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104 Cards in this Set
- Front
- Back
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Factors exclusive to the intrinsic pathway.
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8,9,11,prekallikrein, hwmk
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Factors exclusive to the extrinsic pathway
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3,7
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Common pathway factors
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1,2,5,10,13
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factor 1
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fibrinogen
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factor II
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prothrombin
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factor IV
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calcium
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factor III
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tissue factor
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factor V
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proaccelerin, labile factor
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factor VII
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proconvertin, Stabile factor
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Factor VIII
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AHF, antihemolitic factor A, antihemophilic globulin
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Factor IX
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Plasmin thromboplastin component, Christmas factor, antihemophilic factor B
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Factor X
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Stuart factor, stuart prower factor
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Factor XI
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plasma thromboplastin antecedant, antihemophilic factor C
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Factor XII
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Hageman, contact factor
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Factor XIII
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Fibrin stabilizing factor, FSF
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Fletcher factor
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prekallikrein
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fitzgerald factor
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High molecular weight kininogen
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Fibrinogen group, aka
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thrombin sensitive group
factors I, V, VIII, XII plasma - present serum - absent vitamin K and Absorption - no Stability - V & VIII unstable Increased in stress, pregnancy, inflammation, fear, oral contraceptives |
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Prothrombin group
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Factors II, VII, IX, X
Plasma - present Serum - present Vitamin K and absorption - yes stability - stabile increased in pregnancy, oral contraceptives decreased, coumadin aka, vitamin K dependant group |
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Contact group
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XI, XII, Prekallikrein and HMWK
Plasma - present Serum - present Vit K and absorption - no Stabile |
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Positive feedback
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Factor VIIz can activate both X & IX, Xa can activate II and more VII, factor IXa activated more X and VII
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Negative feedback
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Thrombin/thrombomoduline activation of protein C, ultimately stops the formation of the new thrombin
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Plasminogen
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glycoprotein,
absorbed into clot with fibrin converted to plasmin by activators |
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Intrinsic plasminogen activators
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In blood
HMWK, XIIa, Kallikrein |
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Extrinsic plasminogen activators
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tPA, tissue plasminogen activators, from endothials
Urokinase, from kidneys |
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Therapeudic plasminogen activators
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tPA - promotes fibrinolysis
Streptokinase, from strep B Urokinase, from urine Staphylokinase, from staph all used in MI and PE clotting |
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Aspirin induced petechiae
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aspirin inhibits vasoconstriction leading to pinpoint hemorrhages
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Ehler-Danlos syndrome
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Abnormal collagen reduces platelet adhesion
increases vascular fragility Inherited |
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Hereditary hemorrhagic telangiectasia
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deficiency of elastic fibers results in dilation of capillaries
disorganized patterns bleeding tendencies ensue |
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Scurvy
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Vitamin C deficiency
Decreases hyaluronic acid (cement between endothelials) |
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Senile purpura
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loss of elasticity in aging
causes bruising in elderly |
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Henoch-Schonlein purpura
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GI hemorrhage and joint swelling
most common in kids follow upper respiratory infection Caused by immunologic damage to endothelials, drugs, infectious agents |
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platelet count
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normal 150 to 450 X 10 to 9th
2 to 4 micrometers |
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Platelet aggregation test
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bleeding time
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Platelet aggregrating studies
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add aggregating agent to platelet-rich plasma.
