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33 Cards in this Set

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1˚ Hemostasis
1˚ hemostasis= platelet adhesion and aggregation and vessel wall integrity
ie-1st response- form a first ‘glob’ to plug a hole.

Problems= muco-cutaneous bleeding and immediate surgical bleeding

Causes: Isolated Thrompocytopenia: ITP (gpIIb autoantibody), TTP (ADAMS13), DIC (2˚to chronic disease), Glanzmann thrombasthenia (gpIIb/IIIa receptor defect), Bernard Soulier syndrome (Ib/V/IX receptor defect)
3 actions of platelets:
1. Adhesion- after exposure of the subendothelium (collagen and vWF) which attract the platelets to bind to the vWF via glycoprotein (gp)-Ib-V-IX
2. Aggregation- binding of platelets to other platelets (Gp IIb/IIIa receptor on the platelet surface binds to fibrinogen which in turn binds to a platelet)-forms the platelet plug. Also the release of granules from platelets. 2 types: _ (factor V, vWF and fibrinogen)and dense (contain Ca2+, ADP, ATP and serotonin)
3. Activation- platelet changes and special phospholipids are expressed on the surface of the platelet- start coagulation cascade
cell based model of hemostasis
three phases:
Initiation: occurs in the tissue factor bearing cell (and a little bit of Va) TF binds to circulating VII and activates X. Xa can bind to Va and generate a small amount of thrombin (Factor II) enough for priming. TF-VIIa complex also activates IX
Priming: The small amount of thrombin released is enough to activate the platelets- V in the _ granule is released and expressed on the activated platelet surface. Thrombin 1) releases VIII from its carrier protein vWF 2) activates XI on the activated platelet surface
Propagation: form the fibrin clot. IXa from TFBC migrates over to VIIIa and binds. IXa can also be activated by XIa on the activated platelet surface. IXa-VIIIa together form what is called the Ten-ase (X-ase) complex. Xa binds its cofactor Va forming the prothrombinase complex- activates II(thrombin) resulting in a burst of thrombin that can form the fibrin clot
Functions of Thrombin
Procagulant: 1)Aggregate and activate platelets
2)Activate cofactors V and VIII
3)Activate factor XI
4)Cleave fibrinogen to form fibrin
5)Activate factor XIII – cross-linking fibrin and forming a stable fibrin clot
Anti-coagulant- Activate protein C
2˚ Hemostasis
2˚ hemostasis= platelet activation and coagulation reactions as well as clot stabilization
ie.- the ‘nice, normal’ clot forms to prevent bleeding for an extended period of time

Problems= muscle hematomas, hemarthrosis and delayed surgical bleeding.
Mixing Studies
1st step in working up an abnormal aPTT/PT (deficiency vs. inhibitor)
* 50% presence of a specific clotting factor is enough to fully correct a deficiency.
The process: Two test tubes, one containing the patient’s plasma and the other containing normal pooled plasma (NPP) are mixed together (a 50:50 mix). Then aPPTs are run again to look for correction
1)Correction= deficiency (patient’s plasma contains 0%, when mixed should be 50% presence, enough to correct the deficiency)
2) Repeate prolonged aPPT= Inhibitor (Lupus Antibody is bound)
Factor VIII and IX, or VWD-type 2N (VIII carrier) deficiency
X-linked disorder
delay in secondary hemostasis:
Joint and muscle bleeding- hemarthrosis
Intracerebral hemorrhage
Delayed post surgical bleeding
Bleeding with trauma
3 Anti-coagulation mechanisms
1. Plasminogen is activated by tissue plasminogen activator (tPA) into plasmin, which degrades fibrin
2. Antithrombin III (AT-III) circulates, binds heparan, and inactivates activated serine proteases (Factors XIa, IXa, Xa, and IIa)
3. thrombin (Factor IIa) is activated, binds thrombomodulin and activates Protein C, then C complexes with Protein S on the platelet surface to inactivate Factor Va
Virchow's Triad with associated causes
1. Decreased blood flow- Venous stasis, Hyperviscosity, Myocardial dysfunction, pregnancy
2. Inflammation of vessels- Vasculitis, Homocysteinuria (damaging vessel walls), Behçet Disease, Endothelial Damage
3. Hypercoagulitable state- factor V leiden, malignancy, elevated Lp (a), elevated VIII, pregnancy (Estrogen), DIC, Lupus Anticoagulant, prothrombin mutation, Polycythemia Vera, essential thrombocythemia
Platelet disorders that lead to thrombosis
DIC (secondary to chronic disese)
HIT (Heparin induced antibody)
Lupus Anticoagulant (antibody to cardiolipan)
Paroxysmal nocturnal hemoglobinuria (complement activation)
Essential thrombocythemia (overproduction)

* all can cause clotting (over activation) or bleeding (consuming faster than producing)
5 common causes of thrombophilia
1. Antithrombin III deficiency (don't give Heparin)
2/3. Protein C deficiency and Protein S deficiency (don't give coumadin first)
4. Factor V Leiden (extremely common)
5. Prothrombin 20210 A (twenty two-ten A) mutation

