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Cardiorespiratory 2 > Venous Thromboembolism > Flashcards

Venous Thromboembolism Flashcards

1
Q

What is a thrombosis

A

pathological clot (thrombus) formation within a blood vessel.

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2
Q

What is an embolism

A

clot breaks off and travels through circulation until obstructed by vessels of smaller diameter.

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3
Q

What is the difference between a thrombus and a blood clot

A

a thrombus may be soft and jelly like thread whereas a blood clot is hard and firm to the touch

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4
Q

what is the difference between venous thrombi and arterial thrombi

A
  • Venous thrombi – red colour - red cells in a fibrin mesh. (more common form of VTE)
  • Arterial thrombi - white colour - platelets and fibrin. (less common-no valves in arteries)
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5
Q

what are the types of venous thrombi

A
  1. Deep vein thrombosis (DVT): thrombus formed in uninjured vein: almost always occurs in leg veins
    a) Distal – confined to calf veins
    b) Proximal – involve popliteal vein or above
  2. Pulmonary embolism (PE): due to disloged thrombus (embolus) migrating into pulmonary arteries
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6
Q

what veins do most VTEs occur in

A
  • Popliteal v
  • Anterior tibial
  • Posterior tibial
  • Peroneal veins
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7
Q

how is the popliteal vein formed

A

the anterior and posterior tibial and the peroneal –join as a trifurcation behind the knee to form the popliteal vein

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8
Q

describe what the venous system is like after the popliteal vein

A
  • Above the knee the popliteal vein continues as the femoral vein which is a deep vein.
  • In the upper thigh the (superficial) femoral vein is joined by the deep femoral vein to form the common femoral vein.
  • At the level of the inguinal ligament the femoral vein becomes the external iliac vein and is subsequently joined by the internal iliac vein draining the pelvic organs to form the common iliac vein.
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9
Q

How does a DVT occur

A
  • Activated by 12 spontaneous factors in contact with a charged surface that triggers the intrinsic system
  • Stagnant blood triggers the intrinsic system
  • Upstream of the valve you can get little pools of blood
  • When there is no or very little flow through a vein blood can form a stagnant pool in the recesses just above the venous valves;
  • (the same thing can happen in the auricles of the atria in patients with atrial fibrillation).
  • The stagnant blood then forms a thrombus due to activation of the intrinsic system. The thrombus can then get dislodged and form an embolus.
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10
Q

what can trigger the intrinsic system

A
  • Stagnant blood triggers the intrinsic system
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11
Q

why do you not get DVTs as much in superficial veins

A
  • Deep veins rely more on muscle contractions to squeeze the vein and propel the blood centrally. If the muscles are inactive (eg during prolonged sitting) this reduces the blood flow and increases the probability of a thrombus formation.
  • Also superficial veins have more smooth vascular muscle and greater innervation of this muscle; they contract and dilate under the control of the sympathetic nervous system to regulate body temperature by increasing or decreasing flow
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12
Q

how do emboli travel round the body from the legs to form a pulmonary emboli

A

Emboli from the legs enter larger and larger vessels as they progress centrally; they normally pass easily through the right heart and into the pulmonary circulation; however as the pulmonary arteries branch and decrease in size, eventually the embolus gets stuck and forms a pulmonary embolus

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13
Q

DVT and PE can be part of….

A

Thus DVT & PE are part of the same pathological process

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14
Q

a PE may occur in a DVT patient without..

A

A PE may occur in a DVT patient without obvious extra symptoms. (40% of patients with DVT but no features of PE have evidence of PE on lung scan).

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15
Q

describe the percentage of DVT that lead to PE

A

– 25% extend proximally to popliteal vein or above
– 40% of those reaching popliteal vein (10% of total) embolise
- 20% of those that embolise (2% of total) cause fatal PE.

