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Physiology > L2-4: Blood > Flashcards

L2-4: Blood Flashcards

1
Q

What percentage of blood makes up the total body weight?

A

8%

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2
Q

Where is the blood distributed in the body?

A

The lungs
Systemic venous circulation
In the heart, systemic arteries, arterioles and capillaries

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3
Q

What functions does the blood have?

A

Gas transport and exchange
Distributing solutes
Immune functions
Maintains body temperature
Regulates blood clotting
Preserving acid-base homeostasis
Stabilising blood pressure

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4
Q

What solutes does plasma transport?

A

Ions
Nutrients
Hormones
Metabolic waste

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5
Q

How does the blood maintain body temperature?

A

By carrying heat away

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6
Q

What is the pH of blood?

A

7.35-7.45

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7
Q

How is the pH of blood maintained?

A

Using buffering systems

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8
Q

What factor majorly determines blood pressure?

A

Blood volume

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9
Q

What are the blood constituents?

A

Erythrocytes (RBCs)
Leukocytes (WBCs)
Thrombocytes (platelets)

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10
Q

What percentage of blood is WBCs and platelets?

A

1%

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11
Q

What is haematocrit?

A

It is the packed cell volume - total blood volume occupied by RBCs

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12
Q

What percentage of blood is the soluble materials?

A

55%

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13
Q

What is serum?

A

Plasma minus clotting factors

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14
Q

What cellular elements are in blood?

A

RBCs, WBCs and platelets

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15
Q

What is plasma composed of?

A

Water, ions, organic molecules, trace elements and vitamins & gases

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16
Q

What organic molecules are in blood?

A

AAs, proteins, glucose, lipids and wastes

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17
Q

What different proteins are in blood?

A

Albumins, globulins and fibrinogen

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18
Q

What are the different WBCs in blood?

A

Lymphocytes, monocytes, neutrophils, eosinophils and basophils

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19
Q

What are the 2 main functions of plasma?

A

Thermoregulation and transport

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20
Q

What is the approximate percentage of water in plasma?

A

~90%

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21
Q

What are the main functions of water in plasma?

A

High heat capacity - small temp changes
Heat not needed lost to environment
Percentage determines blood viscosity

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22
Q

What is the main plasma protein?

A

Serum albumin

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23
Q

How is serum albumin used in plasma?

A

Maintains osmotic pressure
Assists in transport of lipids + steroid hormones

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24
Q

Where is albumin synthesised?

A

Liver

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25
Q

How are globulins used in plasma?

A

Bind to and transport ions, hormones and lipids - incompatible with water
Immune proteins - Abs/gammaglobulins made by leukocytes

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26
Q

How are globulins used in plasma?

A

Essential for blood clotting

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27
Q

What are the remainder proteins in plasma?

A

Regulatory proteins like enzymes, proenzymes and hormones

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28
Q

What technique can be used to identify plasma proteins?

A

Electrophoresis

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29
Q

How can electrophoresis be used to diagnose conditions?

A

Different patterns and change in number of bands on gel

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30
Q

What dissolved small molecules are in plasma?

A

Nutrients
Waste products
Dissolved gases
Hormones, vitamins and minerals

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31
Q

What dissolved gases are in plasma?

A

Oxygen and carbon dioxide

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32
Q

What waste products are stored in plasma?

A

Creatinine, bilirubin and urea

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33
Q

What nutrients are stored in urea?

A

Glucose, AAs, lipids and vitamins

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34
Q

What is the structure of an erythrocyte?

A

Biconcave disc containing cytosol enzymes and haemoglobin

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35
Q

What is the primary function of RBCs?

A

Oxygen transport

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36
Q

What is the approximate life span of an RBC?

A

~120 days

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37
Q

How many RBCs are there in one person at any one time?

A

25-30 trillion

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38
Q

What is MCV?

A

Mean Cell Volume

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39
Q

What is the total volume of erythrocytes?

A

80-96 femtolitres (fl)

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40
Q

How is MCV used as a clinical index?

A

Small RBCs - iron deficiency anaemias
Large RBCs - folate deficiency (vitamin B9) anaemias

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41
Q

What are blood cells synthesised from?

A

Multipotential hematopoietic stem cell

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42
Q

What are the different stages of erythropoiesis?

