DVT AND PTE Flashcards

1
Q

Favorable environment for venous thrombi

A
  1. Stasis
  2. Low oxygen Tension
  3. Upregulated pro-inflammatory genes
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2
Q

is the most common preventable cause of death among hospitalizedpatients

A

Pulmonary thromboembolism or PE

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3
Q

Chronic thromboembolic pulmonary hypertension

A

causes breathlessness, especially with exertion

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4
Q

(also known as chronic venous insufficiency) damages the venous valves Of the leg and worsens the quality of life by causing ankle or calf swelling and leg aching, especially after prolonged standing

A

Post thrombotic syndrome

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5
Q

it’s-most severe form, postthrombotic syndrome causes

A

skin ulceration

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6
Q

Virchow’s triad

A

venous stasis,
hypercoagulability
endothelial injury

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7
Q

Prevention of VTE , most common in-hospital prophylaxis :

A

Low dose UFH OR LMWH

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8
Q

May possibly cure pulmonary hypertension and indicated mgt for chronic thromboembolic pulmonary hypertension

A

PULMONARY THROMBOENDARTERECTOMY

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9
Q

Approve clinical use of Fibrinolysis which is effective up to 14 days post PE

A

Massive PE

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10
Q

Additional indication for fibrinolysis:

A

Submissive PE
if with preserved BP
WITH MODERATE OR SEVERE RV DYSFUNCTION

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11
Q

Preferred fibrinolytic treatment

A

rtPA 100mg continuous 2 hour IV INFUSION

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12
Q

1st line inotropic agents for treatment of PE related shock

A

Dopamine, dobutamine

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13
Q

Principal indications of inferior vena cava IVC filters:

A
  1. Active bleeding precluding anticoagulation

2. Recurrent venous thrombosis despite intensive anticoagulation

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14
Q

Duration of anticoagulation: if DVT of upper extremity or calf provoked by surgery, trauma, estrogen exposure, in dwelling device/catheter:

A

3 months

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15
Q

Duration of anticoagulation:

provoked proximal leg DVT or PE

A

3-6 months

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16
Q

Duration of anticoagulation:

Cancer and VTE use

A

Use LMWH indefinitely until cancer free

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17
Q
Duration of anticoagulation:
Idiopathic VTE (unprovoked, ex long haul flight) has high recurrence rate after stopping anticoagulants
A

Indefinite anticoagulation to INR 2-3

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18
Q

Duration of anticoagulation:

Moderate or high levels of antiphospholipids antibodies

A

Indefinite anticoagulation

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19
Q

Duration of anticoagulation:

Heterozygous factor V LEIDEN and prothrombin gene mutation

A

Not at increased risk of recurrent VTE

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20
Q

Most serious adverse effect of anticoagulation:

A

HEMORRHAGE

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21
Q

Treatment for anticoagulation hemorrhage sec to HEPARIN or LMWH

A

PROTAMINE SULFATE

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22
Q

Treatment for anticoagulation hemorrhage sec to dabigatran

A

IDARUCIZUMAB

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23
Q

Treatment for anticoagulation hemorrhage sec to APIXABAN, BETRIXABAN, RIVAROXABAN

A

Andexanet

24
Q

Treatment for anticoagulation hemorrhage sec to warfarin and major bleeding

A

Prothrombin complex concentrate

25
Q

Treatment for anticoagulation hemorrhage sec to WARFARIN and less serious bleeding

A

FFP or IV vitamin k

26
Q

Treatment for anticoagulation hemorrhage sec to WARFARIN and minor bleeding

A

Oral vitamin k

27
Q

Treatment for heparin induced thrombocytopenia or HIT for patients with renal insufficiency

A

Argatroban

28
Q

Treatment for heparin induced thrombocytopenia or HIT for patients with hepatic failure

A

Lepirudin

29
Q

Treatment for heparin induced thrombocytopenia or HIT for patients in the setting of PCI

A

BIVALIRUDIN

30
Q

Resistance to activated protein c which inactivated factors 5 and 8

A

Factor 5 Leiden

31
Q

Most common case of acquired thrombophilia

A

APAS

32
Q

The usual cause of death from PTE

A

Progressive right Heart failure

33
Q

10x more common than upper extremity DVT

A

Lower extremity DVT (from calf proximally to popliteal, femoral and iliac veins)

34
Q

Most common symptom of the great masquerader / PE

A

Breathlessness

35
Q

Presentation: erythema , tenderness and palpable cord

A

Superficial venous thrombosis

36
Q

Most common symptom of DVT

A

Cramp or

Charley horse in the lower calf that persists and intensified over several days

37
Q

Often present with marked THIGH swelling, tenderness and erythema

A

massive DVT

38
Q

True or false

If leg is diffusely edematous, unlikely to be DVT

A

True

39
Q

consists of clot dissolution with pharmacomechanical therapy that usually includes low-dose catheter-directed thrombolysis.

