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ESA2 > MoD 5 + 6 (Haemostasis, Thrombosis & Atherosclerosis) > Flashcards

MoD 5 + 6 (Haemostasis, Thrombosis & Atherosclerosis) Flashcards

1
Q

Define haemostasis:

A

The process of stopping bloodflow

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2
Q

Haemostasis depends on what 4 factors?

A
  • Vessel wall (changes in tone and secretion)
  • Coagulation cascade
  • Platelets
  • Fibrinolytic system
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3
Q

What changes occur to endothelial cells to stop bleeding?

A
  • Vasoconstriction
  • Stop secreting coagulation/aggregation inhibitors
  • Secrete von Willebrand factor, ADP, Factor III and Endothelins
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4
Q

What substances are secreted by damaged endothelial cells to promote haemostasis?

A
  • von Willebrand factor
  • Factor III
  • ADP
  • Endothelins
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5
Q

What cell are platelets derived from?

A

Megakaryocytes

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6
Q

What do platelets contain?

A

alpha granules - von Willebrand factor, thrombin

dense granules - ADP

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7
Q

What do platelet alpha granules contain?

A

von Willebrand factor
Thrombin
Fibrinogen

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8
Q

What do platelet dense granules contain?

A

ADP
Serotonin (5HT)
Ca2+

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9
Q

What 4 substances can activate platelets?

A
  • Collagen
  • Thromboxane
  • Thrombin
  • ADP
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10
Q

What causes platelets to change shape, allowing them to adhere to each other to form a platelet plug?

A

Activation = exocytosis of alpha and dense granules

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11
Q

Activated platelets express receptors for what substances?

A
  • von Willebrand factor

- Fibrinogen

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12
Q

What protein cleaves fibrinogen into fibrin?

A

Thrombin

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13
Q

What test could be done to obtain a platelet count?

A

Complete blood count

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14
Q

What co factor is required for prothrombin to be cleaved into thrombin?

A

Activated factor V

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15
Q

What conditions may a low Factor V assay indicate?

A
  • Factor V deficiency
  • Disseminated Intravascular Coagulation
  • Liver disease
  • Primary fibrinolysis
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16
Q

What is an ideal prothrombin time?

A

25-30 secs

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17
Q

What is Prothrombin time?

A

Time it takes for blood to clot

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18
Q

What may an abnormally long prothrombin time indicate?

A
  • Blood thinning drugs
  • Haemophilia
  • Malabsorption
  • Liver disease
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19
Q

Name 5 (endogenous) Thrombin inhibitors:

A

1) Anti thrombin III
2) alpha-1-antitrypsin macroglobulin
3) Protein C
4) Protein S

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20
Q

What is the role of anti-thrombin III in the fibrinolytic system?

A

Degrades thrombin and factor Xa

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21
Q

Which enzyme is required for the degradation of fibrin?

A

Plasmin

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22
Q

List some anti-thrombotic factors released from healthy endothelial cells:

A
  • Plasminogen activators
  • Prostacyclin
  • Nitric oxide
  • Thrombomodulin
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23
Q

What are the anti-thrombotic roles of prostacyclin?

A
  • Vasodilation

- Inhibits platelet activation

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24
Q

What are the anti-thrombotic roles of nitric oxide?

A
  • Vasodilation

- Inhibits platelet aggregation

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25
Q

What is the anti-thrombotic role of thrombomodulin?

A

Converts thrombin into an anticoagulant

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26
Q

What class of drug is Streptokinase?

A

Fibrinolytic

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27
Q

How does Streptokinase and tPA cause the lysis of fibrin?

A

Increase plasmin formation

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28
Q

Define Thrombosis:

A

The formation of a solid mass of blood within the circulatory system, during life

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29
Q

What is Virchow’s Triad?

