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BOD > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is anaemia?

A

Reduction in total circulating red blood cell mass

Reduction in oxygen carrying capacity of blood

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2
Q

How is anaemia measured?

A

Haemoglobin concentration of blood

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3
Q

How does anaemia arise?

A

Imbalance between rate of production of RBCs and rate of destruction

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4
Q

What does the megakaryocyte/erythroid precursor (MEP) give rise to?

A
  1. Erythrocytes

2. Platelets

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5
Q

What does the granulocyte/macrophage progenitor (GMP) give rise to?

A
  1. Macrophages
  2. Neutrophils
  3. Eosinohils
  4. Basophils
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6
Q

What does the common myeloid progenitor give rise to?

A
  1. MEP

2. GMP

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7
Q

What does the common lymphoid progenitor give rise to?

A
  1. B cells and plasma cells
  2. T cells
  3. Natural killer cells
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8
Q

What are the erythroid progenitors?

A
  1. Erythroblasts (normoblasts)

2. Reticulocytes

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9
Q

What is the diameter of a normal RBC?

A

6 - 9.5 µm (7µm average)

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10
Q

What is the RBC life span?

A

120 days

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11
Q

Where are RBCs destroyed?

A

Spleen

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12
Q

What is the minor form of haemoglobin?

A

HbA2

α2 δ2 chains

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13
Q

What are the signs and symptoms of anaemia?

A
  1. Thin skin and nails
  2. Pale mucous membranes
  3. Hypoxic damage in viscera
  4. Compensatory changes
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14
Q

What are the results of hypoxic damage in viscera in anaemia?

A
  1. Weakness, malaise and easy fatiguability
  2. Angina pectoris
  3. Dimness of vision, headache, faintness
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15
Q

What are the compensatory changes in anaemia?

A
  1. Hyperplasia of haematopoietic tissue in bone marrow
  2. Increased heart rate and cardiac output
  3. Increased breathing rate
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16
Q

What causes anaemia?

A
  1. Dyserythropoiesis
  2. Increased destruction of RBCs
  3. Haemorrhage
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17
Q

What is dyserythropoiesis?

A

Impaired generation of RBCs or their constituents

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18
Q

What causes dyserythropoiesis?

A
  1. Stem cell abnormalities

2. Abnormalities of erythroblasts and red cell production

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19
Q

What is aplastic anaemia?

A

Anaemia caused by stem cell abnormality

Little or no functional bone marrow

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20
Q

What is megaloblastic anaemia?

A

Anaemia caused by defective DNA synthesis

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21
Q

What is iron deficiency anaemia?

A

Anaemia caused by defective haem synthesis

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22
Q

What is thalassaemia?

A

Anaemia caused by defective globin synthesis

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23
Q

What causes haemolytic anaemias?

A
  1. Intrinsic abnormalities of the red blood cell (usually hereditary)
  2. Extrinsic abnormalities (usually acquired)
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24
Q

What causes megaloblastic anaemia?

A

Deficiency of vitamin B12 or folic acid, which are coenzymes in the synthesis of thymidine

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25
Q

What are the features of megaloblastic anaemia?

A
  1. Ineffective haemopoiesis leads to pancytopenia
  2. Expansion of haematopoietic tissue
  3. Megaloblasts - may appear in blood
  4. Macrocytosis
  5. Anisocytosis
  6. Poikilocytosis
  7. Iron deposition in organs
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26
Q

What are the effects of megaloblastic anaemia on other cells and tissues?

A
  1. Neutrophils and megakaryocytes are large with hypersegmented nuclei
  2. Enlarged nuclei in gut epithelial cells
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27
Q

What are megaloblasts?

A

Enlarged RBC precursors

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28
Q

What is macrocytosis?

A

Enlarged RBCs

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29
Q

What is anisocytosis?

A

RBCs are different sizes

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30
Q

What is poikilocytosis?

A

RBCs are different shapes

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31
Q

What is the role of vitamin B12?

A

Coenzyme required for conversion of transport form of folic acid to tetrahydrofolate (FH4)

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32
Q

What is the transport form of folic acid?

A

methyl-tetrahydrofolate

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33
Q

What is the role of tetrahydrofolate (FH4)?

A

Enables transfer of one-carbon units

Required for thymidine synthesis

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34
Q

Where does vitamin B12 come from?

A

Entirely diet

Animal sources

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35
Q

What is the minimum daily requirement of vitamin B12?

A

1µg

Average diet has hundreds of µg per day

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36
Q

Where is vitamin B12 absorbed?

A

Terminal ileum

Requires intrinsic factor from gastric mucosa

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37
Q

Where is vitamin B12 stored?

