Q
what is acquired haemolytic anaemia
A
haemolytic syndrome in newborns (Rh), autoantibodies, compliment, drug induced
19
Q
inherited haemolytic anaemia is caused by what
A
2 types
defect in the RBC cytoskeleton is caused by mutations in a or b spectrin (hereditary spherocytosis)
defects in haemoglobin production which occur in sickle cell and thalassaemia
20
Q
what happens in A-thalassaemia
A
large deletions in a globin
21
Q
what happens in beat thalassaemia
A
mutation in the B globin
22
Q
what are the three ways to stop bleeding
A
vasoconstriction (thromboxane, serotonin, angiotensin, vasopressin)
haemostasis
23
Q
what is the difference between arteries and vein
A
arteries take heart from the blood to organs and tissues except the pulmonary artery
veins return blood from the tissues and organs to the heart and then to the lungs
24
Q
describe the functions of blood
A
hydration of tissues and organs delivery of oxygen provision of nutrients fight infection regulation of body temp distribution of endocrine hormones prevent blood loss via blood clot
25
which components of the blood fight infection
white blood cells contribute to immune response against infection and allergic reactions
blood plasma, compliments system and activated ti fight infection by pathogen
26
which components of the blood are involved in clotting
platelets, small anuclealted cells that join together
| different tissue factors and cofactors coagulate which results in fibrin clot through formation of thrombin
27
which cell do wall blood cells come from
stem cells made in the bone marrow
28
why are the two lineages of blood cells
lymphoid - produces lymphocytes and NK cells
| myeloid - RBC's, platelets, mast cell and white blood cells
29
how many types of blood cell are there
11
30
what is the difference between blood plasma and blood serum
plasma is 55% blood volume - contains important clotting factors, immunoglobulins, albumin and fibrinogen
serum is plasma but has already had clotting factors removed
31
what is the composition of blood
55% plasma
| 45 % cells
32
how are blood groups classified and why is it bad if they are fro the wrong person
blood groups are based off different antigens present on the RBS cell membrane - if blood groups are incompatible then antibodies react and cause haemolysis
33
which blood types work with other
O is the universal donor and AB is the universal recipient
34
what is the difference in transfusion of RBC vs Platelets
same as normal for RBC but if its platelets AB can go to all, A = A and O, B = B and O and O can only go to O
(its the direct opposite)
35
how does the Rhesus blood group lead to haemolytic syndrome of the newborn
Rh is a transmembrane protein antigen present on the membrane you can either be Rh+ or RH-
a woman who is Rh- but has a Rh+ baby can create antibodies that cross the placental barrier and causes haemolysis of the baby and lethal anaemia (only affects the second pregnancy)
36
what are some examples of blood plasma vs blood cells
plasma = bleeding, thrombosis, hereditary angioedema, compliment deficiency
blood cells = cancer, sickle cell anaemia, thalassaemia, leukopenia, thrombocytopenia, mononucleosis
37
what are the main causes of bleeding
severe blood loss, we can't lose more than 10% of our blood - can be due to injury, disease, coagulation deficiency, drugs, vit K deficiency, liver disease, sepsis
38
what are the main causes of thrombosis
formation of blood clot. can be venous or arteriole caused by atherosclerosis, cancer, surgery, immobilisation, factor V leiden, hypercoaguability
39
how are haematological malignancies are classed with examples
classified according to blood cell lineage and location
they can be a myeloid neoplasm or lymphoid neoplasm
Leukaemia (blood) or lymphoma (lymph nodes)
can be acute (week) or chronic (years)
40
what are the main causes of acquired aenemia and how can these be recognised on film
it is the loss of O2 delivery and it is caused by abnormalities in Hb or RBC
mild froms involve thalassaemia and sickle cell
41
what is iron deficiency and why is it bad
it is essential element of haem which binds O2 - lack of iron leads to pale and small RBC due to reduced Hb production
42
what is Vit B12/ folate deficiency
involved in DNA replication - causes problems with mitosis or proerythroblast - causes large RBC and low count
it is caused by reduced absorption from poor nutrition or certain drugs
43
what is the difference between haemolytic anaemia and anaemia affecting production of RBC
haemolytic anaemia is due to increased RBC destruction from 120 days to 20 days as the bone marrow is unable to replace sufficient RBC - can be acquired or inherited
anaemia that affects production of RBC's is caused by reduced growth factors
