Thrombosis And Embolism Flashcards

1
Q

2 types of non laminar blood flow

A

Turbulent and stagnant

caused by thromboembolism, atheroma, hyperviscosity, spasm, external compression, vasculitis, vascular steal

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2
Q

Virchow’s triad

A

Changes in blood vessel wall
Changes in blood constituents
Changes in pattern of blood flow

Factors causing thrombosis (formation of a solid mass of blood within the vascular system during life)

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3
Q

Specific changes in Virchow’s triad causing thrombosis

A

Endothelial injury
Stasis or turbulent blood flow
Hypercoagulability of blood

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4
Q

What direction does thrombus propagate in

A

Direction of flow

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5
Q

Causes of changes in blood flow

A

Stasis eg flights

Turbulence eg atheromatous plaque or aortic aneurysm

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6
Q

Common clinical scenarios of thrombosis

A

DVT, ichaemic limb, MI

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7
Q

Positive outcomes of thrombosis

A

Resolution

Organisation/recanalization

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8
Q

Negative outcomes of thrombosis

A

Death

Propagation to embolism

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9
Q

Definition of embolism

A

Movement of abnormal material in bloodstream and it’s impaction on vessel, blocking the lumen

Mostly dislodged thrombi

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10
Q

Systemic / arterial thromboembolus

A

Mural thrombus (MI or AF with LAD)
Aortic aneurysm
Atheromatous plaque
Valvular vegetations

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11
Q

Venous thromboembolism

A

Paradoxical emboli, originate from DVT, most common cause of thromboembolic disease

Travel to pulmonary arterial circulation and may occlude bifurcation (saddle)
Often multiple, over time these cause pulmonary hypertension and right ventricular failure

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12
Q

Consequences of systemic thromboembolus

A

Travel to wide variety of sites most commonly lower limbs, then brain and organs

Consequences depend on vulnerability of tissues to ischemia, calibre of occluded vessel, collateral circulation

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13
Q

Risk factors for DVT and pulmonary thromboembolism

A

Cardiac failure, trauma/burns, post op or partum, nephrotic syndrome, disseminated malignancy, oral contraceptives, age, bed rest, obesity, PMH of DVT

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14
Q

Prophylaxis of surgery patients at risk for DVT

A

Ted’s (stockings), heparin

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15
Q

Fat embolus

A

After major fractures, brain kidneys and skin affected

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16
Q

Gas Embolus

A

From decompression sickness (N2 forms as bubbles which lodge in capillaries

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17
Q

Air embolus

A

Head and neck wounds, surgery, CV lines

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18
Q

Tumour embolus

A

From spread

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19
Q

Trophoblast embolus

A

Pregnant women, placenta goes to lungs

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20
Q

Septic embolus

A

Eg infective endocarditis

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21
Q

Amniotic fluid embolus

A

Cause of collapse in childbirth

22
Q

Bone marrow embolus

A

Fractures or cpr

23
Q

Foreign body embolus

A

Intravascular cannulae tips, sutures etc

24
Q

Rheumatic fever

A

Disordered immunity
Inflammation in heart and joints sometimes neuro
5-15y
Flitting pains in joints plus skin rashes and fever
Pancarditis in acute phase with heart murmurs
Patients have had a recent sore throat usually A beta haemolytic streptococcus
Damage to heart by Ab and T cell reactions