A

Liver

5 year store

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38
Q

What causes vitamin B12 deficiency?

A
  1. Inadequate intake, eg. vegans
  2. Increased requirements
  3. Malabsorption due to gastric causes
  4. Malabsorption due to pancreatic insufficiency
  5. Malabsorption due to ileal disease
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39
Q

What is pernicious anaemia?

A

Intrinsic factor deficiency due to autoimmune destruction of gastric mucosa

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40
Q

Where does folate come from?

A

Entirely diet

Vegetables and fruit

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41
Q

What is the minimum daily folate requirement?

A

50µg

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42
Q

Where is folate absorbed?

A

Jejunum

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43
Q

How long does folate storage provide for?

A

100 day reserve

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44
Q

What causes folate deficiency?

A
  1. Inadequate intake, eg. elderly, alcoholics
  2. Increased requirements
  3. Inadequate absorption in small bowel disease
  4. Impaired utilisation
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45
Q

What is methotrexate?

A

Folic acid antagonist

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46
Q

What is the commonest anaemia in the UK?

A

Iron deficiency anaemia

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47
Q

What are the features of RBCs in iron deficiency anaemia?

A
  1. Microcytic
  2. Poikilocytic
  3. Hypochromic
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48
Q

What is the daily iron requirement?

A

7mg for male

15mg for female

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49
Q

What are dietary sources of iron?

A
  1. Organic (haem) in animal produce (25% absorbed)

2. Inorganic (non-haem) in vegetables (5% absorbed)

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50
Q

What is ferritin?

A

Intracellular protein that binds iron and stores it

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51
Q

What is haemosiderin?

A

What ferritin is converted to in cases of iron overload

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52
Q

How is iron balance maintained?

A

Regulation of iron absorption in the duodenum

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53
Q

What is hepcidin?

A

Released by liver when hepatic iron levels rise

Prevents iron absorption

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54
Q

What are the causes of iron deficiency?

A
  1. Impaired absorption
  2. Increased demand
  3. Chronic blood loss, eg. ulcer or malignancy
  4. Low dietary intake
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55
Q

What are the effects of severe iron deficiency?

A
  1. Loss of function of iron-containing enzymes
  2. Malabsorption
  3. Changes in nails, hair, tongue, etc.
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56
Q

Give two examples of iron-containing enzymes

A
  1. Catalase

2. Cytochromes

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57
Q

What is extravascular haemolytic anaemia?

A

Removal of RBCs by macrophages, largely in spleen

Causes splenomegaly

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58
Q

What is intravascular haemolytic anaemia?

A

Lysis of RBCs within the circulation

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59
Q

What is the physiological response to haemolytic anaemia?

A
  1. Increased erythropoiesis
  2. Expansion of red marrow
  3. Extramedullary haemopoiesis
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60
Q

What are some features of the blood in haemolytic anaemia?

A
  1. Increased numbers of reticulocytes

2. May contain erythroblasts

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61
Q

What are the features of intrinsic haemolytic anaemia?

A
  1. Hereditary
  2. Deformed erythrocytes cannot travel through spleen sinusoids
  3. Trapped RBCs are phagocytosed by macrophages
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62
Q

What are the intrinsic causes of haemolytic anaemia?

A
  1. Structural defects
  2. Enzyme defects
  3. Haemoglobin abnormalities
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63
Q

What is hereditary spherocytosis?

A

Defects in RBC skeleton lead to abnormal spheroidal cells

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64
Q

What enzyme defects cause haemolytic anaemia?

A

Pyruvate kinase deficiency causes reduced ATP production from glycolysis

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65
Q

What are the extrinsic causes of haemolytic anaemia?

A
  1. Immune
  2. Physical
  3. Chemical
  4. Infection
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66
Q

What is haemolytic anaemia of the newborn?

A

Immune reaction between maternal antibodies and fetal red blood cells

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67
Q

What physical factors cause haemolytic anaemia?

A

Valve replacement

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68
Q

What chemical factors cause haemolytic anaemia?

A

Lead poisoning

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69
Q

What infectious factors cause haemolytic anaemia?

A

Malaria

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70
Q

What causes sickle cell disease?

A

Point mutation

Changes glutamic acid to valine

Changes polar amino acid on external surface of β globin protein

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71
Q

What are the effects of sickle cell disease in homozygotes?

A

HbS aggregates and polymerises due to infection, dehydration, decreased pO2, decreased pH

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72
Q

What are the consequences of sickle cell disease?

A
  1. Haemolysis
  2. Occlusion of small blood vessels
  3. Tissue hypoxia/infarction
  4. Chronic tissue hypoxia
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73
Q

Where does haemolysis mostly occur in sickle cell disease?