44
what produces erythropoietin
fibroblasts the the kidney
45
what is the role of EPO
emo increases due to low RBC and stimulates RBC production - when tissue pO2 increases emo reduces to slow RBC production
can be made artificially fro people with kidney problems and anaemia
46
what are the causes for acquired haemolytic anaemia
syndrome of the newborn, autoantibodies, complement, drug-induced, snake venom, mechanical heart valves, infections
47
what are some causes of inherited haemolytic anaemia
RBC cytoskeletal defects (mutations), RBC enzyme defects, haemoglobin defects (sickle cell/thalassemia)
48
what are the underlying mechanisms that cause sickle cell
point mutation in Hb globing gene - Glu6 - Val
polymerisation of Hb distorts RBC causes sickling and formation of sticky patch on exterior which causes them to stick together and cause clots
49
what is the cause of sickle cell crisis
sticky patch causes blockage in blood vessels causes severe pain prevents o2 reaching organs and tissues causes damage
50
what is the difference between adult and foetal Hb
adult = 2 alpha 2 beta
foetus = 2 alpha 2 gamma
2 alpha genes on one chromosome and one beta on another chromosome
51
what are the underlying mechanisms of thalassaemia
large deletions of alpha globin (2 alpha genes on chromosome) - if there are large deletions then it can be fatal
beta thalassaemia is caused by mutations in the beta globin genes
if both copies are affected then the patient has foetal haemoglobin or beta thalessamia major
52
why are sickle cell and thalassaemia common in africa
more common in malarial areas as provides protection against malaria
plasmodium parasite cannot get into sickled RBC or incompatible with RBC physiology
53
what two processes occur in the stemming of bleeding
```
vasoconstriction = peptides/hromones lead to contraction of smooth muscle in vessel wall
haemostasis = platelet activation and aggregation then coagulation pathway
```
54
what are the differences between primary and secondary haemostasis
primary - platelets activated by collagen and thrombin - once activated undergo shape change and clump together to form coagulum
secondary - cascade of proteolytic enzymes in plasma that activate one another first activated by tissue factor or contact - produces fibrin clot network
55
what is the trigger for primary haemostasis
injury exposes collage to which the inactivated platelets bind activating them - activated platelets then release ADP and thromboxane which activate more platelets
56
describe the structure of platelets
smallest cell in the blood but second most abundant after RBC - no nucleus and produced by megakaryocytes in the bone marrow - they contain alpha granules and dense granules
57
describe the function of platelets
alpha granules contains lots of clotting factors and growth factors
dense granules contain ADP, 5HTP Ca and polyphosphate
58
what are the three stages of clotting via platelets
activation, adhesion and aggregation
59
what happens in activation of platelets
vascular damage exposes sub-endothelia collagen
| planets bind to collagen directly via GPVI and a2b1 and via GPIV and vWF activating the platelets
60
how do platelets activate further platelets
platelets release ADP and thromboxane which bind to P2Y and TP receptors
61
what molecules are involved in platelet aggregation
a2b3 binds fibrinogen and vWF which hold the plug together
62
which type of receptors are platelets activated through
receptor ligand interactions based on trans membrane protein receptor
GPVI and a2b3 interact with collagen
63
```
what do these receptors do in platelets
GPIb
Thrombin
PY2
TP
```
interact with vWF
bind with thrombin which cleave protease activated receptors and activate
PY2 is receptor for ADP
TP is receptor for thromboxane
64
what role does limited proteolysis have in initiation of coagulation
after injury FVII from blood binds to TF expressed on membrane of cells surrounding blood vessel
FVII once auto-activated it cleaves and activate FX - FXa then converts prothrombin to thrombin which converts fibrinogen to fibrin
65
initial amount of thrombin generated by pathway is not enough so what happens in the consolidation phase in coagulation
initial thrombin activation activates FXI FVIII and FV which are co factors - these overall increases cross links of fibrin to stabilise network and increase resistance to fibrinolysis
66
what is the difference between intrinsic and extrinsic coagulating pathways
extrinsic - triggered by Tissue factor (TF) on cell membrane of perivascular cells
intrinsic - triggered by negatively charged surfaces such as glass, polyphosphates which are released by platelets and misfiled proteins
67
```
define these terms:
major
