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Semester 2: Cardiorespiratory Fitness > PBL Topic 2 Case 8 > Flashcards

PBL Topic 2 Case 8 Flashcards

1
Q

Identify the clinical features of a massive pulmonary embolism

A
  • Severe central chest pain (cardiac ischaemia)
  • Shock, pale, clammy, syncope
  • Tachypnoeic, tachycardic, hypotension
  • Gallop rhythm and widely split second heart sound
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2
Q

Explain how thrombin is removed from the blood

A
  • Adsorbed by fibrin filaments
  • Combines with antithrombin III which inactivates thrombin
  • Heparin binds to antithrombin III, which removes Factors XII, XI, X and IX
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3
Q

Identify two other factors found in the cytoplasm of a platelet

A
  • Growth factor

- Fibrin-stabilising factor

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4
Q

Why are immobilised patients more at risk of a deep leg vein thrombosis?

A
  • Reduced calf muscle contraction
  • Reduction in pressure
  • Reduced venous return
  • Increased risk of stagnation and hence DVT
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5
Q

How are platelets formed from megakaryocytes?

A
  • Megakaryocytes fragment either in the bone marrow or soon after entering the blood
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6
Q

Outline type 2 von Willebrand’s disease

A
  • Inherited autosomal dominant condition
  • Partial qualitative abnormality of vWF
  • Minor clinical features such as bleeding following minor trauma or surgery
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7
Q

Why is there vasoconstriction following trauma to a vessel?

A
  • To reduces the blood flow through the damaged vessel

- To prevent blood loss

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8
Q

What is the diameter of a platelet?

A
  • 1 - 4 uM
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9
Q

What is the role of the mitochondria in platelets?

A
  • Formation of ATP and ADP
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10
Q

Why is warfarin not given in the later months of pregnancy?

A
  • It can cause inter-cranial haemorrhages in the baby during delivery
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11
Q

Explain why aspirin potentiates the effects of warfarin

A
  • Inhibition of platelet function
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12
Q

What is Prekallikrein also known as?

A
  • Fletcher Factor
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13
Q

Outline the clinical features of immune thrombocytopenia purpura

A
  • Mucosal bleeding
  • Purpuric rash
  • Skin bruising
  • Menorrhagia in females
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14
Q

What is international normalised ratio?

A
  • Used to determine prothrombin time

- Which measures the effect of warfarin

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15
Q

What is an embolism?

A
  • Mass of material
  • That is able to lodge in a vessel
  • And block its lumen
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16
Q

What are thrombocytes?

A
  • Platelets
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17
Q

What is heparin?

A
  • Injectable Anticoagulant
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18
Q

Why is heparin not typically given subcutaneously?

A
  • Delay of up to 60 minutes
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19
Q

What does a CXR show with a a massive pulmonary embolism?

A
  • Oligaemia

- Dilation of pulmonary artery

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20
Q

Explain why cephalosporins potentiate the effects of warfarin

A
  • Inhibit the reduction of Vitamin K
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21
Q

Outline the pathophysiology of a pulmonary embolism

A
  • Va/Q = infinity
  • Intrapulmonary dead space
  • Reduced surfactant as a result of reduced perfusion
  • Alveolar collapse
  • Hypoxaemia
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22
Q

What is the normal Activated Partial Thromboplastin time?

A
  • 26 - 37 seconds
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23
Q

Outline the pathophysiology of immune thrombocytopenia purpura

A
  • Antibodies coat platelet

- Which binds to Fc receptors of macrophages

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24
Q

Where do the majority of venous thrombi lodge?

A
  • Pulmonary circulation as a pulmonary embolism
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25
Q

Identify the main unwanted effect of warfarin

A
  • Haemorrhage
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26
Q

What is the most common cause of embolism?

A
  • Thrombus
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27
Q

Identify three treatments of immune thrombocytopenia purpura

A
  • Corticosteroids as immunosuppressive therapy
  • IgG infusion to block Fc receptors
  • Splenectomy
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28
Q

Why are diuretics and vasodilators avoided in the treatment of pulmonary embolism?