A

Spleen

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74
Q

Which microvascular beds are most likely to be occluded in sickle cell disease?

A

Where flow is slow

  1. Spleen
  2. Bone marrow
  3. Sites of inflammation
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75
Q

How much Hb is HbS in heterozygotes?

A

40%

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76
Q

Why does HbS protect against malaria?

A

Only in heterozygotes

Increased clearance of parasitised red blood cells following sickling

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77
Q

What is thalassaemia?

A

Absent or reduced synthesis of globin chains of HbA

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78
Q

What RBC conditions protect against malaria?

A
  1. Sickle cell trait

2. Thalassaemia

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79
Q

What are the two consequences of thalassaemia?

A
  1. Reduced RBC production

2. Relative abundance of other globin chain

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80
Q

What are some features of RBCs in thalassaemia?

A
  1. Hypochromic
  2. Microcytic
  3. Anisocytosis
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81
Q

What is the effect of relative abundance of other globin chain in thalassaemia?

A
  1. Precipitates as inclusions
  2. Damages cell membrane
  3. Impaires DNA synthesis
  4. Destruction of erythroblasts
  5. Destruction of RBCs
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82
Q

Which chromosome codes for β chain?

A

Single gene on chromosome 11

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83
Q

What do mutations in β chain cause?

A
  1. Loss of β chain (β0)

2. Inadequate synthesis of β chain (β+)

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84
Q

What processes might β chain mutations affect?

A
  1. Gene transcription
  2. RNA splicing
  3. Translation
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85
Q

What is thalassaemia major?

A

Both β chain genes are mutated

β0/β0, β+/β+, β0/β+

Severe anaemia

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86
Q

What is thalassaemia minor?

A

Only one β chain gene is mutated

β0/β or β+/β

Mild anaemia

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87
Q

What are the physiological consequences of thalassaemia?

A
  1. Bone marrow expansion with erosion of cortical bone
  2. Extramedullary haemopoiesis
  3. Excessive absorption of dietary iron
  4. Iron overload
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88
Q

What are α chains encoded by?

A

Two duplicated genes on each chromosome 16

Each gene contributes 25% of α globin protein

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89
Q

What causes α thalassaemia?

A

Deletion of α chain genes

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90
Q

Which thalassaemia is more severe?

A

β thalassaemia

Free β and γ chains are more soluble than free α chains

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91
Q

What is HbH (β4) disease?

A

–/-α

Severe anaemia

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92
Q

What is Hb Barts (γ4) disease?

A

–/–

Lethal in utero

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93
Q

What is pancytopaenia?

A

Reduced numbers of RBCs, WBCs and platelets in blood

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94
Q

What is a reticulocyte?

A

Immature red blood cell that no longer contains a nucleus

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95
Q

What is an erythroblast?

A

Early nucleated red blood cell precursor

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96
Q

What is a normoblast?

A

Late nucleated red blood cell precursor

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97
Q

What is normal haemostasis?

A

Physiological response of blood vessels to injury, to prevent blood loss

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98
Q

What accomplishes haemostasis?

A
  1. Platelets
  2. Proteins of plasma-based coagulation cascade
  3. Endothelial cells
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99
Q

What are platelets?

A

Discoid anuclear bodies

Produced by cytoplasmic fragmentation of megakaryocytes in bone marrow

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100
Q

What is the lifespan of a platelet?

A

7 days

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101
Q

How are platelets activated?

A

By extracellular matrix proteins

Especially collagens exposed when endothelial layer is monolayer damaged

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102
Q

How do platelets adhere to collagen?

A

Strongly

Via von Willebrand factor

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103
Q

What do platelets do once they adhere to collagen?

A
  1. Change their shape
  2. Shoot out long processes
  3. Secrete chemical signals
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104
Q

What chemical signals do platelets secrete?

A
  1. Thromboxane A2
  2. Vasoactive amines, eg. 5HT
  3. ADP
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105
Q

What do platelet signals promote?

A
  1. Vasoconstriction

2. Platelet aggregation

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106
Q

What forms the primary haemostatic plug?

A

Aggregated platelets in damaged blood vessel

Platelet membranes drawn into close apposition with eventual fusion

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107
Q

What molecules mediate platelet contraction in the haemostatic plug?

A
  1. Integrins, eg. aIIbβ3
  2. Ig superfamily junctional adhesion molecules
  3. Endothelial cell specific adhesion molecules
  4. Kinase-ligand combination of eph and ephrin families
108
Q

What are the effects of integrins and eph/ephrins?

A
  1. Cytoskeletal alterations
  2. Myosin-dependent contraction
  3. Retraction of blood clot
109
Q

What are the effects of haemostasis with reduced platelet number?

