Coagulation Flashcards
Name the steps for hemostasis.
Adhesion
Activation
Aggregation
Fibronylisis
1/2 of our plts are stored in the spleen? T/F
F. 1/3
Primary hemostasis is when?
plug forms (AAA) 3 steps
Secondary hemostasis is when?
reinforce or stabilize the clot (enzyme clotting cascade)
Vasopressin/ DDAVP increases vWF.
DDAVP
What replaces vWF
DDAVP, cryo, FFP, and factor 13 concentrate (Humate)
Once plt is activated what does it release?
TXA and ADP
What is the cascade with ADP?
phospholipase turns phospholipid –> Arachidonic Acid then Cyclooxygenase (COX) coverts AA–>Prostaglandins & Thromboxane A2
What makes plt adhesion start?
inj and the attachment of vWF to college and plt receptor.
Describe the stage of plt adhesion.
Once vWf attaches to plt, it changes shape (activate) and release TXA and ADP. This a + feedback loop that increases plt activation.
Describe the stage of plt aggregation.
Fibrinogen then attaches its self to 2 differet ptl receptor GpIIb/IIIa= now 2 plts linked together.
Where is plasminogen synthesized?
- Is plasminogen active or inactive? if not active what activates it?
- Plasminogen turns into____ which breaks down clots.
- Liver
- inactive; activated by tPA and uorokinase
- plasmin
vWF is Factor 8. T/F
F. vWF is not a factor it does attach to this receptor.
vWF dz Type I; tx
- Type II
- Type II
- I: mild reduction (most common): DDAVP~0.3mcg/kg – stimulates release
- II: what is produced is not effective: DO NOT GIVE DDAVP it can result in thrombocytopenia
- III: Severe reduction: give Humate-P (vWF concentrate)` 50-80u/kg FFP or cryo
Tell me how they work in general..build up or breakdown clot
- anitcoagulants:
- antiplatelets
- thombolytics aka fibrinolytic or plasminogen activators
- Anti-fribrinolytic
- block clotting factors from the coscade
- inhibit platelet aggregation
- breakdown existing clots
- prevent clot breakdown
Name anticuagulants:
What factors do they inhibit?
Xa: xaban drugs
IIa: Troban and rudin
Xa and IIa: parin
Heparin is an acid/base with a positive/negative charge high/low molecular weight and lipd/water soluble. It also enhances____ activity. It blocks the extrinsic/intrinsic pathway along with the common pathways so this includes factors_____. You stop it ___hr/days/wks b4 sx if needed. Lab to check is PT/PTT with goal of ____. If pt unresponsive to heparin then pt can be treated w/____ and given cryo/FFP/AT 3 concentrate.
acid; negative; high; water; AT 3; intrinsic- 12, 11, 9, 10, 2, 1 ; 4-6h; PTT, 1.5-2.5x; warfarin; FFP and AT 3 concentrate
HIT appears ____ (time) after admin but shows severe SE in ____ (time) after admin. A way to know that the pt has HIT is by checking that_____ are less than ____.
hours/ 4-5 d; plts <50% or 100K
Protamine is an acid/base wi/ a neg/pos charge that over powers/neutralizes heparin. It does/not work with LMWH. SE of protamine. Can cause allergy if pt has?
base; pos; neutralizes; not (all the way). SE: pulmonary HTN -> RVH, hypotN, rebound heparinazation due to lower duration of action 20m vs 1h(heparin). Fish allergy already uses protamine products (NPH).
LMWH is 1/3 or 1/2 size of heparin. You hold it ___(time) b4 surgery.
1/3; 12h
Fandaparinux blocks what factors? This drug has no metabolism. T/F. It is eliminated by the lungs. T/F
Xa only. T; F (kidneys)
Warfarin works by? It’s onset is fast. T/F. If INR is ____, then tx it w/__ and if emergent ___. M, E. DOA
Blocking vit k (VKR1). F, it takes days to become active(8-10h). 5, no tx needed. 5, Vit K ( phyntonadione 4-8h); FFP, factor 7a or PCC. M: liver E: urine, bile. DOA 3-7d after d/c.
Prothrombin complex concentrate (PCC) is made of : PCC 3 vs PCC 4 . What is special about PCC. What is a risk w/ its use?
2,9, 10 vs 2, 7, 9, 10. No T &C needed and can dec INR ~ 30 min. ^ R for thrombosis.
Clopidrogrel and Ticagrelor are both ____ that block ___ and are reversible/irreversible. Clopidrogrel is prodrug/not ticagrelor is prodrug/not. These agents should be stopped ___ (time) b4 sx.
Thienopyridines-antiplatelets; ADP (aggregation): irreversible; prodrug; not prodrug. 7d
