Coagulation Flashcards
What are BVs made of
epithelial cells
First step after BV is injured
Platelets circulate in the body and go to fill the injury
Fibrin
strands that join together at the injury and seal the plug
Fibrinogen
covers the active part of fibrin until converted at the site of injury so the fibrin does not clot in the blood
What causes fibrinogen to turn into fibrin
proteins in the blood—thrombin
thrombin
active form that helps convert fibrinogen into fibrin; helps make plasmin from plasminogen; breaks up fibrin to prevent constant clotting
tissue factor
Joins with VII to make factor X
prothrombin
inactive form of thrombin
How is the extrinsic pathway activated?
by initial BV insult
intrinsic pathway
workhorse that gets most of the cascade done
What is blood?
mostly plasma–water, also proteins and solutes
plasma proteins
most is albumin and globulins, clotting factors, electrolytes
albumin
control water/solutes in BVs vs cellular space
globulins
HDLs, prothrombin, hormone-transporting proteins
Most plentiful clotting facto
fibrinogen
Where are most clotting factors made?
liver
Natural killer cells
WBCs, defense against tumors and viruses
Serum
plasma w/o clotting factors
Primary activator of cascade
Platelets
Platelet function
hemostasis, coag, release clotting factors; normally circulate as smooth platelets–inactive until find damage
Platelets
not true cells–contain cytoplasmic fragments that can release adhesive pros, coag, and growth factors when they sense a vessel injury
Thrombocytopenia
low platelets–under 100k; high risk for bleeds
Where are extra platelets stored?
spleen
Steps of activation of clotting system
inc platelet adhesion at site of injury (active dendritic platelets), platelet degranulation (active platelets release prothrombotic molecules like ADP, ADP binds and induces agg as platelet-vasc wall and platelet-platelet adherence inc, activation of clotting system
Thromboxone
helps recruit platelets to the site
blood clot
meshwork of fibrin strands and platelets; plug damage and stop bleeding–hemostasis
hemostasis
stopped bleeding
Which pathway is thrombin more active in?
Intrinsic
Target of clot medication
thrombin
How does body know to stop the clot?
anti-thrombin 3 is a circulating thrombin inhibitor, tissue factor pathway inhibitor inhibits factor Xa after body is clotted
fibrinolysis
natural removal of clot; b/d of fibrin; tissue plasminogen activator turns plasminogen into plasmin which b/d fibrin and releases the caught blood cells, breaking the mesh up into fibrin degradation products
u-PA
Also tells plasminogen to activate plasmin and break up fibrin
Clot risk factors
DVT, immobility, afib, heart attack, heart failure, stroke history
coag goals
prevent clot formation, break apart existing clot, help inc circ and perfusion, dec pain, prevent further tissue damage
heparins and coags biggest concern and NC
bleeding–ext or int; monitor Hgb and HCT, need to know where your pt is at risk of bleeding from and why they are on an anti-coag, VS change
sx of bleeding
tachy (first sign), dec BP, resp chx, bruising; bright blood after surgery
antithrombotics
prevent clot/thrombus
anticoags
prevent action of clotting factors and prevent clots
antiplatelets
prevent platelet plugs from forming by dec platelet agg; best for preventing heart attack and stroke
Heparin MOA
prevent clots by activating anti-thrombin which indirectly inactivates thrombin and factor Xa (and more clotting factors); inhibits fibrin formation
enoxaparin (low molecular weight heparin)
prevents clots by inactivating factor Xa; takes large Hep mol and cleaves them into smaller mol that adhere to Xa and become more bioavailable with larger half life
Giving Heparin
only IV or SQ; parenteral only; in 5000 unit injection 2-3x/day or as IV drip with bolus; wt based in kg ONLY
Heparin indications
acts very fast and effectively so for condx that need prompt activity (evolving stroke, big DVT, heart attack, adjunct for dialysis); low dose SQ injection for prophylaxis against post-op DVT, DIC
Protamine sulfate
Heparin and enoxaparin antidote that binds with Heparin and immediately stops it; give IV SLOWLY to avoid BP drop
Heparin is HIGH RISK
check with other RN before giving, rate change or bolus; check labs first
SE of Heparin
bleeding, hematoma, anemia, thrombocytopenia
Bleeding sx
VS, bruising, petechiae (red dots on skin), hematomas, black tarry stool
Heparin induced thrombocytopenia
sim to allergix rxn; low platelet count and inc dev of thrombi caused by antibody dev
What to do if suspect HIT
monitor platelet count, STOP platelet immediately if count gets below 100k, switch to non-hep anticoag
What is IV heparin dose based on?