external
internal
minor
caused by
```
significant blood loss which requires treatment eg plasma, platelets, coagulation factors
truma
haemophilia, aneurysm rupture, drug induced
mild bleeding doesn't usually require treatment
bruising, nose bleeds, heavy periods
68
what are common causes of major bleeding
trauma, surgery, aneurysm rupture, sepsis, drugs
69
what are the main underlying causes of spontaneous bleeding
coagulation factor deficiency or haemophilia, vit k deficiency or thrombocytopenia
70
what occurs in disseminating intravascular coagulation
infection occurs which leads to sepsis and the infection enters the blood stream
causing intravascular tissue factor exposure causing both consumption of clotting factors and platelets leading to bleeding - as well as systematic coagulation activation leading to microvascular clots
both lead to multiple organ failure
71
how can Vit K deficiency lead to bleeding - what is it caused by
vit K undergoes Glu - Gla translation via vit K epoxide reductase
may clotting factors are vit k dependant such as FVII, FIX FX and prothrombin
caused by fat malabsorption
72
how does warfarin work
warfarin tamest the enzyme vit k epoxide reductase which inhibits it which means Glu cannot be modified to Gla and it cannot bind to Ca2+ to phospholipids and so factors do not work
73
what are the differences between haemophilia A and B
Haemo A - deficiency of FVIII, cofactor of FIX in conversion of FX to FXa
X linked recessive
female carrier but male offspring at risk - relatively rare
haemolytic B - deficiency of FIX, FIXa converts FX to FXa
also X linked recessive
74
how do x linked diseases work
women will never be homozygous X linked and will always have one normal X chromosome by they can be carriers - males cannot be carriers but if they have the chromosome they will always be affected - if a mother is a carrier there is 50% chance the daughter is a carrier and 50% son is affected
75
describe what von Willebrand disease is and the various types
caused by a deficiency of vWF
type 1 = heterozygous (autosommal dominant) non - severe
type 2 = functional deficiency (autosomal dominant) - mild
type 3 = complete deficiency (autosomal recessive) - more severe
76
what is/are the primary causes of thrombocytopenia
loss of function of platelets
can be acquired through leukaemia, blood loss, drug induced or immune disease
or inherited = bone marrow failure, mutations, cancer, deficiency affecting platelets
77
describe the structural differences between arteries and veins
```
vein = larger diameter, thin wall, thin smooth muscle, low pressure, valves
artery = small diameter thick wall thick smooth muscle high pressure no valves
```
78
what are the differences between venous and arterial thrombosis
venous - DVT and pulmonary embolism
| arterial - myocardial infarction, atrial fibrillation, peripheral vascular disease stroke
79
how does deep vein thrombosis occur
occurs under low blood flow, stasis causes clots to form develops around valves in deep veins (arms/legs), may lead to pulmonary embolism if part of clot breaks off and travels to lungs
thrombus is RBC and fibrin rich
80
how does a pulmonary embolism develop
small part of DVT clot breaks off
embolus travels through veins, right stream, right ventricle into the lung
blocks artery in lung leading to lung tissue infection, schema of the lung
81
what are the main risk factors of venous thrombosis
immobilisation, surgery, cancer, pregnancy, oral contraceptives, deficiencies in coagulation inhibitors, factor V Leiden mutation
82
how do natural anticoagulants work
| give an example
antithrombin binds to active sites of factors and blocks them - antithrombin blocks thrombin, FXa and FIXa
83
how does fibrolysis work
products of fibrin used in test to see if DVT
| clot busting drugs such as tPA and uPA sued t dissolve them - plasminogen goes to plasmic which degrades fibrin
84
how does an aerial thrombosis develop
plaques form over many years from atherosclerosis, inflammation of the vessel wall with infiltration of macrophages and fat deposits - triggered by rupture of plaque - thrombosis is platelet rich - can lead to MI and stroke
85
what are the main risk factors associated with arterial thrombosis
advanced age, smoking, diabetes, hypertension, cholesterol, poor diet, lack of exercise
86
what are the treatments for arterial thrombosis
aspirin - inhibition of cox1 and thromboxane production
anti ab3 - block receptor of fibrinogen and vWF
anti P2Y - block receptor for ADP induced platelet aggregation
use fibrinolytic (rarely used)
87
what are the treatments for venous thrombosis
heparin which has a quick onset - risk of anaphylactic shock but aids antithrombin
dabigatran - direct thrombin inhibitor