A

-Hematopoietic stem cell
-Erythrocyte-CFU
-Proerythroblast (requires erythropoietin)
-Early erythroblast (haemoglobin synthesised)
-Late erythroblast (nucleus ejected)
-Reticulocyte (last organelles ejected)
-Erythrocyte

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43
Q

Where does erythropoiesis take place?

A

In the red bone marrow

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44
Q

How is erythrocyte synthesis stimulated?

A

Hypoxia due to decreased RBC count/ Hb count or decreased O2 availability

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45
Q

Which organs release the hormone erythropoietin?

A

Kidney and liver

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46
Q

How long does erythrocyte synthesis take?

A

~26 days

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47
Q

Where are erythrocytes phagocytosed at the end of life?

A

In the liver and spleen

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48
Q

What is the haem recycled into?

A

Heam:
converted into biliverdin to bilirubin and secreted f=in bile from the liver
Iron:
transported in the blood using transferrin and stored by protein ferritin in the liver

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49
Q

How are RBCs damaged over their lifespan?

A

From squeezing through capillaries they become fragile and easily rupture

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50
Q

How does haemoglobin allow oxygen transport?

A

Oxygen is able to bind to the haemoglobin to be transported rather than travel in the plasma as it has poor solubilty

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51
Q

What are the 2 different parts of a haemoglobin molecule?

A

The globin - 4 protein chains
Four iron containing haem groups iron can reversibly bind 1 O2

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52
Q

What does the haem group consist of?

A

A porphyrin ring with iron at the centre

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53
Q

What provides the colour of blood?

A

Iron in the haem group makes it appear red when oxygenated and blue when deoxygenated

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54
Q

What are the different forms of globins that exist?

A

Alpha
Beta
Gamma
Delta

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55
Q

What is HbA?

A

Hb with 2 alpha and 2 beta globins

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56
Q

What is HbA2?

A

Hb with 2 alphas and 2 deltas

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57
Q

What is foetal Hb?

A

2 alpha and 2 gamma globins

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58
Q

What is oxygen binding governed by?

A

Partial pressure of oxygen
Number of free oxygen binding sites available - positive cooperativity

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59
Q

What are the 2 different forms Hb can exist in?

A

Tant (t) and relaxed (r)

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60
Q

What are the components of the r form Hb?

A

High O2 affinity
High pO2 - firmly binds O2
e.g. in the lungs

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61
Q

What are the components of the t form?

A

Low O2 affinity
Low pO2 - releases oxygen readily
e.g. in peripheral tissues

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62
Q

What other substances is Hb able to bind?

A

Carbon dioxide
Acidic hydrogen portion of carbonic acid - tissues from CO2, buffers acid
Carbon monoxide - toxic
Nitric oxide - regulatory

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63
Q

What are the 2 major classes of inherited disorders in Hb?

A

Haemoglobinpathies - abnormal globin chains made (sickle cell anaemia)
Thalassaemias - decreased or absent globin chains (defects in gene expression)

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64
Q

What is sickle cell anaemia?

A

A genetic disease: mutation in the beta globin gene - glutamate replaced by valine creating sticky patches
Results in HbS which polymerises at low pO2 forming long crystals of HbS

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65
Q

How does sickle cell anaemia cause deprivation of oxygen to tissues?

A

They become trapped and block small blood vessels

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66
Q

How long is the life span of a sickled RBC?

A

10-20 days

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67
Q

What is the sickle cell trait?

A

Heterozygotes of the disease

68
Q

What disease does HbS overlap with?

A

P. falciparum - the parasite that causes malaria

69
Q

How is the sickle cell trait advantageous?

A

It is protective against mild malaria

70
Q

What are thalassemias?

A

Disease where synthesis of one/both alpha/beta globins is reduced
Disease severity varies
RBCs prone to damage & short lived - anaemia
Recessive genetic disease - gross deletion 1/more globin genes or gene mutation
Hb fails to form correctly

71
Q

What are the 2 different classes of thalassemias?

A

Alpha and beta

72
Q

What are the factors of alpha thalassemia?

A

Production of alpha globin is deficient
Excess beta chains, unstable tetramers of four beta chains HbH
Abnormal O2 dissociation curves + RBC damage
Short lived RBC - anaemia

73
Q

What are the factors of beta thalassemia?

A

Production of beta globin is deficient
Excess alpha chains - no tetramers form
Bind to and damage RBC membranes
High conc toxic aggregates form
RBCs fragile and short lived - anaemia
Results in iron overload

74
Q

Which class of thalassemia is clinically most important?