A
  1. Purpura

2. Spontaneous haemorrhage

110
Q

What is purpura?

A

Bleeding from skin capillaries

111
Q

Where does tissue factor come from?

A
  1. Damaged tissues

2. Surface of activated endothelial cells

112
Q

What is the role of thrombin?

A
  1. Catalyses conversion of fibrinogen into fibrin monomers, which then polymerise into fibrin strands
  2. Activates platelets
  3. Catalyses earlier steps in coagulation cascade
113
Q

What accelerates reactions of activation of factor X?

A

If carried out on phospholipid-rich surface, eg. platelets or other microparticles

114
Q

What are so-called ‘microparticles’?

A

Fragments of monocyte or platelet plasma membrane

115
Q

What forms the secondary haemostatic plug?

A

Meshwork of fibrin strands with fused platelets

116
Q

What is the role of the fibrinolytic system?

A

To dissolve the fibrin plug

117
Q

What is plasminogen?

A

The inactive precursor of the fibrinolytic system

Precipitated along with fibrin in interior of thrombus

118
Q

What is the role of plasmin?

A

Activated form of plasminogen

Protease

Breaks down fibrin

119
Q

What is the role of endothelial cells in normal blood vessels?

A

Inhibit haemostasis

Insulate tissues from blood

Produce enzymatic and chemical inhibitors

120
Q

What enzymatic and chemical inhibitors are produced by endothelial cells in healthy blood vessels?

A
  1. Nitric oxide
  2. Prostacyclin
  3. Antithrombin
  4. Tissue factor pathway inhibitor
  5. Thrombomodulin
  6. Protein S
121
Q

What do nitric oxide and prostacyclin do?

A

Potent inhibitors of platelet activation

122
Q

What does antithrombin do?

A

Expressed on cell surface

Binds and inactivates thrombin

Complexes then released from endothelial cells and cleared in liver

123
Q

What does tissue factor pathway inhibitor do?

A

Blocks activation of factor X by tissue factor

124
Q

What does thrombomodulin do?

A

Expressed on cell surface

Changes conformation of thrombin so that it is less able to cleave fibrinogen during coagulation cascade

Enables thrombin to activate protein C

125
Q

What is protein C?

A

Inhibits coagulation cascade

Inactivates factor V and factor VIII

126
Q

What is protein S?

A

A co-factor for protein C

127
Q

What is the role of damaged endothelial cells?

A

Promote haemostasis

Underlying tissue activates platelets and coagulation cascade when endothelial layer is breached

128
Q

How do endothelial cells promote haemostasis?

A
  1. Synthesis of necessary enzymes and chemical mediators

2. Express binding sites that increase activity of factors X and IX

129
Q

What enzymes and chemical mediators are produced by damaged endothelial cells?

A
  1. von Willebrand factor

2. Tissue factor (thromboplastin)

130
Q

What is von Willebrand factor?

A

Promotes platelet adhesion to matrix proteins, such as collagen, following injury

131
Q

What does tissue factor (thromboplastin) do?

A

Activates coagulation

132
Q

What is thrombosis?

A

Inappropriate activation of haemostasis

133
Q

What is a thrombus?

A

Mass formed from blood constituents in the circulation during life

134
Q

What is a thrombus made of?

A

Fibrin and platelets, with entrapped red and white blood cells

135
Q

Where might thrombi form?

A
  1. Cardiac chamber

2. Blood vessel

136
Q

How do thrombi cause damage?

A
  1. Obstruct lumen of vessels in which they form

2. Break off and form emboli

137
Q

What is a blood clot?

A

Formed in static blood

Involves coagulation system without interaction of platelets with vessel wall

138
Q

What is the structure of a blood clot?

A

Soft, jelly-like and unstructured

Random mixture of blood cells suspended in serum proteins

139
Q

What is Virchow’s triad?

A

Factors predisposing to thrombosis

  1. Changes in vessel wall
  2. Changes in blood flow
  3. Changes in constituents of blood
140
Q

What causes changes in vessel wall?

A
  1. Ischaemic hypoxia
  2. Infection
  3. Physical damage
  4. Chemical damage
  5. Immunological damage
141
Q

What might cause physical damage to a vessel wall?

A
  1. Rupture of atherosclerotic plaque
  2. Crushing of veins
  3. Haemodynamic stress in hypertension
142
Q

What might cause chemical damage to a vessel wall?

A
  1. Lipids
  2. Bacterial LPS
  3. Toxins from cigarette smoke
143
Q

What is the effect of disruption of laminar flow?

A
  1. Platelets come into contact with endothelium
  2. Impaired removal of pro-coagulant factors
  3. Impaired delivery of anti-coagulant factors
  4. Direct injury or activation of endothelium
144
Q

What causes a change in blood flow in the arteries or cardiac chambers?

