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Phase 1 Med (Liv) > Cardiovascular (summary Sheets) > Flashcards

Cardiovascular (summary Sheets) Flashcards

1
Q

What are the two phases of blood?

A
  • Cellular component

- Fluid component

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2
Q

What does the cellular component of the blood consist of?

A

Red cells (99%), white cells and platelets

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3
Q

What does the fluid component of the blood consist of?

A

Plasma

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4
Q

What is an estimate of the volume of blood in the body?

A

5 litres

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5
Q

What is a haematocrit?

A

The volume of red blood cells i.e. haemoglobin in the blood

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6
Q

What is a normal haemocrit level?

A

0.45

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7
Q

What is haemopoiesis?

A

The process of production of blood cells and platelets which continues throughout life

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8
Q

Where does adult haemopoiesis occur?

A

Bone marrow

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9
Q

Where does embryonic/early life haemopoiesis occur?

A

Sites other than the bone marrow

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10
Q

What are the most primitive cells in the blood?

A

Stem cells

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11
Q

What do stem cells do in the bone marrow?

A

Proliferate and differentiate into mature cells

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12
Q

What is an erythrocytes lifespan?

A

120 days

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13
Q

What is a platelets lifespan?

A

7-10 days

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14
Q

What is a white blood cell lifespan?

A

6 hours

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15
Q

Name two cells of the blood which are anucleate

A

Erythrocytes and platelets

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16
Q

Where are the precursor cells of erythrocytes located?

A

Bone marrow

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17
Q

In which bones is the bone marrow stored, which contains the precursor to erythrocytes in adults?

A

Axial skeleton - skull, ribs, spine, pelvis and long bones

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18
Q

In which bones is the bone marrow stored, which contains the precursor to erythrocytes in children?

A

All bones

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19
Q

In which bones is the bone marrow stored, which contains the precursor to erythrocytes in utero?

A

Yolk sac, then liver and spleen

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20
Q

What abnormality of the blood could be a sign of leukaemia?

A

If precursor cells are found in the blood - they shouldn’t be in the blood of someone healthy

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21
Q

What is the function of hormonal growth factors?

A

Stimulate precursor stem cells to proliferate and differentiate

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22
Q

What is the hormonal growth factor for erythrocytes and where is it made?

A

Erythropoietin - made in the kidney

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23
Q

What is the hormonal growth factor of white cells?

A

G-CSF (granulocyte colony stimulating factor)

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24
Q

What is the hormonal growth factors for platelets?

A

TPO

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25
Q

Give 2 times when the oxygen dissociation curve shifts right

A
  • Decrease in pH

- Increase in temperature

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26
Q

Give two times when the oxygen dissociation curve shifts left

A
  • Increase in pH

- Decrease in temperature

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27
Q

Why do simple cells have a short life span?

A

They have no nucleus or mitochondria, therefore can’t repair themselves

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28
Q

What is the name of a young red blood cell?

A

Reticulocyte

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29
Q

What does a reticulocyte consist of?

A

A membrane (to enclose haemoglobin), enzymes of glycolysis and haemoglobin

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30
Q

What is the primary function of haemoglobin?

A

Carries oxygen from lungs to tissues, where it transfers oxygen to myoglobin in muscles

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31
Q

How does binding occur in haemoglobin?

A

Oxygen binds to Fe2+ in haem reversibly

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32
Q

What is the structure of haemoglobin?

A
  • 2 alpha and 2 beta chains & 4 haem groups

- quaternary structure due to more than 2 tertiary structures

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33
Q

Which antibodies do those with type A blood have? Is this blood type dominant?

A
  • Anti-B antibodies in the blood

- A antigen in co-dominant

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34
Q

Which antibodies do those with type B blood have? Is this blood type dominant?

A
  • Anti-A antibodies in the blood

- B antigen is codominant

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35
Q

Which antibodies do those with type AB blood have?

