hemostasis drugs Flashcards
what is hemostasis
process that halts bleeding after injury to a blood vessel
- formation of platelet plug
- production of fibrin
(clotting cascade with many plasma proteins)
hemostasis modifier agents
- anticoagulants
- inhibit the action of clotting factors
- prevent clot formation - antiplatelet drugs
- inhibit platelet aggregation
- prevent platelet plugs - thrombolytic drugs
- break down existing clots - hemostatic agents
- promote blood coagulation
coagulation pathway simplified
- 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)
anticoagulants “blood thinners”
used prophylactically to prevent:
- clot formation (thrombus)
- embolus
does not break existing clot just stops one from getting bigger
anticoagulants indications
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
types of anticoagulants
- heparin
- low molecular weight heparins (LMWH)
- warfarin (PO)
- direct acting oral anticoagulants (DOAC - factor X and thrombin)
anticoagulants contraindications
- known drug allergy
- acute bleeding process
- thrombocytopenia (decreased platelets in circulation)
anticoagulants adverse effects
bleeding risk:
- gum bleed
- nosebleeds
- unusual bleeding
- anemia/low Hct
- tarry stools (GI bleeding, ulcers)
heparin
indirectly inhibits activity of multiple proteins on cascade
- thrombin
- factor Xa
- other factors in intrinsic pathway
from natural pathway
why is heparin dosage unpredictable
all molecules are a different lengths and size
- want to inhibit coagulations to the right degree
how is heparin dosage monitored
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
heparin characteristics
- given parenteral (SC or IV)
- effective within minutes
- short half life (1-2 minutes)
heparin adverse effects
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)
LMWHs
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)
which plasma protein does lmwh inhibit
factor X
other anticoagulants
danaparoid
- alternative to heparin
- SC or IV
fondaparinux
- synthetic
- SC or IV
client implications: heparin
- double check dose with another nurse
- give SC in areas with more fat (abdomen)
- rotate injection site
- protamine sulphate antidote
client implications: LMWH
- SC in abdomen
- rotate sites below umbilicus
- protamine sulphate antidote
oral anticoagulants: warfarin
- 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)
warfarin continued
- 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)
PT/INR values
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)
what does excessive dietary vitamin k do to warfarin effectiveness
warfarin less effective bc more vitamin k to help clotting factors
what happens to warfarin effectiveness when too little vitamin k
dosage becomes too high (INR levels too high)
what happens if there is warfarin excess
give an antidote (vitamin k)
- IV slow infusion: 4-8 hour effect
- PO: within 24 h
warfarin contraindications
pregnancy
- risk of fetal bleeding, teratogenicity, spontaneous abortion
- can cross BBB
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)
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
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
DOACs: direct thrombin inhibitor
Dabigatran
- po administration (with LMWH for DVT)
- GI disturbance (N&V, pain, bloating)
DOACs: direct factor Xa inhibitors
rivaroxaban
- apixaban
- betrixaban
- edoxaban
PO administration
anticoagulant adverse effectse
increased bleeding (mild to life threatening)
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)
antiplatelet agents
taken prophylactically
- stop agents that activate platelets (ADP, TXA2)
- prevent platelet action
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
clopidogrel (prasugrel, ticlopidine)
- irreversible ADP receptor blocker (antagonist)
- effect lasts lifetime of platelet
ticagrelor
reversible ADP receptor blocker (antagonist)
antiplatelet drugs indications
antithrombotic effects
- reduce MI risk
- reduce stroke risk
aspirin + clopidogrel combination
produces additive antiplatelet activity
- increased bleeding potential
thrombolytic agents
drugs that break down preformed clots
- recombinant tissue plasminogen activator (tPA)
- activate plasminogen to become plasmin which eats away existing clots
thrombolytic agents examples
- alteplase
- tenecteplase
- reteplase
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)
thrombolytic agents: indications
- acute MI
- arterial thrombolysis
- DVT
- occlusions of shunts or catheters
- pulmonary embolus
thrombolytic agents contraindications
- allergy
- concurrent use of other anticoagulation
thrombolytic agents adverse effects
bleeding
- internal
- intracranial
- superficial
other effects: N&V, hypotension, anaphylactoid reactions, dysrhythmias
