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Cardiovascular phase 1 > 2.4 The blood > Flashcards

2.4 The blood Flashcards

1
Q

What is hyperaemia?

A

An increased blood flow to tissues.

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2
Q

What is the cause of active hyperaemia?

A

When blood flow increases due to increased metabolic activity.

Increased metabolic activity - decreased oxygen - increased metabolites - arteriolar dilation - increases blood flow.

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3
Q

What is the cause of reactive hyperaemia?

A

When blood flow increases following blockage (occlusion) to arterial flow.

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4
Q

Describe the composition of blood…

A

Plasma - 55%
Body cells - 45%

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5
Q

What is the structure of Hb?

A

2 alpha and 2 beta chains. 4 haem groups.

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6
Q

What is the process of the production of RBC’s?

A

Erythropoiesis

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7
Q

Describe the hormonal factor of erythropoiesis…

A

Hormonal stimulating factor: Erythropoietin

Made in the kidneys
Constant low level release but also in response to hypoxia.

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8
Q

What is the process of the production of WBC’s?

A

Myelopoiesis

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9
Q

Describe the hormonal factor of myelopoiesis…

A

Hormonal factor: Granulocyte - macrophage colony

Will only stimulate production of myeloblastic WBC and not lymphoid cells.

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10
Q

What is the process of the production of platelets?

A

Thrombopoiesis

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11
Q

Describe the hormonal factor of thrombopoiesis…

A

Hormonal factor: thrombopoiesis

Leads to increased production of megakaryocytes which platelets bud off from.

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12
Q

What is anaemia?

A

Deficiency of heamoglobin.

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13
Q

Describe anaemia levels for males and females…

A

Male hb level <130g/L
Female hb level <110g/L

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14
Q

What are the signs and symptoms of anaemia?

A

Pallor (paleness),
tachycardia (increased HR),
hyperventilation (rapid breathing),
angina in older people,
malaise (discomfort feeling).

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15
Q

What are the causes of anaemia?

A

acute blood loss,
increased removal of RBC,
deficiencies of iron, folate, or vitamin b12.

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16
Q

What are leukocytes?

A

White blood cells which defend the body against disease.
There are 2 main groups: Granulocytes and lymphocytes.

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17
Q

Describe granulocytes…

A

Neutrophil - the most abundant WBC. Phagocytic and release chemo and cytokines to induce inflammation.

Monocytes - Mature into either macrophages or dendritic cells which are both antigen presenting cells.

Basophils - mature in to mast cells. Release histamine and has a role in allergies and immunity.

Eosinophils - role in fighting parasitic infections and a range of regulatory functions.

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18
Q

Describe lymphocytes…

A

Comprise of B and T cells.
They are differentiated based on the site of maturation and the receptors and glycoprotein markers they express leading to function.

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19
Q

Describe T lymphocytes:
Origin and site of maturation
Proportion in blood
Surface receptors
Function

A

Origin : Bone marrow
Site of maturation: Thymus gland
Proportion in blood: 80%
Surface receptor: T cell receptor
Functions: cytotoxic, helper cells, regulatory functions

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20
Q

Describe B lymphocytes:
Origin and site of maturation
Proportion in blood
Surface receptors
Function

A

Origin and site of maturation: Bone marrow
Site of maturation: 20%
Surface receptor: B cell receptor
Functions: Generation of antibodies.

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21
Q

What are the roles of lymphatics in acute inflammation?

A

Lymphatics drain exudate(fluid that leaks out of blood vessels) and carry antigens.

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22
Q

Describe plasma…

A

A transportation medium which contains water, salt, glucose and proteins.

55% of blood fluid component

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23
Q

What are the proteins in blood plasma?

A

Albumin,
carrier proteins,
coagulation proteins,
immunoglobulins.

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24
Q

Describe Albumin…

A

Produced in the liver
Determines oncotic pressure of blood.
Keeps intravascular fluid within that space.

Lack of albumin leads to oedema.

