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Pathological Processes > Session 5 > Flashcards

Session 5 Flashcards

1
Q

What is haemostasis and what does it involve?

A
  • Stopping of a haemorrhage to prevent blood loss

- Involves vasoconstriction and platelet plug formation

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2
Q

What is clotting?*

A

The process of blood becoming a solid mass when it makes contact with connective tissue

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3
Q

What controls clotting?

A
  • Activation and release of different clotting factors

- Production of thrombin which acts on fibrinogen and produces insoluble fibrin filaments that trap RBCs

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4
Q

When will blood clot?

A
  • As soon as spilled from a vessels

- Only cells that will not clot then are endothelial cells, RBCs and WBCs

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5
Q

What are the 3 steps of haemostasis?

A

1) Severed artery contracts to decrease pressure downstream
2) Primary haemostatic plug of activated platelets forms at the hole in the vessel to control bleeding
3) Secondary haemostatic plug as fibrin filaments stabilise the blood clot (30 mins)

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6
Q

What activates platelets?

A
  • Collagen surfaces
  • ADP released by activated platelets and RBCs
  • Thromboxane A2 (platelet aggregator)
  • Thrombin (informs platelets that clotting is activated)
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7
Q

What happens when platelets are activated?

A
  • Stick to the exposed endothelium (von Willebrand factor) on basement membrane
  • Aggregate with other platelets to form platelet plug
  • Fibrinogen sticks platelets together
  • Platelets swell and change shape
  • Secrete factors from platelet granules that help aid clotting (Thromboxane A2/fibrinogen)
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8
Q

How does aspirin decrease platelet aggregation?

A

Irreversibly inactivates cyclooxygenase which is responsible for producing thromboxane A2

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9
Q

Why must thrombin be activated and how is that done?

A
  • Must be activated as blood would otherwise be solid

- Activated by proenzymes known as clotting factors

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10
Q

Which clotting factors need vitamin K for synthesis?

A

II, VII, IX, X + protein C and protein 5

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11
Q

What are proenzymes?

A

Biologically inactive enzyme precursors that must be activated to function as enzymes

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12
Q

What is the intrinsic clotting pathway?*

A

Pathway that involves factors, all of which are in the blood. Vessel break not needed to occur as triggered by a negatively charged surface.

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13
Q

What is the extrinsic clotting pathway?*

A

A pathway that needs a clotting factor (thromboplastin) which is present outside the blood, and is triggered by thromboplastin release from damaged cells that are adjacent to area of haemorrhage.

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14
Q

How does the vascular wall contribute to haemostasis?

A
  • Arterial tunica media contracts
  • Subendothelium traps platelets
  • Secretes plasminogen activator and thrombomodulin that oppose clotting as well as von Willebrand factor which favours it when there is damage
  • Exposure collagen and initiate clotting factor activation
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15
Q

What are the main natural anticoagulants?

A
  • Antithrombin III
  • Protein C
  • Protein S
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16
Q

What happens when someone is deficient in natural anticoagulants?

A

More prone to repeated thrombosis

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17
Q

How does the clot retract?

A
  • Platelets in clot die and cling to fibrin
  • Pull by actin-myosin filaments similar to muscle contractions to retract the clot
  • Toughened by squeezing out fluid
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18
Q

What is fibrinolysis?

A

The process of dissolving the clot once the hole in the vessel is repaired

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19
Q

How is the clot broken down?

A
  • Recognised by macrophages

- Broken down by plasmin

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20
Q

How is plasmin activated?

A
  • Circulates as plasminogen made in liver

- Activated by tissue plasminogen factor (blood), urokinase (urine) and streptokinase (bacteria, not in body)

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21
Q

Why are plasminogen activators used therapeutically?

A

Dissolving fibrin (thrombi and thromboemboli)

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22
Q

Why is tPA preferred over streptokinase ?

A
  • Streptokinase can only be given once as it is antigenic

- tPA has a higher affinity for fibrinogen, is not antigenic and can be given multiple times

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23
Q

Where can bleeding occur from treatment with plasminogen activators?

A

Gums, nose, (serious) brain

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24
Q

What activates fibrinolysis?*

A
  • Fibrin increasing activity of tPA
  • tPA produces plasmin
  • Plasmin breaks fibrin down to the fibrin degradation products (FDPs)
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25
Q

Where are FDPs increased?

A

Conditions with thrombosis, eg. DIC, DVT, pulmonary embolism

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26
Q

What happens to a clot in the end?

