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48 Cards in this Set

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  • Back
4 factors that promote anticoagulation in small vessels
1. Heparin - Enhances ATIII (inactivates thrombin, IX, X, XI)
2. PGI2 (prostacyclin)- Vasodilator, inhibits platlet aggregation; synthesized from INTACT endothelial cells from PGH2 by prostacyclin synthase (this enzyme is NOT inhibited by ASA)
3. Protein C and S - Inactivate factors V and VIII, enhance fibrinolysis
4. tPA - activates plasminogen to release plasmin, which goes on to degrade coag factors and lyse fibrin clots (thrombi)
5 factors that promote coagulation
1. TXA2 - Vasoconstrictor, enhances platelet aggregation; synthesized by platelets from PGH2 by thromboxane synthase, but PGH2 formation is INHIBITED IRREV by ASA and REVER by other NSAIDS (Inhibits COX)
2. vWF - Binds to exposed collagen and then platelets adhere to vWF promoting platelet adhesion, prevents degradation of VIII:C; synthesized by endothelial cells and megakaryocytes - platelets carry vWF in the alpha granules
3. Tissue thromboplastin (Factor III) - activates factor VII in the extrinsic pathway
4. Exposure of thromobogenic subendothelial collagen - activates XII
5. Decreased (intact) endothelial synthesis of antithromogenic substances - NO, PGI2, tPA
What are the 2 platelet receptors
GpIb - binds vWF
GpIIb/IIIa - binds fibrinogen
What Rx affect GpIIb/IIIa receptors
Ticlopidine and clopidogrel inhibit ADP-induced expression of the receptor

Abciximab - monoclonal Ab against GpIIb/IIIa receptor
What is contained within the alpha granules of platelets
vWF and fibrinogen
What activates XII and what is the fxn of XIIa
1. Exposed subendothelial collagen

1. Activates XI
2. Activates plasminogen - produces plasmin and activated plasminogen converts C3 to C3a
3. Activates kiniogen system - produces kallikrein from prekallikrein and bradykinin (incr vasodilation, permeability, pain)
Fxn of factor XIII
Cross-links insoluble fibrin monomers
Fxn of vit K
Activated in liver by epoxide reductase (majority of vit k is syn by colonic bacteria) - activated vit K gamma-carboxylates the vit K dependent factors - Ca can then bind the carboxylated factors
MA of warfarin

Time period of anticoag
Inhibits epoxide reductase and makes vit k nonfunctional

Anticoag doesn't immediately occur b/c still gamma carboxylated factors present - protein C and S decrease first, but prothrombin last - therefore heparin too (immediate anticoag by enhancing ATIII)
What are the 2 main factors that activate plasminogen?
XII and tPA, which cause the release of plasmin
What factors are consumed in the formation of a clot
Fibrinogen (I), prothrombin (II), V, and VIII
What does plasmin produce
D-dimers = fragmented cross-linked fibrin monomers
Sequence of events that occurs in response to injury
Vascular, platelet, coagulation, and fibrinolytic
What characterizes the vascular phase
1. Transient vasoconstriction mediated by endothelin, exposure of tissue
2. Thromboplastin activates VII
3. Exposure of subendothelial collagen activates XII
What characterizes the platelet phase of coag
vWF adheres to subendothelial collagen - platelets adhere to vWF by GpIb receptor - Platelets degranulate (release alpha granules and dense bodies i.e. ADP) - ADP promotes platelet agreggation (bind each by binding fibrinogen which binds IIb/IIIa) - platelets synthesize and release TXA2 - formation of temporary platelet plug
What does bleeding time test
Platelet function to formation of temporary plug
What does the Ristocetin cofactor assay test for
What are the 7 causes of prolonged bleeding time?
2. Bernard-Soulier syndrome
3. Glanzmann's Dz
4. Renal failure
5. Scurvy
6. Thrombocytopenia
7. von Willebrand Dz
Bernard-Soulier Dz
Deficiency of GpIb receptor for vWF
Defective platelet adhesion
Thrombocytopenia and giant platelets
Glanzmann's dz
GpIIb/IIIa receptor deficiency for fibrinogen
Defective platelet aggregation
von Willebrand Dz
Absent or defect vWF
Platelet adhesion defect
Decreased VIII survival

