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BSMS 103 > Thrombotic disorders > Flashcards

Thrombotic disorders Flashcards

1
Q

what is the main presentation of DVT and why is this?

A

leg swelling due to reduced venous return

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2
Q

what location is a DVT usually found?

A

Above the knee - in the iliac or femoral vein

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3
Q

what is the location of clots in a DVT that are silent?

A

below the knee (popliteal or tibial vein) and have high risk of PE

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4
Q

what is the main test for DVT?

A

D-Dimer

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5
Q

what test would be done for DVT if D dimers are raised?

A

US of leg to look at venous blood flow using a doppler

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6
Q

what are differential diagnoses for DVT?

A

cellulitis, bakers cyst behind the knee or muscular pain

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7
Q

name 6 thrombotic risk factors

A

post operative, long term bed rest, cancer, pregnancy/oral contraceptive, long haul flights, obesity, IV drug use

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8
Q

what kind of picture is produced by US?

A

a real time 2D image of soft tissue structures

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9
Q

which two tests are used together to assess likelihood of DVT and what do these indicate?

A

D dimers and wells risk score

  • D dimers show activation of the clotting cascade
  • wells score assesses risk factors that indicate the likelihood of having a DVT
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10
Q

what is the initial treatment for DVT?

A

anti-coagulation with LMW heparin eg tinzaparin or enoxaparin

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11
Q

what is a requirement to administer LMW heparin?

A

good renal function (creatinine clearance > 30ml/min)

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12
Q

how would a patient with poor renal function be anti coagulated?

A

using IV unfractionated heparin (not LMW) and ensure APTT is maintained

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13
Q

what is the subsequent treatment for DVT?

A

load patients with oral warfarin for 3-5 days

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14
Q

when is LMW heparin stopped?

A

when INR (clotting) is more than 2 for 2 days

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15
Q

what would be the long term treatment for a first DVT?

A

6 months of warfarin

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16
Q

what would be the treatment for a second DVT/PE?

A

llifelong warfarin

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17
Q

what does a PE cause in relation to VQ?

A

VQ mismatch

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18
Q

micro emboli in a PE may be asymptomatic but what symptom can they cause?

A

dyspnoea

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19
Q

how will PE patients present O/E?

A

tachycardia, tachypnoeic (rapid RR) and hypotensive, shock

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20
Q

what would someone presenting with a PE and shock be urgently treated with?

A

thrombolytics and IV heparin

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21
Q

what are the three main symptoms of an acute PE?

A

pleuritic pain, dyspnoea and haemoptysis

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22
Q

what are the three main symptoms of a severe PE?

A

syncope, death, signs of shock (hypotension and acute dyspnoea)

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23
Q

what is the gold standard test for a PE?

A

CT pulmonary angiogram to look for filling defects

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24
Q

what is a saddle embolism?

A

blockage at the bifurcation of the pulmonary trunk

25
Q

after a CTPA what other investigations can be done for a PE?

A
  • VQ scan (inject and inhale a radioisotope to examine air and blood flow in the lungs)
  • ECG - look for sinus tachycardia (increased pulse rate), AF, right heart strain due to right bundle branch block
  • CXR - usually normal (rarely see linear atelectasis or small effusions)
26
Q

what is a limitation of a VQ scan for PE?

A

most patients have underlying lung disease so cant be done

27
Q

apart from LMW heparin and warfarin what other treatments can be given for PE?

A
  • IVC filters to prevent embolisation to lungs

- direct oral anti coagulants (DOACs) eg dabigatran and rivoroxaban

28
Q

What drug treatment for PE is the most safe in pregnancy and cancer?

A

LMW heparin

29
Q

how many deaths per year are due to PE?

A

25,000

30
Q

what condition do young patients get a thrombophilia screen for?

A

venous thrombo embolism

31
Q

what inherited factors will be looked for in a thrombophilia screen?

A
  • Factor V leiden (increases likelihood of clots)
  • prothrombin gene variant
  • anti thrombin deficiency
  • protein C or protein S deficiency
32
Q

what is the role of protein S and protein C and what would a deficiency in them lead to?