A

1) Abnormalities of vessel wall
2) Abnormalities of blood composition
3) Abnormalities of blood flow

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30
Q

Give some examples of causes of abnormalities of the vessel wall which may lead to thrombosis:

A
  • Atheroma
  • Trauma
  • Inflammation
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31
Q

Give some examples of causes of abnormalities of blood composition, which may lead to thrombosis:

A
  • Pre/Post-partum
  • Post-surgery
  • Smoking
  • Oral contraceptive pill
  • Cancer and/or Chemotherapy
  • Central obesity
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32
Q

Give some examples of abnormalities of blood flow, which may lead to thrombosis:

A
  • Stagnation

- Turbulence

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33
Q

Why do smokers have an increased risk of thrombosis?

A

More coagulable blood

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34
Q

Describe the appearance of an arterial thrombus:

A

Pale

Lines of Zahn

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35
Q

What makes arterial thrombi pale?

A

Low cell content, high levels of fibrin

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36
Q

What are Lines of Zahn, and where are they seen?

A

Layers of fibrin and platelets, alternating with layers of red blood cells.
Seen in arterial thrombi, formed in areas of rapid blood flow

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37
Q

Describe the appearance of a venous thrombus:

A

Deep red
Gelatinous
Soft

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38
Q

Name the possible outcomes of thrombosis:

A

1) Lysis/Resolution
2) Propagation
3) Organisation
4) Recanalisation
5) Embolism

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39
Q

What is the most likely outcome of small thrombi?

A

Lysis/Resolution

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40
Q

What is meant by propagation of a thrombus?

A

Progressive spread of a thrombus

  • distally in arteries
  • proximally in veins
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41
Q

What is meant by organisation of a thrombus?

A

Invasion of fibroblasts and endothelial cells into the thrombus, which form granulation tissue, and convert the thrombus into fibrous scar-like tissue, may contain tiny capillaries

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42
Q

What is meant by recanalization of a thrombus?

A

Organised thrombus with small blood vessels running through the fibrous tissue, incompletely restoring flow

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43
Q

Why may a venous thrombus cause congestion and oedema?

A
  • Thrombus blocks vein, preventing venous drainage of tissue

- Tissue fluid pressure increases, until equal to arterial pressure

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44
Q

Define embolism:

A

The blockage of a blood vessel by a solid, liquid or gas at a site distant from its origin

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45
Q

Define Deep Vein Thrombosis:

A

Thrombus in a deep vein, composed mainly of fibrin

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46
Q

Why is central obesity a risk factor for hypercoagulable blood?

A

Central obesity causes an increase in adipocytokines in the blood, which increases the coagulability of blood

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47
Q

Give 2 risk factors of endothelial damage:

A
  • Trauma
  • Hypertension
  • Cigarette smoking
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48
Q

Why does immobilisation increase the risk of DVT formation?

A
  • Deep veins of the legs are dependent on the muscle-pump action to return blood to the heart
  • If no muscle pump action, blood pools in the veins = change in blood flow = increased risk of thrombosis
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49
Q

What is the classical presentation of a patient with a DVT?

A
  • Limb oedema
  • Pain
  • Warm or red skin
  • History of immobilisation or long-haul flight
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50
Q

What is the most dangerous complication of a DVT?

A

Pulmonary embolism

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51
Q

What can be used for DVT prophylaxis?

A
  • Subcutaneous heparin

- Leg compression

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52
Q

How does heparin prevent the formation/growth of a thrombus?

A
  • Binds to and activates Anti-thrombin III

- This inactivates Thrombin and Factor Xa

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53
Q

What is the treatment of a DVT?

A
  • IV Heparin

- Oral Warfarin

54
Q

How does Warfarin prevent the formation/growth of a thrombus?

A
  • Inhibits vitamin K Reductase

- Prevents formation of vitamin K dependent clotting factors: II, VII, IX, X

55
Q

The formation of which clotting factors is vitamin K dependent?

A

Factors II, VII, IX, X

56
Q

What is Trousseau syndrome?

