Coag Final Exam Study Guide

Platelets sticking to a surface

Adhesion

VWD and Bernard-Soulier are characterized as platelet ____ disorders

adhesion

Platelets sticking to each other

aggregation

Breakdown of clot

Fibrinolysis

Keeps the surface of endothelial cells slick and promotes vasodilation

prostacyclin and nitric oxide

First recognizable precursor to platelets using light microscopy

megakaryoblast

Compound is released by active platelets and serves as a potent stimulator of platelet aggregation

thromboxane A2

Nuclear doubling without cytoplasmic divisions

endomitosis

Outer region of platelet that contains the glycolax

peripheral zone

Region of platelet that contains actin and myosin which helps platelet maintain or change shape

sol-gel/structural zone

Metabolic region of the platelet that contains dense and alpha granules

organelle zone

Components required for platelet adhesion

VWF and GPIb/IX

Individuals with Bernard-Soulier Disease have a deficiency of ______

GPIb/IX

Inhibited by aspirin, therefore preventing platelet aggregation

cyclooxygenase

Methodology used by most analyzers for counting cells; measures change in electrical currents as platelets pass through an aperture

electrical impedance

Term for presence of platelets gathered around the neutrophils causing a false decrease in platelet count

platelet satellitism/satellitosis

Factor in highest concentration in plasma

Fibrinogen/ Factor I

Common name for factor 2 (II)

prothrombin

Labile Factors

V and VIII (5 and 8)

Factor in extrinsic pathway

VII (7)

Cofactor for factor 10 (X)

5 (V)

Cofactor for 9 (IX)

8 (VIII)

What factor is deficient in Hemophilia A?

Factor VIII (8)

What factor is deficient in Hemophilia B?

Factor XI (9)

What factor is deficient in Hemophilia C?

Factor XI (11)

What group contains factors 2 (II), 7 (VII), 9 (IX), and 10 (X)?

prothrombin group

This group contains factors 12 (XII), 11 (XI), PK, and HMWK

contact group

The vitamin K-dependent factors are

2,7,9,10, Protein C & S

In the presence of _______________a_____________, antithrombin inhibits ______________b______________

a. heparin or heparin-like molecules like heparin sulfate proteoglycans

b. 12,11,10,9,7, thrombin and plasmin

Anti-hemophilic factor

Factor 8

An inactive enzyme

zymogen

Composed of factors 10a, 5a, phospholipid, and Ca

prothrombinase complex

Composed of factors 8a, 9a, phospholipid, and Ca

intrinsic tenase

Acts as both a procoagulant and anticoagulant

thrombin

Serine protease that breaks down fibrin and/or fibrinogen

plasmin

Primary inhibitor of TPA (tissue plasminogen activator)

plasminogen activator inhibitor (PAI)

Major inhibitory mechanism, that acts as an inhibitor of factors 5 and 8

activated protein C

Biochemical inhibitor that neutralizes all serine proteases, thrombin, and plasmin

antithrombin (AT-III)

Lab test that screens for deficiencies in extrinsic and common pathways

PT

Lab test that screens for deficiencies in intrinsic and common pathways

PTT

Used to monitor patients on Coumadin therapy

INR (value calculated from PT result)

Lab test that measures the conversion of fibrinogen to fibrin; used to monitor heparin contamination

thrombin time (TT)

Lab test that is specific for fibrinolysis

D-dimer

Primary way to differentiate DIC from primary fibrinogenolysis

D-dimer

Small, pinhead size spots seen in patients with quantitative platelet disorders

petechiae

Most common form of thrombocytopenia caused by platelet autoantibodies; often in children following a viral infection

Idiopathic Thrombocytopenic Purpura (ITP)

Immune mediated destruction of platelets, in which antibody binds to a heparin-platelet complex

Heparin Induced Thrombocytopenia (HIT)

Disease characterized by decreased platelet count, fever, renal dysfunction, bleeding and bruising

Hemolytic Uremic Syndrome (HUS)

Disease characterized by decreased platelet count, fever, neurological symptoms, bleeding, and bruising

Thrombotic Thrombocytopenic Purpura (TTP)

Disease which the body produces too many platelets, which leads to increased risk of thrombosis

Essential Thrombocythemia

Removal of which organ is sometimes useful in treating chronic thrombocytopenia?

spleen

This treatment enhances the neutralization of thrombin and Factor Xa

heparin

Vigorous exercise or a splenectomy can cause this disorder

reactive thrombocytosis

Characterized by decreased platelet count, prolonged bleeding time, no platelet aggregation with ristocetin, and macroplatelets

Bernard Soulier Disease

Characterized by prolonged bleeding time, no platelet aggregation with ristocetin, and a prolonged PTT

von Willebrand Disease

Individuals with ________ have a deficiency of GPIIb/IIIa

Glanzmann Thrombasthenia

Deficiency of alpha granules

gray platelet syndrome

As aspirin ingestion, platelet aggregation will only be normal with

ristocetin

Hereditary disorder which an individual has a resistance to activated protein C

Factor V Leiden

Injection with _______ reverses the effects of Coumadin

Vitamin K

What conditions are associated with excessive bleeding and hemarthrosis?

hemophilias

A patient with an acquired circulating inhibitor of factor 8 would have the same symptoms as a patient with

Hemophilia A

Mechanism of action of Coumadin/warfarin

inhibit the activity of Vitamin K to prevent the carboxylation of the Vitamin K dependent factors (2,7,9,10), making them non-functional and unable to participate in the secondary cascade

Factor deficiency in which abnormal bleeding will occur following trauma or surgery, but cannot be detected by common coagulation tests

Factor XIII deficiency

Inhibitor that causes very prolonged APTT in the lab, but may lead to thrombosis in the body

Lupus-like anticoagulant

Mixing studies are performed to distinguish _a_ from _b_

a. factor deficiency

b. factor inhibitor

Increased tendency for development of a thrombus

thrombophilia

Anticoagulant that enhances the activity of AT

heparin

The ACT (activated clotting time) or APTT are the best ways to monitor which anticoagulant therapy

heparin

Most common oral anticoagulant ____a____; this therapy is detected in which pathway(s)?

a. Coumadin (warfarin)

b. Intrinsic and Extrinsic

Explanation for why a patient starting Coumadin initially needs a co-administration of heparin

Because Coumadin renders all Vitamin K dependent factors non-functional, including Protein C & S, which play an anticoagulant role. Impairment of these proteins impacts the body’s natural anticoagulant mechanisms, so patients starting Coumadin are initially hypercoagulable. Coadministration prevents this until Coumadin can sufficiently make 2,7,9,19 non/less functional

Thrombolytic therapy that induces plasmin lysis of fibrin within a clot _______a________. A complication of this type of therapy is ______b_____

a. tissue plasminogen activator (tPA), streptokinase, urokinase

b. bleeding

What components are required for the proper formation of a stabilized clot?

All coagulation factors, including Factor 13, as well as calcium and a phospholipid surface (which primarily comes from the platelet surface)

Explain why people with inherited defects of coagulation (clotting or bleeding) may never display any symptoms.

Because there are a vast number of heritable genetic mutations that can affect coagulation, including mutations that may only slightly affect the quantity or functionality (quality) of a factor, people with only “mild” mutations, may not ever show any symptoms or may only be symptomatic after a hemostatic challenge like a surgery or a long plane ride. Only 40% of normal factor levels needs to be present for hemostasis to occur normally.