Haemostasis and thrombosis Flashcards

1
Q

Desribe the 2 clotting mechanisms

A

Intrinsic — occurs when blood passes over roughened damaged endothelium causing collagen to be exposed e.g due to hypertensive damage

Results in release of clotting factors

Extrinsic - occurs when damage to tissue e.g via cut releases thromboplastin

What occurs after activation of factor X is the same for both :

Prothrombin —> thrombin + factor XIII (via factor X)

Thrombin converts fibrinogen —> fibrin

Factor XIII converts fibrin to stable fibrin

Mediated by serine proteases

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2
Q

Describe the action of platelets

A

Clotting factors and platelets work in conjunction

Adhere to damaged smooth muscle below endothelial cell of damaged/disease vessel via vWF

Release aggregation factors - ADP and thromboxane (vasoconstrictor)

This leads to expression of glycoproteins IIb-IIIa which allow cross-linking of platelets via fibrinogen and vWF

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3
Q

Describe the lab tests used to investigate platelet dysfuncton and thrombocytopenia (not enough platelets)

A

Incision to forearm with venous cuff

Increased time for coagulation to occur (denoted by INR)

Healthy INR is 1

Also measure liver function as liver produces many clotting factors

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4
Q

Compare venous and arterial thrombosis

A

Venous thrombosis are a problem of the coagulation factors event due to blood stasis - anticoagulants used

Arterial thrombosis are a platelet event due to atheroma - antiplatelet drugs

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5
Q

What is a transient ischaemic attack*

A

Temporary reduction of blood flow to brain
Vascular cause
Symptoms last <24h
No evidence of infarction on imaging

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6
Q

pathophysiology of AF

A

Spontaneous firing of non pacemaker cells in atria

Abnormal discoordination of ventricular contraction

Disrupted SAN —> AVN conduction

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7
Q
Haemophilia 
What is it 
Causes
Symptoms 
Treatment
A

Genetic - males predominantly affected and female carries
Low/no factor VIII of clotting cascade
Haemorrhage and prolonged bleeding risk
Treated with factor VIII from blood donors or analogue of vasopressin (this increases factor VIII release) ; new monoclonal antibody drug available now as well

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8
Q
Von willebrands disease 
What is it 
Causes 
Symptoms 
Treatment
A

Hereditary lack or defect of vWF
Symptoms - increasing bruising, nose bleeds, mucosal bleeding
Treatment - analogue of vasopresssin, factor VIII or vWF from donors

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9
Q

Liver disease can result in reduced synthesis of ____ ____

This leads to increased _____

A

Clotting factors

Bleeding

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10
Q

Thrombocytopenia
What is it
Causes
Symptoms

A

Reduced platelet number
Spontaneous skin bleeding
Causes - idiopathic, viral, drug-induced, toxins

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11
Q

What is disseminated intravascular coagulation

A

Large amount of fibrin made by procoagulant material such as amniotic fluid/infection or massive trauma
Results in widespread haemorrhage and large consumption of platelets/clotting factors but also may be thrombosis
Treat by giving platelets and fresh plasma

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12
Q

What condition increases risk of venous thrombosis

A

Factor V Leiden mutation

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13
Q

Why does atheroma formation only occur in arteries

A

Low pressure of blood in veins ; less turbulence

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14
Q

What are the different types of ischaemic strokes ?

A

Small vessel disease
Large artery atherosclerosis
Cardio-embolic stroke (due to AF)
Unknown causes

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15
Q

Haemorrhagic stroke
Causes
Symptoms

A

Caused by rupture of artery in brain
Intracebral or subarachnoid (on surface)

Symptoms - headache, nausea, vomiting, reduced consciousness/weakness in one part of body

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16
Q

What are the risk factors of stroke

A
Hypertension 
Diabetes mellitus
Hyperlipidaemia 
Cardiovascular disease 
Haematological conditions such as factor VIII/sickle cell
Inflammatory issues
Obesity 
Alcohol/smoking
17
Q

The hearts normal rhythm is called ___ ____

A

Sinus rhythm

18
Q

What are the causes of AF

A
Cardiovascular causes :
Hypertension 
Atherosclerosis 
Congenital heart disease 
Heart valve disease

