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cardiovascular system > Blood > Flashcards

Blood Flashcards

1
Q

explain the processes from stem cell to platelet production

A

endomitosis, increase in internal membrane system , formation of granules
increase in cell size (megakaryocyte)
increase expression of platelet surface receptors e.g. integrins

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2
Q

where does haematopoiesis occur in the first 0-6weeks of embryo development?

A

yolk sack mesoderm layer (primitive haematopoiesis)

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3
Q

where does definitive haematopoiesis begin after 6 weeks?

A

AGM region aorta-gonad-mesonephros

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4
Q

where does haematopoiesis migrate too from the AGM in the foetus?

A

liver, thymus and spleen
2-7months

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5
Q

where is haematopoiesis primarily in the foetus after 8 months of growth?

A

bone arrow

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6
Q

how to platelets enter the blood stream?

A

cytoplasmic fragmentation, cytoplasmic extent ions called podosomes release paltelets into the blood stream

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7
Q

what soluble signals and how do they activate platelets?

A

thrombin, ADP (released from damaged cells), etc bind to G protein coupled receptors
coagulation cascade activates integrins

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8
Q

what vessel wall signals activate platelets?

A

collagen, von Willebrand factor ( released upon wall damage and bind to collagen to aid platelet adhesion)

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9
Q

what are the 3 main ways platelets change once activated?

A

change shape, become sticky, secrete granules

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10
Q

how do activated platelets in suspension change shape?

A

cytoskeleton rearrangement, filipodia extended from cytoplasm = larger surface area for coming into contact with other platelets / adhesion

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11
Q

how do platelets activated by adhesion change shape

A

cytoskeleton rearrangement cell membrane spreads increasing surface area from adhesion / blocking of blood vessel walls

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12
Q

what are the 2 types of granules platelets release upon activation?

A

alpha and dense granules

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13
Q

what do alpha granules contain / what is their role?

A

haemostatic factors e.g. coagulation factors
platelet receptors adhesion proteins
leukocyte recruitment (signalling molecules)

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14
Q

how do platelets become sticky?

A

αllbβ3 integrins become activated
(via outside in signalling e.g. come into contact with collagen, or inside out e.g. come into contact with thrombin)
these integrins have a high affinity for fibrinogen and VWF = high affinity for primary platelet plug

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15
Q

what do dense granules contain?

A

platelet agonist e.g. ADP - positive feedback platelet activation
haemostatic factors

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16
Q

what material holds the primary haemostatic plug together?

A

fibrinogen

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17
Q

how is the secondary haemostatic plug formed?

A

thrombin cleaves fibrinogen to convert it to fibrin
also activates cofactors such FXIII and FXIIIa, resulting in a fibrin mesh as the end result

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18
Q

what is the final stage of haemostasis?

A

fibrinolysis (the breakdown of the fibrin clot)

19
Q

how does fibrinolysis occur?

A

plasminogen is recruited to fibrin by factors released in response to blood vessel damage
a fibrin bound protease then converts plasminogen to plasmin
plasmin breaks down fibrin

20
Q

what is plasma vs serum?

A
  • Plasma - liquid component after cells, platelets have been removed. Prepared by centrifuging with an anticoagulant such as EDTA or heparin. This means blood doesn’t clot and clotting factors remain in the suspension
  • Serum - liquid component minus cells, platelets and clotting factors. No anticoagulant is added as the blood is centrifuged meaning it clots and take the factors with it out of the liquid
21
Q

how does blood behave differently from a Newtonian fluid?

A

viscosity changes depending on shear rate (increased rate, decrease viscosity)
blood flow is at a constant rate diastole/ systole
walls (blood vessels) can taper and deform

22
Q

what are the intrinsic and extrinsic factors that effect blood viscosity?

A

intrinsic factors (major - haematocrit, plasma viscosity, minor - red cell deformation, red cell aggregation)
extrinsic factors (flow conditions - velocity depends on shear rate)

22
Q

what is the equation for average blood pressure (to do with resistance)?

