Term
| What is the standard diluation factor for WBC counts? What diluent is used? What is the counting area in sqmm? |
|
Definition
|
|
Term
| What is the dilution factor for RBC counts? What diluent is used? What is the counting area in sqmm? |
|
Definition
|
|
Term
| What is the dilution factor for platelet counts? What diluent is used? What is the counting area in sqmm? |
|
Definition
1:100
Ammonium oxalate
1 sqmm |
|
|
Term
| What is a normal leukocyte count per microliter? |
|
Definition
| 4500-11,000 cells/microliter |
|
|
Term
| A differential with an increased lymphocyte count indicates...? |
|
Definition
|
|
Term
| A differential with an increased PMN count indicates...? |
|
Definition
|
|
Term
| A left shift on a differential indicates? What cells are likely to be present? |
|
Definition
| The start of an infection typically seen with immature wbc's (bands, pre-lymph cells, etc.) |
|
|
Term
| On a differential how does the absolute count differ from the relative count? |
|
Definition
Absolute count is the total cells per microliter
Relative count is the percentage seen on the first 100 cells |
|
|
Term
| What is a normal red cell count for an adult male? Female? |
|
Definition
Male - 4.5-6.0 million/microliter
Female 4.0-5.0 million/microliter |
|
|
Term
| How does absolute anemia differ from relative anemia? |
|
Definition
| Absolute anemia is a true decrease in RBC mass while relative anemia is due to an increase in plasma. |
|
|
Term
| How does appropriate erythrocytosis differ from inappropriate erythrocytosis? |
|
Definition
Appropriate - caused by high altitude, pulmonary disease, hemoglobin issue
Inappropriate - tumors/cysts, androgen abuse, epo abuse |
|
|
Term
| How do you calculate the MCV, MCHC, and MCH? |
|
Definition
mcv = pcv/rbc *10
mchc = hb/pcv *100
mch = hb/rbc *10 |
|
|
Term
| What is the purpose of the erythrocyte sediment rate test? |
|
Definition
|
|
Term
true or false,
erythrocyte sediment rates are invalid for anemics. |
|
Definition
|
|
Term
| what is the normal value for erythrocyte sediment rate tests in males and females? |
|
Definition
male - 0-10 mm/hr
female - 0-20 mm/hr |
|
|
Term
| What is significant about toxic granulation? toxic vacuolization? |
|
Definition
| These are reactive responses by the body in response to infection or inflammation |
|
|
Term
| What is the pelger huet anomaly? |
|
Definition
| cells remain fully functional but their morphology is skewed. Seen as heterozygous or 2 lobed or homozygous and no lobed. |
|
|
Term
| what is the alder reilly anomaly? |
|
Definition
| large granules in the cytoplasm. caused by enzyme deficiency. Presence of mucopolysaccharides |
|
|
Term
| What is the may hegglin anomaly? |
|
Definition
| RNA bodies similar to dohle bodies. platelets are giant. these cause excessive bleeding |
|
|
Term
| What is the chediak higashi anomaly? |
|
Definition
| Fatal anomaly with large gray/green bodies. These bodies signify the fusion between primary and secondary granules. Seen in albinos |
|
|
Term
|
Definition
| process of forming a barrier to blood loss and limiting it to the injured site. |
|
|
Term
| What is primary hemostasis? |
|
Definition
| Formation of the platelet plug by way of adhesion, actibvation, aggregation, and secretion |
|
|
Term
| What is secondary hemostasis? |
|
Definition
| Formation of fibrin through the coagulation cascade |
|
|
Term
During secondary hemostasis where do the coagulation factors come from?
Where does vWF protein come from? |
|
Definition
the liver
endothelial cells throughout the body and megakaryocytes |
|
|
Term
| Which coagulation factors are associated with the prothrombin group aka vitamin k dependent factors? What is needed in order to bind for activation |
|
Definition
|
|
Term
| What coagulation factors are associated with the fibrinogen group? What is unique about this group? |
|
Definition
1, 5, 8, 13
these factors are consumable, therefore not present in serum |
|
|
Term
| What coagulation factors are associated with the contact group? What is another name for this group? |
|
Definition
11, and 12
prekallikrein and high molecular weight kininogens |
|
|
Term
| What coagulation factor is essential in in-vivo coagulation? |
|
Definition
|
|
Term
| Where can the intrinsic pathway coagulation factors be found? |
|
Definition
| All within the bloodstream |
|
|
Term
Whats coagulation factors are associated with the intrinsic pathway?
