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Cardiac Physiology > Blood > Flashcards

Blood Flashcards

1
Q

Name the two phases of the blood.

A 
Cellular component (45%) i.e. red cells, white cells, platelets
Fluid component (55%) i.e. plasma
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2
Q

How many litres of blood do we have?

A

5 litres

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3
Q

What term is given to the volume of red blood cells we have?

A

Haematocrit

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4
Q

What is the normal haematocrit?

A

0.45

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5
Q

What is haemopoiesis?

A

The process of the production of blood cells and platelets which continue through life

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6
Q

Where does haemopoiesis occur in adults, children and in utero?

A

Bone marrow of axial skeleton in adults.

Bone marrow of all bones in children.

In utero occurs in yolk sac, liver and spleen

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7
Q

Give the lifetime of red blood cells.

A

120 days

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8
Q

Give the lifetime of white blood cells.

A

6 hours

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9
Q

Give the lifetime of platelets.

A

7-10 days

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10
Q

What condition will a patient have if precursor cells of red blood cells are found in blood?

A

Leukaemia

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11
Q

Which hormones stimulate red blood cells, white blood cells and platelets to proliferate?

A 
RBC = erythropoietin 
WBC = G-CSF (granulocyte colony stimulating factor)
Platelets = Tpo
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12
Q

Will the oxygen dissociation curve of RBC shift right or left when PH is decreased/temperature increased?

A

Shifts to the right. Hb’s affinity for oxygen decreases as it becomes denatured by acidic PH and higher temp.

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13
Q

Will the oxygen dissociation curve of RBC shift right or left when PH is increased/temperature decreased?

A

Shifts to the left. Hb’s affinity for oxygen increases when there is a lower partial pressure of CO2 and the cells will not need as much oxygen.

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14
Q

What term is given to a young red blood cell?

A

Reticulocyte

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15
Q

What does oxygen reversibly bind to within haemoglobin?

A

Fe2+ in haem

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16
Q

Describe the quaternary structure of haemoglobin.

A

2 alpha chains
2 beta chains
4 haem groups

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17
Q

Name the 4 blood groups and rank them in order of most common to least.

A

Most common: O
A
B
Most rare: AB

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18
Q

Which antibodies do type A individuals have?

A

Anti-B antibodies

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19
Q

Which antibodies do type B individuals have?

A

Anti-A antibodies

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20
Q

Which antibodies do type AB individuals have?

A

Neither anti-A nor anti-B antibodies as type AB has A + B antigens. Individuals are universal recipients.

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21
Q

Which antibodies do type O individuals have?

A

Both anti-A and anti-B antibodies as type O have no A or B antigens. Individuals are universal donors. O antigen is recessive.

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22
Q

What does rhesus positive mean?

A

D antigen is present

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23
Q

What general condition means a reduction in haemoglobin in blood?

A

Anaemia

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24
Q

What general condition means an increase in haemoglobin in blood?

A

Polycthaemia

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25
Q

Give the normal haemoglobin range.

A

12.5 - 15.5 g/dl

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26
Q

What are the symptoms of anaemia?

A

Tiredness
Malaise (discomfort)
Shortness of breath
Angina

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27
Q

What are the signs of anaemia?

A 
Glossitis (sore tongue)
Kylonychia (spoon shaped nails caused by iron deficiency) 
Angular stomatitis (cracking at corners of mouth)
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28
Q

Name some classifications of anaemia.

A

Iron deficiency
B12/folate deficiency
Haemolysis
Bone marrow failure

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29
Q

Describe iron deficiency anaemia.

A

Iron is needed for haemoglobin production. Lack of iron leads to reduced red cell production.

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30
Q

What is MCV (mean cell volume) a measure of?

A

Red cell size

Normal range = 82-6 fl

31
Q

What are the causes of iron deficiency anaemia?

A

Bleeding:
Occult gastrointestinal
Menorrhagia (heavy periods)

Diet

32
Q

Describe B12/folate deficiency anaemia.

A

Vitamin B12 and folate are needed for DNA synthesis. Without them, red cells cannot be made in the bone marrow.
Can lead to macrocytic anaemia.

33
Q

What are the causes of B12 deficiency?

A
  1. Stomach damage. Intrinsic factor produced by the parietal cells in the stomach is required for the absorption of B12
  2. Pernicious anaemia - an autoimmune condition. Causes antibodies to be made against parietal cells so less intrinsic factor is produced.
34
Q

What are the causes of folate deficiency?

A

Malabsorption e.g. coeliac disease

Diet - lack of fruit + veg

35
Q

What is haemolysis?

A

Normal or increased red cell production BUT decreased life span (<30 days)

36
Q

What are the causes of haemolysis?

A
  1. Congenital
    - Spherocytosis - blood cells are spherical so get stuck in vessels
    - Sickle cell anaemia - sickle shaped red cells, get trapped in vessels
    - Thalassaemia - mutation in haemoglobin chains
  2. Acquired
    - Immune system attacks own red cells - triggered by blood transfusion
    - Fragmentation of red cells by mechanical heart valve
    - Pregnancy - if mother has rhesus negative blood, and baby has rhesus positive, the mother will make antibodies that destroy the baby’s red cells i.e. rhesus disease
37
Q

Which hormone regulates the production of white blood cells?

38
Q

Name the most abundant white blood cell.

A

Neutrophil

39
Q

What is the lifespan of a neutrophil?

40
Q

What are the actions of neutrophils?