Respiratory diseases
asthma , COPD, lung cancer

Diabetes
Overactive thyroid gland

19
Q

Treatment of AF

A

Anticoagulants to reduce stroke risk
Beta blockers / anti-arrhythmics drugs to control AF
Electric shock treatment (cardio version)
Catheter ablation - involves placing a tube through the blood vessels to the heart
Pacemaker

20
Q

Symptoms of stroke

A

Sudden weakness and numbness in face arm or leg (specificallyy one side of body)
Sudden confusion and difficulty spreaking

Sudden vision problems

Sudden loss of balance

Loss of memory

Sudden difficulty swallowing

Personality changes

21
Q

Describe the process of diagnosis of stroke

A

History
BP,HR,cholesterol chest

Neurological examination

If right hemisphere affected symptoms : difficulties with attention, perceptions, memory, learning

If left hemisphere affected symptoms : language, and logical functions such as analytical thinking and maths

22
Q

How do ischaemic and haemorrhagic strokes look like on CT scans ?

A

Haemorrhage seen as bright white area

Ischaemic area is slightly darker grey

23
Q

How is ischaemic stroke treated ?

A

Recombinant tissue plasminogen activator
Mechanical thrombectomy - physical removal of blood clot
Carotid endarterectomy - removal of carotid plaques (arteries that delver blood to brain)

24
Q

Describe briefly how thrombosis occurs

A

Damaged vessel wall exposes collagen
Circulating platelets aggregate and release coagulation factors
Fibrinogen —> fibrin
Long fibrin molecules bind together platelets and trap RBC/WBC

25
Q

Describe normal fibrinolysis

A

Plasminogen is an inactive pro enzyme within the plasma ; plasminogen —> plasmin by tissue plasminogen activator (t-PA) secreted by endothelial cells

Plasmin breaks down fibrin dissolving the thrombus

The fragmented bits of fibrin are called fibrin degradation products (FDPs)

26
Q

Pathological thrombosis occurs when …

A

The thrombus enlarges past vessel healing requirements

27
Q

What is the D-dimer test?

A

Breakdown product of a fibrin mesh, stabilised by factor XIII

Increased blood levels in thrombosis

28
Q

What arr the 3 factors that predispose thrombus formation?

A

1) damage to vessel wall
2) stasis (slow or turbulent flow)
3) change in character of blood (increased platelets/RBCs/viscosity)

29
Q

What are the main predisposing factors in :

Arteries , veins, ventricles, atrium, heart valves

A
Arteries- vessel wall damage
Veins-stasis
Ventricles-chamber wall damage 
Atrium-stasis 
Heart valves - valve surface damage
30
Q

Infarction

A

Tissue death due to ischaemia

31
Q

Consequences of DVT

A

Congestion (swelling from the accumulation of fluid in nearby tissue )
Infarction may occur ; typically haemorrhagic in nature

32
Q

When would a thrombus occur on the wall of a heart chamber ?

A

Post MI - scarring of heart wall makes thrombus formation more likely to occur due to stasis of the blood (scarred vessel walls can’t contract as well)

33
Q

What might happen to a thrombus ?

A

Broken down by intrinsic fibrinolysis
Occlusion - completely block the lumen
Organisation and recanalisation (formation of new blood vessels, through an obstruction such as a clot )
Propagate
Thromboembolism - break off and travel elsewhere

34
Q

What two materials typically embolise?

A

Thrombus and cancer cells (we would call this metastasis)

35
Q
Thromboemboli in the following regions are called:
A)Lower limb arteries 
B)Mesenteric arteries
C)Renal arteries
D)Splenic artery
A

A)gangrene of legs
B)bowel necrosis
C)kidney infarct
D)splenic infarct

36
Q

What increases the risk of venous thromboembolism ?

A
Use of hormone replacement therapy 
Oestrogen-containing contraceptive therapy 
Varicose veins 
Pregnancy or post partum <6 weeks
Obesity 
Dehydration 
Being bed bounds 
Thrombophilias 
Age >60 
Cancer 
Comorbidities
37
Q

What other materials are capable of embolising ?

A

Fat and bone marrrow
Air (from putting in a central line or lung surgery)
Nitrogen (form diving)
Amniotic fluid (abortion or placental abruption)