A
  • Neither anti-A nor anti-B antibodies in the blood

- Has A & B antigens on surface of red blood cells

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36
Q

Which antibodies do those with type O blood have? Is this blood type dominant?

A
  • Has both anti-A and anti-B antibodies in the blood

- O antigen is recessive

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37
Q

What are the anti-A and anti-B antibodies known as?

A

Anti-erythrocyte (natural) antibodies

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38
Q

In a wrong transfusion, what causes issues?

A

The destruction of transfused cells

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39
Q

In terms of the D antigen, what does it mean if someone is rhesus positive?

A

The D antigen is present

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40
Q

In terms of the D antigen, what does it mean if someone is rhesus negative?

A

The D antigen isn’t present

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41
Q

What is anaemia?

A

Reduction in haemoglobin in the blood

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42
Q

What is a normal level of haemoglobin?

A

12.5-15.5 g/dL

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43
Q

What happens when levels of haemoglobin are lower than they should be?

A

Anaemia

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44
Q

What happens when levels of haemoglobin are higher than they should be?

A

Polycthaemia

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45
Q

Give 3 symptoms of anaemia

A
  • Tiredness
  • Lethargy
  • Shortness of breath on exertion
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46
Q

Give 3 signs of anaemia

A
  • Pink hands
  • Sore tongue
  • Cracking at corners of the mouth
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47
Q

What are the different classifications of anaemia?

A
  • Iron deficiency
  • Folate deficiency
  • Haemolysis
  • Bone marrow failure
  • Of chronic disorder
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48
Q

What is the principle behind iron deficiency anaemia?

A
  • Iron needed for haemoglobin production

- Reduced production of red blood cells

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49
Q

What is a red cell size also a measure of?

A

Mean cell volume

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50
Q

What is a normal MCV level?

A

82-96 fl

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51
Q

What are the two conditions for iron deficiency anaemia?

A
  • Low haemoglobin

- Lower than normal MCV

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52
Q

Give the two main causes of iron deficiency anaemia

A
  • Bleeding

- Dietary

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53
Q

What is Macrocytic anaemia?

A

When erythrocytes are larger than normal

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54
Q

What causes Macrocytic anaemia?

A

A folate/B12 deficiency

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55
Q

What is the pathology behind Macrocytic anaemia?

A

Less B12/folate —> RBCs can’t be made by bone marrow —> less are released —> anaemia

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56
Q

Name a cause of B12 deficiency in the stomach

A
  • Intrinsic factor is required for B12 absorption

- Damaged stomach —> less parietal cells —> less intrinsic factor —> less B12 —> anaemia

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57
Q

What is pernicious anaemia?

A

Causes antibodies to be made against parietal cells, so less intrinsic factors

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58
Q

Give 3 causes of folate deficiency

A
  • Malabsoprtion
  • Dietary e.g. not enough fruit/veg
  • Increase in need e.g. haemolysis/increased cell division
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59
Q

What is haemolysis?

A

Normal/increased cell production but decreased life span

60
Q

Give 3 causes of congenital haemolysis

A
  • Membrane issues
  • Enzyme issues
  • Haemoglobin issues
61
Q

Give 3 causes of acquired haemolysis

A
  • Autoimmune
  • Mechanical
  • Pregnancy
62
Q

What is rhesus disease of pregnancy?

A
  • Mum RhD negative and 1st baby RhD positive
  • RhD positive seen as foreign to mother —> antibodies made. Doesn’t affect this baby.
  • Mother sensitised to RhD positive blood
  • 2nd baby RhD positive —> antibodies work ASAP, giving newborn anaemia/jaundice
63
Q

Where do WBCs mature?

A

Bone marrow

64
Q

What is the pathway to form a WBC?

A

Stem cells —> immature precursor cells —> WBCs

65
Q

How is the rate of production of WBCs controlled?

A

By the hormone G-CSF

66
Q

What is the most numerous WBC?

