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venous thromboembolism Flashcards

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1
Q

define thrombosis

A 
pathological clot (thrombus) formation within a blood vessel
o	Not necessarily hard and firm, can be soft and jelly-like thread
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2
Q

define embolism

A

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

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3
Q

describe what a venous thrombi looks like

A

red colour – red cells in a fibrin mesh (more come form of VTE)

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4
Q

describe what an arterial thrombi looks like

A

white colour: platelets + fibrin. Less common bc no valves in arterioles

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5
Q

define deep vein thrombosis

A

thrombus formed in uninjured vein: almost always occurs in leg veins

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6
Q

where does a DVT form distally and proximally?

A

o Distal – confined to calf veins

o Proximal – involved in popliteal vein or above

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7
Q

what is a pulmonary embolus?

A

due to embolus migrating into pulmonary arteries. Embolus can be from sites above the leg e.g. axillary vein, cerebral vein/sinus, mesenteric vein, portal vein etc.

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8
Q

how does blood enter and leave the leg?

A

enter - femoral artery

leave - external iliac vein

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9
Q

what are the 3 deep main calf veins?

A

anterior and posterior tibial

peroneal

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10
Q

what veins form the popliteal vein?

A

anterior and posterior tibial

peroneal

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11
Q

where do most VTEs occur?

A

popliteal
anterior and posterior tibial
peroneal

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12
Q

when does the femoral vein become the external iliac vein?

A

at the level of the inguinal ligament

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13
Q

how can a venous thromboembolism occur?

A
  • No/little blood through a vein can form a stagnant pool in the gap just above venous valves (happens in the auricles of the atria in people with atrial fibrillation)
  • Stagnant blood forms a thrombus bc of activation of the intrinsic system
  • Thrombus can get dislodged to form an embolus
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14
Q

why do thrombi occur in deep veins rather than superficial?

A

• Thrombi form in deep veins rather than superficial bc
o Deep veins rely on muscle contractions to propel blood  inactive muscles = reduced blood flow = increased chance of a thrombus
o Superficial veins have more smooth vascular muscle and greater innervation of muscle – contraction + dilation controlled by SNS to regulate body temp by increasing or decreasing flow

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15
Q

how does a pulmonary embolism occur?

A

Emboli from legs passes through right heart easily. In the pulmonary circulation vessels get smaller – embolus gets stuck –> pulmonary embolus

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16
Q

where do the majority of DVTs originate?

A

calf veins

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17
Q

how many DVTs that originate in the calf veins cause a fatal PE?

A

2%

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18
Q

why do most deaths occur in PE/VTE?

A

bc of missed diagnosis rather than treatment failure

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19
Q

what are the components of virchow’s triad?

A

reduced blood flow
vessel wall pathology
blood hypercoagulability

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20
Q

what factors can caused reduced blood flow?

A
  • Long-haul flights – muscle pump inactive; blood stasis in veins
  • Immobilisation – bc of conditions e.g. hip/pelvis fracture
  • Obesity – reduced exercise
  • Sickle cell disease – red cell precipitation can occlude vessels
  • Surgery – increased risk in the months following any surgery partly due to immobilisation
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21
Q

what is another name for prostacyclins?

A

prostaglandin PG12

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22
Q

how does PG12 work as a vasodilator?

A
  • binds to and stimulates a platelet prostacyclin receptor - platelet produces cAMP
  • cAMP inhibits platelet activation by VWF and fibrinogen + inhibits entry of Ca2+ to platelets and smooth muscle –> vasodilation
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23
Q

what are the roles of nitric oxide?

A

inhibits platelet activation

powerful vasodilator

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24
Q

how does nitric oxide inhibit platelet activation?

