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c2 > venous thromboembolism > Flashcards

venous thromboembolism Flashcards

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
Q

where is heparan sulphate found in the body?

A

attached to cell surfaces by transmembrane protein backbone

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26
Q

what is the role of heparan sulphate?

A

prevents platelet adhesion

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27
Q

how does heparan sulphate prevent platelet adhesion?

A

Various lengths of heparin sulphate polysaccharides form feathery projections into BV lumen – form a “non-stick” surface on endothelial cells

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28
Q

what can cause vessel wall pathology and a reduction in the vessel wall chemicals?

A

chronic inflammatory diseases
cancer
smoking

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29
Q

what is endothelin?

A

peptide secreted by endothelium that’s a vasoconstrictor

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30
Q

when is endothelin released?

A 
Released by endothelial cells in response to: 
hypoxia
oxidised LDL
pro-inflammatory cytokines 
bacterial toxins
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31
Q

when are plasma endothelin concentrations high?

A

in conditions associated w endothelial cell injury; essential hypertension and congestive heart failure

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32
Q

what are the risk factors for blood hypercoagulability?

A
  • 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
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33
Q

how can cancer increase blood hypercoagulability?

A

Cancerous cells may produce procoagulants + chemotherapy can damage endothelial walls

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34
Q

how does pregnancy increase risk of thrombosis?

A

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

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35
Q

how do VTEs present?

A

Classic signs of distributed inflammation – pain, erythema (redness), tenderness, swelling/oedema, warmth, superficial venous dilation

36
Q

why is correct diagnosis of VTE important?

A
  • many patients w VTE are acc negative when investigated

- drugs used for treatment can cause serious/fatal side effects

37
Q

what are some of the differential diagnoses for VTE?

A 
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
Q

what is a wells score?

A

scoring system for a probability of VTE

39
Q

what wells score indicates that a DVT is likely?

A

2 or more

40
Q

name some of the clinical characteristics of a DVT?

A
  • 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
Q

what further clinical tests should you do if the wells score is more than 2?

A

d-dimer
ultrasound
venography
CT scan, MR venography

42
Q

what is the d-dimer test?

A

blood test measuring fibrin fragments after fibrinolysis. A non-specific marker of fibrin formation

43
Q

when is d-dimer raised?

A

raised in VTE but also in cancer, infection, inflammation, post-op, pregnancy

44
Q

what is the initial treatment for VTE?

A

low molecular weight heparin/fondaparinux

45
Q

how do you administer LMWH?

A

subcutaneously

46
Q

what is the half life of LMWH?

A

4 hours

47
Q

what effect does LMWH have?

A

anti factor Xa effect

48
Q

when do you monitor LMWH treatment?

A

renal failure
pregnancy
obesity

49
Q

when is unfractionated heparin used?

A

where rapid reversibility is needed

50
Q

when is LMWH stopped and what is given afterwards? what is the exception to this?

A

After one week stop LMWH and start warfarin (unless pregnant)

51
Q

what is heparin?

A

anticoagulant protein produced by basophils and mast cells

52
Q

what does heparin do?

A

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
Q

how are natural unfractionated heparin and LWMH different?

A
  • Natural ‘unfractionated’ heparin has molecular chains of diff. molecular weights
  • LMWH only have short chains – more predictable effects than natural heparin
54
Q

what are possible side effects of heparin?

A

o Excessive bleeding

o Heparin-induced thrombocytopenia (HIT

55
Q

when does heparin induced thrombocytopenia develop?

A

5-14 days

56
Q

how is heparin induced thrombocytopenia treated?

A

o Needs to stop all heparin and gets replaced by a non-heparin anticoagulant e.g. hirudin. Potent natural inhibitor of thrombin

57
Q

what is warfarin?

A

vitamin K antagonist

58
Q

what does warfarin do?

A

reduces levels of factors 2, 7, 9 and 10 in plasma

59
Q

how is warfarin administered?

A

orally

60
Q

what is the half life of warfarin?

A

36 hours

61
Q

how must the warfarin dose be adjusted over time?

A

adjusted to maintain INR in range 2.0-3.0

62
Q

why cant warfarin be given during pregnancy?

A

Risks to fetus – teratogenicity, maternal bleeding

63
Q

what can be used instead of warfarin to treat vte?

A

direct oral anticoagulants such as Rivaroxaban Apixaban, Dabigatran

64
Q

what is the acute treatment for VTE?

A

Rivaroxaban and Apixaban – both with no heparin lead in

65
Q

what is the short term treatment for VTE?

A

Dabigatran – heparin lead-in required 5-10 days

66
Q

what is Rivaroxaban?

A

Orally active factor Xa inhibitor that inhibits platelet activation by blocking binding site for Xa

67
Q

when is Rivaroxaban given?

A

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
Q

who is Rivaroxaban contraindicated in?

A

people with significant liver disease and end-stage kidney disease

69
Q

what is apixaban?

A

factor Xa inhibitor - similar in properties to Rivaroxaban

70
Q

what is dabigatran?

A

orally active direct thrombin inhibitor

71
Q

who is dabigatran given to and why?

A
  • 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
Q

what is given as treatment for VTE in pregnancy?

A

use LWMH throughout pregnancy

73
Q

why are DOACs not given to pregnant women?

A

effects unclear - presumed bleeding

74
Q

what is given as treatment for VTE in breastfeeding women?

A

LWMH and warfarin safe but not DOACs

75
Q

what is given as treatment for patients with cancer-associated thrombosis?

A

LMWH more effective than warfarin. DOACs undergoing evaluation

76
Q

what are symptoms of pulmonary embolism?

A
  • Breathlessness, pleuritic chest pain, haemoptysis (65%)
  • Isolated breathlessness (25%)
  • Collapse/syncope, hypotension, shock (10%)
77
Q

what are the signs of a pulmonary embolism?

A
  • Tachypnoea and tachcardia
  • Crepitations and pleural rub
  • Clinical signs of DVT uncommon
78
Q

what are the preliminary exams for pulmonary embolism?

A

ECG
Chest x ray
Arterial blood gas

79
Q

what does an ecg show in someone with pulmonary embolism?

A

sinus tachycardia, right heart strain, T-wave inversion on anterior leads

80
Q

how does a chest x ray look in someone with pulmonary embolism?

A

often normal, focal oligaemia, peripheral wedge shaped density above diaphragm, small pleural effusion

81
Q

what are the arterial blood gases of someone with a pulmonary embolism?

A

often hypoxia
low CO2
but may be normal

82
Q

what are diagnostic tests for PE

A
  • 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
Q

what are the differential diagnoses for 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
84
Q

what are the risk factors for predicting probability of pulmonary embolism?

A
  • 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
Q

what wells score suggests a likley PE?

A

greater than 4

86
Q

how is pulmonary embolism treated?

A

Same as for VTE; ie LMWH initially then warfarin

c2 (37 decks)

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