A

Turbulence

145
Q

What causes turbulence?

A
  1. Narrowing
  2. Aneurysms
  3. Myocardial infarction
  4. Abnormal cardiac rhythm
  5. Valvular heart disease
146
Q

What causes a change in blood flow in the veins?

A

Stasis

147
Q

What causes stasis in veins?

A
  1. Right-side heart failure
  2. Immobilisation
  3. Compressed veins
  4. Varicose veins
  5. Increased viscosity of blood
148
Q

Which veins are most commonly affected by thrombosis?

A
  1. Pelvic veins
  2. Superficial leg veins
  3. Deep leg veins
149
Q

What genetic causes change the constituents of blood?

A
  1. Antithrombin III deficiency

2. Protein C deficiency

150
Q

What acquired causes change the constituents of blood?

A
  1. Tissue damage
  2. Post-operative state
  3. Cigarette smoke
  4. Oral contraceptives
  5. Elevated blood lipid
  6. Malignancy
151
Q

What is the appearance of a thrombus in the arteries or cardiac chambers?

A

Compact mass

Granular and firm

Contains laminations

152
Q

What are lines of Zahn?

A

Laminations in thrombus

Composed of pale branching layers of fibrin and platelets and darker layers with more erythrocytes

153
Q

What is the appearance of a thrombus in the veins?

A

Pale head with long red tail

Tail is red due to enmeshed red cells

Few laminations

154
Q

What is the fate of a thrombus?

A
  1. Lysis
  2. Propagation
  3. Stenosis/occlusion
  4. Organisation
  5. Infection
  6. Embolisation
155
Q

How is a thrombus lysed?

A

Broken down by fibrinolytic system

May be accelerated by streptokinase therapy

156
Q

What is thrombus propagation?

A

Occurs in relatively stagnant blood beyond an occluded vein

Propagates along tail toward heart

157
Q

What is thrombus organisation?

A

Thrombus induces inflammatory reaction and subsequent organisation

  1. Retraction of thrombus and partial digestion by leukocyte enzymes
  2. Monocyte/macrophage phagocytosis of debris
  3. Overgrowth and ingrowth of endothelium, forming new vascular channels
  4. Migration of smooth muscle cells and fibroblasts
  5. Synthesis of extracellular matrix
158
Q

What is the fate of the organised thrombus?

A
  1. Incorporated into vessel wall, narrowing lumen

2. New vascular channels may anastomose and dilate, leading to recanalisation

159
Q

How may a thrombus be infected?

A
  1. During a transient bacteraemia

2. From an infection in adjacent tissue

160
Q

What is an embolus?

A

Intravascular mass carried by blood flow from its point of origin to a distant site

161
Q

What are the different types of embolus?

A
  1. Thrombus
  2. Fat
  3. Air
  4. Atheromatous debris
  5. Bone marrow
  6. Amniotic fluid
162
Q

What are the primary effects of thromboemboli?

A
  1. Stenosis or occlusion of blood vessels
  2. Ischaemia
  3. Infarction
163
Q

Where do emboli from systemic veins or right side of heart lodge?

A

Pulmonary artery

This is a pulmonary embolus

164
Q

What are the effects of a pulmonary embolus?

A
  1. Hypoxia
  2. Reduced cardiac output
  3. Shock
  4. Death
  5. Pulmonary infarction
  6. Right sided heart failure
165
Q

Where do emboli from arteries or left side of heart lodge?

A

Systemic arterial circulation

Brain, spleen, kidney, gut, legs, etc

166
Q

What are the effects of arterial thrombi?

A

Infarction

Subsequent organ failure

167
Q

What are the effects of infected emboli?

A

Pyaemia

Abscess formation where they lodge

168
Q

What are the three layers of the arterial wall?

A
  1. Tunica intima
  2. Tunica media
  3. Tunica adventitia
169
Q

What does the tunica intima consist of?

A

Endothelial cells lying on a basement membrane

170
Q

What functions do endothelial cells perform?

A
  1. Containment of blood
  2. Selective transport of ions, gases, fluids and proteins into tissues
  3. Control of haemostasis
  4. Control of blood pressure
171
Q

Give three features of endothelial cells lining healthy adult blood vessels

A
  1. Long lifespan (~5years)
  2. Rarely divide
  3. Resistant to apoptosis
  4. Retain latent capacity to proliferate and remodel
172
Q

What does the tunica media consist of?

A

Layers of perforated elastic laminae with smooth muscle cells in between

Internal elastic lamina on intimal side

External elastic lamina on adventitial side

173
Q

What does the tunica adventitia consist of?