A
  • Fibrous repair
  • Replaced by granulation tissue
  • Replaced by a tiny scar after
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27
Q

What is haemophilia A?

A

Deficiency of factor VIII

  • X linked recessive
  • Males/homozygous females
  • Decreased amount/activity of factor VIII
  • Inherited but 30% due to new mutations
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28
Q

What are the mild and severe forms of haemophilia A?

A
  • Less than 1% factor VIII activity - very severe

- 6-50% of factor VIII activity - mild

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29
Q

How do patients with haemophilia A present?

A
  • Easy bruising
  • Massive haemorrhaging after trauma and surgery
  • Spontaneous haemorrhages when minor trauma
  • Haemarthrosis
  • Muscle haematomas
  • Prolonged bleeding post dental extraction
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30
Q

What is petechiae?

A

Small pinpoint haemorrhages caused by blood leaking from capillaries (vasculitis/platelet abnormalities)

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31
Q

What are the blood counts of a patient with haemophilia?

A
  • Normal platelet cont
  • Normal bleeding time
  • Normal PT
  • Abnormal APTT (activated partial thromboplastin time; intrinsic pathway that factor VIII is a part of)
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32
Q

What is the treatment for haemophilia A?

A

Recombinant factor VIII infusion

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33
Q

What is haemophilia B?

A
  • Factor IX deficiency
  • X linked recessive
  • Clinically indistinguishable from haemophilia A
  • Same blood counts as haemophilia A
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34
Q

How is haemophilia B treated?

A

Recombinant factor IX

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35
Q

What is von Willebrand disease?

A
  • Bleeding disorder caused by von Willebrand factor deficiency
  • Increased bleeding time and APTT
  • Mucosal bleeding, epistaxis and bruising indicating low platelet function
  • Prolonged bleeding after trauma/menstruation
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36
Q

What are the functions of von Willebrand factor?

A
  • Platelet plug formation by attracting circulating platelets to sites of vessel damage
  • Stabilises factor VIII to protect it form premature destruction
  • Platelet adhesion and aggregation
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37
Q

What is an example of a congenital vessel problem?

A

Hereditary Haemorrhagic Telangiectasia (HHT)

Ehlers-Danlos syndrome

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38
Q

What is HHT?

A
  • Autosomal dominant
  • Dilated microvascular swelling that increases with time
  • GI haemorrhage -> iron deficiency anaemia
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39
Q

What are some acquired problems with vessels?

A
  • Senile purpura (easy bruising in elderly)
  • Steroids
  • Infections
  • Scurvy (defective collagen production)
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40
Q

What is disseminated intravascular coagulopathy (DIC)?*

A
  • Microangiopathic haemolytic anaemia
  • Coagulation activated pathologically so many microthrombi in circulation
  • Consumption of platelets and clotting factors (haemolytic anaemia)
  • Raised PT/INR, APTT, D-dimers, fibrin degradation products, low fibrinogen
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41
Q

What are some triggers for DIC?

A

ALWAYS has a trigger

  • Malignancy
  • Sepsis (gram negative)
  • Severe trauma
  • Transfusion reactions
  • Massive tissue injury
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42
Q

What treatment is needed for DIC?

A
  • Treat underlying cause

- Anticoagulant (heparin)

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43
Q

What can microvascular thrombosis + haemorrhaging cause?

A
  • Gangrene
  • Neurological impairment
  • Renal failure
  • Respiratory distress
  • Intracerebral bleeding
  • Haematuria
  • Epistaxis
44
Q

Why can DIC result in anaemia?

A

Red blood cells often get traumatised and fragmented when squeezing through microthrombi

45
Q

What are thrombophilias?

A

Acquired or congenital defects of haemostasis that can increase a risk of thrombosis

46
Q

What are congenital causes of thrombophilias?

A
  • Natural anticoagulant deficiency

- Abnormal factor V

47
Q

What are acquired causes of thrombophilias?

A

Antiphospholipid syndrome

48
Q

What is PT?

A

Prothrombin time

- Blood test measuring how long it takes for the blood to clot (extrinsic pathway)

49
Q

What is APTT?

A

Activated prothrombin time

- Seeing how well the clotting factors are working

50
Q

What is a thrombus?*

A

Solid mass formed from the constituents of blood within the circulatory system when normal haemostatic activities are inappropriately turned on

51
Q

What is a clot?

A

Mass of blood outside of vessel wall

52
Q

What is Virchow’s triad?*

A

Explanation of what thrombosis depends on and what factors are needed (usually 2):

  • Vessel wall abnormality
  • Blood flow abnormality
  • Blood component abnormality
53
Q

What can cause damage to the vessel wall?*

A
  • Atheromas
  • Direct injury
  • Inflammation
54
Q

Why is there an increased risk of thrombi in pregnancy?

