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IMS > Blood > Flashcards

Blood Flashcards

1
Q

what volume of blood is a human

A

5L

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2
Q

is blood involved in paracrine signalling?

A

no

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3
Q

what is the origin or all blood cells

A

multi potential haematopoetic stem cells

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4
Q

what is the difference between myeloid and lymphoids

A

myeloid = all non-immune blood cells

lymphoid is all immune cells

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5
Q

what is the ration between blood plasma and RBC

A

55% blood plasma - 45% RBC

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6
Q

what does blood plasma contain

A

albumin, immunoglobulins and fibrinogen

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7
Q

what is serum made up of

A

serum = plasma “-“ clotting factor

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8
Q

what is special about AB blood type

A

they have no antibodies so can receive blood from all types

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9
Q

what antibodies does A have and what can they receive to

A

has B antibodies and can receive A and O

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10
Q

what is special about O blood type

A

universal donor of blood but can only receive o blood

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11
Q

what happens when you give the wrong blood type to someone

A

acute haemolytic reaction - hypotension, kidney failure and bleeding

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12
Q

what is haemogloburia

A

free haemoglobin excreted in the urine

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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

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14
Q

what happens to blood in hodgkins lymphoma

A

there is the presence of reed-sternberg cells (giant cells)

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15
Q

what happens when you have iron deficiency

A

main cause of anaemia which leads to microcytic anaemia (pale and small RBC)

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16
Q

what causes large red blood cells (macrocytic anaemia)

A

vitamin B12/folate deficiency

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17
Q

what is normocytic anaemia

A

normal blood loss (doesnt affect RBC)

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18
Q

what is acquired haemolytic anaemia

A

haemolytic syndrome in newborns (Rh), autoantibodies, compliment, drug induced

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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

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20
Q

what happens in A-thalassaemia

A

large deletions in a globin

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21
Q

what happens in beat thalassaemia

A

mutation in the B globin

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22
Q

what are the three ways to stop bleeding

A

vasoconstriction (thromboxane, serotonin, angiotensin, vasopressin)
haemostasis

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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

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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
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25
Q

which components of the blood fight infection

A

white blood cells contribute to immune response against infection and allergic reactions
blood plasma, compliments system and activated ti fight infection by pathogen

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26
Q

which components of the blood are involved in clotting

A

platelets, small anuclealted cells that join together

different tissue factors and cofactors coagulate which results in fibrin clot through formation of thrombin

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27
Q

which cell do wall blood cells come from

A

stem cells made in the bone marrow

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28
Q

why are the two lineages of blood cells

A

lymphoid - produces lymphocytes and NK cells

myeloid - RBC’s, platelets, mast cell and white blood cells

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29
Q

how many types of blood cell are there

A

11

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30
Q

what is the difference between blood plasma and blood serum

A

plasma is 55% blood volume - contains important clotting factors, immunoglobulins, albumin and fibrinogen
serum is plasma but has already had clotting factors removed

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31
Q

what is the composition of blood

A

55% plasma

45 % cells

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32
Q

how are blood groups classified and why is it bad if they are fro the wrong person

A

blood groups are based off different antigens present on the RBS cell membrane - if blood groups are incompatible then antibodies react and cause haemolysis

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33
Q

which blood types work with other

A

O is the universal donor and AB is the universal recipient

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34
Q

what is the difference in transfusion of RBC vs Platelets

A

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)

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35
Q

how does the Rhesus blood group lead to haemolytic syndrome of the newborn

A

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
Q

what are some examples of blood plasma vs blood cells

A

plasma = bleeding, thrombosis, hereditary angioedema, compliment deficiency
blood cells = cancer, sickle cell anaemia, thalassaemia, leukopenia, thrombocytopenia, mononucleosis

37
Q

what are the main causes of bleeding

A

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
Q

what are the main causes of thrombosis

A

formation of blood clot. can be venous or arteriole caused by atherosclerosis, cancer, surgery, immobilisation, factor V leiden, hypercoaguability

39
Q

how are haematological malignancies are classed with examples

A

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
Q

what are the main causes of acquired aenemia and how can these be recognised on film

A

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
Q

what is iron deficiency and why is it bad

A

it is essential element of haem which binds O2 - lack of iron leads to pale and small RBC due to reduced Hb production

42
Q

what is Vit B12/ folate deficiency

A

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
Q

what is the difference between haemolytic anaemia and anaemia affecting production of RBC

A

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
Q

what produces erythropoietin

A

fibroblasts the the kidney

45
Q

what is the role of EPO

A

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
Q

what are the causes for acquired haemolytic anaemia

A

syndrome of the newborn, autoantibodies, complement, drug-induced, snake venom, mechanical heart valves, infections