A

Connective tissue

Contains fibroblasts, leukocytes, nerves, lymphatics and arterial blood supply

174
Q

What is the arterial wall blood supply?

A

Vasa vasorum

175
Q

What are elastic arteries?

A

Large arteries

Prominent elastic laminae in their media

Exposed to high pulsatile pressures

Elastic recoil assists maintenance of continuous flow

176
Q

What are muscular arteries

A

Medium and small arteries

Media composed largely of smooth muscle cells with fewer elastic fibres

177
Q

What is atherosclerosis?

A

Disease of the intima of large and medium sized arteries

The lesions are focal thickenings of intima called plaques

178
Q

What are atherosclerotic plaques?

A

Deposits of fibrous tissues and lipids

179
Q

What is arteriosclerosis?

A

Loss of elasticity and physical hardening of arterial wall of any cause

Often accompanied by calcification of wall

180
Q

Give the four MAJOR positive risk factors for atherosclerosis

A
  1. Hyperlipidaemia
  2. Cigarette smoking
  3. Hypertension
  4. Diabetes mellitus
181
Q

Give some of the minor positive risk factors for atherosclerosis

A
  1. Obesity
  2. Excess alcohol consumption
  3. Advancing age
  4. Family history
  5. Male gender
  6. Stressful/sedentary lifestyle
  7. Low birth weight
  8. Socioeconomic status
  9. Infection, eg. chlamydia
182
Q

Give four negative risk factors for atherosclerosis

A
  1. Moderate alcohol consumption
  2. Female gender
  3. High circulating HDL levels
  4. Cardiovascular fitness
183
Q

What do lipoproteins consist of?

A

Lipid core surrounded by apolipoproteins

184
Q

What is found in the lipid core of a lipoprotein?

A
  1. Triglycerides
  2. Cholesterol
  3. Cholesterol
  4. Phospholipids
185
Q

What are the two pathways by which lipoproteins transfer the proteins they carry into cells?

A
  1. LDL receptor pathway

2. Scavenger receptor pathway

186
Q

What is the LDL receptor pathway?

A

Most active in hepatocytes

Responsible for cholesterol breakdown

187
Q

What does underactivity of the LDL receptor pathway lead to?

A

Hypercholesterolaemia

188
Q

What is the scavenger receptor pathway?

A

Used by macrophages to take up lipoproteins that have been modified

Leads to uncontrolled accumulation of cholesterol

189
Q

What are foam cells?

A

Macrophages containing lost of cholesterol due to the scavenger receptor pathway

190
Q

What is dyslipoproteinaemia?

A

Abnormality in the constitution/concentration of lipoproteins in the blood

191
Q

What causes dyslipoproteinaemia?

A
  1. Genes - familial hypercholesterolaemia

2. Secondary to other diseases - diabetes, hypothyroidism

192
Q

What kind of blood lipid profile increases the risk of atherosclerosis?

A

Increased cholesterol, triglycerides, LDL and lipoprotein A

Decreased HDL

193
Q

What have mice models shown about atherosclerosis?

A

Mice deficient for ApoE or LDL receptors develop advanced atherosclerotic lesions

Mice deficient for scavenger receptors SR-A or CD36 show a modest reduction in lesions

Mice that cannot store cholesterol due to a deficiency in ACAT have a reduction in lesions

194
Q

What initiates atherosclerosis?

A

Endothelial cell injury or dysfunction

195
Q

What does endothelial injury result in?

A
  1. Altered permeability
  2. Adhesion of leukocytes
  3. Activation of thrombosis
196
Q

Which adhesion molecules are expressed in response to endothelial injury?

A
  1. P and E selectin
  2. VCAM-1
  3. ICAM-1
197
Q

Which chemokines are expressed in response to endothelial injury?

A
  1. MCP-1
  2. IL-1 and IL-8
  3. M-CSF
198
Q

Which chemokine receptors do macrophages express inside lesions?

A
  1. CCR2

2. CXCR2

199
Q

What are the roles of macrophages when they migrate to intima lesions?

A
  1. Present antigens to T cells
  2. Activate endothelial cells
  3. Oxidise/take up lipids via scavenger receptors
  4. Modify matrix
  5. Activate smooth muscle cells
  6. Promote coagulation
200
Q

How are smooth muscle cells activated in atherosclerosis?

A

Macrophages, platelets and endothelial cells produce growth factors and ROS

201
Q

What happens to smooth muscle cells activated in atherosclerosis?

A
  1. Migrate to intima
  2. Change phenotype from contractile to synthetic
  3. Secrete ECM
  4. Release enzymes that assist in matrix remodelling
202
Q

What does collagenase do?

A
  1. Breaks down collagen

2. Assists in matrix remodelling

203
Q

What causes lipoprotein oxidation?