A

Stasis is present due to pressure on large veins and blood is hypercoaguable, so there is a higher risk in them occurring in lower limbs

55
Q

What are the problems occurring with blood flow and when do they occur?

A
  • Stasis (slow blood flow common in veins that can lead to hypertension)
  • Turbulent blood flow due to thickening of endothelial wall/atheroma
56
Q

What are the problems with blood components?

A
  • Hypercoaguability (sticky blood caused by increased fibrinogen and factor VIII)
  • Common in smokers, pregnancy, cancer, trauma and post operation
57
Q

What is the appearance of an arterial thrombus?*

A
  • Pale
  • Granular
  • Lines of Zahn present: patterning of RBCs and fibrin and platelets leading to striated patterns
  • Lower cell content
58
Q

What is the appearance of a venous thrombus?*

A
  • Soft
  • Gelatinous
  • Deep red
  • Has higher cell content
59
Q

What is the most crucial component of clotting cascade?*

A

Activation of factor X which will activate factor Xa to cleave prothrombin into thrombin, which can cleave fibrinogen into fibrin.

60
Q

What is the most crucial component of fibrinolysis?*

A
  • tPA activated by a high fibrin presence
  • Cleaves plasminogen into plasmin
  • Plasmin degrades fibrin and degradation products are released
61
Q

What is the difference between parietal and occlusive thrombi?

A
  • Parietal: attached to wall of vessel and restrict lumen

- Occlusive: fill and obstruct lumen

62
Q

What is thrombophlebitis?

A

Painful, superficial thrombi (in superficial veins) associated with inflammation of the vein

63
Q

What is a thrombus on a cardiac valve?

A

Vegetation = 2-3cm long and easy to embolise

64
Q

Where do thrombi on cardiac valves form and why?

A
  • Thrombi form on the valves of the left heart

- Exposed to greater pressures and microtrauma

65
Q

When is lysis of thrombus occurring and what is it?

A
  • Complete dissolution of thrombus to establish blood flow

- Likely when thrombi small

66
Q

What is propagation of thrombus and when does it occur?

A
  • Progressive spread of thrombosis in distal arteries/proximal veins
67
Q

What is organisation of thrombus and when does it occur?*

A
  • Fibrous reparative process
  • Fibroblasts and capillaries grow into thrombus
  • Lumen remains obstructed
68
Q

What is recanalisation of thrombus and when does it occur?*

A
  • Re-establishment of blood flow by the development of new holes in an organising thrombus
  • Smaller capacity than OG vessel
69
Q

What is embolisation?

A
  • Part of the thrombus breaks off and travels through the blood stream
  • Lodges at a distant site in a smaller vessel
70
Q

What are the potential clinical effects of thrombosis?*

A
  • Artery occlusion leading to ischaemia and infarction (MI)
  • Embolisation resulting in occlusion of a distant artery (pulmonary embolism)
  • Congestion and oedema in venous bed
  • Miscarriages (thrombosis of uteroplacental vasculature)
71
Q

Which veins are thrombi most common in?

A

Hepatic, subclavian

72
Q

Which arteries are thrombi most common in?

A

Cerebral, carotid, coronary, mesenteric, renal, femoral/iliac/popliteal

73
Q

What are some appearances of thrombi?*

A

Slide 25/notes.

74
Q

What is an embolism?

A

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

75
Q

How do emboli form?

A
  • Passing from systemic veins to lungs (as blood flow from smaller to larger) - PE
  • Pass from heart via aorta and lodge in arteries
  • Pass from atheromatous carotid artery to brain - stroke
  • Pass from abdominal aorta to leg arteries leading to acute limb ischaemia
76
Q

What is deep vein thrombosis?

A

Clot formation in the veins of the lower limb characterised by unilateral limb swelling.

77
Q

What are some features of pulmonary emboli?*

A
  • Can be small and asymptomatic
  • Multiple can cause pulmonary hypertension
  • If occlude 60% of circulation, can cause sudden death or right-sided heart failure
78
Q

What are saddle emboli?

A

Large emboli that become lodged and bifurcate the artery and block both branches (result in sudden death)

79
Q

Where do thromboemboli in systemic arteries come from?

A
  • Left heart
  • Aneurysms/thrombi on ulcerated atherosclerosis

Embolise to lower extremities/brain/spleen/intestines/kidneys

80
Q

Why are thrombi common in left heart?