A

Neutrophils

67
Q

What are the two function of neutrophils?

A
  • Phagocytose and kill bacteria

- Release chemotaxins (initiates more WBC to come) and cytokines (inflammatory response)

68
Q

What results with a lack of neutrophils?

A

Recurrent bacterial infections

69
Q

What are the two types of lymphocytes?

A

B and T cells

70
Q

What is the function of lymphocytes?

A
  • Vital to immunity
  • Some generate antibodies against specific foreign antigens
  • Immunological memory
71
Q

Where are B lymphocytes produced?

A

Bone marrow

72
Q

Where are B lymphocytes stored?

A

Secondary lymphoid organs

73
Q

How do B lymphocytes work?

A
  • Differentiate into plasma cells

- Produce immunoglobulins when stimulated by exposure to foreign antigen

74
Q

Where are T lymphocytes made and where do they mature?

A
  • Made in bone marrow

- Mature in thymus

75
Q

What are the two types of T cells?

A
  • Antibody generation/cell mediated immunity

- Cytotoxic cells

76
Q

Name 4 white cell conditions

A
  • Acute leukaemia
  • Acute myeloblastic leukaemia
  • Acute lymphocytic leukaemia
  • High grade lymphoma
77
Q

What do platelets determine?

A

Bleeding time —> PT (prothrombin time)

78
Q

What are platelets?

A

Small cytoplasmic anucleate cells that block up holes in blood vessels

79
Q

Where are platelets derived from?

A

Made in bone marrow from megakaryotes?

80
Q

Give two features of platelets

A
  • Spherical

- Enucleate

81
Q

What occurs when there is a reduced number of platelets?

A

Thrombocytopenia —> increased bleeding (main risk cerebral) and spontaneous bleeding

82
Q

What occurs when there is a increased number of platelets?

A

Thrombocytosis —> can lead to arterial/venous thrombosis —> increased risk of heart attack/stroke

83
Q

Name 5 different types of protein in the blood

A
  • Coagulation proteins (enzymes)
  • Plasma proteins
  • Albumin
  • Carrier proteins
  • Immunoglobulins
84
Q

Where are coagulation proteins formed?

A

Liver

85
Q

What is the key coagulation protein and why?

A

Thrombin, as it makes the platelet plug

86
Q

Which coagulation factors require vitamin K for correct synthesis?

A

2, 7, 9, 10

87
Q

What is the function of coagulation proteins and how do they work?

A
  • To make a blood clot
  • Circulate in inactive form
  • Converts soluble fibrinogen into insoluble fibrin polymer
88
Q

What occurs when there is overactivity of coagulation proteins?

A

Thrombosis

89
Q

What occurs when there is underactivity of coagulation proteins?

A

Bleeding

90
Q

Are plasma proteins soluble and where are they found?

A

They are soluble and are found in plasma

91
Q

What is the most numerous protein in the plasma?

A

Albumin

92
Q

Where is albumin produced?

A

Liver

93
Q

Give 2 functions of albumin

A
  • Maintains oncotic pressure

- Carries FA, steroids and thyroid hormones

94
Q

What happens where there is a lack of albumin?

A

Oedema

95
Q

What do carrier proteins carry?

A

Nutrients and hormones

96
Q

Give the 4 types of immunoglobulins

A

IgG, IgM, IgA, IgE

97
Q

What are immunoglobulins?

A

Antibodies produced by plasma cells (differentiated plasma cells)

98
Q

What is the most important immunoglobulin?

A

IgG

99
Q

Which immunoglobulin do all of them start as?

A

IgM

100
Q

When are immunoglobins produced?

A

In response to non-self antigens

101
Q

What is haemostasis and what does it involve?

A

When the blood flow stops. This involves coagulation and contraction of damaged blood vessels

102
Q

Name 3 factors which contributes to blood remaining fluid

A
  • Proteins of the coagulation cascade and platelets circulate inactively
  • Protein and platelets are only activated by tissue factor (on all cells except endothelial). Endothelial punctured —> blood contact with tissue factor and clotting begins
  • Correct balance is vital
103
Q

What is the coagulation cascade?

