Module 4 Part 1 Venous Thromboembolism Flashcards

(45 cards)

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
S+S of PE (7)
• 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
what is a pulmonary embolism?
• Pulmonary Embolus (PE): Clot that gets lodged in vascular system that feeds the lung supply
27
diagnostic tests for VTE are?
• 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
non pharm nursing interventions for VTE (5)
``` • 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
pharm interventions for VTE (3)
• Monitor and treat pain (Tylenol, sometimes narcotics depending on severity) • Administer anticoagulants, thrombolytic -PE: Administer O2! Notify MRP if suspected
30
why would someone be on an anticoagulant? (6)
• 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
anticoagulants are typically used because..?
• 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
does heparin work on intrinsic or extrinsic pathway?
intrinsic clotting pathway
33
what does heparin work on?
works on blocking two clotting factors (thrombin and factor 10A). by blocking these, it suppresses clotting
34
what is the PTT range you wanna be at if pt is on an anticoagulant?
56-70 seconds is the therapeutic range!!
35
what does heparin increase risk for?
increases risk of heparin-induced thrombocytopenia (HIT)
36
what is the major thing to know if someone has HIT?
they can NEVER receive heaprin once they've had HIT
37
what is the antidote for heparin?
protamine sulfate. given if they start bleeding alot
38
does warfarin work on intrinsic or extrinsic pathway?
works on extrinsic pathway
39
how long can warfarin take to reach therapeutic level?
can take 3-5 days!
40
what is bridging and why is it done?
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
what is typical range for INR that you want to see with warfarin?
2-4 seconds
42
antidote for warfarin?
vitamin K
43
what is a common concern with ASA?
anticoagulant properties can last up to a week after one single dose
44
why is liver failure a concern with anticoagulants?
Liver controls the clotting factors. Therefore if there's liver failure, wont be able to produce the clotting factors
45
list patient teaching ideas when pt is on anticoagulant
○ 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