Brainscape's Knowledge GenomeTM

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


See full index

Cardio and Resp diseases > DVT and pulmonary embolism > Flashcards

DVT and pulmonary embolism Flashcards

1
Q

What type of DVT (deep vein thrombosis) can be a big risk?

A

above knee DVT – associated with embolic events

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

What type of risk does DVT have?

A

Multifactorial risk

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

How does DVT form?

A

• Thrombus in deep vein around valves
• Multiple triggers – finely balanced system is destabilised
•

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

What is a pulmonary embolus?

A

fragmentation of proximal clot which travels in venous system until it lodges in the pulmonary circulation

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

Where are the consequences of DVT?

A

Consequences locally in source limb and/or in heart or lungs after embolization

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

What is Virchow’s triad and what does it include?

A

contributing factors to thrombosis:

  • Endothelial injury
  • Stasis
• Blood components
o Platelets
o Coagulation factors
o Coagulation inhibitors
o Fibrinolytic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What happens as we get older?

A

We get more thrombotic as we get older

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does a haemostatic plug form?

A
  • Release of tissue factor from vessel injury
  • Coagulation cascade activated
  • Vessel injury also platelet release reaction and vasoconstriction
  • They all combine to form a stable haemostatic plug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is present at the site of the clot?

A
  • Tissue factor
  • activating factors
  • conversion of prothrombin to thrombin
  • Activated platelets and platelet complexes
  • Fibrinogen converted to fibrin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What forms the clot?

A

Cascade forms a clot

Cascade is self-perpetuating until something stops it

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

What are the phases of the cascade?

A

3 phases of cascade:

  • initiation
  • amplification
  • propagation (this produces clot)

if these phases are interrupted the process is terminated

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

Which pathways can activate the cascade?

A

extrinsic and intrinsic pathways

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

What 2 things are part of the extrinsic pathway?

A

Tissue factor and vessel damage are part of the extrinsic pathway – more important than intrinsic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is crucial in the cascade regardless of the pathway?

A

conversion of factor 10 to 10a

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

What does factor 10a do and how does this lead to the production of a thrombus?

A
  • It acts on prothrombin to thrombin, which activates conversion of fibrinogen to fibrin
  • Activation of factor 13 and cross linked fibrin produces thrombus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What helps control the clotting cascade?

A

There’s inhibitors to balance:

• Proteins C and S – combine to make activated protein C
o Act on factor Va and VIIIa

• Anti-thrombin acts on X and thrombin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What can change the homeostatic point for the clotting cascade?

A

Defects in protein and C or S change the homeostatic point for clotting cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why does the haemostatic plug form? and how does it form?

A

Haemostatic plug formation: Response to injury

  1. Vessel constriction
  2. Formation of unstable platelet plug
    • platelet adhesion
    • platelet aggregation
  3. Fibrin stabilisation of the plug with fibrin
    • blood coagulation
  4. Dissolution of clot and vessel repair
    • Intrinsic fibrinolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens in fibrinolysis?

A
  • Tissue plasminogen activator converts plasminogen into plasmin
  • It breaks down fibrin cross linking strands into D-dimer
  • Raised D-dimer levels suggest tissue inflammation or active breakdown of fibrin clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where are clotting factors, fibrinolytic factors and inhibitors synthesised?

A
  • liver
  • endothelium
  • megakaryocytes (platelets)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some measurements used in DVT/PE/clotting cascade?

A
  • Prothrombin time – PT = PTR
  • Partial thromboplastin time – APTT =APTTR
  • Thrombin time - TT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the risk factors for venous thrombosis?

A

Stasis
• Prolonged immobility eg surgery, travel
• Stroke
• Cardiac failure

Coagulation abnormality
• Surgery or major trauma
• Pregnancy and puerperium
• Oestrogen medication
• Malignancy
Others
• Age
• Past history or family history of VTE
• Obesity
• COVID-19
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the clinical features of DVT?

A
  • Pain, tenderness of veins
  • Limb swelling
  • Superficial venous distension
  • Increased skin temperature
  • Skin discoloration
  • All reflect obstruction to the venous drainage
  • There are multiple differential diagnoses for these presenting features
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How is DVT diagnosed?

A
  • Risk assessment
  • Evidence based pre-test probability score (well’s score) – combines clinical factors in an evidence based way (determines role for diagnostic imaging vs use of blood test for exclusion)
  • D dimer for exclusion
  • Diagnostic tests
  • Compression ultrasonography
  • Venography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the clinical features of pulmonary embolism?

A

Depends on where it lodges
• Peripheral: problems with ventilation perfusion mismatch
• Centrally in bigger vessels: pressure effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the symptoms of PE?

A
  • Dyspnoea
  • Pleuritic chest pain
  • Cough and haemoptysis
  • Dizziness
  • Syncope
  • Importantly the patient may be very unwell or very well – some patients get very few symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the signs of PE?

A
  • Tachypnoea, tachycardia
  • Hypoxia
  • Pyrexia
  • Elevated jugular venous pressure
  • Hypotension – due to proximal pulmonary artery occlusion
  • ECG changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the physiology of symptoms and signs of PE?

A
  • Symptoms and signs determined by thrombus size and burden
  • Multiple small peripheral thrombi produce a different clinical picture to large proximal thrombus
  • Pulmonary infarction is not common – remember the bronchial circulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How is PE diagnosed?

A
  • Risk assessment and diagnostic algorithm
  • D – dimer for exclusion in low risk cases only
  • Mortality stratification - PESI score
  • Assessment of compromise - Pa02 (gas exchange) + D dimer + ECG + increase troponin and BNP indicate damage to myocardium and strain on heart
  • Consider echocardiogram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What diagnostic tests are used if other tests don’t give a certain diagnosis?

A
  • CT pulmonary arteries – CTPA

* Ventilation Perfusion Scan – used for pregnant patients to avoid radiation to pregnant breasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What are the long term consequences of venous thromboembolism?

A
  • 10% of all hospital deaths
  • 30% recurrence at 10 years
  • 30% post phlebitic syndrome at 10 years
  • Chronic thromboembolic pulmonary hypertension (CTEPH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the treatments of VTE?

A
  • Anticoagulants
  • Thrombolysis
  • Surgery
33
Q

What are the main targets of the VTE treatment?

A

• The thrombus

• Two approaches:
o Lyse the thrombus
o Prevent further thrombus formation

34
Q

What is the problem with lysis?

A

Lysis has the problem that if given systemically it lyses all thrombus everywhere

35
Q

What do most treatments aim for?

A

Most treatment aims to:

  • prevent thrombus propagation and formation of new thrombus
  • while allowing the body to concentrate lysis in the place where it is required
36
Q

What are the usual risk of VTE treatments?

A

Risks are short term impact of thrombus burden and damage to vessels while thrombus remains

37
Q

Treatment of acute cardiovascularly stable VTE?

A

– Anticoagulate
o Immediate anticoagulant effect
o Heparin then warfarin/DOAC or immediate DOAC- Rivaroxaban or apixaban

38
Q

Treatment when there is a circulatory collapse due to PE or severe DVT?

A

– Thrombolysis
o Alteplase (tissue plasminogen activator)
o (Streptokinase)
o Followed by heparin and warfarin or other – prevent recurrence

39
Q

What investigations are done pre-treatment?

A

• Clotting screen
o Prothrombin time (INR)
o Partial thromboplastin time
o Thrombin time

• Full blood count – make sure theyre not anaemic

• Urea and electrolytes
o usually part of routine screen – to know creatinine clearance

• Liver function tests
o If clinical suspicion of liver disease – can affect drug excretion

40
Q

What does thrombin time tell?

A

tells time from fibrinogen to fibrin formation – tells how heparin works

41
Q

What does prothrombin time tell?

A

tells about extrinsic pathway, how long it takes to clot after you add tissue factor. important if:

o patients have liver disease affects clotting factor synthesis
o if patients is on warfarin
o if patient has vitamin k deficiency

42
Q

What does partial thromboplastin time tell?

A

tells about intrinsic pathway, tells if
o Patient has clotting factor deficient
o Patient has sepsis

43
Q

What is heparin (UFH)?

A
  • It’s a Glycosaminoglycan
  • Irreversible in binding
  • Immediate action
  • Parenteral administration, iv or sc
  • Renal excretion
44
Q

How is UFH monitored?

A

Activated Partial Thromboplastin Time Ratio – APTTR

45
Q

What prolongs the baseline levels of UFH?

A

o baseline level prolonged by

  • antiphospholipid antibodies
  • combined Rx with warfarin or thrombolytics
  • congenital factor deficiencies
46
Q

What shortens the baseline levels of UFH?

A

o baseline level shortened by

- high Vlll

47
Q

What is a challenge with UFH?

A

actually difficult to achieve reliable anticoagulation

48
Q

How does UFH bind?

A

Binds irreversibly to thrombin and other molecules

Different people have different balance between components – causes different effects in people

49
Q

Where is unfractionated heparin (UFH) synthesised and what does it do?

A
  • biosynthesis: mast cells
  • accelerates inhibition of thrombin (IIa) and Xa
  • bioavailability 30%
  • t ½ 1-2 hours
50
Q

How is low molecular weight heparin (LMWH) made and what does it do?

A
  • fractionation from UFH
  • accelerates inhibition of Xa from converting to thrombin (IIa)
  • bioavailability 90%
  • t ½ 4-12 hours
51
Q

How is LMWH cleared?

A

Renally cleared

52
Q

When is anti-Xa monitoring needed?

A

• Anti Xa monitoring performed under certain circumstances
o Pregnancy
o Renal failure
o Obesity

53
Q

What are the side effects of heparin?

A

• Bleeding
o LMWH: less major bleeding (more even control)
o stop heparin if there’s bleeding when UFH is given
o If LMWH causes bleeding give protamine sulphate – LMWH is harder to reverse

• Heparin induced thrombocytopenia (HIT)
o minor platelet drop at 5 days
- transient
o HIT with thrombosis syndrome (HITTS)
- Thrombocytopenia -IgG antibody to heparin + platelet factor 4 complexes
- Thrombosis - venous and arterial and gangrene
- Timing - 4-5 days after starting heparin
- other cause for thrombocytopenia not found

54
Q

What is the mechanism of action of Warfarin?

A
  • Acts on a number of different places
  • Vitamin k dependant clotting factor – antagonises vitamin k
  • Causing synthesis of Non Functional Coagulant and Anticoagulant Factors
55
Q

Sites of actions for VKA?

A
  • Because it acts on both anti-coagulant and coagulant factors – doesn’t produce anti-coagulation immediately
  • Pro-coagulant state happens first the anti-coagulant
56
Q

Side effects of Warfarin?

A

• skin necrosis - give heparin at first with warfarin for risk of VTE

57
Q

How is warfarin eliminated?

A
  • Rapidly absorbed t½ 36 - 42 hours

* Eliminated by liver

58
Q

What can affect intraindividual dose variation of Warfarin?

A 
• Intraindividual dose variation
o genetic factors 
o compliance / comprehension
o diet 
o co-morbid conditions eg right heart failure
o numerous drug interactions
59
Q

What genes can affect the intraindividual dose variation of Warfarin?

A
  • CYP2C9 – ↑ sensitivity

- VKORC1 – principal genetic modulator

60
Q

How is Warfarin administered?

A
  • Tablets

* Dosing -Loading algorithms and maintenance dose/they track their doses

61
Q

Why is tracking doses of Warfarin important?

A

Because Interruptions are necessary for surgical procedures

62
Q

What are the 2 ways of testing INR?

A
  • Venous sample

- Near patient testing (NPT) finger prick

63
Q

Pros/cons of venous sample

A
  • labour intensive
  • accurate
  • cheap
64
Q

Pros/cons of near patient testing

A
  • capillary whole blood
  • quick
  • patients prefer
  • immediate advice
  • 0.5 variation in INR
  • Expensive
65
Q

What can other drugs do/how they interact with warfarin?

A

Drugs can:
• impair absorption of vitamin K
o increase anticoagulant effect

• compete for plasma protein binding sites
o increase anticoagulant effect

• be hepatotoxic
o increase anticoagulant effect

• induce hepatic enzymes
o reduce anticoagulant effect

• have antiplatelet activity
o cause increased bleeding

66
Q

What are the annual risks of bleeding due to warfarin?