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25
Q

What is serum?

A

Blood plasma without any clotting factors.

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26
Q

Why might someone with liver injury experience prolonged bleeding time?

A

Because the liver produces clotting factors.

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27
Q

What is exposed if you damage the endothelium of a vessel?

A

Underlying connective tissue and collagen.

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28
Q

What are platelets made from, and where are they made?

A

Made in the bone marrow from megakaryocytes.

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29
Q

Why is blood a fluid inside vessels?

A

Platelets and proteins of the coagulation cascade circulate in an inactive state

Endothelial cells, anticoagulant pathway and fibrinolytic pathways ensure fluidity.

30
Q

What is thrombosis

A

Clotting inside the vessel

31
Q

Describe haemostasis

A

Process to stop bleeding.

There are 2 phases:
- Primary haemostasis - forms an unstable platelet plug at the site of injury.

  • Secondary haemostasis - coagulation cascade
32
Q

How do platelets adhere to collagen fibres?

A

Via intermediary Von Willebrand factor (vWF) through the platelet receptor, GP1b.

33
Q

What factors cause platelet activation?

A

Binding of platelets to collagen fibres triggers the release of the contents of their secretory vesicles via exocytosis

Platelet binding to collagen leading to the release of thromboxane a2

Thrombin binds to PAR1 leading to the release of ADP from dense granules and PAR4

Autocrinal or free thromboxane a2 binds to TPalpha

34
Q

What are the effects of platelet activation?

A

The change shape: smooth to spiculated.

This increases their surface area.

New platelets adhere to old ones = platelet aggregation.

This forms a platelet plug.

35
Q

What do activated platelets synthesise?

A

Thromboxane A2.

36
Q

What is the function of Thromboxane A2 (TXA2)?

A

It leads to further platelet aggregation.

37
Q

What is the role of vWF?

A

vWF binds to collagen and platelets bind to vWF.

38
Q

Briefly describe primary hemostasis (platelet plug formation):

A
  1. Endothelial injury- healthy endothelium releases 2 things which keep blood vessels open (NO and prostacyclin) causing vasodilation.
    Injured endothelium release endothelin-1 which causes vasoconstriction.
  2. Exposure- when the blood vessel is damaged, collagen fibres below endothelium is exposed. The damaged cells release VWF which binds to collagen.
  3. Adhesion - VWF (factor 8) binds to collagen using glycoprotein 18 (GPB1) receptor.
  4. Activation- platelet changes shape which releases more VWF, Ca2+, serotonin, ADP, thromboxane A2, resulting in GP11B/IIA expression.
  5. Aggregation - GP11B/11A binds to fibrinogen which links platelets together = platelet plug.
39
Q

What does the coagulation cascade do?

A

Helps stabalise the plug by forming a mesh of fibrin over the primary platelet plug.

It converts soluble fibrinogen into fibrin which then forms a stable fibrin clot.

40
Q

What are the platelet receptors for fibrinogen?

A

glycoprotein IIb/IIIa. Fibrinogen forms ‘bridges’ between platelets.

41
Q

What is the essential component of a blood clot?

A

Fibrin

42
Q

Describe the extrinsic pathway of the coagulation cascade…

A

Damage to the endothelial tissue exposes the tissue factor to the blood which activates factor vii.

Factor vii then has a direct effect on factor x to initiate the common pathway of the coagulation cascade.

43
Q

Describe the intrinsic pathway of the coagulation cascade…

A

Factor xii is exposed to collagen.

Factor x is then activated by ixa along with co-factors (ca2+, phospholipids and viii).

44
Q

What is the common pathway in the coagulation cascade?

A

Xa converts prothrombin (factor ii) into thrombin (factor iia).
Thrombin converts fibrinogen (i) into fibrin (ia) and activates factor xiii.
Fibrin and factor xiii leads to the cross linking of fibrin and a clot.

45
Q

Briefly describe the Fibrinolytic system.