A

Medical sign of a rare form of thrombo-embolism, associated with pancreatic, gastric and lung cancer. Multiple migratory thrombi form in superficial veins, chest wall and arms, and present as tender palpable nodules.

57
Q

What medical sign is associated with the thrombo-emboli which may form due to pancreatic, lung or gastric cancer?

A

Trousseau syndrome

58
Q

Define pulmonary embolism:

A

Occlusion of a pulmonary artery caused by a fragment of a thrombus carried by the blood stream.

59
Q

Why does a pulmonary embolism cause changes in a patients ECG?

A
  • PE causes pressure in pulmonary arteries to increase
  • This increases the afterload of the right ventricle
  • Right ventricle must work harder to eject blood = right ventricle hypertrophy, detectable on ECG
60
Q

What is a saddle embolism?

A

A pulmonary embolism which lodges in the pulmonary artery, and bridges and extends into the left and right pulmonary arteries

61
Q

What are the symptoms of a significant pulmonary embolism?

A
  • Pleuritic chest pain (sharb stabbing pain in lateral chest and upper back)
  • Breathlessness
  • Hypoxia
62
Q

Describe pleuritic chest pain:

A

Sharp, stabbing pain in lateral chest and/or upper back

63
Q

What is a paradoxical embolism?

A

An arterial embolism of venous origin

64
Q

Why is a paradoxical embolism rare, even when an atrial/ventricular septal defect is present?

A

The pressure difference between the RH and the LH prevents blood entering the LH from the RH

65
Q

List some substances which may form an embolism:

A
  • Air
  • Thrombus (blood)
  • Amniotic fluid
  • Nitrogen
  • Bone marrow
  • Fat
  • Medical equipment
  • Tumour cells
66
Q

What are the 2 types of Haemophilia?

A

1) Haemophilia A

2) Haemophilia B

67
Q

What is the inheritance pattern of Haemophilia A?

A

X-linked

68
Q

Is Haemophilia A more common in males or females?

A

Males - as follows X-linked inheritance pattern

69
Q

What is Haemophilia A?

A

Deficiency of clotting Factor VIII, therefore unable to clot normally

70
Q

Why are people with Haemophilia A unable to clot normally?

A

Deficiency of clotting Factor VIII

71
Q

What is the inheritance pattern of Haemophilia B?

A

X linked

72
Q

What is Haemophilia B?

A

Deficiency of clotting Factor IX

73
Q

What is the name of the disease in which the person has a deficiency of the clotting Factor IX?

A

Haemophilia B

74
Q

What is the name of the disease in which the person has a deficiency of the clotting Factor VIII?

A

Haemophilia A

75
Q

What is the inheritance pattern of von Willebrand disease?

A

Autosomal recessive

76
Q

What is von Willebrand disease?

A

Deficiency of von Willebrand factor (required for normal blood clotting)

77
Q

Name some risk factors of Disseminated Intravascular Coagulation:

A
  • Cancer
  • Inflammation ie liver disease, pancreatitis
  • Infection ie recent surgery, septicaemia, tissue injury
78
Q

How does Disseminated Intravascular Coagulation lead to multiple thrombi and serious bleeding?

A
  • Systemic activation of clotting cascade = microvascular thrombi in various organs
  • Over time clotting factors are ‘used up’ = high risk of serious bleeding (cannot clot)
79
Q

What does DIC stand for?

A

Disseminated Intravascular Coagulation

80
Q

What is Thrombocytopenia?

A

Low platelet count (below lower limit)

81
Q

What may cause Thrombocytopenia?

A
  • Inherited mutation (congenital)
  • Viral infection
  • Drugs
  • Neoplasm malignancy to bone marrow
  • Autoimmune disease
  • DIC
  • (Miliary) TB
82
Q

What is the name given to the disorder characterised by a platelet count lower than the lower limit?

A

Thrombocytopenia

83
Q

What is Thrombophilia?