A

they are natural anti-coagulants that keep clotting in check
- deficiency leads to more prone to clotting

33
Q

what acquired syndromes will be looked fora on a thrombophilia screen?

A

anti phospholipid syndromes (phospholipid is required in prothombinase)

34
Q

what is the mechanism of action of warfarin?

A
  • antagonises vitamin K
  • prevents gamma carboxylation of factors II, VII, IX and X
  • inhibits protein C and protein S
35
Q

how is warfarin monitored

A

using the INR - how long it takes blood to clot

36
Q

what is the target INR for DVT, PE and AF?

A

2.5

37
Q

what is the target INR for recurrent venousthrombo embolism or metal heart valves?

A

3.5

38
Q

what is warfarin metabolised by and where?

A

metabolised by P450 in the liver

39
Q

what is patient usually loaded with before prescribing warfarin?

A

LMW heparin

40
Q

what effect do cytochrome P450 inhibitors have on warfarin?

A

increase its power

41
Q

what are some examples of P450 inhibitors?

A

carbamazepine, azathioprine, allopurinol, erythromycin, fluconazole

42
Q

what effect do P450 enhancers have on warfarin and why?

A

inhibit warfarin as P450 breaks down warfarin in the liver

43
Q

what are some examples of P450 enhancers?

A

rifampicin, amiodarone, citalopram

44
Q

what are five side effects of warfarin?

A

teratogenic (use LMW heparin instead), risk of haemmorhage, minor bleeding, skin necrosis and alopecia

45
Q

in what situation would warfarin need to be rapidly reversed and how is this done?

A

needs to be reversed in rapid bleeding by giving vitamin K

- if bleed is life threatening then give octaplex (prothrombin complex) or fresh frozen plasma

46
Q

what is octaplex and when it is it given?

A

a prothrombin complex containing factors II, VII, IX and X

- given in a bleeding emergency to reverse warfarin as vitamin K wouldn’t work fast enough

47
Q

what is the mechanism of action of heparin?

A
  • promotes anti-thrombin
  • irreversibly inactivates factors IIa (thrombin) and Xa
  • this means no fibrinogen to fibrin and no clotting
48
Q

how is heparin administered?

A

Parenterally (any way but oral so bypasses GI tract)

  • LMW even as a sc injection
  • unfractionated given as IV infusion
49
Q

how is unfrationated heparin monitored and how can it be partially reversed ?

A

monitored using APTT and can be part reversed by protamine sulphate

50
Q

what are rare complications of using unfractionated heparin and what can they result in?

A

thrombocytopenia and WTE which results in heparin induced thrombocytopenia

51
Q

what is LMW heparin prescribed according to?

A

patients weight

52
Q

does LMW heparin need to be monitored using APTT?

A

no - but can be monitored by an anti Xa assay

53
Q

what drug were NOACs developed as an alternative to?

A

warfarin

54
Q

what are three advantages of NOACs?

A

orally available, no monitoring needed and good safety profile

55
Q

give examples of two NOACs and their action

A

1) dabigatran - direct thrombin inhibitor (factor IIa)

2) rivoroxaban - direct factor Xa inhibitor

56
Q

does rivaroxaban require good renal function?

A

yes

57
Q

name four anti plat drugs and their mechanism of action

A

1) Aspirin - cox inhibitor which prevents plat aggregation
2) prostacyclin prevent formation of cAMP therefore no plat aggregation
3) clopidogrel - ADP receptor blocker (P2Y inhibitor)
3) glycoprotein IIb/IIIa inhibitors - prevent clots in patients with cardiac stents

58
Q

how do fibrinolytic agents work and when are they given?

A
  • convert plasminogen to plasmin
  • given systemically in acute MI, recent PE, thrombotic stroke, major PE or iliofemoral thrombosis
  • given in stroke to minimise neurological damage but must be given within 6 hours
59
Q

give two examples of fibrinolytic agents

A

tissue plasminogen activator (alteplase) and streptokinase

BSMS 103 (23 decks)

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