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16
Q

what is the 3rd most common cause of cardiovascular death

A

VTE/PE

Most deaths are due to missed diagnosis rather than treatment failure

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17
Q

what are the causes of VTE

A
  1. Reduced blood flow
  2. Vessel wall pathology
  3. Hypercoagulability of blood
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18
Q

what is another term that is used to describe hyper coagulable blood

A

thrombophilia is the term often used to describe hypercoagulable blood

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19
Q

what can cause reduced blood flow

A
  • Long-haul flights especially >8hours (prolonged sitting ) means muscle pump inactive: blood stasis in veins
  • Immobilisation in bed due to other conditions eg hip/pelvis fracture
  • Obesity causing reduced exercise
  • Sickle cell disease: red cell precipitation can occlude vessels
  • Surgery there is a significant increased risk in the months following any form of surgery (partly due to immobilization)
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20
Q

how does prostacyclin PG12 work

A
  • Prostacyclin (also called prostaglandin PGI2) inhibits platelet activation.
  • PG12 binds to and stimulates a platelet prostacyclin receptor.
  • This makes the platelet produce cAMP.
  • cAMP inhibits platelet activation by von Willebrand factor and fibrinogen and also inhibits entry of calcium into platelets and vascular smooth muscle.
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21
Q

why is PG12 also an effective vasodilator

A

PG12 is also an effective vasodilator because it inhibits calcium entry into smooth muscle.

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22
Q

how does nitric oxide prevent the formation of VTE

A
  • constantly released from healthy endothelium.
  • It inhibits platelet activation by stimulating production of cAMP in the platelets
  • also acts as a powerful vasodilator to keep blood moving.
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23
Q

how does heparan sulphate prevent the formation of VTE

A

(different to low-molecular weight heparin) is expressed on the surface of healthy endothelial cells.

  • It is attached to the surface of the cells by a transmembrane protein backbone.
  • Various lengths of heparin sulphate polysaccharides form feathery projections into the lumen of the blood vessel. - These projections create a “non-stick” surface on the endothelial cells that prevents platelet adhesion
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24
Q

what 3 substances in the endothelium prevent the formation of clots

A

PG12 prostacyclin
nitric oxide
heparan sulphate

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25
Q

what can damage the endothelium wall and reduce the amounts of anticoagulation

A
  • chronic inflammatory disease (eg rheumatoid arthritis, IBS etc) and cancer
  • smoking - free radicals damage the system
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26
Q

what is endothelin

A

Endothelin is a peptide secreted by endothelium that is a powerful vasoconstrictor

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27
Q

when does the endothelium release endothelin

A
  • However endothelial cells can release endothelin in response to hypoxia, oxidized LDL, pro-inflammatory cytokines, and bacterial toxins.
  • Plasma endothelin concentrations are high in conditions associated with endothelial-cell injury, as well as in essential hypertension and congestive heart failure
28
Q

what are the risk factors for blood hyper coagulability causing VTE

A
  • Genetic factors include overactive coagulation factors such abnormal factor V (Factor V Leiden)
  • Blood group O individuals are at a reduced risk relative to groups A, B, &AB due to reduced levels of von Willebrand factor & factor VIII
  • Cancer of any sort, but especially when there are metastases. Cancerous cells may secrete procoagulants. Also chemotherapy can damage endothelial walls, bone marrow etc.
  • Pregnancy is associated with an increased risk of thrombosis (Estrogen, when used in the combined oral contraceptive pill and in perimenopausal hormone replacement therapy, is associated with a significant increased risk of venous thrombosis).
29
Q

what is the symptoms and signs of a VTE

A
  • Pain
  • Erythema (redness)
  • Tenderness
  • Swelling/oedema
  • Warmth
  • Superficial venous dilation
30
Q

why is the diagnosis of VTE important

A

1) Many patients with suspected VTE are actually negative on investigation
2) 2) Drugs used to treat VTE can cause serious/fatal side-effects.