*Thrombophilias are additive- this includes inherited and environment risk factors (smoking, oral contraceptives, plane rides)
Acute Leukemia

Clincal Presentation
clonal, neoplastic proliferation of immature hematopoietic cells characterized by arrested differentiation causing an impaired production of normal blood cells
ALL= kids AML= adults
Clincally: roaring in the ears, diffuse bone pain (esp at night), fatigue, low-grade fever, infections, bruising, bleeding, Hyperviscosity (CHF, blurred vision, etc), gingival hyperplasia
Pancytopenia (or elevated WBC)
Immunophenotyping (flow cytometry) for Acute Leukemia
1. Myeloid (AML): CD13, CD33, CD117
2A. T-cell markers (T-ALL): CD2, CD5, CD4, CD8
2B. B-cell markers (B-ALL most common): CD10 (precursor), CD19, CD20
* All leukemias express DR+ except FAB-M3
Acute Leukemia Prognostic Factors
1. Cytogenetics-* most important factor
2. WBC at presentation: Higher white count is associated with a poorer prognosis.
3. Age. Younger age is associated with a better prognosis.
4. Subtype of AML/ALL. M3 (Promyelocytic leukemia) is very curable. M6/M7 is rarely curable.
5. LDH is an indirect marker of cell turnover. High values indicate a rapidly proliferating tumor (>700).
6. Expression of early antigens CD34 (stem cell marker/undifferentiated leukemia) and CD 56.
7. Poor initial response to chemotherapy.
8. Gene expression profile.
Cytogenetics of Acute Leukemia as prognostics
Good Prognosis (chemo alone)
AML: t(15,17); t(8,21); Inv 16
ALL: hyperdiploidy (>50 chromosomes); t(12,21)

Poor Prognosis (offer bone marrow transplant)
Chromosomes 5, 7, 8, 11, complex cyto, t(9,22)
Acute Leukemia Tx
ALL: 2 year of therapy involving 5 drugs
AML: 6 months of therapy involving 2 drugs
* if poor prognostics/no response to Tx consider bone marrow transplant

Complications to Consider:
1. Assume Infection at ANY sign of fever (esp Gram -)
2. Tumor lysis syndrome
3. DIC profile
4. Irradiated blood products (GVHD)

Clinical Presentation
clonal proliferation with NO maturation arrest
Ph+ t(9:22)

Chronic Phase- asymptomatic (4-6 years)
Intermediate Phase- unstable WBC count (1 year)
Acute Leukemia- conversion to acute form

Clincal Presentation: Fatigue, early siety (spenomegaly)
All based upon eradication of bcr-abl

1. Targeted Tx (Gleevec, etc-resistance exists)
2. Chemo/INF-A
3. Bone Marrow Transplant
B Cell Maturation and markers
B cells arise from the lymphoid progenitor and progress from pre-B cells (CD 10), to B lymphocytes (CD20 and CD22 only), to plasma cells (CD138).
Burkitt's Lymphoma

t(8;14)- myc oncogene and immunoglobulin heavy chain enhancer gene.
Follicular Lymphoma
Anti-apoptotic- slow growing

t(14;18)- anti-apoptotic gene and immunoglobulin heavy chain enhancer gene.
Mantle Cell Lymphoma

t(11;14) cyclin D1 (cell cycle regulatory gene) is overexpressed
Diffuse Large B-Cell Lymphoma Tx
Tx Rituximab (targets CD 20)

genotype for germinal vs active
Multiple Myeloma
Plasma Cell Proliferation- IgG

Bone pain, renal dysfxn, amyloid, M protein, etc

t(11;14) (4;14) and (14;16)= aggressive phenotypes
3-5% of all 60-70 yr olds

low plasma count and an M-spike with NO symptoms

Risk of progression to MM is only 1% per year
Waldenstroms macroglobulinemia
Plasma cells proliferation- IgM
Most rare B cell lymphoma
Bleeding Time
Platelet function

1. Platelets below 20,000,
2. Aspirin intake
3. uremia
4. VWD
*2-4 platelet count is not diminished but bleeding time is prolonged due to dysfunctional platelets

*ITP has marked decline in platelet count, but bleeding time is not prolonged
Prothrombin time (PT)
extrinsic pathway

Isolated PT= Factor VII
Activated partial thromboplastin time (aPTT)
intrinsic pathway

Isolated aPTT= Factors 8 or 9

* can also include Factors 11 (asymptomatic) and 12 (hypercoaguable!!)
Thrombin/reptilase time
activates thrombin and determines the rate of reaction of cleavage of fibrinogen to fibrin
Clot stability tests
measure the time it takes for a clot to dissolve.

Clot instability= Factor XIII
Ristocetin platelet aggregation studies
Ristocetin should cause spontaneous platelet aggregation

Does not occur= VWD
B Symptoms
night sweats
unexplained high temperatures (fever)
weight loss