A
  • Patients are already hypotensive

- These will further reduce cardiac output

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29
Q

What does a CXR show in multiple recurrent pulmonary emboli

A
  • Oligaemia

- Enlarged pulmonary arterioles

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30
Q

von Willebrand factor as a carrier protein for what molecule?

A
  • Factor VIII
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31
Q

How are ventilation and perfusion assessed in Va/Q scanning

A
  • Ventilation is assessed using radioactive xenon

- Perfusion is assessed by injection of micro-aggregates of 99mTc-albumin

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32
Q

What is Factor V also known as?

A
  • Proaccelerin

OR

  • AC-globulin

OR

  • Labile Factor
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33
Q

What is the role of thrombomodulin?

A
  • Prevents clotting in the normal vascular system:
  • Binds to thrombin and slows the clotting process
  • Activates protein C that inactivates Factor Va and Factor VIIIa
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34
Q

How is Prothrombin Time performed?

A
  • Addition of tissue factor and calcium to patient’s plasma
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35
Q

What will ABGs show in pulmonary embolism?

A
  • Normal or reduced PaO2 and PaCO2

- That becomes markedly abnormal (metabolic acidosis) in massive pulmonary emboli

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36
Q

Explain why co-trimoxazole potentiates the effects of warfarin

A
  • Inhibition of hepatic drug metabolism
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37
Q

What occurs if emboli lodge in smaller peripheral vessels?

A
  • Gangrene
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38
Q

Platelets are derived from which type of cell?

A
  • Megakaryocyte
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39
Q

What is meant by individual empowerment?

A
  • Giving people responsibility for their health
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40
Q

How do either of these pathways result in prothrombin activator formation?

A
  • Cascade of clotting factors
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41
Q

What is Factor XI also known as?

A
  • Plasma Thromboplastin Antecedent

OR

  • Antihaemophilic Factor C
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42
Q

What is Factor XII also known as?

A
  • Hageman Factor
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43
Q

What is the first-line diagnostic test for pulmonary embolism and why?

A
  • CT pulmonary angiography
  • Shows extent of emboli
  • Highlights alternative diagnosis
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44
Q

What is the difference between theory of reasoned action and planned behaviour?

A
  • Theory of planned behaviour includes behavioural control as an additional determinant of intentions and behaviour
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45
Q

Outline the developmental approach to theories of eating behaviour

A
  • Exposure refers to neophobic responses that shapes view of food
  • Social learning refers to food choices changes through watching others eat
  • Associative learning refers to rewards for eating behaviour or food as a reward for other behaviour
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46
Q

Outline two functions of warfarin

A
  • Oral Anticoagulant

- Vitamin K antagonist

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47
Q

Is joint bleeding a feature of a platelet defect (e.g. thrombocytopenia) or a coagulation defect (e.g. haemophilia)

A
  • Coagulation defect (e.g. haemophilia)
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48
Q

What does Activated Partial Thromboplastin Time measure?

A
  • Factors XII, XI, IX, VIII, X, V, prothrombin and fibrinogen
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49
Q

Outline the mechanism of action of heparin

A
  • Activation of antithrombin III
  • To inhibit thrombin, heparin must bind to AT3 and thrombin
  • To inhibit factor Xa, heparin must bind to AT3 only
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50
Q

What is thrombocytopenia?

A
  • Spontaneous bleeding

- When blood platelet count falls

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51
Q

Outline type 4 von Willebrand’s disease

A
  • Autosomal recessive condition
  • Complete deficiency of vWF
  • Severe bleeding
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52
Q

How can females be affected by Haemophilia

A
  • Lionisation towards the abnormal X chromosome
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53
Q

What is the normal Prothrombin time?

A
  • 12 -16 seconds
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54
Q

Outline the cognitive approach to theories of eating behaviour

A
  • Attitudes towards foods

- Perceived behavioural control

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55
Q

What is Factor VIII also known as?

A
  • Antihaemophilic Factor

OR

  • Antihaemophilic Globulin

OR

  • Antihaemophilic Factor A
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56
Q

When is prothrombin formed?

