Session 5 ILOs - Haemostasis, thrombosis and embolism Flashcards
Define and describe the principles of haemostasis i.e the role of the vessel wall, platelets and the platelet plug, the coagulation system, the fibrinolytic system and plasmin, the production of thrombin and fibrin and the role of thrombin inhibitors
3 main steps of haemostasis:
- Vasoconstriction
- Platelet plug
- Fibrin clot
Describe and begin to interpret the common tests in a coagulation screen
3 main coagulation tests :
- ATTPP (activated partial thromboplastin time)
- Reflects the intrinsic pathway
- Prolonged PT is most commonly due to a deficiency in factors: 8, 9, 11, 12
- Deficiency in 8 (haemophilia A)
- Deficiency in 9 (haemophilia B) - PT (prothrombin time)
- Reflects the extrinsic pathway
- Prolonged PT is most commonly due to factor 7 deficiency - TCT (thrombin clotting time)
- Reflects the final step of the common pathway = conversion of fibrinogen to fibrin (via action of thrombin)
Discuss some common inherited bleeding disorders e.g. Haemophilia A & B and von-Willebrand disease
Haemophilia A:
- X-linked recessive
- Factor 8 deficiency (affects the intrinsic pathway)
- Symptoms: easy bruising, massive haemorrhage after trauma, can get haemoarthroses
- KEY: petechiae are absent
- Prolonged APTT and a normal PT
Haemophilia B = ‘Christmas’ disease:
- X-linked recessive
- Severe factor 9 deficiency (affects the intrinsic pathway)
- Symptoms: clinically indistinguishable from haemophilia A
- Prolonged APTT and a normal PT
- Treated with recombinant factor 9
Von-Willebrand disease:
- Autosomal dominant
- Symptoms: spontaneous bleeding from mucous membranes, excess bleeding from wounds
- Defective or deficient Von-Willebrand factor
- Diagnosed by a normal platelet count with prolonged bleeding time (defective platelet function)
Discuss the pathophysiology, causes, investigation, treatment and complications of some common acquired bleeding disorders e.g disseminated intravascular coagulation
Disseminated intravascular coagulation:
- Always a secondary disease (there is another underlying aetiology)
Pathophysiology:
- Excessive activation of coagulation which leads to the formation of micro-thrombi in the microvasculature
- Consumption of platelets, fibrin, coagulation factors and secondarily activation of fibrinolysis
- This can then lead to leading catastrophe
Causes:
- Sepsis
- Rhabdomyolysis
- Cancer
- Trauama
- Burns
Investigation:
- Blood test would show low levels of platelets, low levels of fibrinogen, high levels of D-Dimers and a high INR
Treatment:
- Treat underlying cause first!!
- Give platelets in the meantime to help improve coagulation
- If let untreated, can get haemorrhages and bleeding from end organs and mucosae
Describe the mode of action of commonly used anticoagulants, how they might be monitored and the complications of anticoagulants
Acute treatment:
- Clot in brain = recombinant tPA (tissue plasminogen activator) helps fibrinolytic process
- Clot in heart = streptokinase, also helps fibrinolytic process
Prophylactic treatment:
- Treatment with low molecular weight Heparin (sometimes oral warfarin)
- New DOACs (novel oral anticoagulants) e.g. Rivaroxaban or Apixaban
Explain the principles of thrombosis
Thrombosis is the formation of a solid mass of blood within the circulatory system
Risk of forming from abnormality in the following (Virchow’s triad)
- Vessel wall e.g. atherosclerosis
- Blood flow e.g. turbulent flow or stasis
- Blood components e.g. hypercoagulative states i.e. increased fibrinogen levels
Explain the principles of embolism and the sources types of embolism
An embolism is the blockage of a blood vessel by a solid, liquid or gas at a distant site from the origin.
Embolisms can be caused by:
- Thombo-emboli (thrombi)
- Air
- Amniotic fluid
- Nitrogen (diving)
- Cancers/tumours
- Fat
Explain the outcomes and complications of thrombosis and embolism
Thrombi can arise in following places and lead to embolisms in the following places (complications):
- Veins = pulmonary embolism
- Heart (left) = ischaemic stroke, bowel ischaemia, renal infarcts etc. (systematic effects)
- Heart (right) = pulmonary embolism (different severities)
- Carotid artery = ischaemic stroke
- Abdominal aorta = acute limb ischaemia
Explain the treatments and preventative methods available for dealing with thrombosis and embolism
Prevention:
- Individuals who are identified as hypercoagulative could be given prophylactic drugs e.g. heparin or DOACs
- Individuals in hospital who are at risk of DVT can be given ‘Flowtron’ boots to assist venous lower limb circulation
- During any penetrative treatments, the patient should lie flat to prevent air flowing into the veins due to negative pressure gradient
Treatments:
- Immediate treatment for acute thrombosis or embolism is clot busters (ateplase or streptokinase) which activates tissue plasminogen activators
