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Physiology and Pharmacology > Blood and Clotting > Flashcards

Blood and Clotting Flashcards

1
Q

what is blood?

A
  • complex fluid containing cellular and fluid parts

- contains erythrocytes (rbc) and leukocytes (wbc)

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2
Q

how can blood be separated?

A

Centrifugation at 10000Gs

  • anticoagulant prevents clotting
  • dense parts form at bottom of tube = rbcs
  • thin layer of wbcs and platelets in middle
  • at top is cell free plasma = liquid
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3
Q

what is haematocrit?

A
  • the amount of rbcs in blood
  • can be measured by measuring height of centrifuge tube and height of rbc portion
  • divide rbc portion by height of tube to find haematocrit as a %
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4
Q

what is plasma?

A
  • watery solution of electrolytes, plasma proteins, carbohydrates and lipids
  • ECF
  • contains plasma proteins involved in coagulation cascade:
  • albumin: prevalent but low molecular weight
  • fibrinogen: important in clotting
  • globulins: 10x size of albumin
  • other coagulation factors
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5
Q

how can plasma be separated?

A
  • electrophoresis
  • pass current through sample and proteins are separated based on molecular weight and charge
  • turn gel 90 degrees after first run to further separate out the proteins
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6
Q

what are erythrocytes (rbcs)?

A
  • most abundant element in blood = haematocrit
  • non-nucleated biconcave cells to maximise SA:V
  • shape maintained by cytoskeleten being anchored to plasma membrane via glycophorin and Band 3 Cl/HCO3 exchange
  • cytoskeleton made of spectrin, actin, p55 and protein 4.1
  • forces exerted on rbc via capillaries can damage cell, but anchoring system maintains its integrity
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7
Q

what are the functions of erythrocytes?

A
  • O2 carriage from lungs to systemic system
  • CO2 carriage from tissue to lungs
  • buffering of acids and bases
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8
Q

what are granulocyte leukocytes (wbcs)?

A
  • granular in nature
  • neutrophils: phagocytose bacteria
  • eosinophils: combat parasites and viruses
  • basophils: release IL-4, histamine, heparin and peroxidase
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9
Q

what are non-granular leukocytes?

A
  • lymphocytes: mature into T cells and B cells

- monocytes: macrophages and dendritic cells

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10
Q

what are platelets?

A
  • they bud off from megakaryocytes in bone marrow (TPO (Thrombopoietin) and IL-3 dependent)
  • sinusoidal capillary has megakaryocytes extending through them
  • there are 150,000-450,000 platelets/um of blood
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11
Q

what is the negative feedback mechanism of platelet budding?

A
  1. each platelet budding from megakaryocyte has a receptor for TPO
  2. abundant platelets bind to abundant TPO receptors so that TPO binds to platelet surface
  3. no more TPO is available to generate megakaryocutes
  4. there are less megakaryocytes for platelets to bud off from, so less platelets are ade
  5. less platelet receptors bind to TPO so TPO stimulates megakaryocytes to increase platelet production
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12
Q

what is the structure of platelets?

A
  • nucleus-free fragments
  • contains microtubules, mitochondira, lysosomes, peroxisomes, a-granules and dense core granules
  • external coat rich in platelet receptors for TPO
  • inner skeleton is a circumferential band of tubulin microtubules
  • tubulin maintains spherical shape when platelet is resting and reorganises them when they are activated
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13
Q

what are alpha-granules?

A
  • secrete fibrinogen and von Willebrand Factor (vWF) and clotting factor 5
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14
Q

what do dense core granules contain?

A
  • ATP
  • ADP
  • serotonin - causes recruitment of other platelets
  • Ca2+
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15
Q

what is blood viscosity?

A
  • resistance of a fluid to a change in shape (opposition to flow)
  • measures resistance to sliding of shear fluid layers
  • there is a shear force generated when layers slideover one another
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16
Q

what 5 factors does blood viscosity depend upon?

A
  1. haematocrit
  2. fibrinogen plasma concentration
  3. vessel radius: as vessel radius changes, viscosity changes
  4. linear velocity: speed at which blood passes through vessel
  5. temperature
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17
Q

how does haematocrit affect blood viscosity?