A

Primary therapy for DVT

40
Q

secondary prevention of VTE

A

Anticoagulation or placement of an inferior vena caval (IVC) filter

41
Q

For patients with swelling of the legs when acute DVT is diagnosed, below-knee graduated compression stockings may be prescribed, to lessen patient discomfort. Theyshould be replaced every 3 months because they lose their elasticity. What is the pressure needed?

A

usually 30–40 mmHg (secondary prevention)

42
Q

Effective anticoagulation is the foundation for successful treatment ofDVT and PE. There are three major strategies:

A

1) the classical but waning strategy of parenteral anticoagulation with unfractionated heparin(UFH), low-molecular-weight heparin (LMWH), or fondaparinux“bridged” to warfarin, (2) parenteral therapy switched after 5 days to a novel oral anticoagulant such as dabigatran (a direct thrombininhibitor) or edoxaban (an anti-Xa agent), or (3) oral anticoagulation monotherapy with rivaroxaban or apixaban (both are anti-Xa agents)with a 3-week or 1-week loading dose, respectively, followed by a maintenance dose without parenteral anticoagulation

43
Q

For patientswith VTE in the setting of suspected or proven heparin-induced thrombocytopenia, one can choose between two parenteral direct-thrombin inhibitors:

A

argatroban and bivalirudin

direct-thrombin inhibitors:

44
Q

UFH anticoagulates by binding to and-accelerating the activity of antithrombin, thus preventing additional thrombus formation. The most popular nomogram uses an initial bolus of____, followed by an initial infusion rate of ____ in patients with normal liver function

A

80 U/kg

18 U/kg per h

45
Q

UFH is dosed to achieve a target activated partial thromboplastin time (aPTT) of

A

60–80 seconds

46
Q

These fragments of UFH exhibitless binding to plasma proteins and endothelial cells and consequently have greater bioavailability, a more predictable doseresponse, and a longer half-life than does UFH. No monitoring ordose adjustment is needed unless the patient is markedly obese orhas chronic kidney disease.

A

LMWH

47
Q

An anti-Xa pentasaccharide, is administered as a weight-based once-daily subcutaneous injection in a prefilled syringe. It does not cause heparin-induced thrombocytopenia.

A

FONDAPARINUX

48
Q

This vitamin K antagonist prevents carboxylation activation of coagulation factors II, VII, IX, and X.

A

WARFARIN

49
Q

Increased d-dimER but low specificity

A
Pneumonia
Pregnancy 2nd and 3rd trimester
AMI
Post surgery 
SEPSIS
Cancer
50
Q

Most frequently cited ECG abnormality

A

Sinus tachycardia
S1Q3T3
T wave in V1 to V4 (most common due to RV strain and ischemia)

51
Q

True or false:

Wells Point Score criteria help estimate the clinical likelihood of DVTand PE. Patients with a low-to-moderate likelihood of DVT or PE should undergo initial diagnostic evaluation with d-dimer testing alone without obligatory imaging tests

A

True

52
Q

True or false:
However, patients with a high clinical likelihood of VTEshould skip d-dimer testing and undergo imaging as the next step inthe diagnostic algorithm.

A

True

53
Q

Second line diagnostic tests for PE

A

Lung scanning

54
Q

equantitative plasma d-dimer enzyme-linked immunosorbent assay (ELISA)rises in the presence of DVT or PE because of the breakdown of fibrin by

A

plasmin

55
Q

Chest X-ray PE abnormalities

A

focal oligemia (Westermark’s sign),
a peripheral wedged-shaped density usually located at the pleural base (Hampton’s hump),
and an enlarged Right descending pulmonary artery (Palla’s sign)

56
Q

Primary therapy consists of clot dissolution with pharmacomechanicaltherapy that usually includes low-dose catheter-directed thrombolysis. This approach is reserved for patients with extensive

A

femoral
iliofemoral
upper extremity DVT

57
Q

Risk stratification:

portend a high risk of an adverse clinical outcome despite anticoagulation.

A

Hemodynamic instability
RV dysfunction on echocardiography
RVenlargement on chest CT
or elevation of the troponin level due toRV microinfarction