A

by stimulating production of cAMP in platelets

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25
where is heparan sulphate found in the body?
attached to cell surfaces by transmembrane protein backbone
26
what is the role of heparan sulphate?
prevents platelet adhesion
27
how does heparan sulphate prevent platelet adhesion?
Various lengths of heparin sulphate polysaccharides form feathery projections into BV lumen – form a “non-stick” surface on endothelial cells
28
what can cause vessel wall pathology and a reduction in the vessel wall chemicals?
chronic inflammatory diseases cancer smoking
29
what is endothelin?
peptide secreted by endothelium that’s a vasoconstrictor
30
when is endothelin released?
``` Released by endothelial cells in response to: hypoxia oxidised LDL pro-inflammatory cytokines bacterial toxins ```
31
when are plasma endothelin concentrations high?
in conditions associated w endothelial cell injury; essential hypertension and congestive heart failure
32
what are the risk factors for blood hypercoagulability?
- thrombophilia - genetic factors - blood group o: reduced levels of VWF and factor 8 - cancer: cancerous cells may produce procoagulants + chemotherapy - pregnancy - increased risk of thrombosis - previous history of vtes
33
how can cancer increase blood hypercoagulability?
Cancerous cells may produce procoagulants + chemotherapy can damage endothelial walls
34
how does pregnancy increase 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
35
how do VTEs present?
Classic signs of distributed inflammation – pain, erythema (redness), tenderness, swelling/oedema, warmth, superficial venous dilation
36
why is correct diagnosis of VTE important?
- many patients w VTE are acc negative when investigated | - drugs used for treatment can cause serious/fatal side effects
37
what are some of the differential diagnoses for VTE?
``` o Musculo-tendinous injury- trauma, haematoma, myositis, tendinitis o Superficial thrombophlebitis o Cellulitis o Compression of iliac veins o Congestive cardiac failure o Hypoalbuminaemia o Lymphoedema, lymphangitis o Synovitis, osteoarthritis, osteomyelitis, fracture, tumour o Acute arterial occlusion ```
38
what is a wells score?
scoring system for a probability of VTE
39
what wells score indicates that a DVT is likely?
2 or more
40
name some of the clinical characteristics of a DVT?
- active cancer within the last 6 months - paralysis, paresis, recent plaster immobilisation - recently bedridden, major surgery - localised tenderness along distribution of deep veins - entire leg swollen - pitting oedema confined to symptomatic leg - collateral superficial veins - previous DVT - alternative diagnosis at least as likely as DVT
41
what further clinical tests should you do if the wells score is more than 2?
d-dimer ultrasound venography CT scan, MR venography
42
what is the d-dimer test?
blood test measuring fibrin fragments after fibrinolysis. A non-specific marker of fibrin formation
43
when is d-dimer raised?
raised in VTE but also in cancer, infection, inflammation, post-op, pregnancy
44
what is the initial treatment for VTE?
low molecular weight heparin/fondaparinux
45
how do you administer LMWH?
subcutaneously
46
what is the half life of LMWH?
4 hours
47
what effect does LMWH have?
anti factor Xa effect
48
when do you monitor LMWH treatment?
renal failure pregnancy obesity
49
when is unfractionated heparin used?
where rapid reversibility is needed
50
when is LMWH stopped and what is given afterwards? what is the exception to this?
After one week stop LMWH and start warfarin (unless pregnant)
51
what is heparin?
anticoagulant protein produced by basophils and mast cells
52
what does heparin do?
prevents conversion of fibrinogen to fibrin • Acts to prevent formation of clots and extension of existing clots within the blood • Doesn’t break down clots that have already formed – stimulates body’s natural clot lysis mechanisms
53
how are natural unfractionated heparin and LWMH different?
* Natural ‘unfractionated’ heparin has molecular chains of diff. molecular weights * LMWH only have short chains – more predictable effects than natural heparin
54
what are possible side effects of heparin?
o Excessive bleeding | o Heparin-induced thrombocytopenia (HIT
55
when does heparin induced thrombocytopenia develop?
5-14 days
56
how is heparin induced thrombocytopenia treated?
o Needs to stop all heparin and gets replaced by a non-heparin anticoagulant e.g. hirudin. Potent natural inhibitor of thrombin
57
what is warfarin?
vitamin K antagonist
58
what does warfarin do?
reduces levels of factors 2, 7, 9 and 10 in plasma
59
how is warfarin administered?
orally
60
what is the half life of warfarin?
36 hours
61
how must the warfarin dose be adjusted over time?
adjusted to maintain INR in range 2.0-3.0
62
why cant warfarin be given during pregnancy?
Risks to fetus – teratogenicity, maternal bleeding
63
what can be used instead of warfarin to treat vte?
direct oral anticoagulants such as Rivaroxaban Apixaban, Dabigatran
64
what is the acute treatment for VTE?
Rivaroxaban and Apixaban – both with no heparin lead in
65
what is the short term treatment for VTE?
Dabigatran – heparin lead-in required 5-10 days
66
what is Rivaroxaban?
Orally active factor Xa inhibitor that inhibits platelet activation by blocking binding site for Xa
67
when is Rivaroxaban given?
treatment of DVT or PE • Indicated for prophylaxis of DVT in patients of knee or hip replacement surgery • Used to prevent blood clots in atrial fibrillation
68
who is Rivaroxaban contraindicated in?
people with significant liver disease and end-stage kidney disease
69
what is apixaban?
factor Xa inhibitor - similar in properties to Rivaroxaban
70
what is dabigatran?
orally active direct thrombin inhibitor
71
who is dabigatran given to and why?
* Delayed onset of action so indicated for treatment of DVT and PE in patients who’ve had anticoagulants for 5-10 days * Also used to prevent blood clots after hip/knee replacements + in those w prior clots
72
what is given as treatment for VTE in pregnancy?
use LWMH throughout pregnancy
73
why are DOACs not given to pregnant women?
effects unclear - presumed bleeding
74
what is given as treatment for VTE in breastfeeding women?
LWMH and warfarin safe but not DOACs
75
what is given as treatment for patients with cancer-associated thrombosis?
LMWH more effective than warfarin. DOACs undergoing evaluation
76
what are symptoms of pulmonary embolism?
* Breathlessness, pleuritic chest pain, haemoptysis (65%) * Isolated breathlessness (25%) * Collapse/syncope, hypotension, shock (10%)
77
what are the signs of a pulmonary embolism?
* Tachypnoea and tachcardia * Crepitations and pleural rub * Clinical signs of DVT uncommon
78
what are the preliminary exams for pulmonary embolism?
ECG Chest x ray Arterial blood gas
79
what does an ecg show in someone with pulmonary embolism?
sinus tachycardia, right heart strain, T-wave inversion on anterior leads
80
how does a chest x ray look in someone with pulmonary embolism?
often normal, focal oligaemia, peripheral wedge shaped density above diaphragm, small pleural effusion
81
what are the arterial blood gases of someone with a pulmonary embolism?
often hypoxia low CO2 but may be normal
82
what are diagnostic tests for PE
* CT Pulmonary Angiogram (CTPA) * Isotope lung scan (V/Q scan), * Echocardiogram - diagnostic at bedside in massive PE * Pulmonary angiogram - gold standard, invasive * Leg ultrasound especially if symptomatic * D-dimer – use in conjunction with low Wells score
83
what are the differential diagnoses for a pulmonary embolism?
* 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
84
what are the risk factors for predicting probability of pulmonary embolism?
- clinical signs and symptoms of DVT - alternative diagnosis less likely than PE - pulse >100 - immobilisation or surgery in previous 4 weeks - previous DVT or PE - haemoptysis - cancer within last 6 months
85
what wells score suggests a likley PE?
greater than 4
86
how is pulmonary embolism treated?
Same as for VTE; ie LMWH initially then warfarin

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