Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Haematology > VTE > Flashcards

VTE Flashcards

1
Q

What are the components of Virchow’s triad?

A

Hypercoagulable state

Vascular wall injury

Circulatory stasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What can cause a hypercoagulable state?

A 
Malignancy 
Pregnancy 
Oestrogen therapy 
Surgery 
Increased inflammatory proteins i.e. IBD and sepsis 
Nephrotic syndrome 
-decreased albumin in BV means less fluid present= increases haematocrit i.e. blood becomes more sticky 
Thrombophilia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can increase the risk of blood stasis?

A 
Atrial fibrillation 
LV dysfunction 
Immobility or paralysis 
Varicose veins 
Venous obstruction 
MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What stages of blood clot formation are common to the extrinsic and intrinsic pathways?

A

Both cause activation of factor X
Factor X converts prothrombin -> thrombin
Thrombin converts fibrinogen-> fibrin
Fibrin forms blood clot with the aid of factor XIII

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What can venous and arterial thrombi lead to? Why is there a difference?

A

Venous -> pulmonary emboli due to venous circulation returning to RA and being pumped to lungs

Arterial -> peripheral emboli due to arterial vessels leading to systemic circulation
NOTE: can lead to MI is formed in LA/LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When can a VTE cause a stroke?

A

When patient has septal defect
Clot can move from right side of heart to left side
Therefore emboli can ascending into common carotids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are important risk factors to consider for DVT/PE?

A 
Immobility
Recent surgery 
Long-haul flights 
Pregnancy 
OCP/HRT i.e. exogenous oestrogen
Polycythaemia i.e. increased haematocrit (sticky blood)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the signs of a DVT?

A

Calf swelling with pitting oedema
Pain
Erythema
Tenderness (especially over the areas of deep veins)
Warmth
Dilated superficial vessels i.e. trying to compensate for blocked deep vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the possible differentials for DVT?

A 
Cellulitis 
Superficial thrombophlebitis
Venous obstruction 
Acute arterial ischaemia 
Lymphoedema 
Baker’s cyst 
Torn muscle 
Fracture
Haematoma i.e. bleeding into the knee joint
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What imaging technique can be used to diagnose DVT?

A

Ultrasound Doppler
Can visualise the vein and artery
-can see the clot in the vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the Well’s score and what is its role in VTE?

A

Predicts the risk of patients presenting with symptoms of DVT/PE actually having them i.e. in terms of likelihood

DVT= >2 points -> DVT LIKELY
<2 points -> DVT UNLIKELY

PE= >4 points -> PE LIKELY
<4 points -> PE UNLIKELY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Why is D-dimer tested for in VTE?

A

Fibrinolytic response occurs shortly after thrombus formation which leads to production of D-dimer as fibrin degradation product (D dimer not usually present)

Negative D-dimer has >90% negative predictive value to exclude DVT/PE when there is low suspicion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why is D-dimer not diagnostic of DVT/PE?

A

Can be raised due to other causes i.e. is only an indication that there has been fibrin degradation

Raised d-dimer in:

  • liver disease
  • infection/inflammation
  • malginancy
  • pregnancy
  • trauma
  • recent surgery
  • MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why does a PE occur?

A

Large emboli blocks pulmonary vessel i.e. smaller emboli are filtered out by the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why can PE lead to RV hypertrophy?

A

Blockage of pulmonary vessel leads to increased pressure across pulmonary system so pressure in pulmonary arteries increases= PULMONARY HYPERTENSION
Increased after load for RV to contract against

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

There are 3 different forms of PE. How can you differentiate based on the clinical presentation?

A

Acute minor PE:

  • sudden onset of dyspnoea
  • chest pain
  • haemoptysis

Acute massive PE:

  • right heart strain
  • haemodynamic instability
  • syncope
  • signs of shock

Chronic
-gradual dyspnoea leading to pulmonary hypertension

17
Q

What signs might be someone suffering from PE present with?

A

Dyspnoea i.e. V/Q mismatch
Pleuritic chest pain (worse on deep breathing) i.e. irritation of parietal pleura due to inflammation associated with emboli
Cough
Haemoptysis i.e. due to ischaemic parenchymal necrosis
Dizziness/syncope i.e. vaso-vagal due to decreased ABP

18
Q

What might you find on clinical examination which implies PE?

A

Tachypnoea
Tachycardia
Hypotension
Evidence of DVT
Pleural rub i.e. due to inflammation
Cyanosis i.e. decreased O2 content of blood due to V/Q mismatch
Raised JVP i.e. due to RHF due to pulmonary hypertension

19
Q

What ECG signs are associated with PE?

A

Sinus tachycardia
S1Q3T3
Right axis deviation
RBBB

20
Q

What are the possible changes seen in a CXR of someone with PE?

A

Wedge-shaped pulmonary infarct
Atelectasis (partial or complete lung collapse)
Small pleural effusions
Oligaemai i.e. lack of blood vessels

NOTE: can rule out differentials i.e. pneumothorax

21
Q

What blood tests can be done with suspected PE? What would you expect to see?

