Module 4 Part 1 Venous Thromboembolism Flashcards

1
Q

what is the principle indication for antiplatelet drugs?

A

prevention of thrombosis in arteries

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2
Q

what are the 2 main adverse effects of aspirin?

A
  • Even in low doses, aspirin inc. risk for GI bleed and hemorrhagic stroke
  • Enteric-coated or buffered aspirin may not reduce risk of GI bleeding
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3
Q

should dosing for aspirin be high or low?

A

should be low when preventing cardiovascular events.

-Doses higher offer no greater benefit but do inc. risk for bleeding and stroke

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4
Q

what dose of aspirin is used for initial treatment of MI? why?

A

higher dose of 325mg/day is used for initial treatment to establish full anti platelet effects rapidly and then return to 81mg/day for maintenance dosing

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5
Q

what is hemostasis and what are the two stages it occurs in?

A

process by which bleeding is stopped.

  1. formation of a platelet plug
  2. reinforcement of the plug with fibrin (coagulation). Both are set in motion by blood vessel injury
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6
Q

how does your body protect against widespread coagulation?

A

-body must inactivate any clotting factors that stray from site of vessel injury (inactivation is done with antithrombin)

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7
Q

what is necessary in order for an injured BV to heal?

A

removal of a clot

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8
Q

define thrombosis

A

blood clot formed within a BV or within the heart

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9
Q

what are the 3 major drug groups for thromboembolic disorders?

A
  1. anticoagulants

2. antiplatelets, thrombolytic drugs

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10
Q

what makes up a venous thromboembolism (VTE)?

A

deep vein thrombosis (DVT) and pulmonary embolism (PE) collectively make up VTE

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11
Q

do DVT and PE’s usually show mnfts?

A

no, they are often clinically silent!

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12
Q

what are the 3 factors (virchow’s triad) of VTE?

A
  1. stasis of blood (venous stasis)
  2. vessel wall injury
  3. altered blood coagulation
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13
Q

formation of thrombus usually accompanies… ???

A

PHLEBITIS (inflammation of vein walls)

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14
Q

venous thrombosis usually occurs in what veins?

A

veins of lower extremities, (therefore upper extremity thrombosis is not as common)

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15
Q

although upper extremity venous thrombosis is less common, when would you see this in patients?

A

would see in patients with IV catheters or for those who have underlying disease that causes hypercoagulability

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16
Q

risk factors of endothelial damage for DVT and PE? (7)

A
• Trauma
• Surgery
• Pacing wires
• Central venous catheters
• Dialysis access catheters
• Local vein damage
-Repetitive motion injury
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17
Q

risk factors of venous stasis for DVT and PE? (5)

A
• Bed rest or immobilization
• Obesity
• History of varicosities
• Spinal chord injury
-Age greater than 65yrs
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18
Q

what are preventative measures for VTE? (4)

A

• Increasing mobility (getting them walking)
• Compression stockings
• Intermittent pneumatic compression devices (once these come off, then PAT can be done)
-Prophylactic Anticoagulant Therapy (PAT)

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19
Q

what are objectives of treatment for DVT?

A

prevent the thrombus from growing and fragmenting (thus risking PE), recurrent thromboemboli, and prothrombotic syndrome

20
Q

what two types of drug therapy can you combine to possibly eliminate DVT

A

-combining anticoagulation therapy with thrombolytic therapy
This may eliminate venous obstruction, maintain venous patency, and prevent postthrombotic syndrome (caused by early removal of the thrombus)

21
Q

how can you provide a patient with comfort with DVT?

A
  • warm, moist packs applied to affected extremity reduce discomfort
  • pt encouraged to walk once anticoagulation therapy has been initiated
  • bed exercises (repetitive dorsiflexion of the foot) are recommended
22
Q

whats the worst thing that could happen with VTE (aka DVT)?