ONLY one of the qualitiative platelet disorders that has an affect on coag as well - shows as an incr PTT
MC hereditary coag disorder
What does PT evaluate
VII (extrinsic down to formation of fibrin clot)
X, V, II, I
What does PTT evaluate
XII, IX, IX, VIII (intrinsic down to formation of fibrin clot)
X, V, II, I
Heparin, NOT LMWH
5 causes of thrombocytopenia
ITP (Acute and Chronic)
Acute ITP
MCC of thrombocytopenia in childern
Occurs after URI
IgG Ab against IIb/IIIa receptors (Type II)
Platelets are destroyed in the spleen by macrophages
Respinds to CS
Chronic ITP
MCC of thrombocytopenia in adults
SLE (1st manifestation), HIV
IgG Ab against IIb/IIIa receptor (Type II)
Heparin-induced thrombocytopenia
Marcophage removal of platelets - IgG Ab against heparin attached to PF4 (Type II)
HIV Thrombocytopenia
MC hematologic abn in HIV
Deficiency in vWF-cleaving metalloprotease - excess of vWF incr platelet adhesion to areas of endothelial cell injury

Platelets are consumed in formation of thrombi - causes thrombocytopenia

Renal failure
Microangiopathic hemolytic anemia (schistocytes)
Varying neuro Sx

Lab:Decr platelet count - prolonged bleeding time
Nml PT and PTT

TX: plasmophoresis
Lab values for ITP
Decr platelet count- prolonged bleeding time

Nml PT and PTT

Increased megakaryocytes in bone marrow biopsy
What does Fibrin degradation products (FDP) test
Fibrinolytic system
Increased in DIC
NOT specific for DIC (like D-dimer) b/c FDP incr with lysis of fibrinogen AND fibrin thrombi (clots)
D-dimer specific for fibrin thrombi
Causes of primary thrombocytosis
Causes of secondary thrombocytosis
Chronic iron deficiency
Lab values in DIC
Decr Platelet count
Incr bleeding time
Incr PT
Incr PTT
Difference in clinical finding b/w platelet and coagulation defects
Platelet - microhemorrhage: petechia, purpura, nose bleeds, Incr bleed time

Coag - Macrohemorrhage: Hemarthroses, easy bruising, Incr PT and/or PTT
Hemophilia A
X-linked recessive
Factor VIII deficiency
Hemarthroses, easy bruising
Nml platelet / bleeding time
Nml PT
Incr PTT
Tx: Factor VIII
Hemophilia B
X-linked recessive
Factor IX deficiency
Clinical identical to Hemophilia A
Clinical findings of Von willebrands
easy bruising
Associated with angiodysplasia of the right colon
Lab values of von Willebrands =
Incr bleeding time
Incr PTT
Abd ristocetin test
Tx of von Willebrands Dz
Desmopressin acetate (ADH analogue) - increases vWF and VIII
OCP - estrogen has similar action to desmopressin
What is the 50:50 Mix test used for
Distinguish b/w circulating anticoagulants (Abs that destory coag factors) and decreased production of coag factors

No correction of PT and/or PTT = immune destruction

Correction of PT and/or PTT = decreased production of anticoagulants
Causes of vit K deficiency
1. Decreased syntheses
a. Newborn lack colonic bacteria, require IM vit K
b. Abx
2. Malabsorption of fat soluble vit - celiacs
3. Cirrhosis - decr activation by epoxide reductase and decr synth of other factors
Lab findings in liver Dz
Incr PT and PTT
Incr FDP and D-dimers
Incr bleeding time
Pathogenesis of DIC
Activation of coag system via tissue thromboplastin and exposed subendothelial collage

Thrombi develop and consume coag factors and platelets

Fibrinolytic system is also activated by XII
3 main factors involved in thrombus formation
Virchow's traid:
Endothelial injury
Alteration in laminar flow
Hypercoaguable state
Acquired hypercoagulable states
1. Antiphospholipid syndrome - Associated with SLE and HIV, AP Ab contain anticardiolipin Ab and therefore get a false + to syphilis test
2. Malignancy
3. Folate or vit B12 deficiency - due to incr homocysteine
4.OCPs - estrogen increase syn of coag factors and decr ATIII
5. Pregnancy
6. Hyperviscosity - ET, PCV, Waldenstroms
Inherited hypercoaguable states
Hx DVTs and PEs at early age

1. Factor V Leiden - MC, Mutant factor V cannot be degraded by protein C and S
2. ATIII deficiency - No prolongation of PT after injection of STD dose of heparin
3. Protein C and S deficiency - Cannot inactivate factors V and VIII
What pts are at an increases likelihood of developing hemorrhagic skin necrosis when placed on warfarin
Protien C deficiency (inc heterozygote carriers (Asx)) - Protein C falls - incr V and VIII - causes cutaneous vessel thrombosis and skin necrosis