deep venous thrombosis and pulmonary embolism Flashcards

1
Q

what is a thrombus?

A

a pathological clot

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2
Q

what are the three things a clot is made up of?

A

fibrin
platelets
RBCs
(different ratios for different types of clot)

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3
Q

describe the pathway for the formation of a clot in an artery?

A
  1. damage to endothelium
  2. tissue factor produced
  3. prothrombin converted to thrombin
  4. thrombin converts fibrinogen into fibrin
  5. firbrin foms corss-linked fibrin
  6. along with platelets to form a white thrombus
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4
Q

what kind of clots thombi form in arteries?

A

white thrombi, contain few RBCs

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5
Q

what kind of thrombus forms in veins?

A

red thrombus

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6
Q

describe the formation of a red thrombus

A
  1. tissue factor and the contact pathway cause the production of thrombin
  2. thrombin converts fibrinogen into fibrin
  3. fibrin traps RBCs forming a red thrombus
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7
Q

what is the most common cause of white (arterial) thrombus?

A

rupture of atherosclerotic plaque

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8
Q

what are the locations of arterial thrombi?

A

arteries and left heart chambers

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9
Q

what are the consequences of arterial thrombi?

A

ischaemia and infarction

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10
Q

what are the disease caused by arterial thrombi?

A

ACS
ischaemic stroke
limb claudication and ischaemia

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11
Q

what is the composition of an arterial thrombus?

A

white thrombus- platelets and fibrin

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12
Q

what is the mechanism for the formation of venous thrombi?

A

combination of Virchow’s triad especially stasis and hypercoagulability

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13
Q

what is the location of origin of venous thrombi?

A

venous valves and venous sinusoids of muscle

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14
Q

what is Virchow’s triad?

A

stasis
hypercoagulability
endothelial damage/dysfuntion

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15
Q

what do venous thrombi result in?

A

back pressure

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16
Q

what are the diseases caused by venous thrombosis?

A

DVT

pulmonary embolism

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17
Q

what is the composition of a venous clot?

A

red thrombus- RBCs and fibrin

18
Q

what can cause stasis (in Virchow’s triad)

A

immobility

long haul travel

19
Q

what can cause vessel damage/dydfunction in Virchow’s triad?

A
dysfunction:
hypertension
smoking
hypercholesterolaemia
damage:
-indwelling venous catheters
-trauma
-surgery
20
Q

what can cause hypercoagulabilty (in Virchow’s triad)?

A

-inherited causes
-acquired:
pregnancy
cancer
sepsis

21
Q

what is an embolism?

A

intravascular material that migrates from its original location to a distal vessel

22
Q

what is thromboembolism?

A

movement of blood clot along a vessel

23
Q

give 4 examples of venous thromboembolism?

A

limb DVT
pulmonary embolism
visceral venous thrombosis
intracranial venous thrombosis

24
Q

what are the symptoms of DVT?

A

unilateral limb swelling
persisting discomfort
calf tenderness

25
Q

what are the signs of DVT?

A

warmth
redness
prominent collateral veins
unilateral pitting oedema

or may be clinically silent

26
Q

when may DVT cause bilateral signs and symptoms?

A

when there is obstruction of the IVC

27
Q

what are the long-term consequences of DVT?

A
post thrombotic syndrome
causing damage to venous valves. 
This causes:
swelling
discomfort
pigmentation
ulceration of veins in severe form
28
Q

how is DVT diagnosed?

A
  1. clinical assessment and pretest probability score (Wells score)
  2. Blood test: D-dimer if low pre-test probability score
  3. imaging compression ultrasound if positive D-dimer or high pre-test probability score
29
Q

what is D-dimer test, in terms of sensitivity and specificity?

A

-high sensitivity for VTE
-low specificity for VTE
as positive in:
trauma
malignancy
sepsis
bleeding
cancer
recent surgery

30
Q

what are the symptoms of PE?

A

pleuritic chest pain
dysmpnoea
haemoptysis

31
Q

what are the signs of PE?

A

tachycardia

pleural rub in ausculatation (due to pulmonary infarction)

32
Q

what are the symptoms of massive pulmonary embolism

A

severe, sudden dyspnoea

collapse

33
Q

what are the signs of massive pulmonary embolism?

A
cyanosis (blue lips and tongue)
tachycardia
hypotension
raised JVP
may cause sudden death
34
Q

how is PE diagnosed?

A
  1. clinical assessment and pretest probability score (Wells or Geneva)
  2. D-dimer test if low pretest probability score
  3. imaging if D-dimer positive or high pre test probability score
    - isotope ventilation/perfusion scan
    - CT pulmonary angiogram
35
Q

what are the potential long-term consequences of pulmonary embolism?

A
  • most recover fully

- pulmonary arterial hypertension

36
Q

what are the aims of treatment of VTE?

A

prevent clot extension
prevent clot embolism
prevent recurrent clot

37
Q

what are anticoagulation treatments for VTE?

A
parental options:
-unfractioned heparin
-low molecular weigth heparin
Enteral options:
-Warfarin
-direct oral anticoagulants (DOACs)

Thrombolysis reserved for massive PE
eg. alteplase

38
Q

what are the prevention methods for VTE in hospital?

A
  • early mobilsation
  • anti-embolism stockings
  • other mechanical methods of thromboprophylaxis
  • pharmacological thromboprophylaxis
39
Q

why is pulmonary infarction rare in PE?

A

dual vascular supply to lungs with anastomoses;
Pulmonary vascular system
Bronchial vascular system

40
Q

what causes infarction in PE?

A
  1. blockage in branch of pulmonary artery
  2. leads to increase in pressure within pulmonary vasculature
  3. force within bronchial artery may be insufficient to overcome this
  4. leakage of blood into alveolar space occurs and leads to infarcion.