Clotting times–anti-Xa or aPTT; drawn q6h, change rate based on response
How to draw Hep labs
pause for several minutes and flush with saline before drawing blood
Therapeutic dose for Heparin
When labs show that you don’t need a bolus 2x in a row–found therapeutic dose and only need to draw labs in the morning prob
Enoxaparin indications
prophylaxis and tx
Enoxaparin NC
can be given at home–pre-dosed; only SQ; DON’T give with heparin or other anticoagulants except oral warfarin when treating PE or DVT; do not expel the air bubble: will remain in plunger to ensure whole dose is given; slower onset of action compared to heparin but LONGER half-life; rotate injection sites
Enoxaparin SE
bleeding, thrombocytopenia, HIT
Black box for enoxaparin
potential spinal hematoma if patient has epidural catheter
Warfarin (coumadin) MOA
Vitamin-K inhibitor; prevents the synthesis of four coagulation factors (VII, IX, X, prothrombin)
Warfarin indications
prevention VTE/DVT/PE, thrombotic events for patients with afib or heart valves, reduce recurrence of TIA or MI
Warfarin SE
bleeding, lethargy, muscle pain, purple toes
Giving warfarin
ONLY given PO, once a day, usually at 5PM; Onset not until 24 hours! Duration 2-5 days
Warfarin antidote
Vit K (IV); if doesn’t work–fresh frozen plasma (FFP) or whole blood
Warfarin NC
NOT for preg or breastfeeding bc DVT risk; Monitor & TEACH for signs of bleeding, HOLD before surgeries, monitor prothrombin time/INR; monitor INR monthly when reach therapeutic; many drug intx; food intx, avoid alc; Wear medic alert bracelet, use soft bristle toothbrush, no electric toothbrush
INR with warfarin
international normalized ratio; normally 1ish, with warfarin we want 2-3.5
Warfarin food intx
avoid foods high in vit K–green leafy veg like lettuce, kale, cucumber, kiwi, cabbage, etc
Apixaban (Eliquis) and Rivaroxaban (Xarelto) MOA
direct inhibitor of factor Xa
Apixaban (Eliquis) and Rivaroxaban (Xarelto) indications
prevent strokes in patients with afib, post-op thrombo-prophylaxis, treat DVT & PE
Apixaban (Eliquis) and Rivaroxaban (Xarelto) SE
bleeding, hematoma, dizziness, rash, gastrointestinal distress, peripheral edema
Black box warnings for Apixaban and rivaroxaban
spinal hematomas if pt has epidural catheter, risk of thrombosis if drugs stop abruptly
apixaban and rivaroxaban NC
Drug intx, don’t give with other coags, watch liver fxn, don’t stop taking abruptly
apixaban and rivaroxaban inc effect of
CYP3A4 inhibitors (amiodarone, erythromycin, ketonazole, HIV meds, diltiazem, verapamil, grapefruit juice)
apixaban and rivaroxaban dec effect of
Decreased effects: phenytoin, carbamazepine, rifampin, and st. johns wort
apixaban and rivaroxaban antidote
andexxa (recombinant factor Xa, inactivated zhzo)
aspirin (as anti-platelet)
Blocks prostaglandin synthesis through the COX
enzyme pathways; also BLOCKS PLATELET AGGREGATION; prevent platelet clumping
aspirin indx
prevent/treat MI, prevent ischemic stroke
How can you take aspirin?
given PO; can chew baby aspirin for acute event if not EC
aspirin SE
GI N/V, drowsy, confused, bleeding
aspirin NC
Reye’s sx, OTC but prescribed by dr for platelet fxn, don’t crush EC
aspirin CI
thrombocytopenia, active bleeding, blood cancers, traumatic injuries, GI ulcers, vitamin K deficiency, recent hemorrhagic stroke
DDAVP (desmopressin)
Antiplatelets antiode—clop, tica, aspirin
clopidogrel (Plavix) and Ticagrelor (Brilinta) MOA
Antiplatelet ADP inhibitor; alters the platelet membrane so it doesn’t receive the signal to
aggregate
Clopidogrel and ticagrelor indx
dec risk of stroke, prophylaxis of TIAs, post-MI
Clopidogrel and ticagrelor CI
thrombocytopenia, active bleeding, blood
cancers, traumatic injuries, GI ulcers, vitamin K deficiency,
recent hemorrhagic stroke
Clopidogrel and ticagrelor SE
chest pain, edema, flu-like symptoms, abdominal pain, diarrhea, nausea, epistaxis, rash, pruritus
Clopidogrel black box warning
patients with certain genetic abnormalities, who may have higher rate of CV events due to reduced conversion to its active metabolite
epistaxis
nose bleed
What dec clopidogrel’s effectiveness?
amiodoarone, calcium channel blocker, NSAIDs, PPIs
Ticagelor black box warning
inc bleeding risk with aspirin dose over 100mg
Ticagelor antidote
DDAVP or platelet transfusion
Argatroban/bivalrudin class MOA and indications
Thrombin (factor IIa) inhibitors; treat HIT, for pt undergoing PCI procedures and at high risk for HIT
Thrombin inhibitors SE and NC
SE—bleeding; IV only, nursing implications—labs (anti-Xa, H&H, platelets), Argatroban—careful in pt with hepatic dysfunction
