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Semester 2 > MoD Session 5 > Flashcards

MoD Session 5 Flashcards

0
Q

What does the success of haemostasis depend on?

A

Vessel wall
Platelets
Coagulation system
Fibrinolytic system

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1
Q

What is haemostasis?

A

Stopping of haemorrhage within seconds to prevent blood loss

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2
Q

What does a severed artery do in haemostasis?

A

Contracts to decrease pressure downstream

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3
Q

What happens after 5 minutes of an artery being severed?

A

Fragile primary haemostatic plug of platelets has formed at mouth of vessel to control bleeding

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4
Q

What happens ~30 minutes after an artery is severed?

A

Secondary haemostatic plug forms w/fibrin which becomes organised forming granulation tissue which develops into a tiny scar

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5
Q

What do all vessels do to limit blood loss?

A

Constrict their vessel walls

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6
Q

How is a platelet plug formed?

A

Platelets adhere to the damaged vessel wall and each other

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7
Q

What is the platelet release reaction?

A

ATP –> ADP
ADP and thromboxane A2 cause platelet aggregation
5HT and platelet factor 3 released

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8
Q

Which molecules are important in platelet coagulation?

A

5HT

Platelet factor 3

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9
Q

What do platelets do after aggregation?

A

Coalesce

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10
Q

Where are the factors used in the intrinsic coagulation system found?

A

Within BV

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11
Q

What is needed to activate the extrinsic coagulation system?

A

Exo-BV factors

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12
Q

Which factors are activated in the intrinsic coagulation system?

A

12a –> 11a –> 9a –> 10a

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13
Q

Which factors are activated in the extrinsic coagulation system?

A

3a –> 7a –> 10a

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14
Q

How does activation of factor 10a by both the extrinsic and intrinsic coagulation systems cause fibrin formation?

A

10a –> thrombinogen –> thrombin –> fibrinogen –> fibrin

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15
Q

Why does the coagulation system have to be tightly regulated?

A

There is enough thrombin in 1 ml of blood to convert all the fibrinogen in the body to fibrin

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16
Q

How is the coagulation system tightly regulated?

A

Balance procoagulant and anticoagulant forces

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17
Q

What can inhibit the activation of fibrinogen by thrombin?

A

Anti-thrombin III
Alpha 1 antitrypsin
Alpha 2 macroglobin
Protein C and S

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18
Q

What are the effects of inherited antithrombin III or protein C and S deficiencies?

A

Thrombosis (thrombophilia)

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19
Q

What is the fibrinolytic system?

A

Conversion of plasminogen to plasmin which can dissolve fibrin

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20
Q

Give two examples of widely used fibrinolytic therapies.

A

Streptokinase A

Tissue plasminogen activator (tPA)

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21
Q

What is needed for the fibrinolytic system to function?

A

Plasminogen activators

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22
Q

What is activated partial thromboplastin time (aPTT)?

A

Time taken to generate fibrin from initiation of the intrinsic pathway

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23
Q

When is aPTT long?

A

Haemophilia A and B

Factor deficiencies

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24
Q

How do you test aPTT?

A

Activate factor XII w/out activating factor VII in phospholipid emulsion

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25
Q

What is prothrombin time (PT)?

A

Time taken to generate fibrin from factor VII

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26
Q

How do you test PT?

A

Add thromboplastin, recalcify and wait for fibrin filaments to form

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27
Q

When is PT long?

A

Inherited factor VII deficiency
Liver disease
Warfarin treatment
Sever bleeding/massive transfusion

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28
Q

How is a long PT rectified in severe bleeding/massive transfusion?

A

1:1 mix w/normal plasma

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29
Q

What is thrombin time (TT)?

A

Time taken for fibrinogen –> fibrin in the presence of thrombin

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30
Q

How is TT measured?

A

Add thrombin and calcium and wait for fibrin filaments to form

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31
Q

When is a long TT seen?

A

Deficient fibrinogen
Abnormal fibrinogen
Presence of inhibitor to reaction

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32
Q

What does the endothelium secrete?

A

Anti-thrombotic molecules e.g. Plasminogen activators, prostacyclin, nitric oxide and thrombomodulin

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33
Q

What is thrombosis?