A

Predisposition to form thrombus, which may lead to thromboembolism

84
Q

Define Atherosclerosis:

A

The thickening and hardening of arterial walls as a consequence of atheroma

85
Q

Define Atheroma:

A

The accumulation of intra- and extracellular lipid in the tunica media and intima of large and medium arteries

86
Q

What is the name given to the thickening and hardening of arterial walls as a consequence of atheroma?

A

Atherosclerosis

87
Q

What is the name given to the accumulation of intra- and extracellular lipid in the tunica media and intima of large and medium arteries?

A

Atheroma

88
Q

Define arteriosclerosis:

A

The thickening of the walls of arteries/arterioles usually as a result of hypertension or diabetes mellitus

89
Q

What conditions cause arteriosclerosis?

A

Diabetes mellitus

Hypertension

90
Q

What name is given to the thickening of the walls of arteries/arterioles as a result of hypertension or diabetes mellitus?

A

Arteriosclerosis

91
Q

What name is given to the thickening or arteries or arterioles, NOT due to atheroma?

A

Arteriosclerosis

92
Q

What are the 4 stages of atherosclerosis formation?

A

1) Chronic endothelial injury
2) Accumulation of LDLs in the tunica intima
3) Recruitment of macrophages and smooth muscle cells
4) Smooth muscle proliferation, collagen, matrix and extracellular lipid deposition, and neovascularisation

93
Q

How does lipid get into the tunica media during atherosclerosis formation?

A

Macrophages and smooth muscle cells engulf the lipid in the tunica intima, and migrate into the tunica media

94
Q

What are the 3 types of atherosclerosis, characterised by macroscopic appearance?

A

1) Fatty streak
2) Simple (stable) plaque
3) Complicated (unstable) plaque

95
Q

What are the macroscopic features of a stable/simple plaque?

A
  • Small necrotic core
  • Thick fibrous cap
  • Yellow/white
  • Raised
  • Irregular outline
96
Q

What are the macroscopic features of a fatty streak?

A
  • Yellow
  • Slightly raised
  • Lipid deposition in tunica intima
97
Q

What are the macroscopic features of an unstable/complicated plaque?

A
  • Large necrotic core
  • Thin fibrous cap
  • Thrombosis
  • Calcification
  • Haemorrhage
  • Aneurysm formation
98
Q

Define aneurysm:

A

Abnormal blood-filled bulged blood vessel (usually artery), due to a weakening of the vessel wall

99
Q

What are the microscopic changes of early atherosclerosis?

A
  • Smooth muscle cell proliferation
  • Extracellular lipid deposition
  • Accumulation of foam cells
100
Q

What are the microscopic changes of later atherosclerosis?

A
  • Fibrosis
  • Necrosis
  • Cholesterol clefts
  • Disruption of internal elastic lamina (extends into media)
  • Ingrowth of blood vessels
  • Plaque fissuring/rupture
101
Q

What are cholesterol clefts, seen in later atherosclerosis microscopically?

A

Areas of cholesterol crystals in later atherosclerosis, which are removed by the staining process, leaving clefts

102
Q

Name some common sites of atherosclerosis:

A
  • Thoracic/Abdominal aorta
  • Coronary arteries
  • Carotid and cerebral arteries
  • Iliac, femoral and popliteal arteries
103
Q

Atherosclerosis in the coronary arteries causes what disease?

A

Ischaemic Heart Disease (or coronary heart disease)

104
Q

What are the modifiable risk factors for ischaemic heart disease?

A 
Smoking
Diabetes
Hypercholesterolaemia
Hypertension
Stress
Obesity
Fruit + Veg intake
105
Q

What are the complications of Ischaemic Heart Disease?

A

Angina
Myocardial Infarction
Heart failure
Arrhythmia

106
Q

Describe the pain associated with Ischaemic Heart Disease:

A

Central tightening chest pain, which may radiate to arms and/or neck

107
Q

What are the non-modifiable risk factors for Ischaemic Heart Disease?

