Coagulation

Question 1

Name the steps for hemostasis.

Answer 1

Adhesion
Activation
Aggregation
Fibronylisis

Question 2

1/2 of our plts are stored in the spleen? T/F

Answer 2

F. 1/3

Question 3

Primary hemostasis is when?

Answer 3

plug forms (AAA) 3 steps

Question 4

Secondary hemostasis is when?

Answer 4

reinforce or stabilize the clot (enzyme clotting cascade)

Question 5

Vasopressin/ DDAVP increases vWF.

Answer 5

DDAVP

Question 6

What replaces vWF

Answer 6

DDAVP, cryo, FFP, and factor 13 concentrate (Humate)

Question 7

Once plt is activated what does it release?

Answer 7

TXA and ADP

Question 8

What is the cascade with ADP?

Answer 8

phospholipase turns phospholipid –> Arachidonic Acid then Cyclooxygenase (COX) coverts AA–>Prostaglandins & Thromboxane A2

Question 9

What makes plt adhesion start?

Answer 9

inj and the attachment of vWF to college and plt receptor.

Question 10

Describe the stage of plt adhesion.

Answer 10

Once vWf attaches to plt, it changes shape (activate) and release TXA and ADP. This a + feedback loop that increases plt activation.

Question 11

Describe the stage of plt aggregation.

Answer 11

Fibrinogen then attaches its self to 2 differet ptl receptor GpIIb/IIIa= now 2 plts linked together.

Question 12

Where is plasminogen synthesized?

• Is plasminogen active or inactive? if not active what activates it?
• Plasminogen turns into____ which breaks down clots.

Answer 12

• Liver
• inactive; activated by tPA and uorokinase
• plasmin

Question 13

vWF is Factor 8. T/F

Answer 13

F. vWF is not a factor it does attach to this receptor.

Question 14

vWF dz Type I; tx

• Type II
• Type II

Answer 14

• 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

Question 15

Tell me how they work in general..build up or breakdown clot

• anitcoagulants:
• antiplatelets
• thombolytics aka fibrinolytic or plasminogen activators
• Anti-fribrinolytic

Answer 15

• block clotting factors from the coscade
• inhibit platelet aggregation
• breakdown existing clots
• prevent clot breakdown

Question 16

Name anticuagulants:

What factors do they inhibit?

Answer 16

Xa: xaban drugs
IIa: Troban and rudin
Xa and IIa: parin

Question 17

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.

Answer 17

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

Question 18

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 ____.

Answer 18

hours/ 4-5 d; plts <50% or 100K

Question 19

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?

Answer 19

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).

Question 20

LMWH is 1/3 or 1/2 size of heparin. You hold it ___(time) b4 surgery.

Answer 20

1/3; 12h

Question 21

Fandaparinux blocks what factors? This drug has no metabolism. T/F. It is eliminated by the lungs. T/F

Answer 21

Xa only. T; F (kidneys)

Question 22

Warfarin works by? It’s onset is fast. T/F. If INR is ____, then tx it w/__ and if emergent ___. M, E. DOA

Answer 22

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.

Question 23

Prothrombin complex concentrate (PCC) is made of : PCC 3 vs PCC 4 . What is special about PCC. What is a risk w/ its use?

Answer 23

2,9, 10 vs 2, 7, 9, 10. No T &C needed and can dec INR ~ 30 min. ^ R for thrombosis.

Question 24

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.

Answer 24

Thienopyridines-antiplatelets; ADP (aggregation): irreversible; prodrug; not prodrug. 7d

Question 25

-ximab drugs are _____receptros antagonists that stop plt _____. You stop them ____ before sx.

Answer 25

GpIIb/IIIa; agreggation; 24-72h

Question 26

Name COX inhibitors. Which one is irriversible? You use the irreversible in combo w/ ___rx class. The irreversible rx stops the formation of ___ and the reversible one____.

Answer 26

ASA and NSAID. ASA (affects plts for 7-10d). Thienopyridiens. TXA; TXA and ADP ( stops AA from binding to COX)

Question 27

Name fibrinolytics vs antifibrinolytics.
What is dose given of TXA?
What are contraindication for TXA use?

Answer 27

Fibrin: streptokinase, urokinase, tPA

• antifibrin: TXA, AA (amicar), Aprotinin
• 1g b4 insicion; recent DVT,PE <12m, cardiac stent or stroke, thrombophilia