A

Beta

75
Q

What treatment is there for beta thalassemia?

A

Iron chelation therapy or accumulate fatal iron levels

76
Q

How are the different thalassemias diagnosed by electrophoresis?

A

Alpha: reduced HbA, presence of HbH
Beta: beta globins reduced/absent, decreased HbA

77
Q

What is haemostasis?

A

It is the arrest of bleeding from a broken bessel

78
Q

What are platelets?

A

Small cell fragments that have budded off from large bone marrow cells (megakaryocytes)

79
Q

What hormone regulates platelet production?

A

Thrombopoietin

80
Q

Where is thrombopoietin produced?

A

The liver and kidneys

81
Q

What are platelets synthesised from?

A

Hematopoietic stem cells

82
Q

What are megakaryotcytes?

A

Massive cells with multiple copies of DNA

83
Q

What does thrombopoietin do to megakaryocytes?

A

It stimulates them to extend arms through bone marrow sinusoids into blood vessels

84
Q

How many platelets are produced a day?

A

10^11

85
Q

What is the structure of a platelet?

A

Composed of:
Granules
Microtubules
Mitochondria
Plasma membrane

86
Q

Where are platelets stored and how are they activated?

A

Stored: spleen
Released by contraction of the spleen and activated by the sympathetic nervous system

87
Q

How long are platelets life span?

A

~7-10 days

88
Q

What happens to platelets after they die?

A

They undergo apoptosis and are phagocytosed in the liver and spleen

89
Q

What is the exterior coat and what is its function?

A

Rich in glycoproteins, allows adhesion, aggregation and activation

90
Q

What is the function of the tubular system of platelets?

A

Site of thromboxane A2 synthesis and release

91
Q

What is the function of microtubules and microfilaments in platelets?

A

To maintain shape

92
Q

What are the functions of alpha granules?

A

They contain clotting mediators including von Willebrand factor, factors V, VIII and fribrinogen

93
Q

What are the functions of delta granules (dense bodies)?

A

They contain ADP, Ca2+ and serotonin for platelet activation and clotting

94
Q

What are the 3 steps of haemostasis?

A

Vascular spasm (blood vessel constriction)
Formation of platelet plug
Blood coagulation

95
Q

What happens during vascular spasm?

A

Cut/tear in blood vessel
Damaged cells + platelets at cut site release potent vasoconstrictors such as serotonin and ADP
Constriction of smooth muscle layer in vessel wall slows the blood flow and minimises blood loss
Endothelial surfaces are pushed together and adhere to each other (platelets stick to exposed collagen)

96
Q

What happens during platelet plug formation?

A

Adhesion: platelets stick using con Willebrand’s factor (vWF)- plasma protein from endothelial cells & platelets
Activation: plug seals the break and becomes compact, further vasoconstricts and stimulates a clotting cascade

97
Q

What is prostacyclin (PGI2)?

A

It is released by normal blood vessel lining
Inhibits platelet aggregation
Limits platelet plug to damaged region

98
Q

What are the steps of platelet plug formation?

A

Exposed collagen binds and activates platelets
Platelet factors are released (vWF)
More platelets attracted
Aggregation into a platelet plug
(prostacyclin stops platelet adhesion to undamaged cells)

99
Q

What happens during blood clotting?

A

Blood coagulates - blood from liquid to solid gel
Clot strengthens and supports platelet plug
Converts fibrinogen to fibrin and RBCs are enmeshed into the fibrin plug
Clotting pathway: cascade of reactions involving plasma proteins (factors)

100
Q

How is the fibrin polymer formed?

A

Fibrinogen to fibrin monomers using thrombin (factor IIa)
Fibrin monomers to fibrin polymer using factor XIIIa and Ca2+

101
Q

What are the 2 different pathways to stimulate thrombin activity?

A

Intrinsic: Initial stimulus is exposed collagen
Extrinsic: Initial stimulus is blood contact with damaged tissue outside of blood vessel which exposes tissue factor (factor III/ tissue thromboplastin)

102
Q

What is the common pathway to stimulate thrombin activity?

A

A combination of intrinsic and extrinsic pathways to activate factor Xa which allows thrombin (factor IIa) production from prothrombin (factor II) to produce fibrin

103
Q

What are the 2 steps of the normal process of blood clotting?