A
  • Male gender
  • Increasing age
  • Family history
  • Ethnicity
108
Q

Which ethnic groups are at higher risk of developing Ischaemic Heart Disease?

A
  • South Asians

- African-Caribbeans

109
Q

What are the risk factors for Cerebral Ischaemia?

A 
Hypertension
Diabetes
Cardiac disease
Hypercholesterolaemia
Carotid stenosis
110
Q

What is Cerebral Ischaemia?

A

Lack of blood to the brain, leading to ischaemic stroke

111
Q

What is Peripheral Vascular Disease?

A

Slow progressive narrowing of blood/lymph vessels outside of the heart and brain, usually caused by atherosclerosis.

112
Q

What is the common presenting symptom of peripheral vascular disease affecting the legs?

A

Intermittent claudication

113
Q

If a patient presents with bilateral intermittent claudication, what is the problem?

A

Occlusion of the abdominal aorta just above the bifurcation into common iliac arteries, due to an atherosclerosis

114
Q

Define claudication:

A

Pain and/or cramping in the leg due to inadequate blood flow to the muscles

115
Q

What is Leriche syndrome?

A

Aortoiliac occlusion due to atherosclerosis, causing bilateral claudication

116
Q

What is an abdominal aortic aneurysm?

A

Focal dilation of the abdominal aorta to 3cm or more (>50%)

117
Q

How does atherosclerosis sometimes lead to an abdominal aortic aneurysm?

A

Atherosclerosis mechanically weakens the aortic wall, causing loss of the elastic recoil, allowing focal dilation

118
Q

What is Rokitansky’s Thrombogenic hypothesis?

A
  • Atheromas form due to repeated thrombi composed of fibrin, platelets and leukocytes
  • Lipid is derived from the thrombi
119
Q

How could you externally localise the site of occlusion in the lower limb, due to peripheral vascular disease?

A

Compare lower limb pulses from distal to proximal

120
Q

What is Virchow’s Insudation theory?

A
  • Atheromas form in response to endothelial injury and subsequent inflammation, which increases the permeability of the endothelial cells to lipid (from plasma)
121
Q

What is Ross & Glomset’s Reaction-to-Injury hypothesis?

A
  • Atheromatous plaques form in response to endothelial injury, due to an increase in oxidised LDLs.
  • The injury increases endothelium permeability, and allows platelet adhesion, followed by monocyte and smooth muscle migration.
122
Q

What is Benditt & Benditt’s Monoclonal hypothesis?

A
  • Atheromas develop from the proliferation of smooth muscle cells, from a single progenitor cell (each plaque is a monoclonal benign tumour)
123
Q

Whose hypothesis for atheroma formation is currently accepted - ‘unifying hypothesis’?

A

Ross & Glomset’s Reaction-to-Injury hypothesis

124
Q

What cells are involved in atherogenesis?

A
  • Endothelial cells
  • Macrophages
  • Smooth muscle cells
  • Neutrophils
  • Platelets
  • Lymphocytes
125
Q

Define atherogenesis:

A

The formation of abnormal fatty or lipid masses in arterial walls

126
Q

Which cells form foam cells during atherogenesis?

A

Macrophages

Smooth muscle cells

127
Q

What cell type involved in atherogenesis can oxdise LDLs?

A

Macrophages

128
Q

Infection of which microbes increase the risk of atherosclerosis formation?

A
  • Chlamydia pneumonia
  • Helicobacter pylori
  • Cytomegalovirus
129
Q

How can you prevent atherosclerosis?

A
  • No smoking
  • Reduce fat intake
  • Treat hypertension
  • Regular exercise
  • Weight control (maintain healthy BMI)
  • Alcohol control (moderate intake)
130
Q

What are the interventions available for atherosclerosis?

A
  • Modify diet
  • Treat hypertension/diabetes
  • Lipid-lowering drugs ie Statins
  • Blood thinners ie Aspirin
  • Percutaneous coronary intervention
  • Coronary artery bypass grafting

ESA2 (27 decks)

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