different agents-different aggregation patterns ADP Collagen Epinephrine Ristocetin |
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Clot retraction
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time it takes for clot to pull away from test tube at 37 degrees
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Platelet retention
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normal platelets with normal vWF adhere to glass beads in column
Platelet count reduced by 75% |
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Antiplatelet antibodies
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Cause thrombocytopenias
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Quantitative platelet disorders
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Primary throbocytosis
Polycythemia vera, essential thrombocythemia, CML Secondary, malignant, inflammatory, fe def.,etc. |
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Thrombocytopenia
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Disorders of production
Megakaryocyte hypoproliferation Ineffective thrombopoiesis Rare heriditary disorders Disorders of increaseed destruction or utilization Non-immune Bleeding, DIC, etc. Immune-Pupura |
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Platelet adhesion disorders
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Bernard-Soulier syndrome
giant platelets, missing plt membrane glycoproteins, no membrane receptor for vWF, increased bleeding time vWF - lack of plasma protein for plt to adhere to damaged vessels mild bleeding, inc. bleeding time, dec. aggregation due to ristocetin |
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Disorders of platelet aggregation
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Glanzmann's thrombosthenia
certain ethnic populations, decreased surface membrane glycoproteins, IIa and IIb, plts can't bind fibrin, abnormal clot retraction |
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Disorders of platelet secretion
Deficiencies of dense granules |
Chediak-Hiagashi syndrome
plts produce giant lysosomes pt albinism, prone to infection and hemorrhage Wiskott-Alkrich syndrome lack of stored or pooled nucleotides, infection, hemorrhage Hermansky-PUdlak syndrome dense core granules albinism, pink eye |
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Gray-platelet syndrome
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Deficiency of alpha granules
large platelets with no granules defective aggregation due to lack of stored ADP |
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Acquired disorders of platelet function
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Myeloproliferative disorders
Paraprotein disorders Autoimmune Uremia DIC Drugs - anticoagulants, etc. Diet fish containing C19 or C21 onions and garlic herbs |
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Inherited coagulation disorders
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Autosomal recessive
deficiencies in I, II, V, VII, X, XI, XII, XIII, prekallikrein, HMWK Sex-linked def. in factors VIII and IX Autosomal dominant males and females, vWF |
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Hemophilia A
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Classic hemophilia - factor VIII:C def
sex linked 50 deletion mutations in the gene for factor VIII small percentage may develop Ab to VIII:C, very bad |
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Hemophilia B
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Christmas disease, factor IX def
sex linked, less severe than A 34 deletion mutations in gene for factor IX |
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von Willebrand
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Autosomal dominant, most frequently inherited
def or defect in VIII:C and VIII vWF severe bleeding that decrease with age |
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Acquired bleeding disorders
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Hepatic disease
dec. synthesis of coag factors impaired clearance and recycling of activated components Vitamin K def. HDN Sterile gut malabsorpion of fats DIC, plts depleted by clotting |
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Primary thrombosis disorders
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inherited
Antithrombin III def. causes thrombophlebitis & PE Treatment: heparin, coumadin Protein C def causes superficial and dvt with PE, Vit K dependant, inactivates V and VIII Protein S def. causes venous thromboses cofactor promotes inactivation of factor V by protein C |
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Secondary thrombosis disorders
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Lupus anticoagulant, auto-ab against plt phospholipids
Postoperative, activation tissue substances exposed during surgery Malignancy, pregnancy, Estrogen, the pill, Morbid obesity results in dec AT-III |
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Coaguation screening procedures
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Clinical history, p.e., meds
Other diseases, liver, renal, cancer, Vit K def., alcoholism Look for bruising, bleeding membranes |
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Principles used to count cellular elements
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Optical detection
Electrical impedance |
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Four basic properties or laser
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1. Monochromatic
2. Low divergence 3. Coherence 4. Brightness |
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N:C angle
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10 degrees
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Lobularity angle
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90 degrees
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Granularity angle
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90 degrees depolarized
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Cell size angle
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O degrees
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RBC histogram, shift to right
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Macrocytes
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Measured values
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WBC, RBC, Plt, Hgb, MCV, MPV
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Calculated values
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HCT, MCH, MCHC, RDW, PDW
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Sweep flow
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Stream of diluent flows behind RBC aperature during RBC/PLT sensing
Keeps cells from swirling back into the sensing zone and being counted as platelets Carries them away to waste |
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L.A.S.E.R.
