| which leukocytes are myelocytes? are they granular or agranular? | granular neutrophils, granular basophils, granular eosinophils, agranular monocytes |
| which leukocytes are lymphocytes? are they granular or agranular? | B and T lymphocytes, both agranular |
| what is the order of most to least abundant leukocytes? | neutrophils, lymphocytes, monocytes, eosinophils, basophils
(never let monkeys eat bananas) |
| describe the characteristics of platelets | platelets are called thrombocytes, cell fragments from megakaryocytes, stick to exposed collagen, adhere to it because of the Von Willebrand factor |
| describe the steps and phases of hemostasis | step 1: vascular spasm
step 2: platelet plug formation
step 3: coagulation
phase 1: intrinsic and extrinsic pathway to prothrombin activator
phase 2: thrombin activation
phase 3: fibrin mesh formation |
| describe the intrinsic pathway of coagulation | activated by negatively charged surfaces (e.g. platelets) -> factor XII -> factor XI -> factor IX -> factor IX/VIII complex -> factor X |
| describe the extrinsic pathway of coagulation | activated by tissue factor released by endothelial cells -> TF/VII complex formed -> factor X |
| describe the coming together of the intrinsic and extrinsic pathway of coagulation and the formation of ...? | the intrinsic and extrinsic pathway both activate factor X in the end -> factor X activates factor V -> factor X, factor V, calcium ions and platelet factor 3 activate prothrombin activator |
| describe phase 2 of coagulation | prothrombin activator transforms prothrombin (factor II) into thrombin |
| describe phase 3 of coagulation | thrombin transforms fibrinogen (factor I) into fibrin
thrombin and calcium ions together activate factor XIII
fibrin and factor XIII form cross-links between the fibrin polymers -> fibrin mesh |
| what are the names of the 13 clotting factors/procoagulants? | factor I = fibrinogen
factor II = prothrombin
factor III = tissue factor /phospholipids
factor IV = calcium ions
factor V = proaccelerin
factor VI = (does not exist)
factor VII = proconvertin
factor VIII = antihemophilic factor (AHF)
factor IX = plasma thromboplastin component (PTC)
factor X = Stuart factor
factor XI = plasma thromboplastin antecedent (PTA)
factor XII = Hageman factor
factor XIII = fibrin stabilizing factor (FSF) |
| what happens during vasular spasm of hemostasis? | the break in the blood vessel causes the smooth muscle to vasoconstrict. this is because of the local pain receptors reflex, the damage to the smooth muscle and the chemicals that are released by the broken endothelial cells and platelets |
| what happens during the platelet plug formation of hemostasis? | platelets attach to the now exposed collagen fibers
a bridge between the collagen and platelets is formed by the Von Willebrand factor
platelets release chemicals (ADP, serotonin, tromboxane A) that attract more platelets |
| what are the cardinal signs of inflammation and how/why do they occur? | heat + redness -> vasodilation of arterioles, more blood to injury site
pain, swelling and possible temporary loss of function -> increased capillary permeability, fluid leaks out of them into tissues |
| what are the steps of phagocyte extravasation? | 1. leukocytosis
2. rolling adhesion
3. margination/tight binding
4. diapedesis
5. chemotaxis/migration |
| what happens during leukocytosis of phagocyte extravasation? | broken tissue sends out leukocytosis-inducing factors, neutrophils migrate into the bloodstream and increase in concentration, vasodilation happens, leukocytes closer to the endothelial cells |
| what happens during rolling adhesion of phagocyte extravasation? | histamine (released by mast cells), TNF-α and LPS cause the release of Weibel-Palade bodies, P-selectin appears on the endothelium.
TNF-α and LPS also cause the appearance of E-selectin.
P- and E-selectin bind loosely to the leukocytes on the Sialyl-LewisX glycoproteins.
the leukocytes roll along the endothelium. |
| what happens during margination/tight binding of phagocyte extravasation? | a chemokine binds to its receptor on the leukocyte, which causes a conformation change of the leukocyte integrins. this increases the adhesiveness of the leukocyte.
endothelial cells release intracellular adhesion molecules (ICAMs), ICAMs bind the leukocyte tightly to the endothelium. |
| what happens during diapedesis of phagocyte extravasation? | the leukocytes flatten and squeeze in between the endothelial cells as a result of chemical signals. the basement membrane is broken down by enzymes that digest extracellular matrix molecules. |
| what happens during chemotaxis/migration of phagocyte extravasation? | the leukocytes are in the tissue space and follow the chemical trail to the injury (positive chemotaxis) |