A
  • plasma is 0% has it has no rbc and has steepest curve: the highest flow of driving pressure (100mL/s)
  • haematocrit of whole blood is 36% and flow is 20mL/s
  • whole blood varies so may have higher haematocrit e.g. 66% so a slower rate
  • haematocrit is usually 30-50%
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18
Q

why are there different linear velocities of blood flow?

A
  • in a cylindrical blood vessel, laminae of blood are concentric cylinders
  • due to sheer forces between vessel wall and blood flow, there are different blood velocities
  • each concentric layer gets faster nearer to the center
  • central layer is faster than outer layer: laminar blood flow
  • layers form a parabolic shape in velocity
19
Q

what is the parabolic profile of blood flow velocity?

A
  • maximal velocity is at the centre (Vmax)
  • the lower the viscosity, the sharper the point
  • low viscosity = extended parabolic shape
  • high viscosity = stunted parabola
20
Q

where do rbc travel in the arteriole?

A
  • in the centre rather than the periphery as they flow faster in the centre
  • Poseuille discovred that rbcs accumulate in the centre of arterioles for faster transportation
21
Q

what does axial accumulation of cells lead to?

A

plasma skimming:

  • around branching vessel is a layer of plasma where there are no rbcs at the edge
  • therefore there is low haematocrit in the periphery of blood vessels
22
Q

how is plasma skimming prevented?

A

axial cushions:

  • invaginations of the vessel wall prevents the plasma layer from forming
  • haematocrit is maintained
23
Q

what is plasma spinning?

A
  • lamina layers are limited to width of rbcs, so there is a limitation to the number of rbcs in small blood vessels
  • rbc membranes rolls around the cytoplasm
  • this causing tank treading where 2 adjacent cells spin the plasma
  • vessels smaller than rbcs cause rbc deformities, so viscosity falls
24
Q

what is laminar blood flow?

A
  • where flow is fastest at the centre
  • extended parabolic profile
  • no murmurs are heard: healthy
25
Q

what is turbulent blood flow?

A
  • at high flow rate, above critical velocity, blood flow is turbulent, not laminar
  • causes the parabolic profile to be blunted
  • occurs if the radius is large, velocity is high and if there is local stenosis (restriction of vessel lumen which increases velocity)
  • clinically significant as murmurs can be heard
26
Q

what is haemostasis?

A
  • prevention of haemorrhage (blood loss)
27
Q

what are the 4 ways in which haemostasis is achieved?

A
  1. vasoconstriction by thromboxane A, serotonin, thrombin, endothelin-10 to reduce blood loss
  2. increased tissue pressure causes decreased transmural pressure (difference between intravascular pressure and tissue pressure)
  3. platelet plug: small branches in vascular endothelium
  4. coagulation/clot formation
28
Q

how does vasoconstriction by thromboxane A, serotonin, thrombin, endothelin-1 cause haemostasis?

A
  • these factors are released by platelets or formed through the release of other factors
  • thrombin causes endothelial cells to release endothelin-1 which is the most potent vasoconstrictor
29
Q

how does increased tissue pressure cause decreased transmural pressure in haemostasis?

A

transmural pressure = difference between intravascular pressure and tissue pressure

  • tissue pressure increases due to loss of fluid from the vasculature into tissue
  • causes tissue fluid accumulation
30
Q

what is the platelet plug in haemostasis?

A
  1. adhesion of platelets
  2. activation
  3. aggregation
31
Q

what is the coagulation cascade/clot formation?

A
  • semisolid mass of platelets and fibrin mesh with trapped rbc, wbc and serum
32
Q

what is platelet adhesion and how is it achieved?

A
  • platelet adhesion mediated by receptors on surface, bound to ligands
  • endothelial cells release vWF which is triggered by:
    • high sheer forces
    • cytokines
    • hypoxia: loss of oxygen
  • injured epithelia expose collagen in the sub-epithelial layers which binds to vWF and activated platelets
  • breach of epithelium exposes collagen, fibronectin and laminin
33
Q

how does platelet activation occur?