A

Initiation: tissue exposure triggers extrinsic pathway leading to thrombin production but amounts are too small for sustained coagulation
Amplification: thrombin produced feeds back and activates intrinsic pathway

104
Q

What are the different anticlotting systems in the body?

A

Anti- thrombin
Tissue factor pathway inhibitor
Thrombin
Thrombomodulin

105
Q

How does anti-thrombin allow anticlotting systems?

A

Inhibits clotting factors like thrombin, activity is enhanced by heparin which is normally present on endothelial cells

106
Q

How does tissue factor pathway inhibitor allow anticlotting systems?

A

It binds to factor III/VIIa complex preventing it from activating its substrates factor IX and factor X, binds to factor Xa directly

107
Q

How does thrombin allow anticlotting systems?

A

Binding to its receptor stimulates production of prostaglandins, nitric oxide and ADP to further inhibit further platelet aggregation

108
Q

How does thrombomodulin allow anticlotting systems?

A

It is expressed by endothelial cells and binds to thrombin, eliminating its coagulant effects and inactivating factors Va and VIIIa

109
Q

What is fibrinolysis?

A

Clot breakdown
Aggregated platelets secrete platelet derived growth factor beta (PDGF beta) with recruits fibroblasts
Fibroblasts form scar tissue
Simultaneously the clot is dissolved by a fibrinolytic enzyme called plasmin

110
Q

What is plasmin?

A

It is activated by tissue plasminogen activator (t-PA) secreted by endothelial cells

111
Q

What does t-PA need to become active to work on the clot?

A

Fibrin

112
Q

Which factors are proteases?

A

III, V, VIII and XIII

113
Q

Which factors are glycoproteins?

A

III, V and VIII

114
Q

Which factor is a transglutaminase?

A

Factor XIII

115
Q

What can disorders of haemostasis be defined as?

A

Excessive/unwanted clotting
Inadequate clotting
Defects of platelets - quantitative/qualitative
Deficiency or dysfunction of coagulation factors
Acquired
Inherited

116
Q

What are examples of acquired disorders of haemostasis?

A

Renal disease- lack thrombopoietin
Hepatic disease - lack fibrinogen
Vit K deficiency - needed for synthesis of clotting (factors II, VII, IX and X)
Drug induced disorders - effects on platelet activity

117
Q

What are examples of inherited disorders of haemostasis?

A

Structural defects to vascular system (narrow veins and pooling blood)
Thrombotic disorder- alteration to haemostasis impairs clot formation
Quantitative (thromboctopaenia) or qualitative (thrombopathy) - defects of platelets
Deficiency or disfunction of coagulation factors (coagulopathy)

118
Q

What is thrombosis?

A

Excessive/ unwanted clotting

119
Q

What is thrombus?

A

A blood clot within a vessel or the heart

120
Q

What is an embolus?

A

Detached mass able to travel in a vessel (solid, liquid or gas)

121
Q

What is an embolism?

A

The lodging of an embolus

122
Q

What is a thromboembolism?

A

Blockage by a thrombus

123
Q

What is stenosis?

A

Abnormal narrowing of a passage in the body

124
Q

What is Virchow’s triad?

A

The three risk factors for thrombosis:
Blood stasis
Changes in vessel wall
Thrombogenic changes in the blood - hypercoagulability

125
Q

What are examples of anticoagulants used in treatment?

A

Warfarin - widely prescribed inhibits vitamin K
Heparin - endothelial cell-derived polysaccharide, by injection which activates antithrombin III

126
Q

When would the likelihood of forming clots be increased?

A

Atrial fibrillation
Aortic valve replacement
Recent surgery
Autoimmune diease

127
Q

What is thrombocytopenia?

A

Low platelet count

128
Q

What is thrombocytopenia caused by?

A

Autoimmune disease
Drug induced

129
Q

What are the clinical manifestations caused by thrombocytopenia?

A

Easy bruising, petechia rash, mucous membrane bleeding or excessive bleeding after minor trauma

130
Q

What is thrombotic thrombocytopenic purpura caused by?

A

Formation of small clots in the circulation resulting in low platelet numbers
Spontaneous aggregation of platelets and initiation of platelet cascade

131
Q

What are examples of coagulopathies?