31
Q

what are some differentiate diagnosis to VTE

A 
Musculo-tendinous injury- trauma, haematoma, myositis, tendinitis
Superficial thrombophlebitis
Cellulitis
Compression of iliac veins
Congestive cardiac failure
Hypoalbuminaemia
Lymphoedema, lymphangitis
Synovitis, osteoarthritis, osteomyelitis, fracture, tumour
Acute arterial occlusion
32
Q

what is WELLS score

A

This is a widely used scoring system for probability of a VTE

33
Q

what are the clinical characteristics for WELLS score for possible VTE

A

Active cancer within last 6 months 1

Paralysis, paresis, recent plaster immobilisation 1

Recently bedridden ≥ 3 days, major surgery <12 weeks 1

Localised tenderness along distribution of deep veins 1

Entire leg swollen 1

Calf swelling ≥ 3 cm (10 cm below tibial tuberosity) 1

Pitting oedema confined to symptomatic leg 1

Collateral superficial veins (non-varicose) 1

Previous documented DVT 1

Alternative diagnosis at least as likely as DVT -2

34
Q

what Total of the wells score is a DVT likely

A

If the total score is greater than or equal to 2 then DVT is likely, if it is less than or equal to 1 then it is unlikely

35
Q

if the wells score is greater than 2 what do you do

A
  • D-dimer

- Ultrasound

36
Q

what is a D dimer blood test

A

blood test measuring fibrin fragments after fibrinolysis. A non-specific marker of fibrin formation (usually raised in VTE but also in cancer, infection, inflammation, post-op, pregnancy)

37
Q

how do you do an ultrasound for a DVT

A
  • Usually compression ultrasound*, as non-invasive
  • Sometimes venography (gold standard) e.g. if looking for calf DVT for which ultrasound is insensitive
  • Other techniques – CT scan, MR venography
38
Q

what does LMWH stand for

A

Low molecular weight heparin (LMWH) or Fondaparinux

39
Q

what is the intinial agent of choice for VTE in most patients

A

LMWH is the Agent of choice for initial VTE treatment in most patients

40
Q

describe the LMWH properties

A
  • Subcutaneous (SQ) administration
  • Half life - about 4 hours
  • Predominantly anti factor Xa effect
  • Fixed, weight-adjusted dose once or twice daily
  • No monitoring (unless renal failure, pregnant, obese
41
Q

what is more powerful than LMWH

A

• Unfractionated heparin may be used where rapid reversibility is needed as it is more powerful

42
Q

what do you use after one week of LMWH

A

After one week stop LMWH and start warfarin (unless pregnant), heparin works straight away but warfarin is easier to control

43
Q

what is heparin produced by and what is it

A

Heparin is a naturally occurring anticoagulant protein produced by basophils and mast

44
Q

what is the difference between heparin and heparin sulphate

A

Heparin sulphate is produced by endothelial cells whereas heparin is produced by basophils and mast cells

45
Q

what does heparin do

A

Heparin prevents conversion of fibrinogen to fibrin thus preventing the formation of clots
- does not break down clots that have already formed but stimulates the body natural clot lysis to break down existing clots

46
Q

what is the difference between natural heparin and LMWH

A
  • Natural (unfractionated`) heparin consists of molecular chains of polysaccharides of varying molecular weights. Low molecular weight heparins (LMWHs), in contrast, consist only of short chains.
  • LMWHs have more predictable effects than unfractionated heparin and can be given subcutaneously rather than i.v. for heparin
47
Q

what are the side effects of heparin

A

1) Excessive bleeding occurs in 1 - 5% patients in first week of treatment
2) Heparin-induced thrombocytopenia (HIT)
- Develops 5-14 days after start of heparin or LMWH. Features onset of moderate thrombocytopenia. Requires discontinuation of all heparin and replacement by a non-heparin anticoagulant, eg hirudin, a naturally occurring peptide in the salivary glands of blood-sucking leeches. It is a potent natural inhibitor of thrombin.