Which are considered contact factors? |
|
Definition
12, 11, 9, 8, hmwk, prekallikrein
11, 12, prekallikrein, hmwk |
|
|
Term
| What initiates the intrinsic pathway? |
|
Definition
| exposure of contact factors to vessel structures beneath endothelium |
|
|
Term
| What is required in order to activate the extrinsic pathway? Where is this found? |
|
Definition
tissue factor aka factor 3
This factor does NOT circulate in the blood and is found in the subendothelial tissues. |
|
|
Term
| In the extrinsic pathway, tissue factor binds with ...? |
|
Definition
| Tissue factor binds with factor 7. This complex then goes on to activate factor 10. |
|
|
Term
| Which coagulation factors are associated with the common pathway? |
|
Definition
|
|
Term
| What are the three reactions of the common pathway? |
|
Definition
1) activation of factor 10
2) conversion of prothrombin to thrombin by activated factor 10
3) cleavage of fibrinogen to fibrin by thrombin |
|
|
Term
| What coagulation factor stabilizes the clot? |
|
Definition
|
|
Term
| How does factor 8 become active? |
|
Definition
|
|
Term
| What happens when blood flow returns to normal after clot formation? |
|
Definition
| Dilution and washing away of factors |
|
|
Term
| Besides enzymes, what controls feedback inhibition during hemostasis? |
|
Definition
|
|
Term
| Liver clearance is activated by...? |
|
Definition
|
|
Term
| Liver clearance is degraded from ...? |
|
Definition
|
|
Term
| What is the most important inhibitor for coagulation? What does it have the most significant effect on? |
|
Definition
|
|
Term
| Anti-serine protease effects which coagulation factors? |
|
Definition
| 12a, 11a, 9a, 10a, 2a, plasmin, and kallikrein |
|
|
Term
| What is heparin cofactor 2? |
|
Definition
| A second line coagulation inhibitor |
|
|
Term
| What does heparin cofactor 2 inhibit? When is it inactive? |
|
Definition
| inhibits thrombin but inactive with other coagulation or fibrinolytic proteases |
|
|
Term
| What increases tissue factor pathway inhibitor? |
|
Definition
|
|
Term
| Where is tissue factor pathway inhibitor produced? Where is it secreted? |
|
Definition
produced by the liver, lung, bladder,
endothelial tissue cells
secreted by platelets |
|
|
Term
| What stimulates the secretion of tissue factor pathway inhibitor? |
|
Definition
|
|
Term
| What does it mean to be a Kunitz-type serine protease inhibitor? |
|
Definition
| pretends to be good substrate for the enzyme, but after binding, enzyme activity slows or ceases |
|
|
Term
| What are the two vitamin K dependent PROTEINS? |
|
Definition
|
|
Term
| What is required for optimal activation of protein c? |
|
Definition
| thrombomodulin and calcium |
|
|
Term
| What is the function of protein s? |
|
Definition
| To enhance the activity of activated protein C by promoting its binding to phospholipid surfaces |
|
|
Term
| What is the function of thrombomodulin? |
|
Definition
| To bind thrombin, in order to prevent its clotting activity |
|
|
Term
| What age group is a2-macroglobulin highest in? |
|
Definition
|
|
Term
| What is the function of c1 inactivators? |
|
Definition
to inhibit the contact factors in the intrinsic pathway
also inhibits esterase activity of C1 from complement cascade |
|
|
Term
| What is plasminogen, and what is its function? |
|
Definition
| A zymogen synthesized by the liver which circulates in the blood and absorbs within the fibrin mass and cleaves into serine protease. (plasmin) |
|
|
Term
| What is the exogenous plasminogen activator? |
|
Definition
|
|
Term
| What is the purpose of the plasminogen activators in the blood? |
|
Definition
| involved in the contact phase of the intrinsic coagulation cascade |
|
|
Term
| What coagulation factors can plasmin digest? |
|
Definition
| Factors 5 and 8 as well as fibrinogen and fibrin |
|
|
Term
| What is the result of the plasmin digestion of factor 12? |
|
Definition
| Decreases coagulant activity but increases prekallikrein activity |
|
|
Term
True or False:
Plasma causes a linear degradation of fibrin or fibrinogen. |
|
Definition
False
The degradation is considered assymetrical and progressive, not linear. |
|
|
Term
| What are the fibrinogen degredation products? |
|
Definition
|
|
Term
| Theoretically, if you were to increase fibrin fragments, what effect would this have? |
|
Definition
|
|
Term
| What are the 5 inhibitors of plasminogen activators and plasmin?(fibrinolytic) |
|
Definition
| a2-antiplasmin, a2-macroglobulin, PAI-1, PAI-2, PAI-3 |
|
|
Term
| What is the function of a2-antiplasmin? What does it complex with? |
|
Definition
| complexes with plasminogen or plasmin and inhibits contact factors, factor 10a, and thrombin |
|
|
Term
| What is the function of a2-macroglobulin? What does it complex with? |
|
Definition
| complexes with plasmin (slowly) in order to neutralize excess plasmin once a2-antiplasmin is saturated |
|
|
Term
| What is the role of PAI-1? |
|
Definition
primary inhibitor of t-PA and tcu-PA
activates protein C |
|
|
Term
| Where does PAI-1 come from? |
|
Definition
| platelet granules, endothelial cells, hepatocytes, tumors |
|
|
Term
| What is the role of PAI-2? Where does it come from? |
|
Definition
inhibits t-PA and tcu-PA but not as strong as PAI-1.
