Haemostasis practical Flashcards

1
Q

Blood has 3 general functions

A
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2
Q

examples of transport function of blood

A

deliver oxygen and nutrients to cells

transport hormones to effector organs

remove metabolic waste products from cells

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3
Q

regulatory function of blood

A

absorb and districute body heat

naintain adequate fluid volume

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4
Q

protective function of blood

A

prevent blood loss via clotting

prevent infection

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5
Q

what is plasma

A

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.

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6
Q

Buffy coat

A

(<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).

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7
Q

erythrocytes

A

make up 45% of volume in males and ~42% in females. This value is called the haematocrit, or packed cell volume (PCV).

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8
Q

a reduced PVC means that

A

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.

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9
Q

what is the structure of a platelet

A

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.

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10
Q

function of platelets

A

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.

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11
Q

collagen binding, activates the platelets via

A

glycoprotein VI (GpVI)

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12
Q

how to activated platelets change?

A
  1. shape
  2. bind to each other
  3. release chemical mediators to support haemostasis
  4. Move PS (phosphatidylserine lipids) from the inner leaflet to the outer leaflet
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13
Q

explain how platelets change shape and spread across damaged tissue

A

they project pseudopodia, giving them a star shaped appearance

they increase their surface area for their interaction with damaged tissues and each other

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14
Q

explain activated platelets binding together- aggregation

A
  • 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
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15
Q

Why do platelets release chemical mediators? what do they release?

A

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

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16
Q

Explain the flipping of phosphatidylserine (PS) lipids

A
  • 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
17
Q

for a venous clot what drugs do you use

A

anticoagulation

18
Q

for an arterial clot what drugs should you use

A

antiplatelet

19
Q

what does haemostasis mean

A

arresting of bleeding

20
Q

what part of the blood vessel is occupied by platelets

A

closer to the vessel wall, away from the centre

21
Q

whta are the 3 steps of haemostasis:

A
  1. vascular spasm
  2. platelet plug formation
  3. coagulation
22
Q

explain vascular spasm

A

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

23
Q

name two chemical mediators relased by platelets that cause vasospasm

A

serotonine

thromboxan A2

24
Q

what are the 3 steps involved on platelet plug formation

A

adhesion

activation

aggregation

25
Q

explain the adhesion step in platelet plug formation

A

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

26
Q

explain the activation step of platelet plug formation

A

when they bind to collagen via the they are activated GPVI, changing shape and spreading out

27
Q

What do alpha granules contain

A

vWF, firbinogen, factor V and GPIIb/IIIa

28
Q

What is thromboxane originated from

A

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

29
Q

what is coagulation

A

the process of changing from a liquid to a solid

means that the primary secondary plug matures into a secondary one

30
Q

An inappropriately formed thrombus is called a

A

thrombosis

31
Q

2 kinds of thrombosis

A

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

32
Q

what is a bleeding diathesis and give 2 examples

A

A bleeding diathesis (predisposition or sensibility) is a tendency to bleed excessively. Inherited bleeding diatheses include:

Von Willebrand Disease and haemophilia A

33
Q

haemostasis pathway from vessel injjury to formation of stable blood thrombus

A

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

34
Q

What is thrombocytopaenia

A

low platelet count

35
Q

antithrombotic factors

A

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