A
  • Following the rupture of a blood vessel
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57
Q

Explain why necrosis in soft tissues may occur in patients taking warfarin

A
  • Thrombosis in venules

- Inhibition protein c synthesis

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58
Q

How is the platelet plug strengthened?

A
  • Fibrin formation

- Between aggregating platelets

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59
Q

Why is warfarin not given in the first months of pregnancy?

A
  • It is able to cross the placenta

- It is teratogenic

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60
Q

Outline the pathogenesis of thrombotic thrombocytopenic purpura

A
  • Reduction in ADAMTS-13,
  • A protease that breaks down large vWF into smaller factors that can interact with platelets
  • Aggregation of platelets to these large vWF
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61
Q

Outline the boundary model of overeating

A
  • Dieters take longer to feel full
  • Dieters set a boundary which limits what they can eat
  • Dieters cross this boundary until they feel full
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62
Q

Why is genotyping necessary when administering warfarin

A
  • VKORC1 gene is polymorphic

- Warfarin is metabolised by CYP2C9, a substate of P450 isoenzymes, which is also polymorphic

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63
Q

What is meant by social engineering?

A
  • Ill health is influenced by poverty, lack of education and poor living conditions
  • Objectives should be to improve these standards
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64
Q

Why are IV fluids given in pulmonary embolism?

A
  • Patients are hypotensive

- Fluids increase right heart pumping

65
Q

What is the most common cause of venous thrombosis?

A
  • Stasis
66
Q

How are platelets removed from the body?

A
  • Macrophages in the spleen
67
Q

What is the role of fibrin-stabilising factor?

A
  • Causes covalent bonds between the fibrin monomers

- Cross-linking of adjacent fibrin fibres

68
Q

Outline five causes of the vascular constriction that occurs following vessel damage

A
  • Myogenic Spasm
  • Autacoid factors
  • Nervous reflexes
  • Myogenic contraction
  • Thromboxane A2 from platelets
69
Q

What is streptokinase?

A
  • Purified fraction of haemolytic streptococci
  • Forms complex with plasminogen to form plasmin
  • Lysis of clots and free fibrinogen
70
Q

What is the significance of Vitamin K in the formation of blood clots?

A
  • Necessary for liver formation of prothrombin, Factor VIII, IX and X, Protein C and S
  • In the absence of Vitamin K the tendency to bleed is enhanced
71
Q

What is the action of thrombin on fibrinogen?

A
  • Removal of four low-molecular weight peptides
  • Forming one molecule of the fibrin monomer
  • Which has the capability to polymerise with other fibrin monomers.
72
Q

When can the diagnosis of pulmonary embolism be excluded?

A
  • If D-dimer is not present
73
Q

What is Factor VII also known as?

A
  • Serum Prothrombin Conversion Accelerator

OR

  • Proconvertin
74
Q

What is the function of phospholipids in the cell membrane of platelets?

A
  • Activate multiple stages in the blood clotting process
75
Q

How can atrial fibrillation increase the risk of a thromboembolism?

A
  • Ineffectual movement of the atria causes stagnation
76
Q

What is Factor XIII also known as?

A
  • Fibrin Stabilising Factor
77
Q

Identify the clinical features of multiple recurrent pulmonary emboli

A
  • Breathless, weakness, syncope and angina
  • Signs of right ventricular overload with right ventricular heave
  • Loud pulmonary second sound
78
Q

Explain the haemolytic anaemia as seen in thrombotic thrombocytopenic purpura

A
  • Red cell fragmentation
79
Q

What is Factor X also known as?

A
  • Stuart-Prower Factor
80
Q

What is the role of glycocalyx?

A
  • Prevents clotting in the normal vascular system

- By repelling clotting factors and platelets

81
Q

What is Factor I also known as?

A
  • Fibrinogen
82
Q

Outline the mechanism of action of warfarin on Vitamin K antagonism

A
  • Competitive inhibtion of Vitamin K epoxide reductase component 1 (VKORC1)
  • Thus inhibiting vitamin K epoxide to its active hydroquinone form

-

83
Q

Outline the two ways in which prothrombin activator is formed

A
  • Extrinsic pathway that begins with trauma to the vascular wall
  • Intrinsic trauma that begins in the blood itself
84
Q

How can a myocardial infarction increase the risk of a thromboembolism?

