hemostasis drugs Flashcards

(44 cards)

1
Q

what is hemostasis

A

process that halts bleeding after injury to a blood vessel
- formation of platelet plug
- production of fibrin
(clotting cascade with many plasma proteins)

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2
Q

hemostasis modifier agents

A
  1. anticoagulants
    - inhibit the action of clotting factors
    - prevent clot formation
  2. antiplatelet drugs
    - inhibit platelet aggregation
    - prevent platelet plugs
  3. thrombolytic drugs
    - break down existing clots
  4. hemostatic agents
    - promote blood coagulation
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3
Q

coagulation pathway simplified

A
  • ends with fibrin (p.p. chain activated)
  • amplification down the chain
  • thrombin changes fibrinogen into fibrin
  • factor 10 activates thrombin
  • intrinsic and extrinsic pathway (converge at common point)
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4
Q

anticoagulants “blood thinners”

A

used prophylactically to prevent:
- clot formation (thrombus)
- embolus

does not break existing clot just stops one from getting bigger

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5
Q

anticoagulants indications

A

prevent clot formation:
- MI (block in cardiac artery)
- unstable angina (clot/block)
- a fib (SVD which increases risk of clot bc slower moving blood)
- DVT
- indwelling devices (mechanical heart valves)
- pulmonary embolism

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6
Q

types of anticoagulants

A
  • heparin
  • low molecular weight heparins (LMWH)
  • warfarin (PO)
  • direct acting oral anticoagulants (DOAC - factor X and thrombin)
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7
Q

anticoagulants contraindications

A
  • known drug allergy
  • acute bleeding process
  • thrombocytopenia (decreased platelets in circulation)
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8
Q

anticoagulants adverse effects

A

bleeding risk:
- gum bleed
- nosebleeds
- unusual bleeding
- anemia/low Hct
- tarry stools (GI bleeding, ulcers)

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9
Q

heparin

A

indirectly inhibits activity of multiple proteins on cascade
- thrombin
- factor Xa
- other factors in intrinsic pathway

from natural pathway

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10
Q

why is heparin dosage unpredictable

A

all molecules are a different lengths and size
- want to inhibit coagulations to the right degree

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11
Q

how is heparin dosage monitored

A

monitored by activated partial thromboplastin times (aPTT)
- measures the intrinsic pathway
- aPTTs need to be 1.5-2.5 x greater than control (40sec)
- blood test to measure how long it takes for coagulation

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12
Q

heparin characteristics

A
  • given parenteral (SC or IV)
  • effective within minutes
  • short half life (1-2 minutes)
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13
Q

heparin adverse effects

A

heparin induced thrombocytopenia (HIT)
- binds to platelets and brings antibodies around it which may activate and bring platelets together
- leading to lower amount of circulating platelets

hypersensitivity reactions
- fever, chills, urticaria

anticoagulant effects reversed by protamine sulfate (antidote)

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14
Q

LMWHs

A

low molecular weight heparins
- enoxaparin
- tinzaparin
- dalteparin

predictable anticoagulant response
- do not require frequent lab monitoring (given at home, SC every 12 hrs)

less thrombocytopenia then heparin (protamine sulphate antidote)

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15
Q

which plasma protein does lmwh inhibit

A

factor X

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16
Q

other anticoagulants

A

danaparoid
- alternative to heparin
- SC or IV

fondaparinux
- synthetic
- SC or IV

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17
Q

client implications: heparin

A
  • double check dose with another nurse
  • give SC in areas with more fat (abdomen)
  • rotate injection site
  • protamine sulphate antidote
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18
Q

client implications: LMWH

A
  • SC in abdomen
  • rotate sites below umbilicus
  • protamine sulphate antidote
19
Q

oral anticoagulants: warfarin

A
  • vitamin K antagonist
  • vit K makes clotting factors ready for action: VII, IX, X, pro-thrombin (liver)
  • warfarin doesn’t effect proteins already in plasma just the cells being made in the liver
  • effects depends on clotting factors turnover (protein degradation)
  • max effect may take 3-5 days (starts within 24 hours)
  • patients may be started on 5 days LMWH + warfarin (then LMWH withdrawn)
20
Q

warfarin continued

A
  • orally only
  • dosage variable between individuals
  • monitored by clotting lab test
    - prothrombin time (PT - coagulation time)
    - INR (international normalization reference ratio - desired goal to be in range)
  • PT/INR (measure activity of extrinsic pathway)
21
Q

