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Mechanisms of Disease > Week 5 - Haemostasis and Thrombosis > Flashcards

Week 5 - Haemostasis and Thrombosis Flashcards

1
Q

Define haemostasis

A

The stopping of a flow of blood by the physiological properties of vasoconstriction and coagulation

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2
Q

What does successful haemostasis require?

A
  • Vessel wall (blood vessels constrict to limit blood loss)
  • Platelets (adhere to damaged vessel wall and each other to form a platelet plug)
  • Coagulation system
  • Fibrinolytic system
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3
Q

How is coagulation regulated?

A

By thrombin inhibitors

  • Anti-thrombin III
  • Alpha-1 anti-trypsin
  • Alpha-2 macroglobulin
  • Protein C and S
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4
Q

Why does coagulation have to be tightly regulated?

A

The balance between procoagulant and anticoagulant forces of various types is essential

  • If the balance tips in favour of the procoagulant forces, thrombosis will occur
  • If the balance tips in favour of the anticoagulant forces, there will be excessive bleeding
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5
Q

What is fibrinolysis?

A

Breakdown of fibrin

  • Plasminogen is converted to plasmin by plasminogen activators
  • Can be used to help break down a thrombus
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6
Q

What is thrombosis?

A

Formation of a solid mass from the constituents of the blood, within the circulatory system, during life

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7
Q

What is Virchow’s triad?

A

Predisposing factors to thrombosis

  • Abnormalities of the flow of blood (stagnation, turbulence)
  • Abnormalities of blood components (smokers, postpartum, post-op)
  • Abnormalities of the blood vessel wall (atheroma, direct injury, inflammation)
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8
Q

What is the appearance of arterial thrombi?

A
  • Pale
  • Granular
  • Lines of Zahn
  • Low cell content
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9
Q

What are the effects of arterial thrombi?

A
  • Ischaemia
  • Infarction
  • Depends on site (e.g. end artery) and collateral circulation
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10
Q

What is the appearance of venous thrombi?

A
  • Soft
  • Gelatinous
  • Deep red
  • Higher cell content
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11
Q

What are the effects of venous thrombi?

A
  • Congestion
  • Oedema
  • Ischaemia
  • Infarction
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12
Q

What are the possible outcomes of thrombosis?

A
  • Lysis
  • Propagation
  • Organisation
  • Recanalisation
  • Embolism
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13
Q

What is lysis? (following thrombus)

A
  • Complete dissolution of thrombus
  • Fibrinolytic system active
  • Blood flow is re-established
  • Most likely when thrombi are small
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14
Q

What is propagation? (following thrombus)

A

Progressive spread of thrombosis due to disruption of flow

  • Distally in arteries
  • Proximally in veins
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15
Q

What is organisation? (following thrombus)

A
  • Reparative process
  • Ingrowth of fibroblasts and capillaries
  • Lumen remains obstructed
  • Converts the thrombus to fibrous tissue
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16
Q

What is recanalisation? (following thrombus)

A
  • Bloodflow is reestablished but usually incompletely
  • 1 or more channels are formed through organising thrombus
  • These channels tend to deliver blood as well as the original vessel
  • Usually occurs in arteries
17
Q

What is embolism? (following thrombus)

A
  • Parts of thrombus break off
  • Travels through bloodstream
  • Lodges at a distant site
18
Q

What is an embolism?

A

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

19
Q

What are the different types of embolisms?

A
  • Air
  • Amniotic fluid
  • Nitrogen (N2 bubbles form in the blood with rapid decompression)
  • Medical equipment
  • Tumour cells
  • Thrombo-emboli
  • Other: cerebral, iatrogenic, fat
20
Q

Where can thrombi-emboli occur?

A
  • Pass from systemic veins to the lungs
  • Pass from the heart, via the aorta, to renal, mesenteric and other arteries
  • Pass from atheromatous carotid arteries to the brain
  • Pass from atheromatous abdominal aorta to arteries of the legs
21
Q

What predisposing factors are there for deep vein thrombosis?

A
  • Immobility/bed-rest
  • Post-operative
  • Pregnancy and post-partum
  • Oral contraceptives
  • Severe burns
  • Cardiac failure
  • Disseminated cancer
22
Q

How can deep vein thrombosis be prevented?

A

Identify high-risk patients and offer prophylaxis

  • Sub-cutaneous heparin
  • Leg compression during surgery (stockings)
23
Q

How can deep vein thrombosis be treated?

A
  • Intravenous heparin (anticoagulant, cofactor for anti-thrombin III)
  • Oral warfarin (interferes with synthesis of vitamin K-dependent clotting factors)
24
Q

What are the different types of pulmonary embolism?

A 
Massive PE:
- >60% reduction in bloodflow
- Rapidly fatal
Major PE:
- Medium-sized vessels are blocked
- Patients are short of breath
- Cough
- Blood-stained sputum
Minor PE:
- Small peripheral pulmonary arteries are blocked
- Asymptomatic, or minor shortness of breath
Recurrent minor PE:
- Leads to pulmonary hypertension
25
Q

What is disseminated intravascular coagulation?

A

Pathological activation of coagulation mechanisms

  • Happens in response to a variety of diseases
  • Small clots form throughout body
  • This disrupts normal coagulation, since they use up all the clotting factors
  • Abnormal bleeding occurs from the skin
  • Triggers = infection, trauma, liver disease, obstetric complications
26
Q

What is thrombocytopenia?

A

When the platelet count is way below the reference range

27
Q

What can cause thrombocytopenia?

A

Failure of platelet production:
- Bone marrow failure due to aplastic anaemia (may be due to chemotherapy/leukaemia/etc.)
- B12 deficiency (important for platelet production since it promotes the maturation of megakaryocytes)
Increase in platelet production:
- Idiopathic thrombocytopenia (autoimmune)
Sequestering of platelets
- By enlarged spleen
Dilution of platelets
- By large blood transfusions, without platelet transfusions

28
Q

What is thrombophilia?

A

Blood has an increased tendency to form clots

  • Sometimes associated with blood clots that are caused by genetic mutations
  • Increases risk of DVT
  • Often mild
29
Q

What is haemophilia?

A
  • X-linked recessive disorder
  • There is a type A (defective clotting factor 8) and a type B (defective clotting factor 9)
  • Can be mild, moderate or severe due to various mutations
  • Due to a nonsense point mutation
  • Treat with self-administered factor replacement therapy
30
Q

What can haemophilia cause?

A
  • Haemorrhage into joints, which may cause synovial hypertrophy, pain and long term damage to the joint
  • Muscle bleeding, which causes pressure and necrosis of nerves (painful)
  • Can haemorrhage into retroperitoneum/urinary tract
31
Q

What are the signs of DVT?

A
  • Tender swollen calf

- Warmth and redness of affected limb

Mechanisms of Disease (11 decks)

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