Blood practical Flashcards

1
Q

Blood’s transport function

A

1) deliver oxygen and nutrients to cells
2) Transport hormones to target organs
3) Remove metabolic waste products from cells

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2
Q

Regulatory function of blood

A

1) Absorb and distribute body heat
2) Maintain adequate fluid volume

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3
Q

Protective function of blood

A

1) Prevent blood loss via clotting
2) Prevent infection

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4
Q

Components of blood

A

Plasma- cell-free, contains proteins, ions and molecules.

Buffy coat- thin white layer seen between RBCs and plasma after centrifution. Contains platelets and leukocytes.

Erythrocytes- haematocrit or packed cell volume

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5
Q

Meaning of a reduced PCV

A
  • Patient has fewer RBCs
  • Blood therefore has a reduced carrying capacity than normal and HR and CO may increase to try and compensate.
  • Reduced viscosity of blood
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6
Q

Structure of a platelet

A

Anucleate cells

Biconcave discs

Contain granules that contain substances crucial for haemostasis

Contain functional mitochondria

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7
Q

Initial function of platelets

A

Rapid response to vessel injury

Accumulate and bind to exposed collagen in wall and surrounding

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8
Q

How are platelets activated?

A

1) Exposed collagen binds via GP Ia/IIa (receptor for collagen)
2) soluble agonists released by activated cells such as
(1) ADP
(2) thromboxane A2 (TxA2)
(3) thrombin

trigger platelet activation through GPCR

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9
Q

How do activated platelets change function?

A

1) Change shape and spread across damaged tissue
2) Activated platelets aggregate (bind together)
3) Release chemical mediators to support haemostasis, promote further platelet activation and recruit adittional circulating platelets
4) Move phosphatidylserine (PS) lipids from the inner leaflet of their memebrane to the outer leaflet.

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10
Q

How do platelets change shape

A

Become activated then become star shaped and increase their surface area

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11
Q

Process of platelet aggregation

A

mediated by fibrinogen binding to platelet receptors GPIIIb / IIIa

Each fibrinogen molecule has 2 spatially distant binding sites for platelets and can therfore bind 2 at once. This cross linking sustains aggregation.

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12
Q

What chemical mediators do platelets produce?

A

Thromboxane (TxA2 )

ADP

Arachidonic acid

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13
Q

Thrombaxane TxA2

A

Produced by platelets during haemostasis

has prothrombotic properties by activating platelets

circulating fibrinogen binds thromboxane receptors on platelets activating them.

Vasoconstrictor

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14
Q

ADP (adenosine diphosphate)

A

Platelet agonist

causes platelet shape change, aggregation and generte thromboxane

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15
Q

Effect of platelets moving PS lipids

A

By flipping PS lipids from the inner leaflet of their membrane to the outside leaflet (Platelets) they are engaging in procoagulant activity.

Negatively charged PS provides a scaffold on wjich coagulation factors accumulate in a Ca2+ dependant manner.

Therefore, platelets help localise and activate coagulation factors at the site of injury

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16
Q

Platelet production

A

Thrombopoietin stimulates megakaryoblasts –> megakarypcyte –> plasma membrane invades cytoplasm, dividing it into compartments

Cell then ruptures and the compartments become cells

17
Q

What part of the vessel are platelets found

A

Borders

18
Q

3 steps of haemostasis

A

1) vascular spasm (vasoconstriction to reduce BF)
2) Platelet plug formation
3) Coagulation

19
Q

Vascular spasm

A

Local vasoconstriction

Triggered by the damage itself as well as chemicals released by endothelial cells and platelets (e.g. serotonine and thromboxane)

20
Q

3 steps of platelet plug formation

A

1) adhesion
2) activation
3) aggregation

21
Q

adhesion step of platelet plug formation

A

platelets are slowed and captured at the site of injury by von Willebrand Factor (vWF simultaneosly bonds to collagen and platelets).

Platelet adhesion to collagen is mediated by the platelet receptor GpVI

22
Q

Activation step of platelet plug formation

A

When platelets bind to collagen, they become activated (mediated by glycoprotein VI receptor)

Change shape and spread out

PS lipids relocate from the inner aspect of the platelet membrane to the outside, creating a negative framweork for the coagulation factors to stick to

23
Q

Arachidonic acid

A

Produced by plateletes

converted to thromboxane A2 by COX and thromboxane synthase

24
Q

Aggregation step of platelet plug formation

A

mediated by the binding of fibrinogen to activated GPIIb/IIIa on the surface of platelets thereby cross-linking them. As more platelets arrive in the circulation, they are activated by released ADP and TxA2, and aggregate to platelets already in the plug. This leads to the formation of a primary haemostatic plug.

25
Q

Arterial thrombosis

A

platelet rich

responsible for the thrombi in coronary arteries

26
Q

venous thrombosis

A

rich in fibrin

red thrombi due to the number of RBC trapped in

DVT and PE

27
Q

Order of events from vessel injury to formation of stable blood thrombus

A

vessel injury

platelets adhere to sub-endothelial collagen

platelet activation

adherent platelets release bioactive mediators (ADP and TxA2)

platelet aggregation with formation of primary haemostatic plug

coagulation factors accumulate on activated platelets

conversion of prothrombin to thrombin

conversion of soluble fibrinogen to insoluble fibrin

28
Q

Name 3 factors or receptors that help platelet adhesion to damaged tissue

A

Integrin a2B1

Glycoprotein Ib (GpIb)

von Willebrand factor

29
Q

Thrombocytopaenia

A

high platelet count

30
Q

thrombocytopenia

A

low platelet count

sign is petechiae

31
Q

Prothrombotic factors

A

Long periods of immobility

Combined oral contraceptive pill

more…?

32
Q

Anti-thrombotic factors

A

Vitamin k deficiency- some coagulation factors are dependant (II, VII, IX and X)

Haemophilias

Aspirin