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Preclerkship > VTE & PE > Flashcards

VTE & PE Flashcards

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
Q

In massive PE you may observe ___ sign

A

Kussmaul (JVP increases during inspiration)

26
Q

PE is characterized by ___ symptom onset with ___ chest pain and cough with potential ____

A

Acute
Pleuritic
Hemoptysis

27
Q

A type of “massive PE”

Presentation?

A

Saddle thrombus

Syncope, obstructive chock, circulatory collapse

28
Q

What medical condition is in the modified Wells criterias for PE and DVT?

A

Cancer

29
Q

How do you assess PTP of PE?

A

Modified Wells Score

30
Q

What is the use of the Pulmonary Embolism Rule-Out Criteria?

A

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
Q

What might you see on ECG in a patient with PE?

A

Sinus tachycardia, bradycardia, AFib

RH strain: new RBBB, R-axis deviation, etc.

32
Q

When might you do pulmonary angiography to diagnose a PE?

A

If concurrently administering endovascular treatment

High PE suspicion and other tests negative

33
Q

What is the most definitive diagnostic test for PE?

Backup if contraindicated?

A

CT pulmonary angiogram (IV contrast)

V/Q scintigraphy can be done if CTPA contraindicated

34
Q

What med might you administer to a pulseless patient with PE?

A

Thrombolytics (tPA)

35
Q

How do you decide whether to give empiric parenteral anticoagulation while awaiting confirmation of PE diagnosis?

A

High PTP –> yes
Low/intermediate PTP but long time till results back –> yes
High bleeding risk –> NO

36
Q

3 tenets of supportive care for PE

A

1) Hemodynamic support (IV fluids, vasopressors)
2) Respiratory support (O2, ventilation)
3) Analgesics (morphine, oxycodone; avoid NSAIDS if on anticoag/thrombolytics)

37
Q

Characteristics of “submassive” PE (2)

A

Positive troponin, RV dysfunction

Systolic BP >90 (stable)

38
Q

Characteristics of “massive” PE (2)

A

Shock, RV failure

39
Q

Why does atelectasis happen in PE?

A

Ischemia –> surfactant deficiency

40
Q

When is a pulmonary infarction most likely to occur in PE?

A

If small arteries occluded because otherwise anastomoses comes to the rescue (use bronchial arteries, which can hemorrhage –> hemoptysis)

41
Q

Treatment of nonmassive or submassive PE

A

Low-mod bleeding risk –> anticoagulation (DVT treatment)

High bleeding risk –> IVC filter

42
Q

Treatment of massive PE if LOW bleeding risk

A 
Systemic thrombolytics (tPA, streptokinase, urokinase)
D/C anticoags during thrombolysis and resume after
43
Q

Treatment of Massive PE if HIGH bleeding risk

A

Catheter-directed thrombolysis (under U/S)

44
Q

Treatment of massive PE if thrombolysis fails or is contraindicated

A

Embolectomy (surgery/catheter)

Last resort!!

45
Q

ACS 3 types of things you want to target during treatment

A

1) Anti-ischemic therapies
2) Antithrombotic therapies (antiplatelets/anticoagulants)
3) Adjunctive therapies (statins, ACEi)

46
Q

Anti-ischemic therapies for ACS

A

B-blockers
Nitrates
+/- CCBs

Preclerkship (25 decks)

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