VTE & PE Flashcards

(46 cards)

1
Q

What is a main physiological difference between VTE & arterial thromboembolism?

A

Arterial usually acute events (stroke, MI, etc) mediated by PLATELETS (aspirin!!).
VTE involves platelets but more RBCs/fibrin

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2
Q

What is Virchow’s triad?

A

1) Stasis
2) Hypercoagulable state
3) Endothelial damage

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3
Q

Why does nephrotic syndrome increase risk of DVT?

A

Reduces antithrombin, increases blood viscosity (fluid extravasatino)

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4
Q

How does pregnancy induce a hypercoagulable state?

A

More clotting factors
Reduced proteins C/S
Venous stasis
Mechanical compression from uterus

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5
Q

Why does malignancy provoke DVT?

A

Excretes procoagulants (e.g. TF)

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6
Q

Difference between provoked/unprovoked DVT?

A

Presence vs absence of risk factors

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7
Q

DVT is usually where?

A

L lower limb

R iliac artery overlies the L iliac vein (May-Thurner syndrome)

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8
Q

DVT usually starts in the __ veins, but when causes symptoms over 80% involve the ___ veins. The majority of calf veins under go _____ but 20% ____

A

Calf (anterior/posterior tibeal, peroneal)
Popliteal or more proximal (femoral, iliac)
Spontaneous lysis
Extend to involve the proximal veins

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9
Q

What is D-dimer and how is it used?

A

Fibrin degradation product
High sensitivity but low sensitivity - can rule DVT out but not in
“Only has high NPV (rule out) at low pretest probability!”

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10
Q

What is the most accurate test for diagnosing DVT?

A

Compression venous duplex ultrasound

  • nonthrombosed veins are compressible w/ probe
  • Doppler evaluates noncompressible veins (shows absent/abnormal venous flow)
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11
Q

AFter DVT some patients will develop….

A

Chronic venous insufficiency (postthrombotic syndrome)

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12
Q

4 types of VTE prophylaxis

A

Exercise/mobilization/physio
Avoid triggering meds if risk factors present (e.g. OCPs)
Anticoagulants
Compression stockings

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13
Q

What is a differential of DVT that typically occurs in varicose veins in the leg?

A

Superficial thrombophlebitis

Can lead to DVT/PE, if RFs then anticoagulation

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14
Q

Signs of superficial thrombophlebitis?

A

Pain/induration (hardening)/erythema over superficial vein, palpable cord vein

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15
Q

General treatment approach to DVT

A

1) Assess/treat PE if present
2) Assess bleeding risk
3) Treat based on extent/etiology
4) Treat underlying cause

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16
Q

What are the 3 stages of DVT treatment

A
Expectant (serial venous US, no anticoag) - rare
Primary treatment (3-6 mo anticoag)
Secondary prevention (extended coagulation based on RFs)
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17
Q

Initial parenteral anticoagulation for DVT: length of time and options

A

5-10 days
LMWH: subcutaneous, rapid onset, don’t need to monitor
UFH: bolus + infusion, req monitoring for heparin-induced thrombocytopenia
Fondaparinux: factor Xa inhibitor (binds/activates antithrombin) - fast onset, don’t need to monitor aPTT

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18
Q

Why do you need to do regular CBCs on a patient on UFH?

A

Looking for heparin-induced thrombocytopenia (if they develop this, try fondaparinux)

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19
Q

Why might UFH be a chosen treatment for DVT?

A

Inadequate subcutaneous absorption

High bleeding risk (fully reversible with Protamine Sulfate!)

20
Q

Long-term anticoagulation in DVT (time and types)

A

3-6 mo
DOAC (Xa/thrombin inhibitors) - first line if nonpregnant!
Vitamin K Antagonists (warfarin) - bridging required, dose adjustments to reach target INR
LMWH (pregnancy or cancer)

21
Q

Why can using warfarin cause INCREASED coagulation at the start?

A

Proteins C/S have shorter halflives and are also Vit K dependent

22
Q

Name 2 factor Xa DOACs, and 1 thrombin DOAC

A

Xa: rivaroxaban, apixaban
Thrombin: dabigatran

23
Q

What substances cause PE?

A

FATAL:

Fat, Air, Thrombus (most common), Amniotic fluid, Less common (bacterial, tumor, etc.)

24
Q

How does the A-a gradient change in PE?

A

Increases (V/Q mismatching)

25
In massive PE you may observe ___ sign
Kussmaul (JVP increases during inspiration)
26
PE is characterized by ___ symptom onset with ___ chest pain and cough with potential ____
Acute Pleuritic Hemoptysis
27
A type of "massive PE" | Presentation?
Saddle thrombus | Syncope, obstructive chock, circulatory collapse
28
What medical condition is in the modified Wells criterias for PE and DVT?
Cancer
29
How do you assess PTP of PE?
Modified Wells Score
30
What is the use of the Pulmonary Embolism Rule-Out Criteria?
If the patient is at LOW risk (according to Wells criteria), clinicians should use the PERC; if a patient does not meet ANY of the eight criteria, the risks of testing are greater than the risk for embolism, and no testing is needed.
31
What might you see on ECG in a patient with PE?
Sinus tachycardia, bradycardia, AFib | RH strain: new RBBB, R-axis deviation, etc.
32
When might you do pulmonary angiography to diagnose a PE?
If concurrently administering endovascular treatment | High PE suspicion and other tests negative
33
What is the most definitive diagnostic test for PE? | Backup if contraindicated?
CT pulmonary angiogram (IV contrast) | V/Q scintigraphy can be done if CTPA contraindicated
34
What med might you administer to a pulseless patient with PE?
Thrombolytics (tPA)
35
How do you decide whether to give empiric parenteral anticoagulation while awaiting confirmation of PE diagnosis?
High PTP --> yes Low/intermediate PTP but long time till results back --> yes High bleeding risk --> NO
36
3 tenets of supportive care for PE
1) Hemodynamic support (IV fluids, vasopressors) 2) Respiratory support (O2, ventilation) 3) Analgesics (morphine, oxycodone; avoid NSAIDS if on anticoag/thrombolytics)
37
Characteristics of "submassive" PE (2)
Positive troponin, RV dysfunction | Systolic BP >90 (stable)
38
Characteristics of "massive" PE (2)
Shock, RV failure
39
Why does atelectasis happen in PE?
Ischemia --> surfactant deficiency
40
When is a pulmonary infarction most likely to occur in PE?
If small arteries occluded because otherwise anastomoses comes to the rescue (use bronchial arteries, which can hemorrhage --> hemoptysis)
41
Treatment of nonmassive or submassive PE
Low-mod bleeding risk --> anticoagulation (DVT treatment) | High bleeding risk --> IVC filter
42
Treatment of massive PE if LOW bleeding risk
``` Systemic thrombolytics (tPA, streptokinase, urokinase) D/C anticoags during thrombolysis and resume after ```
43
Treatment of Massive PE if HIGH bleeding risk
Catheter-directed thrombolysis (under U/S)
44
Treatment of massive PE if thrombolysis fails or is contraindicated
Embolectomy (surgery/catheter) | Last resort!!
45
ACS 3 types of things you want to target during treatment
1) Anti-ischemic therapies 2) Antithrombotic therapies (antiplatelets/anticoagulants) 3) Adjunctive therapies (statins, ACEi)
46
Anti-ischemic therapies for ACS
B-blockers Nitrates +/- CCBs