A

Formation of a solid mass of blood w/in circulatory system

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34
Q

What does thrombosis occur due to?

A

Virchow’s triad

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35
Q

What is Virchow’s triad?

A

Abnormalities of:
Vessel wall
Blood flow
Blood components

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36
Q

What can cause abnormalities of the vessel wall?

A

Atheroma
Direct injury
Inflammation

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37
Q

What can cause abnormalities of blood flow?

A

Stagnation

Turbulence

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38
Q

In what circumstances might a patient be hyper-coaguable?

A

Smoker
Post-partum
Post-op

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39
Q

Why can patients who are post-partum have abnormalities of blood components?

A

Due to over-enthusiastic response to blood loss from childbirth

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40
Q

What is given post-op to reduce the risk of abnormalities of blood components causing hyper-coaguability?

A

Prophylactic treatment

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41
Q

How do arterial thrombi appear?

A

Granular
Pale
Low cell content
Lines of Zahn due to bloodflow - yellow = fibrinous, red = RBCs

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42
Q

How do venous thrombi appear?

A

High cell content
Gelatinous
Deep red
Soft

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43
Q

What are the possible outcomes of thrombosis?

A 
Lysis
Propagation
Organisation
Recanalisation
Embolism
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44
Q

Why is lysis the best outcome of thrombosis?

A

Fibrinolytic system is active so can completely dissolute thrombus to re-establish blood flow

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45
Q

When is lysis the most likely outcome of thrombosis?

A

When thrombi are small

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46
Q

What can aid lysis of a thrombus and help return bloodflow to an ischaemic area?

A

Streptokinase A

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47
Q

Why is propagation when an outcome of thrombosis?

A

Progressive spread of thrombosis which is distal in arteries and proximal in veins

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48
Q

How does a thrombus change as it moves during propagation?

A

Increases in size with increasing venous diameter

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49
Q

What is organisation as an outcome of thrombosis?

A

Reparative process where ingrowth of fibroblasts and capillaries keep lumen unobstructed

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50
Q

What process is organisation as a result of thrombosis like?

A

Formation of granulation tissue

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51
Q

What is recanalisation?

A

One or more channels formed through organising thrombus which re-establish blood flow

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52
Q

Is previous bloodflow usually matched after recanalisation?

A

No, recanalisation is usually incomplete

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53
Q

What is embolism as an outcome of thrombosis?

A

Where part of the thrombus breaks off and travels through bloodstream to a distant site

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54
Q

What is the passage of an embolism in a vein?

A

Encounters larger vessels until it reaches the heart where it passes through to pulmonary circulation and becomes trapped

55
Q

What is the passage of an embolism in an artery?

A

Encounters smaller vessels until it becomes trapped

56
Q

What origin does pulmonary embolism always have?

A

Venous

57
Q

What are the effects of arterial thrombosis?

A

Ischaemia

Infarction

58
Q

What do the effects of arterial thrombosis depend on?

A

Site and collateral circulation

59
Q

What are the effects of venous thrombosis?

A

Congestion
Oedema from obstruction causing high hydrostatic pressure
Ischaemia
Infarction if tissue pressure is high enough to occlude artery

60
Q

What is an embolism?

A

Blockage of a BV by solid, liquid or gas at a site distant from its origin

61
Q

> 90% of emboli are what type?

A

Thrombo-emboli

62
Q

How do thrombo-emboli from the heart enter renal, mesentric and other arteries?

A

Via the aorta

63
Q

Where do thrombo-emboli in the brain originate from?

A

Atheromatous carotid arteries

64
Q

Where do thrombo-emboli caused by an atheromatous abdominal aorta end up?

A

Arteries of the legs

65
Q

What types of emboli are there apart from thrombo-emboli?

A 
Air
Amniotic fluid
Nitrogen
Medical equipment
Tumour cells
66
Q

What can embolism lead to which requires amputation?

A

Coagulation necrosis

67
Q

Why can an amputation due to embolism have to be more proximal than the necrotic tissue?

A

Remaining tissue has increased metabolic demand which the blood supply cannot support

68
Q

What can cause the formation of a thrombo-emboli in the heart?

A

MI

AF

69
Q

How can carotid endarctorectomies decease the risk of cerebral embolism?

