Haemostasis & Thrombosis Flashcards
Define thrombosis.
Formation of a solid mass of blood within the circulatory system (during life)
What are some of the mechanisms which maintain haemostasis?
Blood vessel walls: constrict to limit blood loss (more effective when vessel is completely severed)
Platelets: form a platelet plug by adhering to damaged vessel walls (requires ATP, prostaglandins - 5HT released)
Coagulation: fibrin meshwork
Fibrinolysis: breakdown of fibrin by plasmin (+ streptokinase & tissue plasminogen activator - tPA)
Describe Virchow’s triad.
Abnormalities of vessel wall e.g. atheroma, direct injury, vasculitis
Abnormalities of blood flow e.g. stagnation/turbulence
Abnormalities of blood components e.g. smokers, post-partum, post-op
What is the difference in macroscopic appearance of arterial and venous thrombi?
ARTERIAL:
- pale (fewer RBCs due to fast flow)
- granular (breaks easily)
- lines of Zahn: lines between areas of low and high RBC content
VENOUS:
- soft
- gelatinous
- deep red
- higher cell content
note: hard to tell if it was there before/after death at post-mortem
What are some of the outcomes of thrombosis?
Lysis: complete dissolution of thrombus, therefore bloodflow re-established (most likely when thrombi are small)
Propagation: progressive spread of thrombosis in direction of bloodflow (distally in arteries, proximally in veins)
Stagnation -> Turbulence -> Thrombosis
Organisation: ingrowth of fibroblasts and capillaries which obstructs the lumen
Recanalisation: one or more channels form in thrombus, incompletely re-establishing bloodflow
Embolism: part of thrombus detaches and travels to a distant site via the bloodstream
What is the definition of an embolism?
Blockage of a vessel by solid, liquid, or gas at a site distant to its origin
Majority are thrombo-embolism e.g. pulmonary emboli, aortic (- renal - mesenteric), carotid (- brain), abdominal aorta (- leg arteries)
What is a deep-vein thrombosis? What are some risk factors for it? What is the prophylaxis and treatment? What are some complications?
Obstruction of a vein (in the legs) without preceding inflammation which can cause a pulmonary embolism.
Risk factors:
- immobility/bed rest
- post-op (hypercoagulative blood - stagnation)
- pregnancy & post-partum (hypercoagulative blood - stagnation)
- oral contraceptives/pre-menopausal (oestrogen is coagulative)
- severe burns (hypercoagulative blood + dehydration)
- cardiac failure
- disseminated cancer
Prophylaxis: sub-cutaneous heparin, leg compression during surgery (increases venous return), thromboembolic deterrent (TED)
Diagnosis: ultrasound/venography/D-dimer test (fibrin degradation product)
Treatment: IV heparin (acute), oral warfarin (chronic), filter mesh in inferior vena cava
Complications: thrombus migrates to pulmonary trunk (“saddle embolism”) causing cardiac arrest & lung infarction
Describe the varying levels of severity of pulmonary emboli.
MASSIVE (~60% reduction in bloodflow): rapidly fatal e.g. iliac/femoral veins
MAJOR: medium-sized blood vessels blocked - shortness of breath/cough + blood-stained sputum (haemoptysis)
MINOR: small peripheral pulmonary arteries blocked - asymptomatic or minor shortness of breath
RECURRENT MINOR: pulmonary hypertension
note: produce characteristic ECG changes
In what circumstances does blood become more viscous?
- increase in the no. of cells e.g. immune response to infection, myelomas (increased immunoglobulins)
- increased clotting (trapped RBCs)
- reduced temperature (vasoconstriction increases resistance)
- reduced flow e.g. circulatory shock
How do cells flow through plasma in the blood?
Cells congregate in the middle of the tube (therefore flow faster)
- form rouleaux (stacks of RBCs that form due to biconcave disc shape)
note: blood sticks to edges of vessel due to hydrogen bonds/van der Waals’ (increases resistance)
How do you diagnose and treat MIs? What are some complications of MIs?
Diagnosis: ECG, cardiac troponin, CK-MB (+ check clotting, FBC for anaemia, renal function)
ACUTE:
- aspirin & clopidogrel (antiplatelet -> prevents further clots)
- streptokinase (fibrinolysis -> digests clots)
- heparin (anticoagulant)
- primary coronary intervention (stent)
- O2
- IV nitrates (vasodilation)
- analgesia
- glycoprotein antagonists (inhibits platelet aggregation)
- selective beta-blockers (negative inotropy -> reduced O2 demand -> minimises ischaemia)
CHRONIC:
- statins (lower cholesterol)
- selective beta-blockers
- ACE inhibitors (STEMIs) -> vasodilatation -> reduced afterload
- aspirin
- (warfarin)
Complications: arrhythmias, stroke, aneurysm, heart block, heart failure, mitral regurgitation (reduced integrity of muscle) -> left ventricular hypertrophy -> AF -> stroke, cardiac tamponade (reduced integrity of muscle), pulmonary oedema, pericarditis, VF -> sudden death, cardiogenic shock
What is ischaemic bowel? Why does it happen? How do you treat it?
Thromboembolism of superior mesenteric artery (small bowel) e.g. due to migration of aortic thrombus (exarcebated by hypotension) OR strangulated bowel (volvulus)
Bowel appears black and necrotic -> releases toxins -> peritonitis -> septicaemia
Remove ischaemic part of bowel
What is disseminated intravascular coagulation? How is this detected on a FBC? When can it occur? How can it be treated ?
Systemic activation of coagulation cascade causing multiple microvascular thrombi -> clotting factors run out -> severe bleeding
Lots of prothrombin & thrombin, low fibrinogen and platelets
Causes:
- abruptio placentae (separation of placenta from uterus)
- amniotic fluid embolus
- sepsis (endotoxic shock)
- trauma
- metastatic gastric carcinoma
- meningococcal septicaemia
Treatment:
- replace coagulation factors
- heparin
- activated protein C (clotting factor)
- replace antithrombin
- platelet transfusion (acute)
What is thrombocytopenic purpura? What are the symptoms? What is the treatment?
Abnormal decrease in platelets (thrombocytopenia) accompanied by bruising (pupura) which can be triggered by viral infections (antibodies which stick to platelets accidentally produced - platelets destroyed by immune system)
- petachiae
- bleeding gums
- epistaxis
Treatment: steroids (depress immune system -> reduce platelet destruction) & IV gamma-globulin (reduces platelet destruction)
Describe the pathology of varicose veins.
Perforating veins connect the superficial and deep veins of the leg which run in parallel, penetrating the deep fascia of the lower limb (draining the superficial veins into the deep veins via a one way valve)
Incompetent valves -> deep veins drain into superficial -> high pressure in superficial venous system -> stretching/elongation -> pain/venous ulcers