A
  1. They phagocytose and kill bacteria.

2. They release chemotaxins and cytokines for the inflammatory response

41
Q

Where are B lymphocytes made and stored?

A

Made: Bone marrow
Stored: Secondary lymphoid organs

42
Q

What is the action of a B lymphocyte?

A

Differentiate into plasma cells and produce immunoglobins when exposed to foreign antigen.

43
Q

Where are T lymphocytes made and stored?

A

Made: Bone marrow
Stored: Mature in thymus

44
Q

What is the action of a T lymphocyte?

A

Helper cells i.e. CD4, helps B cells in antibody generation

45
Q

Name some white cell conditions.

A

Acute leukaemia
Acute myeloblastic leukaemia
Acute lymphocytic leukaemia
High grade lymphoma

46
Q

Describe acute leukaemia.

A

Proliferation of precursor white blood cells without differentiation. Replaces normal bone marrow cells. Results in anaemia, neutropenia (infections due to no white cells differentiating) and thrombocytopenia (excessive bleeding).

47
Q

Describe acute myeloblastic leukaemia.

A

Malignant proliferation of the precursor myeloblasts (unipotent stem cells) in the bone marrow.

48
Q

Describe acute lymphocytic leukaemia.

A

Malignant proliferation of the lymphoblast precursor cells in the bone marrow.

49
Q

Describe high grade lymphoma.

A

Lymphocytes in lymph nodes become malignant. Classified as Hodgkins and non-Hodgkins.

50
Q

What are platelets?

A

Cytoplasmic anucleate cells

51
Q

Which cells in the bone marrow make platelets?

A

Megakaryocytes

52
Q

What is thrombocytopenia?

A

Reduced platelet numbers. Leads to increased bleeding

53
Q

What is thrombocytosis?

A

Increased platelet numbers. Leads to arterial and venous thrombosis which increases risk of heart attack and stroke.

54
Q

Which enzyme makes the platelet plug?

A

Thrombin. It cleaves fibrinogen.

55
Q

Which coagulation factors do platelets activate?

A

II, VII, IX, X (2, 7, 9, 10 so remember as 1972)

56
Q

Name some plasma proteins and their functions.

A

Albumin - maintains oncotic pressure
Carrier proteins - for nutrients + hormones
Immunoglobulins - antibodies produced by plasma cells

57
Q

Name some immunoglobulins.

A

IgG (most important)
IgM
IgA
IgE

58
Q

Which term is given to the arrest of bleeding?

A

Haemostasis

59
Q

What is thrombosis?

A

When blood clots inside a vessel

60
Q

What are proteins and platelets activated by?

A

Tissue factor. Present in all cells apart from endothelial cells. When endothelium is punctured, blood comes into contact with tissue factor and starts clotting.

61
Q

What type of genetic disorder is haemophilia?

A

Recessive X-linked

62
Q

What type of genetic disorder is haemophilia?

A

Recessive X-linked - only affects males

63
Q

Describe haemophilia A.

A

1/10,000 males
Deficiency in clotting factor VIII
Causes bleeding in muscles and joints
Treat with factor VIII

64
Q

Describe haemophilia B.

A

1/50,000 males
Deficiency in clotting factor XI
Causes bleeding in muscles and joints
Treat with factor XI

65
Q

What type of genetic disorder is Von Willebrands disease?

A

Autosomal dominant

66
Q

Describe Von Willebrands disease.

A

There is a lack of Von Willebrands Factor (VWF).
VWF is required for platelets to bind to damaged blood vessels. Lack of VWF leads to muco-cutaneous bleeding (bleeding in skin and mucous membranes) - bruises, nose bleeds, prolonged cut bleeding.

67
Q

Which vitamin is needed for the synthesis of coagulation factors?

68
Q

What causes a deficiency in vitamin K and how is this treated?

A

Malabsorption causes deficiency. Treated with IV vitamin K.

69
Q

Name 2 anticoagulant drugs.

A

Heparin and warfarin.

70
Q

Describe disseminated intravascular coagulation (DIC).

A

Involves microvascular thrombosis. This is where coagulation cascade occurs inside blood vessels, resulting in a deficiency of clotting factors and platelets as they’ve been used already.

71
Q

Describe how the platelet plug is formed.

A
  1. When a vessel is ruptured, the endothelium is disrupted.
  2. Collagen fibres are exposed. Platelets adhere to the collagen fibres via VWF.
  3. This binding tiggers the release of platelet dense granules which causes ADP to be released. ADP acts on P2Y1 and P2Y12, causing platelet amplification.
  4. ATP binds to P2X1 which also causes platelet amplification
  5. Thrombin binds to PAR1 and PAR4 receptors inducing platelet activation and further thrombin release - i.e. positive feedback
  6. Platelet activation leads to platelets changing shape from smooth to spiculated (spiky), increasing surface area
  7. Expression of glycoprotein IIb/lla receptors on the platelets increases and these bind to fibrinogen. Platelet aggregation occurs.
  8. All of these actions enable a platelet plug to be formed. Platelet plug seal small breaks in vessels.
72
Q

What is blood coagulation/clotting?

A

Transformation of blood into solid gel i.e. clot or thrombus. Supports platelet plug.

73
Q

Name the two pathways of the coagulation cascade.

A

Extrinsic and intrinsic

74
Q

How is a blood clot broken by the body?

A

Plasminogen is converted to plasmin which breaks fibrin down.

Cardiac Physiology (9 decks)

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