A

breaking of clots (emboli) that can go anywhere in body (usually go to lungs)

23
Q

TRUE OR FALSE: Veins DO NOT have valves

A

FALSE

veins HAVE valves, arteries DO NOT

24
Q

S+S of VTE

A

• Swelling
• Pain
• Cool or warm to touch
Can be non-specific… hard to diagnose

25
Q

S+S of PE (7)

A

• Dyspnea (SOB)
• Tachypnea (rapid breathing)
• Decreased SpO2
• Chest pain of “pleuritic” nature (worsened by breathing)
• Cough
• Hemoptysis (coughing up blood)
-If there’s a lack of blood supply to brain, pt will be typically anxious, sweating, fainting

26
Q

what is a pulmonary embolism?

A

• Pulmonary Embolus (PE): Clot that gets lodged in vascular system that feeds the lung supply

27
Q

diagnostic tests for VTE are?

A

• D-dimer-(blood test) If a D-dimer comes back positive, there is a clot
• PTT, PT-INR, platelets
• Ultrasound-deep veins in legs
-CT of chest to rule out PE

28
Q

non pharm nursing interventions for VTE (5)

A
• Monitor CWMS
• Measure limb and mark it so people measure it at the same place
• Monitor skin integrity
• Monitor for S+S of clots
-Mobilization
29
Q

pharm interventions for VTE (3)

A

• Monitor and treat pain (Tylenol, sometimes narcotics depending on severity)
• Administer anticoagulants, thrombolytic
-PE: Administer O2! Notify MRP if suspected

30
Q

why would someone be on an anticoagulant? (6)

A

• Immobility (post surgical)
• Hx. VTE/pulmonary embolus
• Dysrhythmias (A-fib)
• Mechanical heart valve
• Post MI or stroke (r/t clot and therefore don’t want more clots to form)
-Cancer (some cancers increase chance for clots)

31
Q

anticoagulants are typically used because..?

A

• Increase clotting time (seconds) to prevent thrombi from forming, or growing larger
• Inhibit specific clotting factors in the coagulation cascade
They do NOT breakdown clots, they just help for clots to stop forming

32
Q

does heparin work on intrinsic or extrinsic pathway?

A

intrinsic clotting pathway

33
Q

what does heparin work on?

A

works on blocking two clotting factors (thrombin and factor 10A). by blocking these, it suppresses clotting

34
Q

what is the PTT range you wanna be at if pt is on an anticoagulant?

A

56-70 seconds is the therapeutic range!!

35
Q

what does heparin increase risk for?

A

increases risk of heparin-induced thrombocytopenia (HIT)

36
Q

what is the major thing to know if someone has HIT?

A

they can NEVER receive heaprin once they’ve had HIT

37
Q

what is the antidote for heparin?

A

protamine sulfate. given if they start bleeding alot

38
Q

does warfarin work on intrinsic or extrinsic pathway?

A

works on extrinsic pathway

39
Q

how long can warfarin take to reach therapeutic level?

A

can take 3-5 days!

40
Q

what is bridging and why is it done?

A

starting pt on a fast acting drug (like enoxaparin) as well as a longer acting drug (like warfarin). This is done to reach a therapeutic level!! once the warfarin activates in 3-5 days, fast acting drug (enoxaparin) is d/c

41
Q

what is typical range for INR that you want to see with warfarin?

A

2-4 seconds

42
Q

antidote for warfarin?

A

vitamin K

43
Q

what is a common concern with ASA?

A

anticoagulant properties can last up to a week after one single dose

44
Q

why is liver failure a concern with anticoagulants?

A

Liver controls the clotting factors. Therefore if there’s liver failure, wont be able to produce the clotting factors

45
Q

list patient teaching ideas when pt is on anticoagulant

A

○ Soft toothbrushes
○ Diet (limit foods with high vitamin k)
○ Bracelet that shows they are on warfarin high risk for cranial bleeds
○ They are going to bruise easily/bleeding
-difference between a bruise and active bleeding
**If pt is prone to falls (ex. Parkinson’s), they should not be on warfarin and not allowed if pregnant