A
  • Endothelial lining is lost
  • Underlying collagen is exposed
  • Binding of platelets to von Willebrand factor
85
Q

Identify three causes of thrombocytopenia

A
  • Failure of platelet production e.g. megaloblastic anaemia
  • Increased platelet destruction e.g. autoimmune thrombocytopenic purpura
  • Platelet sequestration e.g. splenomegaly
86
Q

Explain why LMWHs do not increase the action of antithrombin III on factor Xa but not on thrombin

A
  • It is too small to bind to both AT3 and thrombin
87
Q

Identify signs and symptoms of deep vein thrombosis

A
  • Painful, red swelling in calf associated with engorged veins
  • Homan’s sign (calf pain on dorsiflexion)
  • Cyanotic discolouration
  • Gangrene
88
Q

How can you use prothrombin time to distinguish between Haemophilia A, von Willebrand’s disease and Vitamin K deficiency?

A
  • Prothrombin time is increased in Vitamin K deficiency

- It is normal in both haemophilia A and von Willebrand’s disease

89
Q

What does a CXR show with a small/medium pulmonary embolism?

A
  • Atelectasis
  • Pleural effusion
  • Raised hemidiaphragm
90
Q

How does serum differ from plasma?

A
  • Serum does not include fibrinogen and clotting factors
91
Q

Identify two cells that produce heparin and where they are located

A
  • Basophils in the blood

- Mast cells in the connective tissue throughout the body

92
Q

Identify the clinical features of a small/medium pulmonary embolism

A
  • Pleuritic chest pain and dyspnoea
  • Tachypnoeic
  • Pleural rub and coarse crackles
93
Q

Identify the treatment of a deep vein thrombosis

A
  • Heparin
  • Warfarin
  • Bed Rest
94
Q

Haemophilia A is a deficiency of which clotting factor?

A
  • Factor VIII
95
Q

Outline the treatment for thrombotic thrombocytopenic purpura

A
  • Plasma exchange, providing a source of ADAMTS-13

- Rituximab, a monoclonal antibody

96
Q

Outline the function of plasmin

A
  • Proteolytic enzyme
  • Lysis of blood clots
  • Digests fibrin fibres and Factors V, VIII, XIII and prothrombin
97
Q

What occurs if emboli lodge in in the intestine?

A
  • Ischaemia bowel

- Resulting in perforation and peritonitis

98
Q

Outline the general mechanism of blood coagulation

A
  • Clotting cascade activates prothrombin activator
  • Which converts prothrombin into thrombin
  • Which acts as an enzyme to convert fibrinogen into fibrin that enmeshes platelets
99
Q

Is mucosal bleeding a feature of a platelet defect (e.g. thrombocytopenia) or a coagulation defect (e.g. haemophilia)

A
  • Platelet defect e.g. thrombocytopenia
100
Q

Explain how plasminogen is converted into plasmin

A
  • Injured tissues release tissue plasminogen activator (t-PA)
101
Q

What is the normal concentration of platelets in the blood

A
  • 150,000 - 300,000

- Per uL

102
Q

Identify three contractile proteins found in the platelet cytoplasm

A
  • Actin
  • Myosin
  • Thrombosthenin
103
Q

Why are males more likely to be by Haemophilia?

A
  • It is inherited as an X-linked recessive condition
104
Q

What does an ECG show with multiple recurrent pulmonary emboli?

A
  • Signs of pulmonary hypertension
105
Q

How is Haemophilia treated?

A
  • Intravenous infusion of either factor VIII or factor IX
106
Q

Outline the causal model of overeating

A
  • Dieting precedes overeating and contributes to it causally
107
Q

What is high-molecular-weight kininogen also known as?

A
  • Fitzgerald Factor
108
Q

What is the Revised Geneva Score?

A
  • Assess probability of pulmonary embolism
  • Takes into account signs, symptoms and risk factors
  • Risk factors include malignancy, DVT, surgery or fracture and age
109
Q

What does an ECG show with a small/medium pulmonary embolism?