PT/INR values

A

PT therapeutic level is 1.3-1.5 times the control level

target INR range 2-3x control (2.5-3.5 if mechanical heart valves)

22
Q

what does excessive dietary vitamin k do to warfarin effectiveness

A

warfarin less effective bc more vitamin k to help clotting factors

23
Q

what happens to warfarin effectiveness when too little vitamin k

A

dosage becomes too high (INR levels too high)

24
Q

what happens if there is warfarin excess

A

give an antidote (vitamin k)
- IV slow infusion: 4-8 hour effect
- PO: within 24 h

25
warfarin contraindications
pregnancy - risk of fetal bleeding, teratogenicity, spontaneous abortion - can cross BBB
26
client education anticoagulants
- maintain intake of vitamin k constant (tomatoes, dark leafy green vegetables) - wear medical alert bracelt - consult physician before taking other drugs or OTC products (many drug-drug interactions bc its metabolized by CYP enzymes)
27
client education: warfarin
- may be started while client still on heparins (until PT/INR indicate adequate coagulation) - full therapeutic effect takes several days - monitor PT/INR regularly
28
Direct-Acting Oral Anticoagulants (DOACs) advantages
- rapid onset and offset - fixed doses - no blood test - few drug-drug interactions - no dietary concerns - lower risk of bleeds
29
DOACs: direct thrombin inhibitor
Dabigatran - po administration (with LMWH for DVT) - GI disturbance (N&V, pain, bloating)
30
DOACs: direct factor Xa inhibitors
rivaroxaban - apixaban - betrixaban - edoxaban PO administration
31
anticoagulant adverse effectse
increased bleeding (mild to life threatening)
32
all anticoagulants: client education
- importance of regular lab testing where necessary) - signs of abnormal bleeding (gums, nosebleeds, bruising, heavier menstrual bleeding, in vomit/stools/urine/sputum, abdominal pain)
33
antiplatelet agents
taken prophylactically - stop agents that activate platelets (ADP, TXA2) - prevent platelet action
34
acetylsalicylic acid (antiplatelet)
inhibit COX pathway (for thromboxane A2) - irreversible inhibition of COX in platelets risk for stomach problems and ulcers used for heart attack, MI, stroke, cardiac arteries blocked pentoxifylline
35
clopidogrel (prasugrel, ticlopidine)
- irreversible ADP receptor blocker (antagonist) - effect lasts lifetime of platelet
36
ticagrelor
reversible ADP receptor blocker (antagonist)
37
antiplatelet drugs indications
antithrombotic effects - reduce MI risk - reduce stroke risk
38
aspirin + clopidogrel combination
produces additive antiplatelet activity - increased bleeding potential
39
thrombolytic agents
drugs that break down preformed clots - recombinant tissue plasminogen activator (tPA) - activate plasminogen to become plasmin which eats away existing clots
40
thrombolytic agents examples
- alteplase - tenecteplase - reteplase
41
thrombolytic agents: mechanism of action
activate fibrinolytic system to break down clot in blood vessel (plasminogen --> plasmin) re-establish blood flow to - heart muscle (MI) - brain (stroke)
42
thrombolytic agents: indications
- acute MI - arterial thrombolysis - DVT - occlusions of shunts or catheters - pulmonary embolus
43
thrombolytic agents contraindications
- allergy - concurrent use of other anticoagulation
44
thrombolytic agents adverse effects
bleeding - internal - intracranial - superficial other effects: N&V, hypotension, anaphylactoid reactions, dysrhythmias