A
  1. ROS intermediates

2. Enzymes released by platelets, macrophages and endothelial cells

204
Q

What do oxidised lipoproteins do?

A
  1. Chemoattractant for monocytes
  2. Phagocytosed by macrophages
  3. Stimulate various cells in plaque to release cytokines and growth factors
  4. Induce dysfunction in smooth muscle, macrophages, endothelium
  5. May be immunogenic
  6. Inhibit plasminogen activation
205
Q

What do anti-oxidants do?

A
  1. Inhibit formation of oxidised lipids

2. Reduce risk of myocardial infarction

206
Q

Give two examples of anti-oxidant

A
  1. Vitamin E

2. Nitric oxide

207
Q

What is the role of T lymphocytes in atherosclerotic plaque formation?

A

Activate immune responses and cytotoxic killing in plaque

208
Q

What do platelets do in early atherosclerotic lesions?

A
  1. Adhere to injured endothelium

2. Release PDGF

209
Q

What is PDGF?

A

Platelet-derived growth factor

Activates smooth muscle cells

210
Q

What do platelets do in advanced atherosclerotic lesions?

A

Involved in thrombosis in rupture of plaque occurs

211
Q

What are the four types of intimal lesions?

A
  1. Isolated monocytes/macrophages
  2. Fatty dots or fatty streaks
  3. Fibro-fatty atherosclerotic plaques
  4. Complicated plaques
212
Q

Where are fatty streaks found?

A

Throughout vascular tree but particularly at branch points

By second decade of life

213
Q

What are fatty streaks?

A

Clusters of lipid-laden smooth muscle cells and foam cells

214
Q

Where are fibro-fatty atherosclerotic plaques found?

A

Principally in abdominal aorta, coronary arteries, carotid arteries, circle of Willis, arterial branch points

Appear by third/fourth decade in men, later in women

215
Q

What are fibro-fatty atherosclerotic plaques?

A

Raised white-yellow plaques that may coalesce

Atrophic media

Fibrous cap, lipid core and shoulder

216
Q

What is the fibrous cap?

A

On extreme intimal surface of plaque

Composed of collagen, smooth muscle cells, macrophages and T cells

217
Q

What is the lipid core?

A

In plaque

Contains foam cells

May contain necrotic debris and extracellular lipid, esp. cholesterol

218
Q

What is the shoulder of the cap?

A

Contains foam cells, smooth muscle cells, T cells and new blood vessels

219
Q

What are the features of complicated plaques?

A

May be calcified

May expand due to haemorrhage

May rupture/ulcerate

May form aneurysms due to thinning media

220
Q

What is diffuse intimal thickening?

A

Due to build up of smooth muscle cells, collagen and elastin in intima

Associated with ageing, hypertension and chronic inflammation

221
Q

What are the most important clinical sequels of atherosclerosis?

A
  1. Ischaemic heart disease
  2. Peripheral vascular disease
  3. Cerebrovascular disease
  4. Aneurysms
  5. Renal failure
222
Q

What causes intermittent claudication?

A

Peripheral vascular disease

223
Q

What is ischaemia?

A

Insufficient local blood supply to an organ

Insufficient quantity

224
Q

What is infarction?

A

Necrosis due to ischaemia

225
Q

What are the five causes of ischaemia?

A
  1. External occlusion of blood vessels
  2. Internal occlusion
  3. Spasm of vessel
  4. Capillary blockage
  5. Shock
226
Q

What is shock?

A

Circulatory failure with low arterial blood pressure

Causes impaired perfusion of tissues

227
Q

What are the four types of shock?

A
  1. Cardiogenic
  2. Hypovolaemic
  3. Anaphylactic
  4. Septic
228
Q

What causes cardiogenic shock?

A

Heart cannot pump blood due to MI, arrhythmia, outflow obstruction, external compression

229
Q

What causes hypovolaemic shock?

A
  1. Haemorrhage

2. Severe burns

230
Q

What causes septic shock?

A

Gram positive and Gram negative bacterial infection

231
Q

What causes anaphylactic shock?

A

Generalised type 1 hypersensitivity

232
Q

What are the metabolic consequences of ischaemia?

A
  1. Hypoxia
  2. Poor nutrient supply
  3. Failure to remove waste products
233
Q

What are the cellular consequences of ischaemia?

A
  1. Reduced aerobic respiration
  2. Decreased ATP production
  3. Reduced protein synthesis
  4. Damage to DNA, membrane and cytoskeleton
  5. Cell swelling due to failure of sodium pump
234
Q

Which cells are most susceptible to ischaemia?