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Light
Amplification by Stimulated Emission of Radiation |
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Hydrodynamic flow
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Decreases area of flow path, while maintaining the same mass flow rate
Results in increase in the average velocity of fluid |
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Laminar flow
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flow inside flow
different velocities focuses sample stream hydrodynamically |
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VCS
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Volume
Conductivity Scatter |
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VCS - RF
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High voltage current determines cell size based on density
Measures N:C ratio Nuclear density Cytoplasmic granularity |
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M.A.P.S.S
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Multiple
Angles Polarized Scatter Separation |
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Peroxidase stain
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Bayer's Advia, combination of flow cytometry, laser light scattering and cytochemistry
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Four channels of peroxidase stain
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A: Hgb - modified cyanmethemoglobin method
B: RBC, Plt - low angle, size high angle, density C: WBC count and diff - same fluid principles with tungsten light instead of laser lyse RBC's Stain WBC's for peroxidase 1. EOS-stain intensely 2. Neutros - moderately 3. monos - weakly 4. lymphs - unstained dark field - size bright field - amount of stain |
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Peroxidase channel D
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Baophil/lobularity channel
Basophils don't lose cytoplasm, counted Lobularity - cytoplasm stripped cells pass thru flow Low angle (0-5) size of cell High angle (5-10) lobularity |
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RBC histogram
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>36 fl=RBC
<36=frags Right - macrocytes Left - microcytes Bimodal -cold agglutination, post transfusion, agglutination of frags |
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RDW
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red cell distribution width
calculated from histogram =SD/mean size X 100 normal range 11.5 to 14.5 percent |
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WBC histograms
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>35 = leukocytes
<35 = clumped or giant plts, NRBC 35 - 90fl lymphocytes 90 - 160 fl mononuclear cells 160 - 450 fl granulocytes |
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Plt histogram
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Normal 3 - 15 fl
<3 bubbles or dust >15 microcytes |
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MPV
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measure of the average volume of plts
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Scatter plots
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x axis - complexity
y axis - size |
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Automation of retic count
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flourescent dyes
young rbc's with RNA fluoresce more brightly |
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Checks
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RBC X 3 = Hgb
Hgb X 3 = HCT MCH X 3 = MCV |
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Inhibitors of fibrinolysis
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Alpha 2 antiplasmin - present in platelets and plasma
irreversibly attaches to free plasmin rendering plasmin non-functional Alpha 2 macroglobulin - inhibits fibrinolysis after Alpha 2 antiplasmin depleted Alpha 1 antitrypsin - a protease inhibitor |
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Plasmin
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serine protease enzyme
degrades facftors I, V, VIII, XIIa, XIII and fibrin Activates the complement system liberates kinins from kinogen |
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Fibrin split products or
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Fibrin degradation products (D-Dimers)
D fragments of fibrinolysis exert antithrombin effect inhibits hemostasis interferes with platelet aggregation |
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Tissue plasminogen activator inhibitor
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inhibits activation of fibrin-bound plasminogen by inactivating tPA and urokinase
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Control of fibrinolysis
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Regulate so unwanted clots are dissolved, but not broken down prematurely
prevents widespread clotting prevents premature lysis of clot |
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Protective measures against Thrombosis
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Normal blood flow
Removal of activated clotting factors and particulate material by hepatocytes Coagulation inhibitors |
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Coagulation inhibitors
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Antithrombin III
Heparin cofactor Protein C (serine protease) Protein S (cofactor) C1 inactivator Alpha 2 macroglobulin Alpha 1 antitrypsin |
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Antithrombin III
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The major inhibitor of coagulation
inhibits thrombin by forming stable 1 to 1 complex with thrombin Inhibits factor Xa and others Binding of AT-III and thrombin increased 100 fold or greater in presence of heparin |
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Heparin cofactor
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enhance rate of activity of AT-III
naturally occuring heparin and heparin sulfate prevent intravascular clot formation Made by basophils |
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Protein C and Protein S
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Inactivate factors Va and VIIIa
promotes fibrinolysis by inactivating plasminogen activator inhibitors thrombomodulin enhances ability of thrombin to activate protein C |
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C1 activator
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inhibits contact factors by inhibiting C1 esterase in complement pathway
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Alpha 2 macroglobulin
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inhibits coagulation
and fibrinolysis |
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Alpha 1 antitrypsin
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inhibitsx factors XIa and thrombin
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Coag specimens
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9 to 1 ratio
no tissue contamination pts with high or low HCT need correction Lipemic or icteric specimens may interfere with optics |
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Pt detects deficiencies in factors
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I, II, V, VII and X
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aPTT detects deficienies in factors
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I, II, V, VII, VIII, IX, X, XI, XII and HWMK and Prekallikrein
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Peripheral zone
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receptor site
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Sol-gel zone
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contractile system
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Organelle zone
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metabolic system
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Submembrane area
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surface connecting system
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Dense bodies
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ADP, serotonin, calcium
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Alpha granules
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PF4, vWF, fibronectin
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Mitochondria
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ATP synthesis
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Lysosomal granules
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hydrolase enzymes
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