A
  • Infarcts common in LV so thrombi can form on necrotic endothelium
  • AFib = reduced atrial contraction; dilated L. atrium and stagnant flow
81
Q

What are the risk factors for DVT?

A
  • Immobility
  • Post-operative
  • Pregnancy
  • Oral contraceptive pill
  • Burns
  • Cardiac failure
  • Cancer metastases
82
Q

What are the forms of DVT prophylaxis?

A
  • Identify patients with high risk
  • Mobilise early after surgery
  • Give subcutaneous heparin
  • Leg compression during surgery (stockings)
83
Q

What are paradoxical emboli?

A

Thromboemboli that form in systemic veins but embolise to systemic arteries

84
Q

How can paradoxical emboli bypass lungs?

A
  1. able to pass through arterio-venous anastomoses

2. larger emboli can only enter by passing through interventricular septal defects/foramen ovale

85
Q

What is an atheroma?

A

Necrotic material present in atherosclerotic plaques that can be released when the plaque breaks open

86
Q

What is a transient ischaemic attack?

A

An episode of sudden neurological dysfunction that will resolve within 24 hours and is a result of microscopic emboli in the brain that can break up quickly before neurological damage

87
Q

What are fat and bone marrow emboli from?

A

Emboli that are a complication of bone fractures or occur after liposuction

88
Q

How are such emboli formed?

A
  • Fractured bones release bone marrow fat oil droplets

- Droplets coalsece and are sucked into the venules torn by fracture

89
Q

What are the symptoms of fat embolisms and when are they seen?

A
  • Respiratory distress
  • Neurological symptoms
  • Seen 1-3 days after fractures
  • 10-15% mortality
90
Q

What are paradoxical emboli?

A

Thromboemboli that form in systemic veins but embolise to systemic arteries

91
Q

How can paradoxical emboli bypass lungs?

A
  1. able to pass through arterio-venous anastomoses

2. larger emboli can only enter by passing through interventricular septal defects/foramen ovale

92
Q

What is an atheroma?

A

Necrotic material present in atherosclerotic plaques that can be released when the plaque breaks open

93
Q

What is a transient ischaemic attack?

A

An episode of sudden neurological dysfunction that will resolve within 24 hours and is a result of microscopic emboli in the brain that can break up quickly before neurological damage

94
Q

What are fat and bone marrow emboli from?

A

Emboli that are a complication of bone fractures or occur after liposuction

95
Q

How are such emboli formed?

A
  • Fractured bones release bone marrow fat oil droplets

- Droplets coalsece and are sucked into the venules torn by fracture

96
Q

What are the symptoms of fat embolisms and when are they seen?

A
  • Respiratory distress
  • Neurological symptoms
  • Seen 1-3 days after fractures
  • 10-15% mortality
97
Q

What is an air embolism and how does it develop?

A
  • Negative pressure in the veins during inspiration
  • Can draw in air after trauma
  • 100mls fatal as they will form bubbles in heart that will stop circulation
98
Q

What are nitrogen emboli and how do they occur?

A
  • e.g. deep sea divers breathing in nitrogen underwater that is released into the body as bubbles when they rise to the surface too quickly
  • Bubbles distort tissues and cause emboli
  • Can also form painful bubbles in muscles/joints
99
Q

How are nitrogen emboli treated?

A

Prompt compression in a compression chamber to force gas back into solution (patient shouldn’t fly as atmospheric pressure is low and can bring more gas out)

100
Q

What is an amniotic fluid embolism?

A

Complication where amniotic fluid enters the maternal circulation through a tear in the amniotic membrane and can cause sudden respiratory distress, hypertension, DIC (20-40% mortality)

101
Q

What are talcum emboli?

A

Microscopic foreign bodies that drugs are cut with (so found in lungs of drug abusers)

102
Q

How does aspirin work to treat thromboembolic disease?

A
  • Acetylates cyclooxygenase to inhibit prostaglandin synthesis irreversibly
  • Platelets can’t produce thromboxane A2 and formation of platelet plug is inhibited
103
Q

How does heparin work to treat thromboembolic disease?

A

Forms irreversible complexes with antithrombin III to activate it (given intravenously or subcutaneously)

104
Q

How does warfarin work to treat thromboembolic disease?

A

Oral medication that interferes with vit. K synthesis (and vit K needed to make some cofactors)

105
Q

How else can pulmonary emboli be prevented?

A

Putting umbrella-shaped filters in IVC

Pathological Processes (10 decks)

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