A

ABG

  • low pO2
  • low PCO2 (Tachypnoea)

D-dimer
-negative d-dimer can exclude PE

22
Q

What is a CTPA and when is it indicated?

A

CT pulmonary angiogram

Gold standard for investigation PE i.e. can identify SADDLE EMBOLI

Well’s score >4

23
Q

What are the 4 main types of imaging that can be used in suspected PE?

A

CXR
CTPA
CTCA
Isotope lung scans

24
Q

What is a CTCA and when is it indicated?

A

CT coronary angiogram which is a gated-scan meaning it is only done at specific points in cardiac cycle

When patient presents with chest pain i.e. acts as TRIPLE RULE OUT

  • PE
  • coronary HD
  • aortic dissection
25
Q

What is the function of isotope lung scan?

A

Radioisotope used to assess difference between blood flow and gas flow
I.e. embolus causes defect in perfusion but ventilation will be normal

26
Q

When is isotope lung scan indicate instead of CTCA?

A

When patient has renal dysfunction due to CT requiring contrast dye which relies on adequate renal function to clear it

27
Q

What can be done as part of VTE prophylaxis?

A

Graduated elastic compression stockings i.e. improves venous return and reduces venous pooling

LMWH i.e. Enoxaparin 20mg
-unless actively bleeding or already on warfarin or NOAC

28
Q

How would someone presenting with VTE be treated?

A

Initial= Treatment dose of LMWH i.e. enoxaparin/dalteparin
-1.5mg/kg SC for at least 5 days

Switch to long-term anticoagulation:

  • Warfarin= need target INR of 2-3 i.e requires monitoring
  • NOAC/DOACs i.e. Apixaban/Dabigatran/rivaroxaban

Treat for 3 months and then review i.e. may need to continue if cause unclear or irreversible

29
Q

What is the function of inferior vena cava filter? When are the indicated in PE patients?

A

Inserted into IVC to catch blood clots travelling from venous system to heart or lungs whilst still allowing blood to pass

For px with recurrent PEs or if unsuitable for anticoagulation therapy

30
Q

What treatment it indicated in life-threatening PE?

A

Thrombolyis using IV Anteplase

Catheter or embolectomy

31
Q

What should be considered when patient presents with unprovoked VTE? How is this investigated?

A

Cancer

CXR 
HX + examination 
FBC, calcium, LFT
Urine dipstick 
CT abdomen + pelvic >40 yo 
Mammogram >40F
32
Q

What is the classical triad for PE?

A

SOB
Haemoptysis
Pleuritic chest pain (pain on inspiration)

33
Q

Why does a PE cause pleuritic chest pain?

A

Irritation of parietal pleura resulting in inflammation of underlying visceral pleura

34
Q

What are thrombophilias and how are they related to VTE?

Give examples.

A

Group of conditions which predispose patient to blood clot meaning they increase the risk of someone developing VTE

Antiphospholipid syndrome 
Antithrombin deficiency 
Protein C or S deficiency 
Factor V Leiden 
Hyperhomocysteinaemia 
Prothrombin gene variant 
Activated protein C resistance
35
Q

What is the normal function of protein C and S in thrombolysis?
Why would protein C and S deficiency lead to increased risk of VTE?

A

Protein C is normally located on endothelial protein C receptor
Released and protein C is activated by thrombin which has been bound to thrombomodulin receptors on endothelium surface
Activated protein C binds free protein S to form complex which acts to cleave FVa and FVIIIa i.e. cofactors
-FVIIIa= converts FX toFXa
-FVa= converts prothrombin to thrombin

Therefore cleaving these factors promotes anticoagulation

If deficient:
-would induce a hypercoagulable state-> risk factor for VTE

36
Q

Why would factor V Leiden disease lead to increased risk of VTE?

A

Factor V Leiden disease is where there is a polymorphism in factor V leading to it being resistant ot proteolytic action of protein C+S
-induces pro-thrombotic state

37
Q

Why does pregnancy increase the risk of VTE?

A

Pregnancy= state of hypercoagulability

  • increased production of clotting factors
  • decreased fibronolysis
  • increased platelet adhesiveness

Increased venous stasis

  • due to pressure of gravid uterus on IVC + left iliac vein (crosses behind uterus)
  • decreased venous tone
38
Q

Which leg is DVT most likely to happen in pregnancy and why?

A

Left leg

  • due to uterus compressing left iliac vein which passes posterior to uterus
  • increased venous stasis in left leg compared with right
39
Q

What is Budd-Chiari syndrome?
What triad does it classically present with?
How is it managed?

A

Blood clot develops in hepatic vein leading to blockaged of blood outflow
Can cause acute hepatits

Abdo pain
Hepatomegaly
Ascites

Anticoagulation
Investigated hyper-coagulable state
Treat hepatits

Haematology (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions