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Cardiovascular > DVT + Stroke > Flashcards

DVT + Stroke Flashcards

1
Q

What is DVT? What is PE? Presentations of PE?

Clinical features of DVT?

A
  • Thrombi form in sites of venous stasis e.g. venous valve pockets
  • PE - thromboemboli detach and travel through right side of heat to block vessels in the lungs
  • PE - SOB, pleuritic chest pain, haemoptysis
  • DVT - painful, red, swollen leg that is hot to touch
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2
Q

What is distal vein thrombosis? Proximal vein thrombosis? Which DVTs are diagnosed in hospital? Which have higher ris of PE?

A
  • DVT of the calves
  • DVT of the popliteal vein or the femoral vein
  • Proximal - do not scan below knee
  • Proximal (distal do not req treatment)
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3
Q

Why is number of VTE cases expected to rise by over 8% in next 5 years?

A

Due to growing and ageing population

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4
Q

How do patients with VTE/DVT describe their quality of life? (2)
What is VTE?

A
  • Worse perceptions of their health
  • Lower levels of physical functioning
  • VTE includes DVT and PE
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5
Q

Compare the mortality of PE and DVT alone? What is a common complication of DVT? In what percentage of proximal DVTs does this occur?

A
  • PE alone has higher mortality than DVT alone
  • Post Thrombotic Syndrome (PTS)
  • 30%
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6
Q

What factors can lead to hypercoaguable state in virchow’s triad? (6)

A
  • Malignancy
  • Pregnancy and
    peripartum period
  • Oestrogen therapy
  • Inflammatory bowel disease
  • Sepsis
  • Thrombophilia
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7
Q

What factors can lead to circulatory stasis in Virchow’s triad? (4)

A
  • Left ventricular dysfunction
  • Immobility or paralysis
  • Venous insufficiency or varicose veins
  • Venous obstruction from tumour, obesity or pregnancy
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8
Q

What are exposing risk factors for VTE? (6)

A

Acute conditions/trauma, surgery

  • Surgery
  • Trauma
  • Acute medical illness
  • Acute heart failure
  • Acute respiratory failure
  • Central venous catheterisation
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9
Q

What are predisposing risk factors for VTE? (11)

A

Patient characteristics

  • History of VTE
  • Chronic heart failure
  • Advanced age
  • Varicose veins
  • Obesity
  • Immobility or paresis
  • Myeloproliferative disorders
  • Pregnancy/peripartum period
  • Inherited or acquired thrombophilia
  • Hormone therapies
  • Renal insufficiency
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10
Q

Both exposing and predisposing risk factors? (2)

A
  • Cancer

* Inflammatory diseases

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11
Q

What categories can VTE be broken down into? What can provoked VTE be further broken down into? Examples? What are causes of unprovoked VTE?

A
  • Provoked and unprovoked (idiopathic) VTE
  • Transient/reversible factors e.g. surgery or hospitalisation (immobilisation)
  • Continuing/irreversible factors e.g. cancer
  • No identifiable cause
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12
Q

Compare recurrence rates of provoked and unprovoked VTE?

A

More likely to have second clot with unprovoked VTE than provoked

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13
Q

Known consequences of VTE? (5)

A
  • Fatal PE
  • Risk of recurrent VTE
  • Post-thrombotic syndrome (PTS)
  • Chronic thromboembolic pulmonary hypertension (CTEPH)
  • Reduced quality of life
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14
Q

Prevalence of post thrombotic syndrome? Characterised by? (6)

A
  • Occurs in nearly one-third of patients within 5years after idiopathic DVT
  • Pain (nerve-type pain, requires significant amount of analgaesia)
  • Oedema
  • Hyperpigmentation
  • Eczema
  • Varicose collateral veins
  • Venous ulceration
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15
Q

What is thought to be associated with development of PTS?

A

DVT-induced damage to valves in the deep veins and valvular reflux leading to venous hypertension are thought to be associated with PTS

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16
Q

What is CTEPH? Effects of CTEPH? (3) Mortality? Curable?

A
  • Serious complication of PE (up to 5% of PE patients develop this)
  • Dyspnoea, hypoxaemia and right heart failure
  • 4-20%
  • Can be cured through surgery to remove clot
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17
Q

Investigations for VTE? (2)

A

Pre-test probability scores (of there being a clot)
* D-Dimer - test of exclusion

Ultrasound

  • Compressability US
  • Doppler US
  • Venography
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18
Q

What is compressibility ultrasound? Venography?

A
  • If able to compress vein in the groin suggests no clot

* Venography - dye injected into foot which travels to veins in leg

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19
Q

What are D-dimers? Can it be used to diagnose VTE? What can it be used for? In what patients is test used? When should it be used with caution?

A
  • Breakdown product of fibrin
  • No, it has a low positive predictive value for VTE
  • It can be used to exclude VTE as has high negative predictive value (>98%)
  • Used as first line screening test for suspected VTE with low Wells score
  • Used with caution in patients with previous DVT
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20
Q

How is Wells score interpreted?

What are the different scores? (3)

A

Probability

  • Low = Check D-dimer - no imaging if negative
  • Mod/high = need imaging regardless of D-Dimer, negative imaging and positive D-Dimer requires repeat imaging
  • Low - 0 or less
  • Moderate - 1-2
  • High - 3 or more
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21
Q

Modified Wells score for PE?

A
  • Score of = 4 makes PE unlikely

* Score of >4 makes PE likely

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22
Q

What probability scores are used for PE?

A
  • Geneva score and Modified Wells score
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23
Q

Interpreting Geneva score? (3)

A
  • Low risk - 0-3 points (less than 10% incidence of PE, if d-dimer negative might not need investgation)
  • Intermediate risk - 4-10 (need d-dimer to exclude)
  • High risk (60% incidence, regardless of d-imer will need imaging)
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24
Q

Imaging techniques for VTE?

A
  • Ultrasound
  • CT pulmonary angiogram (CTPA)
  • CXR (usually normal in PE)
  • V/Q scan
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25
Q

What is CXR useful for in VTE? V/Q scan? What is the gold standard test for PEs? What is V/Q scan limited by?

A
  • Cannot be used for PE, but can show pleural effusions and occasionally infarct
  • Can be used for small peripheral PEs and pregnancy
  • CTPA gold standard test for PEs
  • Frequency of inconclusive results (false positives and false negatives)
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26
Q

Pharmacological interventions for DVT and PE? (3)

A
  • Anticoagulation (does not destroy clot, prevents propagation of clot)
  • Thrombolysis
  • Analgesia
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27
Q

Mechanical interventions for DVT and PE? (2) Screening? (2) Why screen for cancer?

A

Mechanical interventions

  • Graduated compression stockings
  • IVC filters

Screening

  • Cancer
  • Thrombophilia

Screened for cancer because both exposing and predisposing factor for VTE

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28
Q

Treatment for provoked VTE? Unprovoked? VTE in patients with active cancer?

A
  • LMWH for at least 5 days, VKA within 24 hours and continued for 3 months
  • LMWH for at least 5 days, VKA within 24 hours and continued for 3 months - asses risks for further treatment
  • LMWH for 6 months + reassess for continued treatment
29
Q

Advantages of VKA (Vitamin K antagonists e.g. Warfarin)? (2) Disadvantages? (5)

A
  • Can be used in patients with severe renal impairment
  • Anticoagulation can be reversed (Vitamin K)

Disadvantages

  • Slow onset
  • Numerous interactions with other drugs and food
  • Narrow therapeutic window
  • Inter-individual variability in dose response
  • Need for INR monitoring
30
Q

Advantages of NOACs? (4) Disadvantages? (3)

A

Advantages

  • Predictable pharmacological profiles
  • Absence of major interactions with food or other drugs
  • Do not require routine INR monitoring
  • May shift practice to longer treatment duration

Disadvantages

  • No available antidote
  • No readily available monitoring for special circumstances (e.g. major bleeding, urgent procedure)
  • No long term data
31
Q

Examples of NOACs? (4) Used for?

Why are NOACs generally preferred over Warfarin?

A
  • Apixiban - DVT and prophylaxis
  • Rivaroxiban - DVT, PE and prophylaxis
  • Dabigatran - VTE in hip or knee surgery
  • Edoxaban - prophylaxis of DVT and PE

Just as good as Warfarin with less evidence of bleeding complications

32
Q

What is the reasoning for continued anticoagulant use?

A

Reduces liklihood of recurrent VTE

33
Q

Special cases of VTE? (3) Treatment?

A

Drug-use associated

  • Risk of haemorrhage vs risk of embolic disease (must balance treatment)
  • Rivaroxiban or Fragmin

Cancer Associated
* Fragmin

Phlegmasia (extensive DVT)
* Arterial compromise

34
Q

What patients is thrombolysis treatment for DVT used for? (4)

A
  • Ileofemoral DVT of less than 14 days duration
  • Good functional status
  • Life expectancy of >1 year
  • Low risk of bleeding
35
Q

What patients is thrombolysis treatment for PE used for? Not used for?

A
  • Patients with PE and haemodynamic INSTABILITY

* Do not use for patients with PE and haemodynamic STABILITY

36
Q

What are compression stockings used for? When are they worn? Must it be worn in both legs? Complications?

A
  • Used to prevent post thrombotic syndrome (PTS) - ONLY treatment for this
  • Worn ASAP after diagnosis and for at least 2 years after
  • Only on affected leg(s)
  • Compression can lead to ischaemia due to arterial compromise
37
Q

What are IVC filters? When are TEMPORARY IVC filters used? Why can permanent IVC filters not be used in these patients? When is permanent IVC filter used?

A
  • Mechanical device in IVC designed to catch any clots – prevents death by PE
  • Patients with proximal DVT or PE who cannot have anticoagulation treatment
  • Mechanical device will stimulate clotting and will end up blocking IVC
  • Patients with recurrent proximal DVT or PE despite adequate anticoagulation (only after considering increasing target INR or LMWH)
38
Q

Complications of IVC filter?

A
  • Thrombosis

* Can jut through IVC into aorta causing fistula

39
Q

What is a stroke? Is stroke mortality increasing or decreasing? Incidence and prevalence?

A
  • Acute onset of focal neurological symptoms and signs due to disruption of blood supply to brain
  • Decreasing
  • Increasing
40
Q

Types of stroke? (2)

A
  • Ischaemic (80%) - clot blocks blood flow to an area of brain
  • Haemorrhagic (20%) - bleeding occurs inside or around brain tissue
41
Q

Causes of haemorrhagic stroke? (2)

A
  • Raised blood pressure
  • Weakened blood vessel wall due to:-
  • structural abnormalities like aneurysm, arteriovenous malformation(AVM)
  • inflammation of vessel wall(vasculitis)
42
Q

Causes of ischaemic stroke? (3)

A
  • Thrombotic - clot blocking artery at site of occlusion
  • Embolic - clot blocking artery travelled to artery from somewhere more proximal in the arteries or the heart
  • Hypoperfusion - reduced flow of blood due to stenosed artery rather than occlusion of artery
43
Q

Non-modifiable risk factors for stroke? (5)

A
  • Age - older
  • Family history of CVD
  • Gender - males
  • Race – South Asians
  • Previous stroke
44
Q

Modifiable risk factors for stroke? (11)

A
  • HYPERTENSION
  • Hyperlipidaemia
  • Smoking
  • Prior history of TIA especially if recent and recurrent
  • Atrial fibrillation
  • Diabetes
  • Congestive heart failure
  • Alcohol excess
  • Obesity
  • Physical inactivity
  • Poor socioeconomic status
45
Q

What is a TIA?

A

Artery blocked by clot so region of brain deprived of blood flow, but endothelium able to dissolve small clots so if clot small enough, it is dissolved and within minutes blood flows again

46
Q

Why are hypertension and smoking important risk factors for stroke?

A

Hyper tension

  • 10 mmHg reduction in SBP reduced risk of cardiovascular events by 20%
  • even isolated systolic hypertension can increase stroke risk

Smoking
* doubles risk of ischaemic stroke

47
Q

Treatment for hyperlipidaemia with regards to stroke?

A

Statin therapy in all patients with ischaemic stroke but NOT haemorrhagic stroke

48
Q

What group of patients do rarer causes of stroke normally affect? What are rarer causes of stroke? (7)

A

Younger patients

  • Homocysteinemia (endothelial damage)
  • Vasculitis, Antiphospholipid antibody syndrome (inflammation of blood vessel)
  • Protein S, C, Antithrombin III deficiency (anticoagulants)
  • Paradoxical embolism (venous clot to arterial side) through patent foramen ovale/pulmonary AV shunts
  • Genetic- Factor V Leiden mutation, common prothrombin mutation, MELAS, CADASIL,Fabry’s disease
  • Cardioembolic- mural thrombi, infective endocarditis, myxoma
  • Cervical artery dissection (inside of artery tears)
49
Q

Behavioural modifications for prevention of stroke? (4)

A

Diet

  • Mediteranean, DASH, AHA or USDA
  • Decresed sodium, sugar and calorie intake

Exercise
* Moderate to intense exercise 3-4 times per week

Weight control

  • If obese, goal is BMI <30
  • Overweight, goal is <25
  • If healthy, BMI of 18-25 should be maintained

Smoking cessation

  • Behavioural therapy + counselling
  • Nicotine therapy
  • Bupropion or varenicline
50
Q

How is disability reversed in stroke? How can next stroke be stopped?

A
  • Thrombolysis of thrombectomy in ischaemic stroke

* Identifying what caused the stroke and starting appropriate treatment

51
Q

How can you tell the type of stroke a patient has? Examples? (3)

A

Brain imaging - ONLY way of differentiating between ischaemic and haemorrhagic stroke

  • CT angiography
  • MRI and diffusion weighted imaging
  • MRI and susceptibility weighted imaging (looks for old haemosiderin deposits)
52
Q

What are “stroke mimics”? Examples? (6)

A

Conditions that present acutely with focal neurological signs but are not due to interrupted blood flow

  • Hypoglycaemia
  • Seizure- postictal states
  • Migraine
  • Other metabolic -hyperglycaemia, hyponatremia
  • Space-occupying lesions like brain tumours
  • Functional hemiparesis – patient pretends to have a stroke
53
Q

How to tell difference between ischaemic and haemorrhagic stroke on CT?

A

Darker area = infarct so ischaemia

Lighter area = blood

54
Q

Pics of brain scans

A

…

55
Q

Investigations to find cause of thrombosis or embolism in ischaemic stroke?

A
  • Blood tests - glucose, lipids, thrombophillia screen in young patients
  • Assess for hypertension
  • Any suggestion that patient has blood vessel disease like coronary artery disease or PVD - stroke may be due to blood vessel disease rather than embolic from heart
56
Q

What is an atheroembolism? Which side will infarct be? Cardioembolism? Which side?

A
  • Embolism from thrombus forming on atherosclerotic plaque - platelet rich clots
  • Infarcts same side as affected carotid artery
  • Embolism from a clot formed in the heart(usually left atrium) - clotting factor rich clots
  • infarcts in more than one arterial territory, bilateral
57
Q

Investigations for atheroembolism? (2)

A
  • Carotid scanning

* CT/MR angiography of aortic arch

58
Q

Investigations for cardioembolism? (3)

A
  • ECG - AF, old ischaemic changes (mural thrombus), LVH (suggests uncontrolled hypertension - commonest cause of AF)
  • Echocardiogram - transthoracic, transoesophageal, bubble contrast study to look for interatrial connection
  • 24 hour, 5 a day ECG monitor tests - paroxysmal AF
59
Q

Investigations for cause of bleed in haemorrhagic stroke?

A
  • Hypertensive- usually deep in the brain, older patients
  • If young, not hypertensive and lobar (superficial) haemorrhage- investigate for underlying aneurysm, AVM
  • If multiple haemorrhages- vasculitis, Moya Moya disease, cerebral amyloid angiopathy
60
Q

What can be done to reverse disability in stroke? Why are they time-dependent?

A
  • Thrombolysis- upto 4.5 hrs from onset of symptoms
  • Thrombectomy- upto 6 hrs from symptom onset, usually after having started thrombolysis
  • as brain tissue dies rapidly with any delay
61
Q

Process of thrombolysis? Will there still be some damage? Is thrombolysis an effective treatment for stroke? More effective in treatment of stroke or acute MI?

A
  • t-PA injected intravenously
  • Yes as clot takes ~30 mins to dissolve
  • Very effective
  • Stroke - more effective the earlier stroke is caught
62
Q

Effect of thrombolysis in symptomatic intracerebral haemorrhage?

A

Increased risk of symptomatic bleed within 36 hrs but better fuctional outcome

63
Q

Thrombectomy process? (2)
Is it indicated in every stroke?
Can it be used in older patients?

A
  • Stent retriever pushed through clot then expanded to integrate through the clot
  • Retriever and blood retracted into catheter and removed
  • No, only those in which catheter can reach the clot e.g. proximal large artery, not distal small artery
  • Yes
64
Q

Medical management for stroke caused by thombus/atheroembolic? (5)

A
  • Antiplatelets (Aspirin 75 mg + Dipyridamole MR 200 mg twice daily/Clopidogrel 75 mg daily)
  • Statins to treat high lipids
  • Diabetes management
  • Hypertension management
  • Lifestyle advice
65
Q

Medical management for stroke caused by AF? (3)

A

ANTICOAGULATION ASAP!

  • Warfarin (Vitamin K antagonist)
  • Direct acting oral anticoagulants (act by inhibiting clotting factors directly like factor X and thrombin)
  • Rivaroxaban, Dabigatran, Apixaban, Edoxaban
66
Q

Medical management of stroke caused by hypertension? (2)

A
  • Antihypertensives

* Perindopril + Indapamide reduced recurrence of stroke even when commenced on normotensive patients

67
Q

Surgical management of stroke? (3)

A
  • Haematoma evacuation
  • Relief of raised intracranial pressure
  • Carotid endarterectomy
68
Q

Why are TIAs an emergency?

A

Risk of stroke after TIA

  • 11-15% in first month
  • 24% to 29% in five years
69
Q

If symptoms of TIAs resolve does that mean there is no damage? How can stroke be prevented?

A
  • Studies show evidence of changes on MRI if symptoms last over 1 hr
  • CAN prevent a stroke if cause found by prompt investigation and management of cause

Cardiovascular (28 decks)

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