A

Strip carotid arteries of atheroma so decrease risk of thrombus formation

70
Q

Why must a patient who has presented with a fracture who then goes on to develop SoB and neurological symptoms be treated quickly?

A

They have a fat embolism which has blocked vessels in the brain causing small haemorrhages

71
Q

How does fracture of a long bone cause fat embolism?

A

2-6 days after break bone marrow cells die and release fat into the surrounding broken BV

72
Q

Why does fat embolism cause neurological symptoms?

A

The fat can squeeze through arterial-venous anastomoses in the lungs and therefore enter the arterial system where it is most noticeable in the brain as it causes small haemorrhages

73
Q

What two causes other than long bone fracture can cause fat embolism?

A

Adipose tissue damage

Biochemical disturbance

74
Q

What type of embolism would injection of an oily drug into a vein cause?

A

Iatrogenic

75
Q

What are the predisposing factors for DVT?

A 
Immobility - lack of calf muscle pumping
Post-op
Pregnancy and post-partum
High oestrogen type contraceptives
Severe burns
Cardiac failure
Disseminated cancer
76
Q

What is Trossaeu syndrome?

A

Where tumour cells secrete coagulation factors

77
Q

Can DVT be prevented?

A

No, you can only reduce the risk in identified high-risk patients

78
Q

What is used for prophylaxis in patients with a high risk of DVT?

A

SC heparin
Heparin derivatives w/low molecular weight
ED stockings
Inflatable boots in surgery

79
Q

What treatment is given for DVT?

A

IV heparin followed by oral warfarin

80
Q

What does IV heparin followed by warfarin take a few days to act?

A

Have to irreversibly inhibit all enzyme molecules

81
Q

What method does DVT treatment usually follow?

A

Prevention of thrombus propagation, not breaking it down

82
Q

What determines the outcome of pulmonary embolism?

A

Size of embolism

83
Q

What are the effects of a massive pulmonary embolism?

A

If it causes >60% decrease in bloodflow it is rapidly fatal as it often completely blocks the pulmonary trunk

84
Q

What are the effects of a medium sized pulmonary embolism?

A

Medium sized BV are blocked causing SoB with or without a cough
Blood stained sputum can be caused due to development of a pulmonary infarct

85
Q

What effects does a minor pulmonary embolism cause?

A

Asymptomatic or minor SoB due to peripheral pulmonary artery blocking

86
Q

What do recurrent pulmonary emboli cause?

A

Pulmonary hypertension

87
Q

How fast does the fibrinolytic system destroy blood clots?

A

At the same rate at which they are formed

88
Q

Why does it not matter that a severed vein will not contract as a severed artery does in haemostasis?

A

Pressure in them is already low

89
Q

Which step of haemostasis do patients with a platelet count of <1x10^9/L lack?

A

Formation of a primary haemostatic plug

90
Q

Which step of haemostasis do haemophiliacs lack?

A

Secondary haemostatic plug formation as they have normal platelets but can’t produce fibrin

91
Q

What are the five platelet activators?

A

Collagen surfaces within extravascular areas
Thrombin
ADP released by activated platelets and injured RBC
Adrenaline
Some prostaglandins

92
Q

What do activates platelets do?

A

Swell into sticky spiny spheres and die

93
Q

How do platelets adhere to other surfaces?

A

Stick to von Willebrand factor which is concentrated on the subendothelial basement membrane

94
Q

What is the subendothelium?

A

The basement membrane or collagen where the endothelium is removed

95
Q

What acts as glue between platelets in aggregation?

A

Fibrinogen

96
Q

What factors do platelets secrete to help the platelet plug to grow?

A

Fibrinogen
ADP
Thromboxane A2 - powerful platelet aggregator

97
Q

What are most of the circulating molecules which act to activate thrombin?

A

Proenzymes

98
Q

Give two examples of cofactors used in blood clotting.

A

Phospholipids

Calcium

99
Q

What is clot retraction?

A

When platelets cling to fibrin filaments and pull by their actin-myosin system as they die

100
Q

What is the purpose of clot retraction?

A

Toughen clot by squeezing out fluid?

Helps to pull sides of small wounds together

101
Q

What happens to fibrinolytic activity after surgery?

A

Drops for 7-10 days

102
Q

What is urokinase?

