DVT & PE Flashcards
1
Q
What are the predisposing factors to venous thrombosis?
(Relate to Virchow’s triad)
A
-
endothelial dysfunction of injury
- exposure to collagen, tissue factor
- trauma (direct, surgical, catheters0
- disruption of normal balance between production of pro and anti thrombotics
- exposure to collagen, tissue factor
-
hypercoagulability of blood
- increase in pro/decrease in anti coagulation factors
-
changes in blood flow
- more platelets contacting the endothelium
- slowing
- impaired mobility (leg muscle pump)
- hyperviscosity of blood (polycystemia, dehydration)
- cardiac failure
- turbulence
2
Q
How do predisposing factors for venous thrombosis differ from those leading to thrombosis in the arteries and heart?
A
- in arterial thrombosis, endothelial injury is the main component of importance (Virchow’s triad)
- atherosclerosis, turbulence due to obstruction
- in venous thrombosis, it is due to the slowing of the blood (hypercoagulability is a risk factor)
3
Q
Where can venous thrombosis occur?
A
- most commonly in the leg or pelvic veins (DVT)
- deep veins: anterior and posterior tibial veins and peroneal vein
- superficial veins (subcutaneous tissue): greater saphenous vein (drains into femoral) and lesser saphenous veins (drains into the popliteal)
4
Q
What is the most common site of venous thrombosis?
A
- deep veins of the leg:
- anterior and posterior tibial veins and peroneal vein
- most commonly in veins of the calf
- most clinically significant in more proximal veins (popliteal, femoral, pelvic) because they are more likely to embolise
- up IVC into RA and RV
- can end up in pulmonary system depending on size –> PE
5
Q
What are the risk factors for DVT related to blood flow?
A
changes in blood flow
- slowing
- impaired mobility/leg muscle pump
- hyperviscosity (polycystemia, dehydration)
- cardiac failure
6
Q
What are the risk factors for DVT related to endothelial damage?
A
endothelial dysfunction or injury
- trauma (surgical, direct, catheters)
7
Q
What are the risk factors for DVT related to hypecoagulability of blood?
A
hypercoagulability - more relevant in VT than AT
- post-op, post-trauma, severe burns, post-MI
- malignancy and chemotherapy
- +estrogen (periparyum, oral contraceptives, HRT)
- anti-phospholipid antibody syndrome
- nephrotic syndrome (proteinuria causing oedema)
- obesity (adipose cytokines modify liver function, imbalance of anticoagulants)
- inflammatory disease (bowel, acute infectious diseases eg pneumonia)
- cigarette smoking (weak, via endothelial damage)
- genetic/inherited diseases
- Factor V Leiden mutation (most common)
- prothrombin mutation
- deficiencies of anti-thrombin, protein C, protein S
- high factor VIII
8
Q
What are the clinical features of DVT?
A
- ~50% of DVT is asymptomatic
- odema due to +BP
- buildup of blood in capillaries
- superficial veins can’t drain if clot is in perforating veins
- backs up into the superficial veins giving the legs a red appearance
- variable swelling
- redness
- warmth
- discomfort
- pain
- tenderness
9
Q
What is pulmonary thrombo-embolism?
A
- vast majority arise from thrombi formed in the systemic veins (particularly pelvic and deep femoral veins)
- ~10% of pt die within the firs hour; 30% die from recurrent embolism
- effect depends on size +/- underlying lung or CVD
10
Q
What is the pathophysiology of pulmonary thrombo-embolism?
A
- development of hypoxaemia
- thromboembolis blocks PA –> acute pulmonary hypertension
- air enters but blood can’t flow through capillaries –> V/Q mismatch
- local PA obstruction leading to widespread reflex pulmonary vasoconstricion by platelets releasing thromboxane (++vasoconstriction)
- +RV stress –> dilation –> contractile dysfunction
- secondary defects of the LV
- constriction of airways distal to the bronchi
- decreased pulmonary compliance due to hemorrhage, loss of surfactant
11
Q
What are the clinical features of pulmonary thrombo-embolism?
