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Cardiovascular System > Thrombosis And Embolism > Flashcards

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
Q

Aschoff body

A

Seen in heart in rheumatic fever , a focus of chronic inflammatory cells, necrosis, and activated mq (antischkows cells)

26
Q

Rheumatic heart disease

A

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
Q

Tissue factor that causes prothrombin to turn into thrombin

A

X

28
Q

Tissue factor that causes fibrin to turn into cross linked fibrin

A

XIII

29
Q

components of red venous thrombosis

A

fibrin and RBC

30
Q

Arterial thrombosis

A

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
Q

venous thrombosis

A

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
Q

causes of acquired hypercoaguability

A

pregnancy
sepsis
cancer

33
Q

causes of endothelial dysfunction

A

Hypertension
smoking
hypercholesterol

34
Q

causes of endothelial damage

A

indwelling venous catheters
trauma
surgery

35
Q

examples of VTE

A 
Limb deep vein thrombosis (DVT)
Pulmonary embolism (PE)

Visceral venous thrombosis
Intracranial venous thrombosis

36
Q

Venous Thromboembolism: Epidemiology

A 
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
Q

Risk factors for VTE

A 
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
Q

Symptoms and signs of DVT

A

Unilateral limb swelling
Persisting discomfort
Calf tenderness

[Warmth]
[Redness- erythema]
[Prominent collateral veins]
[Unilateral pitting oedema]

May be clinically silent

39
Q

Potential long-term consequence of DVT

A

Post Thrombotic Syndrome
Damage to venous valves
Incidence of 20-60% within 2 years of DVT

Swelling
Discomfort
Pigmentation
Ulceration in severe form

40
Q

how is DVT diagnised

A

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
Q

wells score for DVT (high is over 2)

A

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
Q

What is a ‘D-Dimer’?

A

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
Q

Symptoms and signs of PE

A 
Pleuritic chest pain
Breathlessness-  dyspnoea
[Blood in sputum- haemoptysis]
Rapid heart rate- tachycardia
Pleural rub on auscultation 
usually due to pulmonary infarction
44
Q

Symptoms and signs of massive pulmonary embolism

A 
Severe dyspnoea of sudden onset
Collapse
Blue lips and tongue - cyanosis
Tachycardia
Low blood pressure
Raised jugular venous pressure
May cause sudden death
45
Q

Diagnosis of pulmonary embolism

A

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
Q

Wells score for PE (high is over 4.5)

A

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
Q

Questions to ask in patients with diagnosed VTE

A

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
Q

anticoagulation treatment options for VTE

A

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
Q

treatment for PE and DVT other than anticoagulants

A

Vascular surgical interventions in massive DVTs
Thrombolysis reserved for massive PE (Collapse, haemodynamic compromise ie. Shocked Patient)
E.g. Alteplase

50
Q

Aims of treatment of VTE

A

Prevent clot extension
Prevent clot embolisation
Prevent recurrent clot

51
Q

Potential long-term consequence of DVT

A

Post Thrombotic Syndrome
Damage to venous valves
Incidence of 20-60% within 2 years of DVT

Swelling
Discomfort
Pigmentation
Ulceration in severe form

52
Q

Potential long-term consequence of pulmonary embolism

A

Most recover fully
Pulmonary arterial hypertension
Serious outcome
4% patients (< 1/20)

Cardiovascular System (33 decks)

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