comes from human placenta and pregnant women plasma |
|
|
Term
| What is the result of increased PAI's? |
|
Definition
| impaired fibrinolysis and increased thrombosis |
|
|
Term
| What do ATIII, a1-antitrypsin, and C1 inactivator all inactivate? |
|
Definition
|
|
Term
| What does the drug heparin do? |
|
Definition
| acts indirectly by enhancing the effect of antithrombin III. (happens immediately upon entering bloodstream) |
|
|
Term
| What does antithrombin III remove? |
|
Definition
| activated serine proteases |
|
|
Term
| How do oral anticoagulants work? |
|
Definition
| by preventing thrombin formation by inhibiting vitamin K |
|
|
Term
| How does one calculate an INR? |
|
Definition
| patient prothrombin time / normal prothrombin time |
|
|
Term
| Combination drug therapy is typically reserved for what two issues? |
|
Definition
| pulmonary embolism and dvt |
|
|
Term
| What type of drug is aspirin and how does it work? |
|
Definition
| Aspirin is an antiplatelet drug which works by inhibiting the synthesis of thromboxane A2 |
|
|
Term
| How does the drug plavix work? |
|
Definition
| inhibits platelet aggregation by direct inhibition of ADP binding to its receptor |
|
|
Term
| Thrombolytic drugs work by...? |
|
Definition
| acting on an existing emboli to break them down |
|
|
Term
| Urokinase is produced by...? |
|
Definition
|
|
Term
| What is apsac? what is the benefit |
|
Definition
complex of streptokinase and plasminogen
has a longer half-life |
|
|
Term
| What is t-PA (tissue plasminogen activator) derived from? |
|
Definition
|
|
Term
| What is the main concern with using thrombolytic drugs? |
|
Definition
| bleeding because they attack circulating fibrinogen as well as the formed clot |
|
|
Term
| Streptokinase works by...? |
|
Definition
| complexing with plasminogen that is absorbed to fibin and activates it to plasmin |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Tissue factor; thromboplastin |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Proacceterin; labile factor |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Proconvertin; stable factor |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| Plasma thromboplastin antecedent |
|
|
Term
|
Definition
| Contact factor; Hageman factor |
|
|
Term
|
Definition
| fibrin stabilizing factor |
|
|
Term
| Prekallikrein factor aka? |
|
Definition
|
|
Term
|
Definition
|
|
Term
| When running a bleeding time coagulation test, what is the purpose and which level of hemostasis are you observing? |
|
Definition
vascular integrity and platelet function
primary hemostasis |
|
|
Term
| What coagulation test is used to observe the function of the extrinsic pathway? |
|
Definition
|
|
Term
| What is the activated partial thromboplastin time test used for? |
|
Definition
| To assess the function of the intrinsic pathway |
|
|
Term
| What test is used to determine factor 13 functionality? |
|
Definition
|
|
Term
| What test is used to determine fibrinogen functionality? |
|
Definition
|
|
Term
| What is used to determine the functionality of fibrinolysis? |
|
Definition
| fibrin/fibrinogen degradation products |
|
|
Term
| What is a d-dimer test used for? |
|
Definition
| specific for factor 13-linked fibrin clot (fibrinolysis) |
|
|
Term
| In the fibrinolytic system plasminogen breaks down into ___________, which breaks down into _________, which breaks down into ___________ |
|
Definition
| plasmin, fibrinogen, fibrin |
|
|
Term
| What are the intrinsic activators of the fibrinolytic system? |
|
Definition
|
|
Term
| What are the extrinsic activators of the fibrinolytic system? |
|
Definition
|
|
Term
| PA1/2/3 all have their function between the break down of what, into what? |
|
Definition
| Between the breakdown of plasminogen into plasmin |
|
|
Term
| a2-antiplasmin and a2-macroglobulin have their function between the breakdown of what, into what? |
|
Definition
|
|
Term
| All fibrinolytic system activators have their function between the breakdown of what, into what? |
|
Definition
|
|