A
- variable presentation
- variable dyspnoea
- haemoptysis
- cough
- syncope
- pleuritic pain (usually indicative of infarct)
12
Q
What are the acute and chronic complications of pulmonary thrombo-embolism?
A
- large or numerous emboli cause:
- occlusion of PA or pulmonary trunk causing sudden collapse and death
- acute cor pulmonale (RHF due to pulmonary HT) with dyspnoea, cyanosis
- medium size:
- dyspnoea, cough, acute cor pulmonale (not as severe)
- pulmonary infarction
- uncommon bc lung is supplied by bronchial arteries
- more common w/underlying lung or CVD (COPD, heart failure) where the patient is hypoxic or anemic
- typically peripheral in lung –> wedge shaped and hemorrhagic (dual blood supply) causing haemoptysis
- pleuritic chest pain and pleural friction rub due to inflammation +/- pleural effusion due to increased secretions
- small:
- may be clinically silent
- pulmonary infarction (as above)
- multiple over time may lead to chronic pulmonary hypertension and tf chronic cor pulmonale
13
Q
What are the long-term outcomes of DVT?
A
- fibrinolysis, organization, complete or partial recanalization of thrombus
- damaged, incompetent valves of deep veins:
- leads to varicose veins (dilation of superficial veins)
- chronic venous insufficiency (impairing venous drainage) –> causes venous stasis
- chronic oedema due to local fibrosis and increased pressure in capillaries
- pigmentation (RBCs in oedema), chronic ulceration due to odema fluid
- legs appear dry and brown
- **DVT is one cause of these by there are others
14
Q
How can DVT be prevented?
A
- pharmacologic prophylaxis with anticoagulants (heparin)
- moblization and exercises to induce muscle pump function
- compression stockings
- lifestyle/activity modifications
15
Q
What is venous thrombo-embolism (VTE)?
A
- mostly arise in deep veins of legs
- potential to embolise to lungs
- one of the 3 major cardiovascular causes of death (stroke, IHD)
- most common preventable cause of death amongst hospitalized patients
16
Q
What is thrombophilia?
A
- inherited or acquired disorders that increase risk of developing VT or AT
- VT predominate
- thromboses may be recurrent, present at unusal sites, or at a young age (eg OCs)
- hypercoagulable state
- causes include:
- genetic/inherited causes of hypercoagluability
- malignancy
- antiphospholipid syndrome
- pregancy and high oestrogens (OCs)
17
Q
What is the structure of normal venous drainage in the leg?
A
- superficial veins drain into the deep veins via the perforating veins
- perforating veins contain valves that prevent flow from the deep veins to the supervicial veins
- thrombus forms in the deep veins due to muscle inactivity and/or hypercoagulables states
18
Q
How does a pulmonary infarct present histologically?
A
- coagulative necrosis (no nuclei) surrounded by haemorrhage (inflammatory reaction around edge)
- week+ see blood in alveoli
- heals in same way as post-MI cardiac tissue (acute inflammation, granulation tissue)
19
Q
How do pulmonary thromboemboli heal?
A
- by orgnaisation:
- ingrowth of smooth muscle cells, fibroblasts, and endothelium into the fibrin-rich thrombus
- and/or recanalisation:
- recanalisation is the formation of blood vessels through the thrombus
20
Q
What are the other sites where venous thrombosis can occur?
A
- veins of the upper limb (eg axillary, causing oedema nad redness of the arm)
- upper limb caths
- cerebral venous sinuses (causing cerebral infarction/stroke)
- mesenteric veins
- portal veins
- hepatic veins
- obstruction can lead to impaired venous flow, oedema in the liver that impinges arterial flow, causing necrosis of liver tissue and subsequent liver failure
- these can occur in younger people especially with genetic defects (Factor V) or other predisposing factors (OCs)
- commonly due to hypercoagulability and thrombophilias, can be due to trauma eg upper limb caths that damage the endothelium
21
Q
What are the complications of venous thrombosis in sites other than the lungs?
A
- infarction
- impairment of venous drainage