A

Plasminogen is converted into plasmin. Plasmin cuts the fibrin at various places leading to the formation of fragments.

46
Q

What is the purpose of the fibrinolytic system?

A

It acts to prevent blood clots from growing and becoming problematic.

47
Q

In haemostasis what is prothrombin converted into?

A

Thrombin.

48
Q

Give 3 functions of Thrombin.

A
  1. Converts fibrinogen into fibrin.
  2. Activates factor XIII into XIIIa.
  3. Has a positive feedback effect resulting in further thrombin production.
49
Q

What does an undamaged endothelium release in order to prevent platelet activation in undamaged areas?

A

Prostacyclin (inhibits platelet aggregation) and NO (inhibits platelet adhesion).

50
Q

What is released upon cell activation and contains a high concentration of a molecule that acts as an agonist at the platelet P2Y12 receptor?

A

Platelet dense granules.

51
Q

What is the role of fibrinogen in platelet aggregation?

A

It forms cross-links between aggregating platelets.

52
Q

Give 2 reasons why the liver is important in clotting.

A
  1. The liver produces many clotting factors.
  2. The liver produces bile salts that are needed for vitamin K absorption. Vitamin K is needed for clotting factor production.
53
Q

When are the platelet receptors for fibrinogen exposed?

A

During platelet activation.

54
Q

What is Virchow’s triad?

A

It describes 3 categories thought to contribute to thrombosis.

55
Q

What are the 3 categories of Virchow’s triad?

A
  1. Stasis of blood flow.
  2. Endothelial injury.
  3. Increased coagulation ability.
56
Q

What are the 2 main erythrocyte antigens?

A

ABO
Rhesus

57
Q

Which of the ABO blood groups is recessive?

A

O, A and B are co-dominant.

58
Q

Why is the O blood group a universal donor?

A

It has no A or B antigens.

59
Q

Describe type A blood…

A

40%
Has anti-B antibodies.
More common than B.
Can be A+ or A-

A+ accepts (A+, A-, O+, O-)

A- accepts (A-, O-)

60
Q

Describe type B blood…

A

12%
Has anti-A antibodies.
Can be B+ or B-

B+ accepts (B+, B-, O+, O-)

B- accepts (B-, O-)

61
Q

Describe type AB blood…

A

3%
Universal acceptor/recipient
Has no antibodies
A and B antigens on RBC

62
Q

Describe type O blood…

A

45%
Universal donor
Has both anti-A and anti-B antibodies.
Has no A/B antigens on RBC.

63
Q

How do you determine ABO blood group?

A

Test using antibodies

64
Q

Describe how testing for the presence of antibodies against A or B antigens will determine someones blood group?

A

The presence of antibodies in the blood will indicate that this person does not have these antigens on their RBC’s. For example, if a persons blood is found to contain antibodies against the B antigen then they can’t be of the AB or B blood groups.

65
Q

Describe how testing using antibodies will determine someones blood group?

A

If the antibodies bind it indicates the presence of a specified antigen. For example, if antibodies against the B antigen bind to the patients RBC then the person must be of either the AB or B blood groups.

66
Q

What is one difference between Immunoglobulin antibodies and rhesus antibodies?

A

Rhesus antibodies can cross the placenta whereas the immunoglobulin antibodies cannot.

67
Q

What antigens are part of the rhesus blood group system

A

C,D, and E antigens.

68
Q

Describe the D/d antigen of the rhesus blood group

A

D/d is the most important
It is a null gene, so no protein (anti-d is non-existent)
15% of the population is dd so they don’t have the protein.

69
Q

What problems can arise if a pregnant lady is found to be rhesus D negative?

A

If exposed to D RBC’s the lady will have antibodies against the D antigen. The antibodies can cross the placenta and cause haemolysis of the babies red blood cells. This can result in in-utero death.

70
Q

What can be given to rhesus D negative mothers to prevent sensitisation?

A

Anti-D.

Cardiovascular phase 1 (9 decks)

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