47
Q

what are some causes of inherited haemolytic anaemia

A

RBC cytoskeletal defects (mutations), RBC enzyme defects, haemoglobin defects (sickle cell/thalassemia)

48
Q

what are the underlying mechanisms that cause sickle cell

A

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
Q

what is the cause of sickle cell crisis

A

sticky patch causes blockage in blood vessels causes severe pain prevents o2 reaching organs and tissues causes damage

50
Q

what is the difference between adult and foetal Hb

A

adult = 2 alpha 2 beta
foetus = 2 alpha 2 gamma
2 alpha genes on one chromosome and one beta on another chromosome

51
Q

what are the underlying mechanisms of thalassaemia

A

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
Q

why are sickle cell and thalassaemia common in africa

A

more common in malarial areas as provides protection against malaria
plasmodium parasite cannot get into sickled RBC or incompatible with RBC physiology

53
Q

what two processes occur in the stemming of bleeding

A 
vasoconstriction = peptides/hromones lead to contraction of smooth muscle in vessel wall 
haemostasis = platelet activation and aggregation then coagulation pathway
54
Q

what are the differences between primary and secondary haemostasis

A

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
Q

what is the trigger for primary haemostasis

A

injury exposes collage to which the inactivated platelets bind activating them - activated platelets then release ADP and thromboxane which activate more platelets

56
Q

describe the structure of platelets

A

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
Q

describe the function of platelets

A

alpha granules contains lots of clotting factors and growth factors
dense granules contain ADP, 5HTP Ca and polyphosphate

58
Q

what are the three stages of clotting via platelets

A

activation, adhesion and aggregation

59
Q

what happens in activation of platelets

A

vascular damage exposes sub-endothelia collagen

planets bind to collagen directly via GPVI and a2b1 and via GPIV and vWF activating the platelets

60
Q

how do platelets activate further platelets

A

platelets release ADP and thromboxane which bind to P2Y and TP receptors

61
Q

what molecules are involved in platelet aggregation

A

a2b3 binds fibrinogen and vWF which hold the plug together

62
Q

which type of receptors are platelets activated through

A

receptor ligand interactions based on trans membrane protein receptor
GPVI and a2b3 interact with collagen

63
Q 
what do these receptors do in platelets 
GPIb
Thrombin
PY2
TP
A

interact with vWF
bind with thrombin which cleave protease activated receptors and activate
PY2 is receptor for ADP
TP is receptor for thromboxane

64
Q

what role does limited proteolysis have in initiation of coagulation

A

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
Q

initial amount of thrombin generated by pathway is not enough so what happens in the consolidation phase in coagulation

A

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
Q

what is the difference between intrinsic and extrinsic coagulating pathways

A

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
Q 
define these terms:
major
external
internal 
minor
caused by
A

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
Q

what are common causes of major bleeding

A

trauma, surgery, aneurysm rupture, sepsis, drugs

69
Q

what are the main underlying causes of spontaneous bleeding

A

coagulation factor deficiency or haemophilia, vit k deficiency or thrombocytopenia

70
Q

what occurs in disseminating intravascular coagulation

A

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
Q

how can Vit K deficiency lead to bleeding - what is it caused by

A

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
Q

how does warfarin work

A

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
Q

what are the differences between haemophilia A and B

A

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
Q

how do x linked diseases work

A

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
Q

describe what von Willebrand disease is and the various types

A

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
Q

what is/are the primary causes of thrombocytopenia

A

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
Q

describe the structural differences between arteries and veins

A 
vein = larger diameter, thin wall, thin smooth muscle, low pressure, valves 
artery = small diameter thick wall thick smooth muscle high pressure no valves
78
Q

what are the differences between venous and arterial thrombosis

A

venous - DVT and pulmonary embolism

arterial - myocardial infarction, atrial fibrillation, peripheral vascular disease stroke

79
Q

how does deep vein thrombosis occur

A

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
Q

how does a pulmonary embolism develop

A

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
Q

what are the main risk factors of venous thrombosis

A

immobilisation, surgery, cancer, pregnancy, oral contraceptives, deficiencies in coagulation inhibitors, factor V Leiden mutation

82
Q

how do natural anticoagulants work

give an example

A

antithrombin binds to active sites of factors and blocks them - antithrombin blocks thrombin, FXa and FIXa

83
Q

how does fibrolysis work

A

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
Q

how does an aerial thrombosis develop

A

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
Q

what are the main risk factors associated with arterial thrombosis

A

advanced age, smoking, diabetes, hypertension, cholesterol, poor diet, lack of exercise

86
Q

what are the treatments for arterial thrombosis

A

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
Q

what are the treatments for venous thrombosis

A

heparin which has a quick onset - risk of anaphylactic shock but aids antithrombin
dabigatran - direct thrombin inhibitor

IMS (20 decks)

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