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Pharmacology > Chapter 27- anticoagulants, antiplatelets, thrombolytics > Flashcards

Chapter 27- anticoagulants, antiplatelets, thrombolytics Flashcards

1
Q

What are the two pathways that lead to coagulation?

A

intrinsic pathway- activated in response to injury

extrinsic pathway- activated when when blood leaks out of a vessel and enters tissue spaces

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2
Q

Steps that initiate the clotting process

A
  • when blood vessel is injured, vessel spasms and constricts (limits blood flow to injured area)
  • platelets become sticky, adhering to each other and to damaged vessel
  • as the bound platelets break down, they release substances that attract more platelets to the area…the flow of blood is reduced, thus allowing the process of COAGULATION
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3
Q

coagulation cascade

A
  • coagulation occurs when fibrin threads create a meshwork that traps blood constituents so that they develop a CLOT
  • two separate pathways lead to coagulation…
    • intrinsic pathway
    • extrinsic pathway
  • near end of cascade, a chemical called prothrombin activator—> prothrombin—-> thrombin—>fibrinogen—>fibrin
  • these fibrin strands provide framework for the clot
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4
Q

REMOVAL of blood clots

A
  • called FIBRINOLYSIS

- initiated within 24-48 hours of clot formation and continues until clot is dissolved

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5
Q

What are the several steps of fibrinolysis?

A
  • when fibrin clot is formed, nearby blood vessels secret enzyme TISSUE PLASMINOGEN ACTIVATOR (TPA)—>plasminogen—> plasmin—>digests fibrin strands and removes clot
  • the body regulates fibrinolysis so that UNWANTED fibrin clots are are removed; fibrin present in wounds is left to maintain hemostasis
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6
Q

thromboembolic disorders occur when…

A
  • the body forms undesirable clots
  • a stationary clot is called a THROMBUS (if in a vessel, it grows larger as more fibrin is added)
  • traveling clot is called an embolus
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7
Q

bleeding disorders are characterized by…

A
  • abnormal clot formation
  • thrombocytopenia- most common bleeding disorder and is a deficiency of platelets
  • hemophilias-bleeding disorder caused by genetic deficiencies in specific clotting factors
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8
Q

what is the most common inherited bleeding disease?

A

von Williebrand’s disease (vWD)

-results in decrease in quantity or quality of von Williebrand factor, which has a role in platelet aggregation

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9
Q

mechanisms of coagulation modification

A
  • prevention of the formation of clots= ANTICOAGULANTS, ANTIPLATELETS
  • dissolve clots, removal of existing clot= THROMBOLYTICS
  • promote formation of clots= HEMOSTATICS
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10
Q

3 examples of anticoagulants

A

warfarin (Coumadin)

heparin

enoxaparin (Levonox)

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11
Q

heparin’s action

A
  • prevents conversion of prothrombin to thrombin and the conversion of fibrinogen to fibrin
  • binds to antithrombin III (which inactivates thrombin)
  • inactivates several clotting factors
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12
Q

action of warfarin

A
  • interferes with the vitamin K dependent factors by reducing synthesis of vitamin K
  • inhibits hepatic synthesis of coagulation factors
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13
Q

Specific points of Coumadin (what does it treat, what route of administration, pregnancy?)

A
  • treatment of atrial fib, CHF, valvular disease, pulmonary embolus, deep vein thrombosis (DVT)
  • takes 3-5 days for therapeutic dose
  • ORAL (long term treatment)

DO NOT TAKE while pregnant

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14
Q

Coumadin (antidote, how to monitor effectiveness)

A

-antidote= VITAMIN K
MONITOR PT

  • how to monitor effectiveness?
    1. 5 to 2 x baseline= therapeutic range

example: normal PT is 2.0-3.0

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15
Q

Heparin (route of administration, antidote, pregnancy?)

A

route of admin= IV and subcutaneous

  • antidote= PROTAMINE SULFATE
  • heparin CAN be used with pregnancy, warfarin CANNOT
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16
Q

Heparin (monitor effectiveness, other facts)

A

-quick onset
-indirect thrombin inhibitor
-how to monitor effectiveness?
1.5 to 2.5 x baseline= therapeutic range
MONITOR PTT
example: normal PTT is 25
so, 25x1.5=37.5 and 25x2.5=62.5
someone taking heparin should have PTT of 37.5-62.5

17
Q

Enoxaparin (monitor effectivess, antidote, route of administration)

A
  • monitor effectiveness: do not really test effectiveness; PTT levels would probably go up, so you could monitor that
  • antidote= protamine sulfate? (b/c cousin to heparin)
  • route of administration= subcutaneous in abdomen (about 2-3 inches away from umbilicus)
18
Q

enoxaparin (facts)

A
  • same as heparin except has a longer half life

- lower molecular weight, doesn’t bind with proteins

19
Q

antiplatelet medications

A

-interferes with platelet aggregation
-affects ADP and TXA2
PLAVIX

20
Q

common antiplatelet medications

A
  • aspirin
  • ticlopidine (Ticlid)
  • clopidogrel (Plavix)
21
Q

When are IV antiplatelets usually given? What is the half life of antiplatelet drugs?