A

A plasminogen activator found in urine

103
Q

Why is the vascular wall not passive?

A

The arterial media contracts and the subendothelium traps platelets

104
Q

Why does smoking cause hypercoaguability of blood?

A

Activates Hageman factor (factor XII)

105
Q

Why are platelets in the veins more concentrated along the endothelium?

A

They are the smallest formed elements in the blood

106
Q

How does a parietal thrombus compare to an occlusive thrombus?

A

Parietal - restricts lumen of vessel

Occlusive - fills and obstructs lumen

107
Q

What is the most important mechanism for limiting spread of thrombus?

A

Blood flow

108
Q

How do thrombi form in a vein?

A

Platelets catch in an eddy behind a valve, form an aggregate, settle on the wall and stick to other platelets as they pass by

109
Q

What do arterial thrombi tend to remain?

A

Parietal

110
Q

When do occlusive arterial thrombi tend to occur?

A

Over an atherosclerotic plaque that has cracked open

111
Q

How can thrombi and post-mortem clots be distinguished?

A 
Thrombi = laminated w/lines of Zahn, opposed to intimal surface
Clots = rubbery and shiny, not laminated, not attached to intima
112
Q

What is a vegetation?

A

2-3 cm long thrombus on a cardiac valve

113
Q

Why do vegetations usually occur on the valves of the left heart?

A

Exposed to greater pressure and therefore microtrauma so exposed subendothelial tissue is thrombogenic

114
Q

What can happen the vegetations?

A

They can become infected

115
Q

How does aspirin work as an antithrombogenic?

A

Irreversibly acetylates an enzyme of prostaglandin metabolism in platelets so they cannot produce thromboxane A2, inhibiting haemostatic plug formation

116
Q

What is a saddle emboli?

A

Large emboli that becomes lodged astride the bifurcation of the pulmonary artery

117
Q

Where do approximately 80% of pulmonary emboli arise?

A

In thrombi in the deep veins of the thigh and popliteal vein

118
Q

How does atrial fibrillation lead to thrombi formation?

A

Decreased atrial contraction –> dilatation of the left atrium –> stagnation of blood in atrium –> thrombus

119
Q

How do paradoxical emboli bypass the lungs?

A

Small emboli pass through arterio-venous anastomoses in the pulmonary circulation
Larger emboli pass through defects in the IV septum or formaen ovale during straining which increases pressure in right side of heart

120
Q

What is a paradoxical embolus?

A

Arise in systemic veins but embolism in systemic arteries

121
Q

What is atheroma?

A

Gruel-like necrotic material in atherosclerotic plaques released into the blood when the plaque breaks open

122
Q

When might an atherosclerotic plaque break open?

A

Spontaneously
During surgery
During catheterisation

123
Q

Why do patients with emboli of atheroma present with abdominal pain?

A

The intestine is often affected

124
Q

How does air embolism arise after trauma or the neck and chest?

A

During inspiration in the upright position veins draw in air due to their negative pressure

125
Q

What approximate amount of air will cause a fatal air embolus?

A

100 ml

126
Q

How can air embolism arise in labour?

A

Enter uterus and be forced into veins open during uterine contraction

127
Q

What happens to air emboli from the lungs when they reach the heart?

A

Gather in right heart as a frothy mass that stops circulation

128
Q

Why is nitrogen a particular problem when a diver resurfaces too quickly and releases dissolved gases into the body as bubble?

A

It is fat soluble and can result in persistent bubbles in lipid-risk tissues e.g. CNS

129
Q

How is the bends treated?

A

Prompt recompression

130
Q

How does amniotic fluid cause embolism?

A

Enters circulation through a tear in amniotic membranes

131
Q

What can amniotic fluid embolism cause?

A

Sudden respiratory distress and collapse

132
Q

What is amniotic fluid embolism a complication of?

A

Labour and Caesarean section

133
Q

Why can emoblisation not occur in veins?

A

Blood runs from smaller to larger vessels so injects will o through heart and embolism pulmonary arteries

134
Q

Why does venous flow favour stenosis?

A

It is slow

135
Q

What can be seen in the lungs of IV drug abusers?

A

Microscopic foreign bodies e.g. talcum

Semester 2 (45 decks)

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