blood and clotting

Question 1

what are the components of blood

Answer 1

-erytrocytes (RBC)
-leukocytes (type of WBC)
-platelets (for clotting blood)

Question 2

what’s plasma

Answer 2

-pale watery solution of electrolytes, plasma portend, carbohydrates and lipids

Question 3

what can colour variation of blood tell us

Answer 3

-pink: Hb released by heamolysis (RBC)
-brown/green: high bilirubin (RBC breakdown), liver or gall bladder issue
-cloudy: cryoglobulins (immunoglobin) which is aboral increase in viscosity leading to vessel obstruction and local thrombosis

Question 4

what are the principle proteins in blood

Answer 4

-albumin(largest protein component in blood): oncotic pressure, binds to steroids, T3, bilirubin, bile salts, FA
-fibrinogen )large role in clotting): precursor of fibrin
-immunoglobulins : humoral immunity from plasma/ B cells

Question 5

what are erythrocytes

Answer 5

-most abundant cell
-non-nucleated biconcave discs ,maximising SA:Vol
-mainly composed of haemoglobin
-shape main†lined by cytoskeleton anchored to plasma membrane

Question 6

what are the 3 functions of erythrocytes

Answer 6

-O2 carriage from lungs to systemic system
-CO2 carriage from tissues to lungs
-buffering of acids/bases

Question 7

what are the two different types of leukocytes

Answer 7

-granulocytes
-non-granular

Question 8

examples of granulocytes

Answer 8

-neutrophils- phagocytose bacteria
-eosinophils- combat parasites and viruses
-basophils- release IL-4, histamine, heparin snd peroxidase

Question 9

examples of non-granular leukocytes

Answer 9

-lymphocytes- matures into T cells and B cells (plasma cells)
-monocytes - macrophages and dendritic cells

Question 10

what is the feedback mechanism for platelets

Answer 10

-platelets also have receptors for TPO
-abundant platelets bind to TPO
-megakaryocytes not generated
-platelets not made
-receptors do not bind to TPO
-TPO stimulates megokaryocyte production
-platelets generated

Question 11

what does haemostasis mean

Answer 11

-prevention of haemorrhage

Question 12

how does haemostats prevent haemorrhage

Answer 12

1) vasoconstriction
2)increased tissue pressure- decreases transmural pressure
3) platelet plug (primary haemostasis)- transient to prevent further blood loss, small breaches in vascular endothelium
a: adhesion
b:activation
c: aggregation
4) clot formation (secondary haemostasis)- stabilisation of weak platelet plug with fibrin lading to semisolid mass of platelets and fibrin mesh with trapped cells and serum

Question 13

what do platelets consist of

Answer 13

-nucleus free-fragments
-mitochondria
-lysosomes
-peroxisomes
-alpha granules (VWF, fibrinogen, clotting factor, platelet derived growth factor)
-dense- core granules (ATP, ADP Ca2+)
-external coat rich in platelet receptors
-tubulin micortubules maintains discoid shape leads to a dynamic shape change in activation
-cytoskeleton contains actin and myosin: dispersed at rest, dynamic shape change in activation and clot retraction

Question 14

what happens during platelet plug formation: platelet adhesion

Answer 14

-rapid temporary seal to prevent further blood loss
-damage to endothelium exposes subendothelial collagen (most thrombogenic)
-plasma VWF binds to exposed collagen and platelet receptors
-platelets adhesion mediated by platelet receptors
-further endothelial cell VWF released leading to additional links
-binding of platelet receptors leads to cascade of IC events and therefore activation

Question 15

what happens during platelet plug formation: platelet activation

Answer 15

-intracellular signalling cascade initiates:
= secretion/ exocytosis of dense and alpha granules: VWF increases platelet adherence and activation, as well as ADP with thromboxane further activation
=secretion platelet derived growth factor leads to cell proliferation/ wound healing
=thromboxane leads to vasoconstriction and inflammation
=cytoskeleton changes: lamellipodium/filopodia
=expression of fibrinogen receptors

Question 16

what happens during platelet plug formation: platelet aggregation

Answer 16

-platelet fibrinogen receptors bind to plasma fibrinogen
-this forms molecular bridges between platelets leading to aggregation (forms a plug)
-plugs breach in endothelium
-eventually actin and myosin contract leading to a more compact platelet plug

Question 17

what happens during blood clot formation

Answer 17

-slower, complex process involving cascade of clotting factors with a more permanent fibrin mesh
-blood clot= semisolid mass
-activation triggers chain reaction converting precursors leading to activated factors
-controlled proteolysis amplifies clotting signals

Question 18

what are the 2 ways clotting can occur

Answer 18

-intrinsic pathways (slower, contact activation)
-extrinsic pathway (trauma/inflammation)

Question 19

what’s the intrinsic pathway

Answer 19

-initiated by factors within blood in contact with the negatively charged membrane surface of the activated platelet
-cascade of protease reactions
-positive feedback acts at several upstream levels, ending in activated factor Xa

Question 20

what’s the extrinsic

Answer 20

-triggered by injury to endothelium which allows tissues factor (receptor) in sub endothelial cells to become activated when blood factor VII in contact
-results in activated factor Xa

Question 21

what’s the common pathway for both intrinsic and extrinsic pathway

Answer 21

-factor Xa from both pathways enters common pathway top generate thrombin (enzyme) and produce stable fibrin

Question 22

how do homeostatic mechanisms prevent haemostasis

Answer 22

-promotion of anti-thrombotic state
-promotion of pro-thrombotic state

Question 23

what occurs in the promotion of anti-thrombotic state

Answer 23

-normal endothelial cells maintain normal blood fluidity through paracrine factors and anticoagulant factors (acting locally)
-paracrine factors- e.g. prostacyclin promotes vasodilation, nitric oxide inhibit platelet adhesion and aggregation
-many anti-coagulant factors (including thrombomodulin- complexes with thrombin)

Question 24

what occurs in the promotion of pro-thrombotic state

Answer 24

-event of vascular damage
-hypoxia (lack of oxygen)- expression of procoagulants (if damage to blood vessels, no blood can be given to them)

Question 25

what happens with normal blood flow

Answer 25

-in a cylindrical blood vessel, laminae of blood form concentric cylinders
-velocities increase from wall to centre (thin layer next to wall cannot move)
-laminar flow leads to parabolic profile with maximal velocity at centre
-abnormal blood flow leads to endothelial injury
-turbulent flow caused by local stenosis, large radius, high velocity

Question 26

what’s thrombus in pathology

Answer 26

-thrombus- intravascular blood clot
-arterial thrombosis- following erosion or rupture of atherosclerotic plaque

Question 27

what’s vichrow triad

Answer 27

-primary risk factors are
=abnormal blood flow
=endothelial injury leading to platelet activation
=hypercoagulability