A

Series of proteolytic enzymes that become activated in a cascade to generate thrombin which cleaves fibrinogen into fibrin —> blood clot

104
Q

Is the coagulation cascade all or nothing?

A

No, so it can be graduated depending on the severity

105
Q

Which cell is responsible for primary haemostasis?

A

Platelets

106
Q

What are the functions of platelets in bleeding?

A
  • Adhere to damaged endothelium

- Aggregate to form platelet plug that blocks hole in vessel

107
Q

What is the pathology of haemophilia A?

A
  • X-linked
  • Bleeding into muscles and joints
  • Deficiency in clotting factor 8
108
Q

What is the pathology of haemophilia B?

A
  • X-linked
  • Bleeding into muscles and joints
  • Deficiency in clotting factor 9
  • Less common compared to A as smaller gene
109
Q

What is the pathology of Von Willebrand’s disease?

A
  • Autosomal dominant inheritance
  • Lack of VWF
  • Muco-cutaneous bleeding (bleeding in skin and mucous membranes)
110
Q

What is VWF used for?

A
  • Required for platelets to bind to damaged blood vessels

- Lack —> platelet dysfunction so muco-cutaneous bleeding

111
Q

Give 5 examples of acquired bleeding disorders

A
  • Anti-platelet/anti-coagulation medication
  • Liver disease
  • Vitamin K deficiency
  • Drugs
  • Disseminated intravascular coagulation
112
Q

How can liver disease cause an acquired bleeding disorder?

A
  • Liver is site of synthesis of coagulation factors and fibrinogen
  • Prolonged prothrombin time
113
Q

How can a vitamin K deficiency cause an acquired bleeding disorder?

A
  • Needed for formation of coagulation factors 2, 7, 9, 10

- A fat soluble vitamin

114
Q

What causes vitamin K deficiency and especially in what condition?

A

Malabsorption - especially in obstructive jaundice

115
Q

How does vitamin K deficiency present and what’s the link to coagulation factors?

A
  • Prolonged PTT

- Coagulation factors are still produced but don’t work

116
Q

How does aspirin work?

A

Affects platelet function

117
Q

How do heparin and warfarin work?

A
  • Inhibits vitamin K

- Affects coagulation cascade

118
Q

What 2 affects can steroids have cardiovascularly?

A
  • Makes tissues thin

- Causes bleeding/bruising

119
Q

What is disseminated intravascular coagulation (DIC)?

A
  • Breakdown of haemostasis

- Simultaneous bleeding and microvascular bleeding

120
Q

Give 3 causes of DIC

A
  • Sepsis
  • Pregnancy
  • Malignancy
121
Q

What happens when the coagulation cascade is activated inside blood vessels?

A
  • Thrombin is produced
  • Fibrinogen is converted to fibrin
  • Platelet plugs are formed
122
Q

What is the pathway when a small vessel is damaged?

A
  • Constricts (due to endothelin-1)
  • Temporarily slows flow of blood to affected area
  • This presses opposed endothelial surfaces of the vessel together
123
Q

What are the interdependent processes of stopping bleeding?

A

Formation of a platelet plug and blood coagulation

124
Q

When does permanent closure of a vessel occur by construction and contact stickiness?

A

In the very small vessels of the microcirculation

125
Q

Briefly describe the formation of a platelet plug

A
  • Injury to vessel disrupts endothelium so exposes collagen fibres
  • Platelets adhere to collagen via VWF (using glycoprotein 1b receptor)
  • This binding to the collagen triggers the platelets to release the contents of their secretory vesicles by exocytosis
  • One of these contents are platelet dense granules. ADP is released from these granules which acts on P2Y1 and P2Y12 causing platelets amplification
  • These actions result in the platelet changing shape from smooth discoid to spiky, which increases SA of platelet (activation)
  • Activation causes an increase in expression in GPIIB/IIIa receptors on platelets which binds to fibrinogen, enabling new platelets to adhere (aggregation)
  • Adhesion rapidly induces thromboxane, which is released into ECF to stimulate further aggregation
126
Q

What does thromboxane A2 do?

