DVT and PE

Question 1

two commonest presentations of venous thrombosis

Answer 1

PE and DVT

Question 2

VTE occurs due to

Answer 2

virchows triad:
- alteration in blood flow (venous stasis)
- injury to the blood vessel wall (vascular endothelial injury)
- hypercoagulable state (inherited or acquired)

Question 3

things that might cause a hyper coagulable state

Answer 3

sepsis
inflammation
oestrogens
malignancy
inherited thrombophilia

Question 4

things that might cause vascular damage

Answer 4

cannula
atherosclerosis
trauma or surgery

Question 5

things that might cause venous stasis

Answer 5

AF
immobility
venous obstruction
venous insufficiency or varicose veins

Question 6

factor V leiden mutation

Answer 6

point mutations in the F5 gene which encodes for factor V in clotting cascade
mutations make factor V resistant to activated protein C (natural anticoagulant) = patient is more likely to clot

Question 7

clinical presentation of DVT

Answer 7

usually unilateral leg
leg erythema
warmth
swelling
pain

Question 8

DDx for DVT

Answer 8

muscle strain/tear
baker’s cyst
cellulitis
lymphatic obstruction
venous insufficiency
leg oedema (heart failure or others)

Question 9

D-dimer is

Answer 9

is a product of clot breakdown
released upon breakdown of polymerised cross linked fibrin

Question 10

high D-dimer levels indicate

Answer 10

that coagulation has been activated
fibre clot has formed, and clot degradation by plasmn has occurred

Question 11

if D-dimer is negative (low)

Answer 11

high negative predictive value
if negative, a blood clot is highly unlikely

Question 12

causes of elevated D-dimer

Answer 12

not just clotting
also:
- severe infection and sepsis
- trauma
- cancer
- thrombolytic therapy
- surgery
- pregnancy
- liver or kidney disease
- DIC

Question 13

doppler ultrasound

Answer 13

if a vein cannot be collapsed or compressed, a DVT diagnosis is made on the assumption that a clot is preventing the collapse
the flow of blood changes the sound waves reverberated via the Doppler effect
an absence of blood flow indicates a blood clot

Question 14

how does warfarin work

Answer 14

prevents vit K dependant coagulation factors from being activated

Question 15

which are the vit K dependant anticoagulation factors

Answer 15

2,7,9,10 (the good analog tv channels)

Question 16

heparin acts on

Answer 16

antithrombin

Question 17

most emboli come from

Answer 17

lower limb proximal veins
iliac, femoral, popliteal

Question 18

how does a PE form

Answer 18

emboli comes from the lower limb proximal veins
clot travels through the right ventricle to pulmonary arteries and lodges

Question 19

once a PE emboli has lodged

Answer 19

results in
1. decreased gas exchange due to mechanical obstruction of the vascular bed. ventilation/perfusion mismatch causes hypoxia
2. infarction in 10% of people where the slot lodges in smaller pulmonary arteries. pleuritic chest pain
3. cardiovascular compromise depending on the clot burden, there can be compromised cardiac output = hypotension

Question 20

saddle PE

Answer 20

if the embolus is large enough
it can lodge in the main pulmonary artery and obstruct flow from the right ventricle to the lung
life threatening

Question 21

clinical presentation of PE

Answer 21

dyspnoea
cough
chest pain

maybe also haemoptysis or calf pain or swelling (due to concurrent DVT)

Question 22

examination findings of PE

Answer 22

tachypnoea
tachycardia
hypoxia
signs of DVT
if ssaddle PE or massive PE: low BP, signs of right heart failure, raised JVP, leg swelling

Question 23

DDx of PE

Answer 23

heart failure
MI
pneumonia
exacerbation of chronic lung disease
pericarditis
MSK pain

Question 24

investigations for PE

Answer 24

blood tests: FBC, U&E, troponin (MI?), d-dimer
CXR: look for another diagnosis
ECG: most commonly you see a tachycardia

Question 25

V/Q scan

Answer 25

ventilation/perfusion scan - nuclear medicine
need to have a normal CXR first
looks at distribution of blood flow compared to alveolar ventilation
pulmonary artery occlusion leads to ventilated areas without perfusion (dead space) leading to V/Q mismatch

Question 26

CTPA

Answer 26

CT pulmonary angiogram
most sensitive and specific test
contrast injected into vein - CT lung to capture contrast moving through the pulmonary arteries

Question 27

thrombophilia screen

Answer 27

protein tests
protein C, ATII levels: reduced in acute thrombosis, anticoagulation
prothrombin gene mutation and factor V Leiden gene mutation
lupus anticoagulant (affected by anticoagulation), antiphospholipid antibodies

Question 28

indication for thrombophilia screen

Answer 28

a patient with unexplained VTE
a patient with strong family history of VTE if it will change management
family Hx of thrombophilia in young women considering COCP

do not do protein C, S and ATII in acute thrombosis and anticoagulation and the levels will be affected

Question 29

choice of treatment for VTE

Answer 29

DOAC: apixaban, rivaroxaban, dabigatran are treatment of choice in most cases
warfarin
LMWH: low molecular weight heparin, may be used in short term initially if in hospital, used in pregnancy

Question 30

treatment duration for VTE

Answer 30

minimum 3 months and then assess ongoing risk factors for thrombosis at the end of three months