Coagulation And Anti-Coagulation + Drugs

Front 1

Hageman Factor is aka ___ and is the 1st step in which coag pathway?

Back 1

Factor 12, Intrinsic

Front 2

Plasminogen is NATURALLY converted to plasmin via stimuation by which 3 things?

Back 2

Factor 12
t-PA (or urokinase-like PA)
Streptokinase

Front 3

What is the main function of plasmin?

Back 3

Fibrinolysis (thrombolysis)

Front 4

What binds plasmin to restrict excess lysing of thrombi?

Back 4

alpha-2 antiplasmin

Front 5

Which factors require Vitamin K?

Back 5

2, 7, 9, 10 (coag)
Protein C & S (anti-coag)

Front 6

Why is Vitamin K required in coagulation?

Back 6

Facilitates binding of factors 2,7,9,10 & proteins C & S to phospholipid surface of platelets

Front 7

Anti-thrombin III inhibits thrombin and which 4 coag factors?

Back 7

9a,10a,11a,12a

Front 8

Protein C inactivates which factors to cause anti-coagulation?

Back 8

5a and 8a

Front 9

Thrombin function:

Back 9

Converts fibrinogen to fibrin

Front 10

Cross-linked fibrin is created by which 2 things:

Back 10

Fibrin + Factor 13a (& Ca2+)

Front 11

The cofactor for Protein C activation is:

Back 11

Protein S

Front 12

Vitamin K is antagonized by which drug? Which factors does this decrease?

Back 12

Coumadin (Warfarin).
2,7,9,10 & Proteins C & S

Front 13

thromboplastin is aka, which activates factor 7 of which pathway?

Back 13

tissue factor/factor 3
Extrinsic

Front 14

Partial thromboplastin time (PTT) is a measure of the function of the proteins in which pathway?

Back 14

INTRINSIC

Front 15

Prothrombin time (PT) is a measure of the function of the proteins in which pathway?

Back 15

EXTRINSIC

Front 16

Injury to the endothelial membrane exposes what?

Back 16

vWF, von Willebrand Factor

Front 17

vWF binds to platelets via which platelet receptor?

Back 17

glycoprotein Ib (GpIb)

Front 18

After platelets bind to vWF, they bind to fibrinogen via which of their receptors?

Back 18

GpIIb-IIIa complex

Front 19

The two granulation products of platelets that aid platelet aggregation (primary hemostatic plug) are:

Back 19

ADP and thromboxane A2 (TXA2)

Front 20

The secondary hemostatic plug is created by interaction of which 3 components:

Back 20

ADP, TXA2, thrombin (then thrombin converts fibriongen to fibrin to increase stability of clot)

Front 21

How does thrombin contribute directly to the inflammatory process?

Back 21

Conversion of fibrinogen to fibrin generates fibrin split products-->causes adhesion of neutrophils and monocytes

Front 22

How does thrombin contribute to anti-coagulation (fibrinolysis)?

Back 22

Stimulates endothelial cells to release tissue plasminogen activator (t-PA)-->plasmin-->cleaves fibrin-->fibrin split products

Front 23

Elevated fibrin split products may be indicative of diagnosing which 3 abnormal thrombotic states?

Back 23

DIC, DVT, pulmonary thromboembolism

Front 24

Factors 5a and 10a mediate which next step in coagulation?

Back 24

Conversion of prothrombin to thrombin

Front 25

Antithrombin III and HEPARIN bind thrombin to do what?

Back 25

inhibit it-->anti-coagulation

Front 26

Treatment for AML (acute myelogenous leukemia):(2 drugs)

Back 26

Anthracycline
Cytarabine

Front 27

What is the function of Anthracycline and Cytarabine?

Back 27

Treats AML by killing off bone marrow cells (BM aplasia).

Front 28

If you suspect a patient has PML (AML-M3), what histological signs would you see? What would you treat with before cytogenetic tests came back? Once confirmed, what else might you treat with?