A

Causes vasoconstriction and platelet activation

127
Q

What enhances the effectiveness of a platelet plug?

A

Contraction - platelets contain a high conc. of actin and myosin, which results in compression and strengthening of the platelet plug

128
Q

What happens to the smooth muscle in the damaged vessel during platelet activation, aggregation and plug formation?

A

It is simultaneously being stimulated to contract - decreasing blood flow to the area and pressure within the damaged vessel (caused by thromboxane A2)

129
Q

Why does vasoconstriction to the area of a ruptured vessel occur?

A

As a result of platelet activation - due to thromboxane A2 release

130
Q

Why doesn’t the platelet plug expand away from the damaged endothelium?

A
  • The undamaged endothelium either side synthesises and releases prostacyclin which inhibits platelet aggregation
  • Also releases nitric oxide which vasodilates, but is an inhibitor of platelet adhesion, activation and aggregation
131
Q

Is the formation of a platelet plug quick?

A

Yes - very quick

132
Q

What is the primary mechanism used to seal breaks in vessel walls?

A

Platelet plug

133
Q

What is blood coagulation?

A

The transformation of blood into a solid gel (clot/thrombus) which consists mainly of fibrin

134
Q

Where does blood clotting usually occur?

A

Locally around a platelet plug - dominant haemostat defence

135
Q

What is the function of a blood clot?

A

To support & reinforce the platelet plug and to solidify blood that remains in the wound channel

136
Q

What are the two divisions of the coagulation cascade?

A
  • Extrinsic (as a cellular element outside to blood is needed)
  • Intrinsic (everything needed is in the blood)
137
Q

Briefly describe the intrinsic pathway of the coagulation cascade

A
  • Factor 12a is activated when it comes into contact with exposed collagen fibres underlying damaged epithelium
  • Eventually get to factor 10a –> converts prothrombin into thrombin
  • Thrombin is the enzyme which converts fibrinogen to fibrin
  • Fibrin can be used to secure the blood clot and build it up
138
Q

Briefly describe the extrinsic pathway of the coagulation cascade

A
  • Begins with tissue factor
  • Blood is exposed to sub endothelial cells when vessel damage disrupts the endothelial lining
  • Tissue factor binds to factor 7, which initiates the formation of more factors
  • Eventually get to factor 10a —> converts prothrombin to thrombin
139
Q

What are the indirect roles that the liver plays in clotting?

A
  • The site of production for many plasma clotting fibres

- Produces bile salts which are needed for the absorption of vitamin K. It is required to produce prothrombin

140
Q

What is fibrinolytic system?

A

A fibrin clot is not designed to last forever, it is a temporary fix until permanent repair of the vessel occurs

141
Q

How are blood clots broke down?

A
  • Plasminogen is converted by plasminogen activators into plasmin
  • Plasmin goes on to break fibrin down, and so the entire clot
142
Q

Where is cardiac muscle found?

A

Only in the heart

143
Q

What does cardiac muscle do in relation to other muscles?

A

Combines properties of both skeletal and smooth muscle

144
Q

What gives cardiac muscle a striated appearance?

A

The regularly repeating sarcomeres composed of myosin-containing thick filaments interdigitating with thin filaments that contain actin

145
Q

What are present in an actin thin filament?

A

Troponin and tropomyosin

146
Q

What are intercalated discs (cardio)?

A
  • Adjacent cells which are joined end to end at structure
  • There are desmosomes which hold the cells together and to which the myofibrils are attached
  • There are also gap junctions

Phase 1 Med (Liv) (13 decks)

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