A

Decreasing order of sensitivity:

  1. Neurons
  2. Renal proximal tubule epithelium
  3. Myocardium
  4. Skeletal muscle
235
Q

Which cells are least susceptible to ischaemia?

A

Macrophages and fibroblasts are insensitive

236
Q

How long does it take for neurons to suffer irreversible damage following anoxia?

A

3 minutes

237
Q

How long does it take for myocardium to suffer irreversible damage following anoxia?

A

20 minutes

Functional impairment after one minute

238
Q

What determines the susceptibility of organs to ischaemia?

A

Anatomy of blood supply to the organ

239
Q

What is the dual blood supply of the lungs?

A

Pulmonary and bronchial arteries

240
Q

What is the dual blood supply of the brain?

A

Circle of Willis

241
Q

What is the dual blood supply of the liver?

A

Hepatic artery and portal vein

242
Q

Which organs are most susceptible to ischaemia?

A

Organs supplied from a single vessel

Kidney and spleen

243
Q

Give eight factors that affect outcome of ischaemia

A
  1. Anatomy of blood supply to organ
  2. Size of block
  3. Degree of block
  4. Speed of onset
  5. Persistence of block
  6. Vulnerability of tissue
  7. Demand of tissue
  8. General adequacy of circulation
244
Q

What causes transient ischaemia?

A

Unstable thrombi that break down

245
Q

What are the outcomes of ischaemia?

A
  1. No effect
  2. Functional defects
  3. Reversible cell damage
  4. Infarction
  5. Ischaemic reperfusion injury
246
Q

What are the microscopic features of infarction?

A
  1. Ischaemic coagulative necrosis
  2. Acute inflammation around the edges after 24 hours
  3. Organisation of infarct
  4. Non-functional fibrous scar after 6 - 8 weeks
247
Q

What are the features of coagulative necrosis?

A
  1. Cytoplasm shows eosinophilia
  2. Nuclei may be pale, shrunken or fragmented
  3. Tissue architecture preserved for several days
248
Q

What is karyolysis?

A

Pale nucleus

249
Q

What is pyknosis?

A

Shrunken nucleus

250
Q

What is karyorhexis?

A

Fragmented nucleus

251
Q

When do macrophages appear in the infarct?

A

3 - 5 days

Granulation tissue starts to develop

252
Q

How does the infarct appear in the early stages?

A

Red due to capillary dilatation and haemorrhage

Poorly defined

253
Q

What is a pale infarct?

A

Infarct in solid tissue

After 24 hours

Well demarcated

254
Q

What is a red infarct?

A

Infarct remains red due to haemorrhage

Result of artery occlusion or venous occlusion

255
Q

What is the shape of an infarct?

A

Determined by blood supply to tissue

Usually cone-shaped

Apex at point of occlusion

Base at organ surface

256
Q

What is on the surface of the infarcted organ in the early stages?

A

Acute inflammation and granulation tissue at margin of infarct

Fibrinous exudate on surface of organ

257
Q

What is the infarct eventually replaced by?

A

Grey scar tissue

258
Q

What is a septic infarct?

A

Secondary infection of infarct that may lead to abscess formation

259
Q

What occurs after an infarct in the brain?

A

Liquefactive necrosis

Necrotic cells digested quickly

Forms cyst containing liquid

Surrounding by reactive glial cells

260
Q

What is ischaemic reperfusion injury?

A

Reversible injury that becomes irreversible due to restoring blood flow to ischaemic tissue

Due to generation of fresh mediators of cell injury

Initiation of acute inflammation by delivery of neutrophils and complement

261
Q

What causes myocardial infarction?

A

Usually coronary artery atherosclerosis

Predominantly affects left ventricle

262
Q

What are the effects of myocardial infarction?

A
  1. Dysrhythmia
  2. Sudden death
  3. Cardiogenic shock
  4. Rupture of infarct
  5. Mural thrombosis
  6. Scarring leading to cardiac aneurysm
  7. Adaptation to inadequate cardiac output
  8. Cardiac failure
263
Q

What causes pulmonary infarction?

A

Thromboembolism from pelvic or leg veins

264
Q

What are the effects of pulmonary infarction?

A
  1. Silent
  2. Impaired lung function
  3. Pressure overload on right heart
  4. Right sided heart failure
  5. Infection
265
Q

What are the causes of cerebral infarction?

A
  1. Cerebral artery thrombosis
  2. Embolism
  3. Shock
266
Q

Where does embolism to brain usually come from?

A

Heart or atheroma

Usually in common carotid arteries

Thrombus or plaque

267
Q

What are the outcomes of cerebral infarction?

A
  1. Liquefactive necrosis and cyst formation

2. Sudden onset of inadequate cerebral function (stroke)

BOD (8 decks)

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