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Pharm 1 > drug therapy for coagulation disorders > Flashcards

drug therapy for coagulation disorders Flashcards

1
Q

what does hemostasis mean

A

heme = blood
stasis = halt
halt of the blood

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2
Q

describe hemostasis

A

-natural process in body response to injury to tissue
-prevention or stoppage of blood loss from injured vessel (maintain vascular integrity)

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3
Q

what mechanisms are involved in hemostasis

A

-vasoconstriction
-formation of platelet plug
-sequential activation of clotting factors
-reparation of the opening in damaged vessel

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4
Q

describe the process of coagulation

A

plasminogin and fibrin form clot -> stop blood flow -> blood vessel is repaired -> plasmin (fibrinolysin) dissolves clot

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5
Q

whats the difference between intrinsic and extrinsic clotting pathways

A

-intrinsic is activated by trauma inside the vessel
-extrinsic is activated by trauma to the tissue around vessel

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6
Q

describe thrombogenesis

A

-formation and dissolving of thrombi
-normal body defense

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7
Q

describe arterial thrombosis

A

-obstruct arterial blood flow
-damaged arterial endothelium = platelet activation
-causes: atherosclerosis, HTN, turbulent arterial blood flow
-incomplete blockage = defificent blood flow = ischemia
-complete blockage = obstruction = necrosis

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8
Q

describe venous thrombosis

A

-reult of venous stasis
-slow venous blood flow = thrombin and procoagulant substances become concentrated
-“embolus”
-less cohesive than arterial embolus = easily detachable = travel
-classic = DVT
-dangerous r/t pulmonary embolism if detached
-1/2 patients are asymptomatic = double dangerous

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9
Q

what are the s/sx of DVT

A

-pain (particularly in lower extremity)
-errythema
-swollen
-hot

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10
Q

what is done to prevent DVT in bed bound hospital pts

A

-scds/TED
-anticoagulants may be given prophylactically

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11
Q

describe atherosclerosis

what is it and what can happen if untreated

A

-elevated lipid serum levels = lipid filled macrophages = fibrous plaques/lesions = sever ulceration and scar tissue build up in arteries
-consequences and clinical implications depend on location and size of thrombi/emobli
-progressive over time is left untreated
-heart = MI
-brain = TIA/CVA/stroke

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12
Q

what are anticoagulants used for

A

-used in thrombotic disorders (more effective in preventing venous thrombus)
-prevention of new formation or management of thromboembolic disorders
-thrombophlebitis, DVT, pulmonary embolism

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13
Q

whare are antiplatelets used for

A

-used to prevent arterial thrombus
-prevents one or more steps in prothromobtic activity of platelets

plt life = 7-10 days

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14
Q

what are thrombolytics used for

A

-dissolve thrombi and limit tissue damage in thromboembolic disorders
-stimulate conversion of plasminogen to plasmin (enzyme that breaks down fibrin)

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15
Q

do anticoagulants dissolve formed clots?

A

nope

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16
Q

describe dosing of anticoagulants

A

dosings to therapeutic levels is challenging

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17
Q

what is the main adverse effect of anticoagulants

A

bleeding

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18
Q

describe what heparin is used for

A

-does not dissolve existing clot
-anticoagulant
-given to prevent new clot formation and extension of clots present
-prevention and management of thromboembolic disorders (afib, DVT, PE)

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19
Q

describe giving heparin IV

what are you monitoring and how

A

-monitor aPTT/PTT per heparin nanogram protocol
-lab drawn approximately one hour before dosing until therapeutic
-bridge to oral anticoagulation (warfarin)

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20
Q

describe giving heparin SQ

A

-prophylaxis for DVT formation prevention in bed restricted hospital patients (dose: 5000units/ml)
-enoxaparin : low molecular weight heparin (prefilled syringe with airlock)

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21
Q

what is the antidote for heparin

A

protamine sulfate

heparin is an acid and protamine sulfate is a base (neutralizes)

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22
Q

describe warfarin

think about monitoring and dosing

A

-regulated by INR
-based on PT and INR
-lab drawn daily until therapeutic
-once therapeutic, drawn every 2-4 weeks for duration of anticoagulant therapy, unless dose adjusted

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23
Q

what is the antidote for warfarin

A

vitamin K

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24
Q

what is important to include in pt teaching for warfarin

A

-avoid foods high in vitamin K (green leafy vegetables and green tea)
-avoid grapefruit and cranberry juice, as well as alcohol (increases effects of warfarin)

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25
Q

describe fondaparinux

A

-factor Xa inhibitor
-SQ injection only (prefilled syringe)
-prevention of DVT post hip/knee surgery
-super expensive
-can be IV in pts with heparin induced thrombcytopenia
-does not require regular blod test monitoring

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26
Q

describe dabigatran

A

-direct thrombin inhibitor
-tx of afib/stroke prevention
-PO twice daily
-does not require regular blood test monitoring

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27
Q

what is the reversal agent of dabigatran

A

idarucizumab

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28
Q

describe rivaroxaban

A

-factor Xa inhibitors
-tx of afib/stroke prevention/ 2ndary DVT prevention
-PO once a day
-does not require regular blood test monitoring

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29
Q

describe apixaban

A

-facotr Xa inhibitor
-tx of afib/stroke prevention
-PO twice daily
-does not require regular blood test monitoring

30
Q

what is the black box warning for all factor Xa inhibitors

A

-do not stop abruptly
-risk for rebound thrombotic event

31
Q

what should you educate pts on when they are taking anticoagulants

A

-ecchymosis (increased bruising)
-prolongation of bleeding episodes
-dizziness, lightheadedness
-hypotension
-low Hgb/Hct
-bloody/dark urine
-CP/SOB
-hemoptysis (bloody sputum)

32
Q

what are some side effects of all anticoagulants

A

-risk for bleeding
-may experience GI issies (dyspepsia (indigestion), nausea, upper abdominal pain, GI hemmorhage, diarrhea)
-NSAID use discouraged (increased risk for GI ulcers/bleeding)
-many meds/dietary interactions with anticoagulation

33
Q

antiplatelets act by a variety of different mechanisms, what are they?