A

ABP= CO x Resistance

23
Q

why is exercise hard for those with anaemia (give 2 reasons)

A

low haematocrit = slow rate of O2 delivery
also decreased viscosity of blood means needs to be an even higher increase in CO to maintain the right pressure
as CO is already high in anaemics at rest, can be hard to match for exercise

24
Q

what is the main determiner of plasma viscosity?

A

plasma proteins e.g. albumin, immunoglobulin

25
Q

what plasma protein contributes to blood viscosity the most?

A

fibrinogen due to its role in blood clotting

26
Q

In what conditions does fibrinogen and therefore blood viscosity increase?

A

atherosclerosis, inflammatory conditions,
diabetes

27
Q

how does viscosity decrease with an increase in shear rate and vie versa?

A

high rate, blood cells deform, align with the flow
low flow rates, rbc aggregate, mediated by proteins such as fibrinogen, increase viscosity

28
Q

what are the symptoms of hyper viscosity syndromes?

A

spontaneous bleeding from mucous membranes, visual disturbances due to retinopathy and neurological symptoms ranging from headaches, vertigo to seizure and coma

29
Q

what is hyperglobulinemia?

A

elevated immunoglobins

30
Q

what is Waldenström macroglobulinemia?

A

cancer of B lymphocytes that can increase blood viscosity up to 10mPa due to them producing excess immunoglobins

31
Q

what is hyperleukocytosis?

A

very high numbers of white blood cells = hyper viscosity

32
Q

what areas are particularly susceptible to atherosclerosis?

A

bifurcations and branch points (due to disturbed flow), areas with increase permeability to macromolecules or increased adhesiveness to monocytes, areas with increased turnover (proliferation/ apoptosis) as well as altered levels of eNOS (Endothelium NO)

33
Q

what is protective against atherosclerosis?

A

shaer stress and lamina flow

34
Q

what are the properties of the red blood cells membrane which aid it to travel through capplries?

A

spectrin in membrane ring like structures allowing deformation, it also provides stability (to withstand flow stress) and controls flexibility
special transporters such as Na/K ATPase, they also control the haemoglobin conc which contols the volume of rbc

35
Q

how does cell geometry effect the cells ability to pass through cell membrane?

A

size / diameter - relative to the capillary how much does it need to deform
surface area/ volume (rbc biconcave disc shape has high surface area to volume ratio, don’t need extra membrane to deform, similarly wbc have ruffles)

36
Q

how does cytoplasm and viscosity effect cells ability to pass through capillaries?

A

higher cytoplasm viscosity e.g. haemoglobin conc, vs packed cytoplasm of wbc effect ability to move through capillaries
also cytoskeleton rearrangement is a factor

37
Q

how does membrane deformability effect a cells ability to move through capillary?

A

rigidity , cant be too rigid, also needs stability to prevent degradation
e.g. spectrin

38
Q

what disease effect the ability of red blood cells to flow through vessels such as capllries?

A

mutations in sceptrin = haemolytic anaemia
mutations in haemoglobin e.g. sickle cell anaemia, leads to formation of S haemoglobin which polymerises at low O2 levels leading to deformed rbc which occlude vessels
malarial parasite falciparum increases rigidity and alters membrane structure

39
Q

what is the main property of blood that contributes to its flow in large vessels?

A

viscosity

40
Q

what is the main component of blood that effects its flow in smaller vessels?

A

cellular properties

41
Q

where to leukocytes exit the blood stream?

A

venules

42
Q

how to leukocytes exit the venules?

A

margination - tbc aggregate in the middle pushing the wbc to the periphery
leukocyte makes contact with the endothelium and slow themselves down via selectins (rolling)
wbc integrins are then activated by signals allowing them to adhere to the endothelium
cytokines attract leukocytes to the site of infection as they squeeze through gaps in the endothelium

cardiovascular system (3 decks)

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