A
  • ligand binding leads to a conformational change in receptors
  • this promotes an intracellular signalling cascade
  • promotes exocytosis of dense storage granules containing ATP, ADP, serotonin, Ca2+, alpha-granules, vWF, clotting factor 5 and fibrinogen
  • promotes cytoskeletal changes where filopodia becomes lamellipodia
34
Q

what happens during platelet aggregation?

A
  1. fibrinogen binds to receptors on platelets
  2. platelets adhere to vWF which attaches to the endothelium
  3. activation causes conformational change in the receptor to allow it to bind to fibrinogen
  4. a molecular bridge is formed between platelets so they can group together
35
Q

what is a blood clot?

A
  • semisolid pass of rbcs, wbcs, serum and mesh of fibrin and platelets
  • activating event triggers chain reaction of converting precursors/factors (F) to activated factors (AF)
  • controlled proteolysis amplifies the clotting signals
  • precursors are cleaved into activating factors, which are then lytic factors for the next part of the cascade
  • thrombus is an intravascular clot
36
Q

what is the process of the intrinsic pathway clotting cascade?

A
  1. surface contact activation on membrane of activated platelets
  2. F12 is activated to AF12
  3. High Molecular Weight Kallikrein (HMWK) acts as cofactor to anchor AF12 to platelet membrane
  4. activation allows cleavage of prekallikrein to kallikrein
  5. releasing kallikrein speeds up reaction, so F11 is cleaved to AF11
  6. this causes F9 to become AF9
  7. thrombin causes F8 to become AF8
  8. these AFs enable accumulation of a tri-molecule with Ca2+ to form Tenase complex
  9. Tenase converts F10 to AF10
37
Q

what is the process of the extrinsic pathway of the clotting cascade?

A
  1. membrane-bound tissue factor activation when blood contacts material from damaged membranes
  2. the cell has a tissue factor receptor which can bind to F7 at injury site
  3. This binding converts F7 to AF7
  4. tissue factor receptor, AF7 and Ca2+ form a tri-molecule
  5. tri-molecule converts F10 to AF10
38
Q

what happens at the end of both the intrinsic and extrinsic pathways?

A
  1. tri-molecule with Ca2+ converts F10 to AF10
  2. AF5 complexes with thrombin and AF10, enabling conversion of prothrombin to thrombin
  3. positive feedback loop where the cascade gets faster and faster once thrombin is released
  4. thrombin cleaves fibrinogen to fibrin
  5. fibrin monomers form polymers to form a stable fibrin
  6. thrombin activates F13 which catalyses fibrin polymer to stable fibrin
39
Q

how are blood clots prevented?

A
  • homeostatic mechanisms prevent haemostasis

- endothelial cells maintain blood fluidity via paracrine factors and anticoagulant factors

40
Q

what is the role of paracrine factors in clot prevention?

A

paracrine factors such as prostacyclin promote vasodilation to increase blood flow and nitric oxide which inhibit adhesion

41
Q

what is the role of anticoagulant factors in clot prevention?

A
  1. Tissue Factor Pathway Inhibitors (TFPI) on endothelial cells maintain antithrombotic surface by binding and inhibiting the complex to prevent downstream cascade
  2. antithrombin intervenes in many points of the cascade and stops activation of factors
  3. thrombomodulin binds to thrombin to stop its effects
42
Q

what is a thrombus?

A
  • an intracellular blood clot that can cause damage when ruptured
  • CVS must balance between pathological states of inadequate and overactive clotting
  • inadequate leads to extensive haemorrhage
  • overactive leads to vasculature problems
43
Q

what are the risk factors of deep vein thrombosis (DVT)?

A
  • venous stasis: slowing of flow in veins
  • vascular injury
  • hypercoagulability: coagulation occurs at heightened rate
44
Q

what is arterial thrombosis?

A
  • following erosion or rupture of atherosclerotic plague

- rupturing and flaking off into blood system will form blockage in smaller arteries

Physiology and Pharmacology (13 decks)

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