48
Q

what is warfarin

A

• Warfarin is a small molecule that acts as a Vitamin K antagonist

49
Q

what plasma proteins does warfarin reduce

A

reduces levels of factors II, VII, IX, X, in plasma

50
Q

what are the features of warfarin

A
  • Can be administered orally
  • Long half-life - 36 hours
  • Delayed onset of action (so start treatment with heparin)
  • Primarily affects INR, & dose must be adjusted to maintain INR in range 2.0-3.0
  • Has multiple drug interactions
  • Risks to fetus – teratogenicity, therefore cant be used in pregnancy maternal bleeding – so never given during pregnancy or suspected pregnancy
51
Q

name the modern treatments for VTE

A

Direct Oral Anticoagulants (DOACs) such as Rivaroxaban, Apixaban, Dabigatran etc can be used instead of warfarin to treat VTE (with initial LMWH if using Dabigatran)

52
Q

what do you initially have to use if you are using the DOACs dabigatran

A

initial LMWH if using Dabigatran

53
Q

what does rivaroxaban do

A

Rivaroxaban is an orally active factor Xa inhibitor that inhibits platelet activation by blocking the active site of factor Xa

54
Q

when is rivaroxaban used

A
  • it is indicated for treatment of DVT or PE
  • It is also indicated for prophylaxis of DVT in patients undergoing knee or hip replacement surgery.
  • It is also used to prevent blood clots in atrial fibrillation.
55
Q

when can rivaroxaban not be used

A

Rivaroxaban is contraindicated in people with significant liver disease and end-stage kidney disease

56
Q

what does apixaban do

A

Apixaban is another factor Xa inhibitor similar in properties to Rivaroxaban

57
Q

what doe dabigatran do

A

Dabigatran is an orally active direct thrombin inhibitor

58
Q

what is dabigatran used

A

It has a delayed onset of action so is indicated for the treatment of DVT and PE in patients who have been treated with a parenteral anticoagulant for 5-10 days.

  • It is also used to prevent blood clots following hip or knee replacement and in those with a history of prior clots.
  • It is used as an alternative to warfarin and does not require monitoring by blood tests.
  • have to start with heparin and then switch over after a week
59
Q

if your pregnant what drugs would you use and wouldn’t use

A

Warfarin and DOACs cross placenta
Warfarin teratogenic 6-12/40 and bleeding risk
DOACs effects unclear – presumed bleeding
Use LMWH throughout pregnancy

60
Q

if you are breasffeeding what drugs you use use

A

LMWH and warfarin safe but not DOACs

61
Q

if you have cancer what drugs would you use

A

LMWH more effective than warfarin

DOACs undergoing evaluation

62
Q

what are the symptoms of a pulmonary embolism

A
  1. Breathlessness, pleuritic chest pain, haemoptysis as blood can go into the airways(65%)
  2. Isolated breathlessness (25%)
  3. Collapse/syncope, hypotension, shock (10%)
63
Q

what are the signs of a pulmonary embolism

A
  1. Tachypnoea and tachcardia
  2. Crepitations and pleural rub
  3. Clinical signs of DVT uncommon
64
Q

what investigations initially should you do for pulmonary embolism

A
  1. ECG – sinus tachycardia, right heart strain, T-wave inversion on anterior leads.
  2. CXR – often normal, focal oligaemia, peripheral wedge shaped density above diaphragm, small pleural effusion
  3. Arterial blood gases – often hypoxia, low CO2, but may be normal
65
Q

what are the diagnostic tests that should you have a pulmonary embolism

A
  1. CT Pulmonary Angiogram (CTPA)
  2. Isotope lung scan (V/Q scan – looks at the ventilation perfusion ratio in different parts of the lung ),
  3. Echocardiogram - diagnostic at bedside in massive PE
  4. Pulmonary angiogram - gold standard, invasive
  5. Leg ultrasound especially if symptomatic
  6. D-dimer – use in conjunction with low Wells score
66
Q

what are the differential diagnosis of a pulmonary embolism

A
  • Pneumonia or bronchitis
  • Asthma
  • COPD exacerbation
  • Acute coronary syndrome
  • Anxiety
  • Pneumothorax
  • Costochondritis
  • Musculoskeletal pain or rib fracture
  • Dissection of the aorta
  • Pericardial tamponade
  • Lung cancer
  • Primary pulmonary hypertension

Cardiorespiratory 2 (43 decks)

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