A
  • IV antiplatelets can be used before a diagnosis (such as MI) is confirmed; patient needs meds immediately so IV antiplatelets may be given (until diagnosis confirmed)
  • half life of antiplatelet medications is the half life of the platelet! (so about 5 days; platelets live about 10 days)
22
Q

what are therapeutic uses of antiplatelet drugs?

A
  • preventing clot formation
  • mainly for the disease processes of heart attack, strokes
  • antiplatelets are used second to treat DVT when patient cannot take anticoagulants
23
Q

contraindications of anticoagulants

A
  • active bleeding
  • head injury
  • recent surgery
  • bleeding disorder
  • advanced liver and renal disease
  • postpartum
  • pregnancy with warfarin (not with heparin)
24
Q

drug interactions with anticoagulants

A
  • any antiplatelet or antithrombotic medication
  • spinal-epidural anesthesia
  • food with high vitamin K content
  • some herbs
  • many drug interactions with warfarin
  • ALCOHOL (alcohol will prolong bleeding)
25
Q

adverse effects of anticoagulants

A
  • BLEEDING
  • hypersensitivity reactions
  • GI (N/V/D, pain)
  • heparin can cause “HIT”, heparin induced thrombocytopenia, and thrombosis (although thrombocytopenia usually leads to excessive bleeding, HIT causes the opposite effect: an increase in adverse thromboembolic events which can lead to thrombosis)
26
Q

Nursing implications/teaching for anticoagulants

A
  • know appropriate labs and values for each med discussed
  • know appropriate route each med is given as well as onset
  • know antidote and have readily available
  • teach to watch for signs of bleeding
  • teach patient to use soft toothbrushes, electric razors, and be careful of injury; NO FLOSSING
  • liver enzymes may elevate, showing cell damage
  • warn patients of effects of alcohol (especially with warfarin and blood tests)
27
Q

Lab values to monitor while on anticoagulation therapy

A
  • prothrombin time (PT)- used to monitor warfarin therapy; INR should be 2-3 to prevent DVT; 2.5-3.5 to prevent arterial thrombosis
  • INR
  • PTT- used to monitor heparin therapy; 25-35 seconds is normal
  • CBC
28
Q

contraindications for antiplatelet drugs

A
  • underlying bleeding disorders
  • sever liver impairment- clotting proteins come from our liver, so if we have liver impairment, do not give antiplatelets because we will have increased bleeding (no clotting)
  • any active bleeding
  • pregnancy
  • aspirin= “allergic triad” caution with renal or otic disease; gout
29
Q

Drug interactions with antiplatelets

A
  • risk of bleeding with anticoagulants
  • any acidifying agents
  • antigout medications
  • NSAIDs (when taking clopidogrel (Plavix))
30
Q

adverse effects of antiplatelets

A
  • bruising and petechiae
  • GI (N/V/D, pain)
  • watch for blood in stool, emesis, etc.
  • headache
  • dizziness
  • weakness
  • aspirin= hearing changes (tinnitus)
  • watch for anaphylactic reactions
  • watch for platelet number (thrombocytopenia)
31
Q

nursing implications/teaching for antiplatelets

A
  • monitor intake and output (dehydration)
  • watch for BLEEDING
  • discontinue meds 7-10 days prior to surgery, dental work
  • watch for hearing loss, dizziness, LOC changes
  • teach patient to take aspirin with food to decrease stomach upset
32
Q

Plavix (clopidigril) drug info

A
  • prevention of thromboembolic events in patients with a recent history of MI, CVA, or peripheral artery disease
  • inhibits platelet aggregation directly inhibiting ADP binding to its receptor
  • onset is 1-2 hr
  • don’t give to people with active bleeding
  • platelet transfusions in treatment of overdose may be necessary to prevent hemorrhage
33
Q

Thrombolytics action

A
  • promote fibrinolysis (clot destruction) by converting plasminogen to plasmin
  • thrombolytics actually DISSOLVE insoluble fibrin within the clot
  • administered for disorders in which an intravascular clot has ALREADY formed (acute MI, pulmonary embolism, acute ischemic CVA, DVT)
  • restore blood flow to tissue served by blocked vessel
34
Q

when do you get the best results with thrombolytics?

A
  • “window of opportunity”- when you give med to patient when they are first experiencing symptoms of MI…go to ER within 6 hours of having symptoms of MI for best results.
  • window of opportunity for strokes is shorter (3 hours)
35
Q

drug interactions for thrombolytics (and antidote)

A

-any anticoagulant or antiplatelet

antidote= aminocaproic acid

36
Q

adverse effects of thrombolytics

A
  • hemorrhage
  • anemia
  • hypersensiticity (esp with streptokinase)
37
Q

nursing implications/teaching for thrombolytics

A
  • thorough history is a must
  • given only IV
  • monitor for anaphylactic reactions
  • watch for bleeding from all portals
  • have antidote ready
38
Q

thrombolytic drug therapy

A
  • start IV lines, arterial line, or Foley catheter prior to beginning therapy (anything involving sticking with needle)
  • monitor vital signs frequently
  • prevent injury
  • assess neurovascular and cardiovascular status frequently
  • monitor lab values

Pharmacology (10 decks)

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