A

Von Willebrand’s disease - lack of vWF so poor platelet aggregation (autosomal dominant)
Haemophilia A: deficiency in factor VIII (X-linked recessive)
Haemophilia B: Deficiency in factor IX

132
Q

What does the severity of haemophilia depend on?

A

Depends on the amount of factor VIII/ IX is in the blood

133
Q

What is the treatment of haemophilia?

A

Replacement of missing clotting factor

134
Q

Who discovered the ABO blood group system?

A

Karl Landsteiner

135
Q

What are blood groups?

A

Classification of blood based on presence of inherited antigenic substances on the surface of red blood cells

136
Q

What are RBC surface antigens?

A

A complex mixture of proteins, glycoproteins and glycolipids found on the surface of all RBCs and a range of other cells in the body

137
Q

How many blood group systems known?

A

43

138
Q

How many different blood group antigens have been described?

A

> 600

139
Q

What is the complete blood group?

A

The set of surface antigens on the individuals RBC

140
Q

How can blood group change?

A

Infection, malignancy, autoimmune disease or after bone marrow transplant

141
Q

What are the 5 sugars contained in the ABO system?

A

Fucose
Galactose
N-acetylgalactosamine
N-acetylglucosamine
Sialic acid

142
Q

What are the 3 enzymes in the ABO system (glycosyl transferases)?

A

Fucosyl transferase (FUT1)
N-acetlygalatosamine transferase (A transferase)
Galactose transferase (B transferase)

143
Q

What are the 2 genes in the ABO system?

A

ABO and H

144
Q

What do the 2 genes in the ABO system encode?

A

Glycosyltransferases - transfer monosaccharides to polysaccharide chains

145
Q

What are the 3 possible alleles of the ABO gene?

A

A and B are dominant to O
O allele encodes a truncated, non-functional protein

146
Q

What does the H gene encode?

A

Fucosyl transferase (FUT1)

147
Q

What phenotype does hh encode?

A

‘Bombay’ phenotype
Can only receive transfusions from others with the same blood group

148
Q

Which chromosome is the ABO gene on?

A

9

149
Q

How did the O allele arise?

A

A deletion in exon 6 which lead to a frameshift to an inactive protein

150
Q

Which transferase enzymes do the A and B alleles code for?

A

A: A-transferase (N=-acetly galactosamine transferase)
B: B-transferase (galactose transferase)

151
Q

Why can’t the hh gene make any ABO antigens?

A

Because they do not have any functional FUT1 so they cannot make any substance H so no ABO antigens

152
Q

What transferase does the O gene encode?

A

It cannot encode a transferase as it doesn’t have A/B transferases so only makes H substance

153
Q

What transferases are added for the AB gene?

A

Both A and B so either galactose or N-acetlygalactosamine is added to the terminal galactose on H substance

154
Q

What are the different genotypes ABO individuals can be?

A

AA, AO - BG A
BB, BO - BG B
AB - BG AB
OO - H substance only

155
Q

Which blood group is the most common in most populations?

A

Blood group O

156
Q

Why are foreign blood groups attacked by the immune system?

A

As people without A or B substances develop antibodies against either or both without ever being exposed

157
Q

What happens during haemolytic transfusion reaction?

A

Agglutination results in RBC lysis
Once RBCs lysed in blood system the complement system is activated leading to kidney failure, uncontrolled clotting and circulatory shock which can be fatal
Abs in donated blood can cause agglutination in recipient RBCs (less significant as diluted)

158
Q

What is the most important rhesus antigen?

A

D antigen

159
Q

Which genotype encodes Rh+?

A

Dd or DD

160
Q

What happens when mismatched rhesus antigens come into contact?

A

Anti-Rh abs destroy Rh+ RBCs they come in contact with
RBC bound by IgG, engulfed by macrophages, transported to liver and spleen for removal
Less serious than intravascular haemolysis

161
Q

Which blood group is a universal acceptor?

A

AB+

162
Q

Which blood group is a universal donor?

A

O-

163
Q

What happens when a newborn has haemolytic disease?

A

If a woman with Rh- antigens has a baby with a man with Rh+ antigens leakage of the antigens in the baby can cause production of antibodies which when impregnated again with a baby with Rh+ antigens it can cause damage to the fetal RBCs

164
Q

How is haemolytic disease combatted in newborns?

A

Mothers (Rh-) are given anti-D immunoglobulin which removed any foetal Rh+ blood from her circulation before antibodies are made

165
Q
A

Physiology (6 decks)

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