Back 28

Auer rods in promyelocytes.
Tx first with ATRA (all-trans retinoic acid) which causes differentiation of promyelocytes. Also can use ARSENIC TRIOXIDE, which causes differentiation AND apoptosis of malig promyelocytes

Front 29

AML with gingival involvement and risk for meningeal involvement:

Back 29

M5, monocytic leukemia

Front 30

Someone recently treated with chemotherapy (cyclophosphamide and doxorubicin) and with a history of refractory cytopenias is at risk for:

Back 30

Secondary AML, which responds poorly to chemo and involves chromosomes 5,7,8

Front 31

Two drugs that treat myelodysplasias by interfering with hypermethylation of DNA

Back 31

5-azacytidine
Decitabine

Front 32

A drug that treats myelodysplasia by decreasing or eliminating abnormal karyotype, especially 5q deletion

Back 32

Lenalidomide

Front 33

Burning & red toes and/or feet (erythromelagia), WAY increased platelets, hypercellular marrow in older pts could be:

Back 33

Thrombocythemia

Front 34

Treatment of choice for pregnant & younger patients with thrombocythemia

Back 34

Interferon

Front 35

Why wouldn't you want to treat a pregnant mother with thrombocythemia with Hydroxyurea?

Back 35

Increases HbF, which is teratogenic to fetus, decreases all blood counts and slightly leukemic

Front 36

AML with abnormal erythrocyte precursors (binucleate and megaloblastic)

Back 36

M6

Front 37

AML associated with megakaryocytes and myelofibrosis due to release of platelet derived growth factor (PDGF)

Back 37

M7

Front 38

RAR-alpha is what? What disease is characterized by its dysfunction?

Back 38

retinoic acid receptor alpha gene; mutated by a translocation t(15;17) in AML-M3

Front 39

Thromboplastic (platelet-making)substances released from hypergranular promyelocytes in AML-M3 leads to what?

Back 39

DIC

Front 40

JAK2 kinase mutations are found in 2/3 of patients with ___ and 50% of patients with ___.

Back 40

Polycythemia vera, Essential thrombocythemia & myeloid metaplasia with myelofibrosis

Front 41

Of the myeloproliferative syndromes, assay of the leukocyte alkaline phosphatase (LAP) activity is __ in CML, but __ in Polycythemia vera, Essential thrombocythemia, and Myelofibrosis w/ myeloid metaplasia

Back 41

decreased in CML
increasead in everything else, including inflammatory disorders

Front 42

The 2 myeloproliferative disorders with hyperuricemia leading to gout are:

Back 42

Polycythemia vera, myelofibrosis w/ myeloid metaplasia

Front 43

On a smear you see: nucleated RBC, granulocyte precursors, teardrop cells, giant platelets and megakaryocyte fragments. What could it be?

Back 43

Myeloid metaplasia w/ myelofibrosis

Front 44

Treatment for myelofibrosis includes __ for anemia, __ to stimulate RBC production, __to control high plts/splenomegaly, __for pain/symptom ctrl, and __to increase lifespan, except in elderly

Back 44

1. androgens, corticosteriods
2. EPO
3. Hydroxyurea
4.Thalidomide/Lenalidomide
5.Splenectomy, transfusions
6. Allogenic stem cell transplant

Front 45

bcr-abl is a fusion protein with ___ kinase activity created by the translocation:

Back 45

tyrosine
9:22

Front 46

In a leukemoid reaction, LAP is high, as in all myeoloproliferative syndromes EXCEPT CML. To make the diff dx b/w an MPS and a leukemoid rxn, you will look for:

Back 46

Basophilia absent in leukemoid reaction, WBC < 50k

Front 47

The best treatment for the bcr-abl tyrosine kinase activity of CML is:

Back 47

Imatinib, prevents phosphorylation by attaching to Tyr kinase

Front 48

3 alternate treatments for CML include:

Back 48

Hydroxyurea, IFN, Allogenic stem cell transplant

Front 49

Abnormal bleeding from the mucous membranes and small vessels in the skin (petechiae, purpura, small eccymoses) indicated a disorder in:

Back 49

Hemostasis, a platelet disorder

Front 50

Abnormal bleeding from large vessels into the deep tissues and joints indicates a disorder in:

Back 50

Coagulation (PT and PTT)