A
  • Sinus tachycardia

- Atrial fibrillation

110
Q

Explain the raised lactic dehydrogenase as seen in thrombotic thrombocytopenic purpura

A
  • Haemolysis
111
Q

How is Thrombin Time performed?

A
  • Addition of thrombin to a patient’s plasma
112
Q

Outline the vicious circle of clot formation

A
  • The clot initiates positive feedback forming clots in the surrounding blood
  • Thrombin acts on many other blood-clotting factors
  • Thrombin has a proteolytic effect on prothrombin to release more thrombin
113
Q

Why is heparin not typically given via intramuscular injections?

A
  • This would cause haematomas
114
Q

Outline the intrinsic pathway

A
  • Trauma activates Factor XII
  • Release of phospholipids from damaged platelets
  • Factor XIIa activates Factor XI in the presence of kininogen and prekallikrein
  • Factor XIa activated Factor IX
  • Factor IX activates Factor X in concert with Factor VIIIA
  • Phospholipids combine with Factor V to form prothrombin activator
  • Prothrombin activator splits prothrombin to from thrombin in the presence of calcium ions
115
Q

Identify two factors that determine when blood will coagulate and when they are expressed

A
  • Anticoagulants, blood does not coagulate in a normal vessel
  • Procoagulants, blood does coagulate in ruptured vessels
116
Q

How does bleeding after surgery differ between a platelet defect (e.g. thrombocytopenia) or a coagulation defect (e.g. haemophilia)

A
  • Immediate in a platelet defect e.g. thrombocytopenia

- Delayed in a coagulation defect e.g. haemophilia

117
Q

Identify two causes of Vitamin K deficiency

A
  • Gastrointestinal disease due to poor absorption of fat
  • Liver disease (e.g. hepatitis, cirrhosis and acute yellow atrophy) due to bile deficiency, as bile also facilitates fat digestion
118
Q

How can you use Activated Partial Thromboplastin Time to distinguish between Haemophilia A, von Willebrand’s disease and Vitamin K deficiency?

A
  • APTT is greatly increased in Haemophilia A
  • APTT is increased or decreased in von Willebrand’s disease
  • APTT is increased in Vitamin K deficiency
119
Q

Identify the investigations carried out to detect a deep vein thrombosis

A
  • D-dimer
  • Iliofemoral Thrombosis = B mode venous compression
  • Below knee-thrombosis = Venography with ultrasound
120
Q

Is purpura a feature of a platelet defect (e.g. thrombocytopenia) or a coagulation defect (e.g. haemophilia)

A
  • Platelet defect e.g. thrombocytopenia
121
Q

How is BMI calculated?

A
  • Dividing an individuals body weight by their square height
122
Q

Identify five factors that contribute to overeating

A
  • Denial
  • High-risk situations
  • Loss of control
  • Lowered mood
  • Cognitive shift
123
Q

What is Factor IV also known as?

A
  • Calcium
124
Q

What is Factor IX also known as?

A
  • Plasma Thromboplastin Component

OR

  • Christmas Factor

OR

  • Antihaemophilic Factor B
125
Q

What is meant by individual prevention?

A
  • Health is influenced by the behaviours and conditions of the individuals
  • Objectives to change health behaviours by education, advertising and specific interventions
126
Q

What is the function of glycoproteins in the cell membrane of platelets?

A
  • Repulse adherence to normal endothelium

- Promote adherence to injured areas of the vessel wall (especially to collagen)

127
Q

Why is protamine sulphate given with heparin therapy

A
  • Haemorrhage is an unwanted side effect

- Protamine sulphate is a heparin antagonist

128
Q

What is the treatment of von Willebrand’s disease

A
  • Analogue of ADH (vasopressin) known as desmopressin

- To stimulate release of vWF from endothelial cells

129
Q

What BMI score is considered as obesity?

A
  • BMI score greater than 30
130
Q

Define and outline Virchow’s triad

A
  • Three predisposing situations that result in a thrombus
  • Changes in the intimal surface of the vessel
  • Changes in the pattern of blood flow
  • Changes in the blood constituents
131
Q

Where is fibrinogen formed?

