Haemostasis practical Flashcards
Blood has 3 general functions
examples of transport function of blood
deliver oxygen and nutrients to cells
transport hormones to effector organs
remove metabolic waste products from cells
regulatory function of blood
absorb and districute body heat
naintain adequate fluid volume
protective function of blood
prevent blood loss via clotting
prevent infection
what is plasma
it makes up 54% of blood volume
is the cell-free component of blood. It contains proteins, molecules and ions. Its pale-yellow colour comes from bilirubin.
Buffy coat
(<1% of volume) is the thin white layer that is observed between plasma and red cells after the centrifugation of blood. It contains leukocytes (white blood cells) and thrombocytes (platelets).
erythrocytes
make up 45% of volume in males and ~42% in females. This value is called the haematocrit, or packed cell volume (PCV).
a reduced PVC means that
Patient has fewer RBCs. Their blood therefore has a reduced carrying capacity than normal and her heart rate and cardiac output may increase to compensate. The viscosity of the blood will also be reduced. Conversely, an increased PCV increases the viscosity increasing the force (afterload) required to pump blood around the body.
what is the structure of a platelet
Platelets are anucleate cells and are the smallest formed element in blood.
They are bi-convex discs (smartie-shaped) with a maximum diameter of approx. 2-3 micrometres. They are approx. 1/10 the size of RBCs by volume. Platelets contain granules that contain a variety of substances important in haemostasis.
They also contain functional mitochondria. Platelet lifespan is approx. 7-10 days.
function of platelets
Play an essential role in haemostasis. They respond rapidly when a blood vessel in injured.
Within seconds, platelets accumulate at the site of injury and bind to exposed collagen in the vessel wall and surrounding tissue.
collagen binding, activates the platelets via
glycoprotein VI (GpVI)
how to activated platelets change?
- shape
- bind to each other
- release chemical mediators to support haemostasis
- Move PS (phosphatidylserine lipids) from the inner leaflet to the outer leaflet
explain how platelets change shape and spread across damaged tissue
they project pseudopodia, giving them a star shaped appearance
they increase their surface area for their interaction with damaged tissues and each other
explain activated platelets binding together- aggregation
- process is mediated by fibrinogen binding to the platelet receptor GPIIb/IIIa
- this receptor is usually present in high concentrations but has a low affinity for fibrinogen until it is activated and changes its conformation
- each fibrinogen molecule can bind to and activate 2 platelets simultaneously- cross linking
- the GPIIB/IIIa receptor is an important target for therapeutic anti-platelet drugs
Why do platelets release chemical mediators? what do they release?
to support haemostasis
promote further platelet activation
recruit additional circulating platelets
most important mediators are:
ADP (released from dense granules)
TxA2 (synthesised de novo by COX and thromboxane synthase enzymes)
they both activate other platelets and cause aggregation at the site of injury- aiding in the production of thr primary haemostatic plug
Explain the flipping of phosphatidylserine (PS) lipids
- moving PS lipids from the inner leflet to the outer membrane exposes the PS lipids
- they are negatively charged and provide a scaffold on whjich coagulation factors can accumulate in a Ca2+ manner
- this supports the localisation and activation of coagulation factors at the site of injury
for a venous clot what drugs do you use
anticoagulation
for an arterial clot what drugs should you use
antiplatelet
what does haemostasis mean
arresting of bleeding
what part of the blood vessel is occupied by platelets
closer to the vessel wall, away from the centre
whta are the 3 steps of haemostasis:
- vascular spasm
- platelet plug formation
- coagulation
explain vascular spasm
local vasoconstriction in response to vessel injury to reduce the speed and volume of blood extravasating
triggered by injury itself as well as chemicals relased from endothelial cells and platelets
name two chemical mediators relased by platelets that cause vasospasm
serotonine
thromboxan A2
what are the 3 steps involved on platelet plug formation
adhesion
activation
aggregation
explain the adhesion step in platelet plug formation
platelets are slowed down and captured at the site of injury via an interaction with von Willebrand factor (bonds to collagen and platelets)
platelets then bind directly to collagen by receptor GPIIIb/IIa
explain the activation step of platelet plug formation
when they bind to collagen via the they are activated GPVI, changing shape and spreading out
What do alpha granules contain
vWF, firbinogen, factor V and GPIIb/IIIa
What is thromboxane originated from
it is synthesised de novo from released arachidonic acid via COX and thromboxane synthase
it is an agonist at TP receptors causing platelet activation and vasoconstriction
what is coagulation
the process of changing from a liquid to a solid
means that the primary secondary plug matures into a secondary one
An inappropriately formed thrombus is called a
thrombosis
2 kinds of thrombosis
arterial- platelet rich (white thrombi) and are responsible for thromboses in coronary arteries resulting in MI and thrombotic stroke
venous- tend to be rich in fibrin (red- due to RBC) and form in deep vein thrombosis, these are the kind that typically cause PE
what is a bleeding diathesis and give 2 examples
A bleeding diathesis (predisposition or sensibility) is a tendency to bleed excessively. Inherited bleeding diatheses include:
Von Willebrand Disease and haemophilia A
haemostasis pathway from vessel injjury to formation of stable blood thrombus
platelets adgere to sub-endothelial collagen
platelet activation via GPIIb/IIIa receptor
adherent platelets relase mediators ADP and TxA2
platelet aggregation with formatin of primary haemostatic plug
coagulation fac tors accumualte on activated platelets
conversion of prothrombin FII to thrombin IIa
conversion of soluble fibrinogen to insoluble fibrin Ia
What is thrombocytopaenia
low platelet count
antithrombotic factors
some coagulation factors are K+ dependant (II, VII, IX and X), having a K+ deficiency can lead to excessive bleeding
haemophilias are genetic disorders that impair the blood’s ability to coagulate
aspirin is an irreversible COX inhibitor- preventinf platelets from synthesising TxA2 from arachidonic acid
