coagulation studies lab med

4 stages of the hemostatic mechanism

vasoconstriction, platelet activation, coagulation cascade, fibrinolysis/clot degradation

cells produced from megakaryocytes that live for 7-10days and whose external membranes contain glycoproteins and granules contain hormones, enzymes, and other chemicals

platelets

first role of platelets in primary hemostasis

adhesion (immediatly adhere to expose collagen and von willebrand factor acts as glue to buind platelets to collagen

2nd role of platelets in primary hemostasis

activation (calcoum makes platelets change shape and stick to each other and release their cytoplasmic granules which mediates aggregation.

how long does aspirin inhibit platelet function

for the whole life of the platelet

if your pt is on apririn what should you tell them before their coag studies are done

they need to be off the aspirin for 48-96hrs before hand so their studies dont get messed up

third role of platelets in primary hematostasis

aggregation (platelet recruiting and attach to other platelets to form a mesh network, platelet-to-platelet cross links stabilized by thrombospondin)

what clotting factors are included in the intrinsic pathway

12, 11, 9, 8

what clotting factors are included in the extrinsic pathway

7

what clotting factors are included in the common pathway

10, 5, 7, prothrombin, thrombin, fibrinogen

defects in hemostasis that can result in abnormal bleeding or clotting

injury to vascular system, inadequate platelets in number or fxn, inadequate clotting pathway mech (not enough clotting factors in cascade), inadequate fibrin clot formation, breakdown and repair

whats the first lab test we do for any blood problems/coagulation studies

CBC

possible causes for thrombocytosis (inc platelets)

myoproliferative disorders, reactive from hemorrhage, malignancy, infection, splenectomy

possible causes for thrombocytopenia (dec platelets)

bone marrow disorders, autoimmune disorders, liver disease

skin redness on pts w bleeding disorders doesnt ___

blanch

skin things you may see in pts w thrombocytopenia

petechiae, purpura, ecchymosis (all non-blanching)

most common cause of poor platelet function

secondary to meds (esp aspirin or clopidogrel)

possibel causes for poor platelet function (which may result in life threatning hemorrhages cause they cant clot)

hereditary, myloproliferative diseases, myelodysplastic disorders, uremia, liver dailure, renal failure, clotting factor deficiency

an automated assay of platelet function that measures time required to build a stable platelet plus and obstain full occlusion (simulated in vitro not tested on body) and reported in seconds

closure time

uses for closure time test

good for theraputic monitoring, not a screening test for bleeding risk, prolonged=bad

measurement of PLT aggregation to various activators in vitro that is recorded by a light transmission aggregometer (will initially look turbid and then clear as platelets aggregate)

platelet aggregation studies

how are platelet aggregation studies recorded

change in transmission of light is recorded as a function of time on a moving strip = looks like a response curve

gold standard in platelet function testing

platelet aggregation studies

the only platelet test that measures platelet function in the body and not in vitro

bleeding time test

a test that measures how long it takes body to stop bleeding by making 2 incisions and recording how long it takes for pt to stop bleeding

bleeding time test

types of coagulation tests

PT, PTT, INR

caogulation test that measures extrinsic and common pathways (factors 2, 5, 7, 10)

prothrombin time (PT)

what increases PT

prolonged in coagulation factor deficiencies

method of choice to monitor warfarin therapy

PT

what is a critical value for International Normalized Ratio (INR)

5+ (want it to be less than 3.5 if theyre on warfarin)

increasing INR=

increased anticoagulation

use for measuring PT

evaluate liver function (bc liver is where coagulation factors are made)

high PT causes

low vit K , liver disease, anti-coag therapy, DIC, hypothermia, massive blood diffusion , meds (erythromycin, allopurinol)

low PT causes

fresh frozen plasma transfusion, vit k supplementation, meds (PCN, doxycycline, rifampin (TB med), aspirin)

coagulation test that measures intrinsic and common pathways (factors 1, 2, 5, 8, 9, 10, 11, 12)

partial thromboplastin time (PTT or APTT)

causes of prolonged/high PTT

coagulation factor deficiency, hereditary, vit k deficiency, liver disease, anti-coagulatoin therapy

causes of shortened/lower PTT

DIC, severe hemorrhage, cancer

critical value for PTT

100+ (indicates bleeding problem, cant clot)

clinical uses of PTT test

eval liver function, monitor heparin therapy, detect factor deficiency, detect lupus anticoagulant, detect specific factor inhibitors, monitor unfractionated heparin therapy, monitor direct thrombin inhibitor

a coagulation test that measures protein concentration (NOT functional activity), usually done when PT/INR and PTT are abnormal or when diagnosing hypo/dysfibrinogenemia/DIC/primary fibronolysis

fibrinogen (factor 1) test

what kind of fibrinogen (factor 1) test is most commonly done

clauss assay is most commpnly performed (modified TT)

critical value for fibrinogen (factor 1) test

under 100

high fibrinogen (factor 1) causes

inflammatory, trauma, cancer, meds (aspirin aka salicylate)

low fibrinogen (factor 1) causes

DIC, liver disease, massive blood transfusion, meds (simvostatin, atenolol, prednisolone)

coag test that measures conversion of fibrinogen to fibrin in the common pathway and is sensitive to circulating anticoagulants (heparin)

thrombin time (TT)

how is a fibrin degradation products test done

serum sample collected in special tubes containing thrombin and a trypsin inhibitor that presents break down of fibrinogen in vitro. serum is added to latex particles coated w anti-fibrinogen antibodies

what do fibrin degradation products cause

visible agglutination

test that detects abnormal clotting in blood (not abnormal bleeding)

D-Dimer assay

how is a D-Dimer assay test done

plasma added to latex particles coated w antibodies specific to D-dimers → causes visible agglutination

negative D-Dimer assay =

clot unlikely (yay)

positive D-Dimer assay =

clot has formed and is breaking down (oh no)

when is a D-Dimer assay test used

when thrombotic event (DVT, PE, etc) suspected or when there are signs of DIC

other things that can falsely raise D-Dimer

preg, heart disease, cancer, recent surgery

which test is best for evaluating a defect in the intrinsic pathway

PTT

first screening tests done when theres bleeding concerns

PT and PTT (if abnormal may be an inhibitor or factor deficiency/abnormality)

what can cause abnormal clot formation

activation of coagulation (surgery/cancer/etc), vascular injury (trauma etc), endothelial cell perturbation (radiation therapy etc), down regulation of coagulation regulatory (inhibitor) systems (APCR, plasmin, etc)

warfarin MOA

inhibits carboxylation of vit K dependent coagulation factors (2, 7, 9, 10)

how do we monitor pts on warfarin

monitor their PT/INR

aim for INR of 2-3 or 3-4 if pt has mechanical prosthetic heart valvues or recurrent systemic embolism

heparin MOA

catalyzes inhibition of thrombin, inhibits factor 10a and 9a, inhibits activation of factor 5 and 7 by thrombin, inhibits activation of platelets

how do we monitor pts on heparin

monitor their PTT (1.5-2.5x pts baseline), can cause heaprin indiced thrombocytopenia if too high

low molecular weight heparin MOA

inactivated factor 10a (but doesnt inactivate thrombin much)

how do we monitor pts on LMWH

monitor by factor 10a inhibition assay