A
  • Liver
132
Q

Explain why colestyramine lessens the effects of warfarin

A
  • Reduce absorption of warfarin
133
Q

Identify five risk factors for deep vein thrombosis

A
  • Surgery
  • Fracture
  • Cardiorespiratory Disease
  • Malignant Disease
  • Increasing age
134
Q

How is Activated Partial Thromboplastin Time performed?

A
  • Addition of a surface activator, phospholipid and calcium to the patient’s plasma
135
Q

How is Va/Q reported and interpreted?

A
  • Reported as a probability

- Interpreted in context of history and other examinations

136
Q

How can you use bleeding time to distinguish between Haemophilia A, von Willebrand’s disease and Vitamin K deficiency?

A
  • Bleeding time is increased in von Willebrand’s disease

- It is normal in both haemophilia A and vitamin K deficiency

137
Q

What is Factor II also known as?

A
  • Prothrombin
138
Q

How do platelets activate nearby platelets?

A
  • Release of ADP, thromboxane A2 and serotonin
139
Q

Haemophilia B is a deficiency of which clotting factor?

A
  • Factor IX

it is also known as Christmas disease

140
Q

How is heparin typically given?

A
  • Intravenously
141
Q

Outline type 1 von Willebrand’s disease

A
  • Inherited autosomal dominant condition
  • Partial quantitative deficiency of vWF
  • Minor clinical features such as bleeding following minor trauma or surgery
142
Q

What is the normal Thrombin Time?

A
  • 12 - 14 seconds
143
Q

Are muscle haematomas a feature of a platelet defect (e.g. thrombocytopenia) or a coagulation defect (e.g. haemophilia)

A
  • Coagulation defect (e.g. haemophilia)
144
Q

Why does the effect of warfarin take several days to develop?

A
  • The degradation of carboxylated clotting factors takes several days
145
Q

What does an ECG show with a massive pulmonary embolism?

A
  • Right atrial dilation with tall P wave in lead II

- Right axis deviation, right bundle branch block and T wave inversion

146
Q

Why is heparin not typically given orally?

A
  • It is not absorbed from the git due to its charge and high molecular weight
147
Q

What is Factor III also known as?

A
  • Tissue Factor

OR

  • Tissue Thromboplastin
148
Q

Identify four mechanisms that are responsible for prevention of blood loss

A
  • Vascular constriction
  • Platelet plug
  • Blood clot
  • Fibrous tissue in the blood clot
149
Q

What is the role of the Golgi apparatus and endoplasmic reticulum in platelets?

A
  • Synthesis of enzymes

- Storage of calcium ions

150
Q

What is the most common cause of arterial thrombosis?

A
  • Atheroma
151
Q

Outline the extrinsic pathway

A
  • Release of Factor III which contains lipoproteins and phospholipids
  • Lipoprotein complex of Factor III complexes with Factor VII
  • Which activates Factor X in the presence of calcium ions
  • Phospholipids combine with Factor Xa and Factor V to form prothrombin activator
  • Prothrombin activator splits prothrombin to from thrombin in the presence of calcium ions
152
Q

Explain why rifampicin lessens the effects of warfarin

A
  • Induces hepatic metabolism of P450 enzyme

- Which increases the rate of degradation of warfarin

153
Q

When is phenidione prescribed

A
  • In patients who suffer adverse reactions to warfarin
154
Q

Identify an advantage of LMWH over heparin fragments

A
  • Longer half life
  • Effects are more predictable
  • Dosing is less frequent
  • Therefore monitoring is less routinely required
155
Q

Explain how platelets adhere to the damaged area

A
  • Secrete pseudopodia
  • Secrete receptors such as Glycoprotein IB-IX-V complex and GIIB-IIA
  • Platelets adhere to underlying collagen via von Willebrand factor
156
Q

What does Prothrombin Time measure?

A
  • Factors VII, X, V, prothrombin and fibrinogen
157
Q

What is the significance of a saddle emboli?

A
  • Located in the bifurcation of the aorta

- Cutting off blood supply to the lower limbs

158
Q

What is the half life of a platelet?

A
  • 8-12 days

Semester 2: Cardiorespiratory Fitness (18 decks)

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