A
  • Fatal 0.1 – 1% pa
  • Major/life threatening 0.5 – 6.5 % pa ie
  • Minor 6.2 – 21.8% pa eg all other bleeds
67
Q

Why warfarin reversal may be needed and how is it done?

A

• When there’s High INR no bleeding

• Emergency reversal with:
o 5mg iv Vit K
o PCC (prothrombin complex concentrate) (octaplex/beriplex): replaces impaired clotting factors
 Factor IX 
 Factor II
 Factor X
 Factor VII
68
Q

How can warfarin affect pregnancy/the foetus?

A

crosses placenta

  • Affects cranial development
  • May cause brain bleeds in foetus
  • Can get problem with bone development
  • coumarin embryopathy

• increased fetal wastage
o intracerebral haemorrhage
o ante partum haemorrhage

69
Q

What are the issues with warfarin?

A

• Narrow therapeutic window
o Frequent monitoring needed (not always available)

  • Risk of bleeding (especially intracranial haemorrhage)
  • Many contraindications and food and drug interactions
  • Lifestyle restrictions
  • Poor compliance and persistence
  • Consequence: many patients are not sufficiently anticoagulated
70
Q

Advantages of direct oral coagulants?

A

• Oral anticoagulant

• Rapid onset/offset of action
o No need for bridging

• Short half life
o Easy to control anticoagulant effect

  • Little or no food-drug interactions
  • Limited drug-drug interactions

•Predictable anticoagulant effect
o No need routine monitoring

71
Q

What are some new anti-coagulants?

A

• Indirect Xa inhibitors - enhance antithrombin
o Fondaparinux
o Idraparinux

• Direct Xa inhibitors (ORAL)
o Rivaroxaban
o Apixaban

• Direct thrombin inhibitors (ORAL)
o Ximelagatran
o Dabigatran

72
Q

What is rivaroxaban?

  • onset?
  • monitoring?
  • how is it excreted?
  • drug/food interactions?
  • side effects?
  • when is it used?
A
  • Direct inhibitor of Xa
  • Oral agent ,once daily dosing
  • Rapid onset of action and half life 4-9 hours
  • Monitoring not usually necessary
  • Renal excretion
  • Few food or drug interactions
  • GI side effects

• in VTE prevention Post hip replacement
o superior to LMWH

• In VTE treatment and secondary prevention of DVT
o non inferior to LMWH and warfarin
o Now first line in many hospitals

73
Q

What study was done on rivaroxaban and what did it show?

A

• SPAF - Rocket AF vs warfarin in 16000 patients
o non inferior
o major bleeding rate similar but less IC bleeding

74
Q

What is apixaban?

  • onset?
  • monitoring?
  • how is it excreted?
  • drug/food interactions?
  • side effects?
A
  • Direct inhibitor of Xa
  • Oral agent
  • Rapid onset of action
  • Half life 9-14hours
  • Monitoring not usually necessary
  • Biliary and renal excretion
  • Few food or drug interactions
  • GI side effects
75
Q

What is dabigatran extexile?

  • onset?
  • monitoring?
  • how is it excreted?
  • drug/food interactions?
  • side effects?
  • cost?
A
  • Direct thrombin inhibitor
  • Oral, fixed doses
  • Monitoring not usually necessary
  • Rapid onset and offset of action
  • Half life 12-17 hours
  • Minimal food and drug interactions
  • Renal excretion
  • Reasonable cost
76
Q

How long are anticoagulants given for VTE?

A

o Variable
o Minimum 6 weeks
o 3-6 months for most indications – in unprovoked thrombosis
o For period of risk

Warfarin can be stopped abruptly

77
Q

What can cause secondary VTE?

A
  • Risk factors related to initial event
  • Idiopathic
  • 20 to 40% percent of those with an unprovoked venous thromboembolism (VTE) experience a recurrence within five years of the initial event
  • This is different in cancer – they’re prothrombotic but don’t respond well to some of the medication
78
Q

What is the relation between COVID-19 and VTE

A
  • Significant numbers of thrombotic events in COVID-19 patients who are unwell
  • Very high D-dimers in many patients
  • Patients appear highly prothrombotic
  • Treatment is the same

Cardio and Resp diseases (29 decks)

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