25
Aschoff body
Seen in heart in rheumatic fever , a focus of chronic inflammatory cells, necrosis, and activated mq (antischkows cells)
26
Rheumatic heart disease
Pancarditis in acute can progress to chronic, manifesting as valvular abnormalities Inflammation of endocardium and left valves results in fibrinoid necrosis of valve cusps/chordae tendinae and vegetations form Deforming fibrotic valvular disease particulatly mitral , CT may thicken and fuse Main cause of MS , can cause MR too.
27
Tissue factor that causes prothrombin to turn into thrombin
X
28
Tissue factor that causes fibrin to turn into cross linked fibrin
XIII
29
components of red venous thrombosis
fibrin and RBC
30
Arterial thrombosis
from rupture of athersclerotic plaque comes from arteries of left heart chambers results in ischaemia and infarction causes ACS, IS, limb claudication/ischaemia composed of platelets and fibrin (white thrombus)
31
venous thrombosis
comes from virchows triad especially stasis and hypercoaguability originates in venous vakves and sinusoids of muscles results in back pressire causes DVT and PE composed of RBC and fibrin (red thrombus)
32
causes of acquired hypercoaguability
pregnancy sepsis cancer
33
causes of endothelial dysfunction
Hypertension smoking hypercholesterol
34
causes of endothelial damage
indwelling venous catheters trauma surgery
35
examples of VTE
``` Limb deep vein thrombosis (DVT) Pulmonary embolism (PE) ``` Visceral venous thrombosis Intracranial venous thrombosis
36
Venous Thromboembolism: Epidemiology
``` DVT: 1 in 1000 pa PE: 1 in 3000 – 5000 pa (chances) Leading cause of direct maternal death in UK Case fatality rate: 1 to 5% Untreated PE: 30% PE in 20% of autopsies young women more then old men more ```
37
Risk factors for VTE
``` surgery late pregnancy caesatian Lower limb problems eg fracture and vv malignancy reduced mobility Congestive HD HT OC COPD hormone replacement therapy neurological disability thrombotic disorders long distance travel obesity ```
38
Symptoms and signs of DVT
Unilateral limb swelling Persisting discomfort Calf tenderness [Warmth] [Redness- erythema] [Prominent collateral veins] [Unilateral pitting oedema] May be clinically silent
39
Potential long-term consequence of DVT
Post Thrombotic Syndrome Damage to venous valves Incidence of 20-60% within 2 years of DVT Swelling Discomfort Pigmentation Ulceration in severe form
40
how is DVT diagnised
Clinical assessment and pretest probability score (Wells score) Blood test: D-dimer if low pre-test probability score Imaging: Compression ultrasound if positive D-dimer or high pre-test probability score
41
wells score for DVT (high is over 2)
Active cancer, or cancer that’s been treated within last six months 1 Paralyzed leg 1 Recently bedridden for more than three days or had major surgery within last four weeks 1 Tenderness near a deep vein 1 Swollen leg 1 Swollen calf with diameter that’s more than 3 centimeters larger than the other calf’s 1 Pitting edema in one leg 1 Large veins in your legs that aren’t varicose veins 1 Previously diagnosed with DVT 1 Other diagnosis more likely -2
42
What is a ‘D-Dimer’?
Breakdown product of cross-linked fibrin Produced during fibrinolysis High sensitivity for VTE Low specificity for VTE Trauma, malignancy, sepsis, bleeding, cancer, recent surgery
43
Symptoms and signs of PE
``` Pleuritic chest pain Breathlessness- dyspnoea [Blood in sputum- haemoptysis] Rapid heart rate- tachycardia Pleural rub on auscultation usually due to pulmonary infarction ```
44
Symptoms and signs of massive pulmonary embolism
``` Severe dyspnoea of sudden onset Collapse Blue lips and tongue - cyanosis Tachycardia Low blood pressure Raised jugular venous pressure May cause sudden death ```
45
Diagnosis of pulmonary embolism
Clinical assessment and pretest probability score (Wells score or Geneva score) Blood test: D-dimer if low pre test probability score Imaging: if D-dimer positive or high pre test probability score Isotope ventilation/perfusion scan CT pulmonary angiogram
46
Wells score for PE (high is over 4.5)
clinical signs and symptoms of DVT = 3 an alternative diagnosis is less likely than PE = 3 heart rate more than 100 = 1.5 immobilisation for 3 or more consecutive days or surgery in the previous 4 weeks = 1.5 previous objectively diagnosed PE or DVT = 1.5 haemoptysis = 1 malignancy (on treatment, treatment in last 6 months or palliative) = 1
47
Questions to ask in patients with diagnosed VTE
Was there a clear cause or precipitant? Recent surgery / hospitalisation Any symptoms or signs to suggest underlying malignancy? Consider risk of recurrence Clinical Risk Cancer patients DASH score/ HERDoo2 etc
48
anticoagulation treatment options for VTE
Anticoagulation is main treatment Provoked – 3/12 Unprovoked and high risk of recurrence- Lifelong Parenteral- low molecular weight heparin, a factor 10a inhibitor eg dalteparin, no monitoring but cant use in sig. renal failure direct oral anticoagulants- 10a inhibitors eg rivaroxaban or direct thrombin inhibitor eg dabigatran, no monitoring but be careful with high BMI and low renal function
49
treatment for PE and DVT other than anticoagulants
Vascular surgical interventions in massive DVTs Thrombolysis reserved for massive PE (Collapse, haemodynamic compromise ie. Shocked Patient) E.g. Alteplase
50
Aims of treatment of VTE
Prevent clot extension Prevent clot embolisation Prevent recurrent clot
51
Potential long-term consequence of DVT
Post Thrombotic Syndrome Damage to venous valves Incidence of 20-60% within 2 years of DVT Swelling Discomfort Pigmentation Ulceration in severe form
52
Potential long-term consequence of pulmonary embolism
Most recover fully Pulmonary arterial hypertension Serious outcome 4% patients (< 1/20)