A

-inhibit platelet activation
-inhibit platelet adhesion
-inhibit platelet aggregation
-inhibit procagulant activity

34
Q

adverse effects of antiplatelets are dependent on…

A

the medication used

35
Q

what are some important things to include with pt teaching on antiplatelets

A

-call platelets can increase risk of bleeding
-following administration instructions is extremely important
-too little = clot
-too much = bleed tf out
-report any signs of bleeding

36
Q

what is clopidogrel and what does it do

A

-ADP receptor antagonist
-antiplatelet
-irreversibly inhibits ADP receptor on the surface of platelets (no antidote)
-taken once daily, without regard for food

37
Q

what is the antidote for clopidogrel

A

there is no antidote silly goose

38
Q

describe the onset of action of clopidogrel

A

-extensive first pass effect
-onset of action is slow so loading dose is required

39
Q

can clopidogrel be use in conjuntion with ASA?

A

yep

40
Q

does everyone respond to clopidogrel the same?

A

nope, there is significant variability in response

41
Q

what are the most common side effects of clopidogrel

A

-pruritus (itching)
-rash
-purpura
-diarrhea

42
Q

who shouldnt take clopidogrel

A

pts with bleeding or peptic ulcer disease

43
Q

name a thromboxane A2 inhibitor

A

aspirin

44
Q

what does aspirin do

A

inhibits synthesis of prostaglandins = prevents formation of thomboxane A2 = prevents platelet aggregation and thrombus formation

45
Q

what dose is used for aspirin when being used for antiplatelt effects and what conditions is it used for

A

-81-325mg
-long term prevention of MI, CVA, and for pts with prosthetic heart valves
-hx of stents that require antiplatelet need
-also given for suspicion of active MI or TIA

46
Q

what is the antidote for aspirin

A

no antidote silly goose
-irreversible platelet effect
-may need platelet transfusion

47
Q

what are some side effects of aspirin

A

-minimal at low dose
-can have risk for bleeding
-stomach ulcers (take with food)

48
Q

when shoulf caution be taken with aspirin

A

caution with NSAID use and other antiplatelet medications

49
Q

give an example of a glycoprotein IIb/IIIa receptor antagonist

A

abciximab

50
Q

describe what abciximab is and what it does

A

-antiplatelet
-monoclonal antibdies that prevent the binding of fibrinogen
-this action will inhibit platelet aggregation

51
Q

what is abciximab used for

A

used for interventional procedures with ASA and heparin

52
Q

what is a side effect of abciximab

A

insertional site bleeding

apply pressure

53
Q

name a phosphodiesterase -3 enzyme inhibitor

A

cilostazol

54
Q

what does cilostazol do

A

inhibits platelet aggregation and produces vasodilation

55
Q

what is cilostazol used for and when should symptoms improve

A

-used for management of intermittent claudication
-sx should improve with tx in 2-4 weeks (can be up to 12)

56
Q

what is intermittent claudication

A

-pain with activity caused by reduced blood flow to a limb, generally in the legs, relieved with rest
-claudication is a sx of PAD or PVD

57
Q

what does anagrelide do

A

inhibit platelet aggregation induced by cAMP, phosphodiesterase, ADP, and collagen

58
Q

what is anagrelide used for

A

reduce platelet counts r/t essential thrombocythemia (excessive numbers of platelets)

59
Q

what conditions are thrombolytics used to manage

A

-management of acute, severe thromboembolic disease
-MI, PE, thromboembolic stroke (not hemorrhagic), iliofemoral thrombosis

60
Q

what is the goal of using thrombolytics?

A

reestablish blood flow as quickly as possible, prevent/limit tissue damage

61
Q

what is the main adverse effect of thrombolytics

A

bleeding

62
Q

who administers thrombolytics

A

-only experienced personnel in ED/ICU or diagnostic/interventional setting with cardiac monitoring in place
-close monitoring is required

63
Q

what is needed preadministration of thrombolytics

A

baseline laboratories
INR, aPTT, platelet count, fibrinogen

64
Q

describe the decision to ass thrombolytics to medication regime

A

-weigh risk/benefit factors
-avoiding invasive procedures
-omitting anticoagulants or antiplatelets during use

65
Q

what is altepase

A

-thrombolytic
-high risk medication
-recombinant plasminogen activator (rtpa or tpa) : protein that will destroy clots

66
Q

what is altepase used to treat

A

-thrombus dissolution post CVA
-massive PE to resotre pulmonary perfusion

67
Q

describe the pharmacokinetics of altepase

A

-IV administration
-metabolized in liver
-excreted by kidneys
-50%+ of the med is cleared from the body in 10 minutes

68
Q

what are some side effects of altepase

A

-systemic bleeding
-HA
-epitaxis
-hemoptysis
-GI bleed

69
Q

what are some nursing implications r/t altepase

A

-monitor for hypotension r/t increased risk for bleeding
-monitor INR, platelet count, fibrinogen

70
Q

what are some contraindications of altepase

A

-allergy
-intracranial surgery/spinal surgery
-severe hypotension
-active bleeding/coagulation issues/anticoagulation medication
-recent surgery
-stroke aneurysm in last 2 months

Pharm 1 (29 decks)

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