NCLEX EXAM 3: HEMATOLOGY STUDY GUIDE (BASED ON EXAM REVIEW SLIDES)

EXAM 3: HEMATOLOGY STUDY GUIDE (BASED ON EXAM REVIEW SLIDES)Exam 3: Hematology Study Guide (Based on Exam Review Slides) Hematology: Erythropoiesis: Erythrocyte Differentiation • Erythropoiesis: formation of new RBCs only (subset of hematopoiesis) • Start w/ erythroid progenitor cell and then w/ erythropoietin (which is synthesized and released by the kidney), its an exocrine hormone, that then helps convert erythroid progenitor cell (stem cell) to a proerythroblast (committed progenitor cell) and then that morphs into a normoblast and then that morphs into a reticulocyte and then that differentiates into an erythrocyte so we’ve got several stages of development • Key points: 1. As the progression goes from left to right the cell becomes much more functional and effective ▪ For ex: the reticulocyte phase, the phase before the differentiation (maturation) into a true erythrocyte (mature cell), is far less effective. It’s not an adult, grown-up, fully functional RBC (like erythrocytes are). 2. The nucleus of the cell shrinks as it moves through this maturation pathway to the point where the reticulocyte no longer has a cell nucleus (it’s a baby cell, it’s still undergoing growth and development) so idk why the nucleus dissolves, but the ribosomes remain, so they are capable of generating globulin and heme (mitochondria are still in the reticulocytes so they are still able to generate Hemoglobin (Hgb)) so the development of Hgb continues even though there’s no nucleus w/in the reticulocyte (Hgb: iron-containing oxygen-transport metalloprotein in RBCS; in the blood it carries oxygen from the lungs to the rest of the body) ▪ If we look at where erythropoietin stimulates bone marrow to make more RBCs (incr output of RBCs) ▪ If problem is back here w/ progenitor cell (erythroid progenitor) then giving erythropoietin isn’t going to help w/ anything and its not w/out side effects, esp exogenous, which is what were going to give. ▪ So you want to be thinking if prob is w/ progenitor cell, if somebody wants to give erythropoietin, you want to ask why? Erythropoietin acts beyond that so it wont have any impact if the pathology is located at the progenitor cell Hemostasis: local control of bleeding (not systemic) 1. Vasoconstriction (limits blood flow): extremely transient cessation of blood flow (about 15 secs) • Ex: skinned shin and wondered why she wasn’t bleeding, though hmm where’s the blood? Then all of a sudden blood starts coming (15 seconds later) • Vasoconstriction extremely transient (temporary), to limit the loss of blood, like 15 secs maybe less than that (not very long) o Have a little bit of time where we limit blood flow 2. Platelet plug: primary hemostasis; prevent further bleeding • Then what happens is we start forming a platelet plug. Platelets are our primary hemostasis (to locally control bleeding) o Everyday we have little microscopic hemorrhages w/in our body. Apoptosis goes awry or we stretch something just a little too far and it creates a little break and it creates a little hemorrhage. We don’t even realize this bc we don’t have any clinical manifestations from it, but the platelets immediately respond when there is bleeding and they form a platelet plug internally (we don’t even know we’ve had a bleed), prevents further bleeding. o Platelet plug is tentative (not certain or fixed), just a bunch of platelets glomming on to where the site is, so the platelet degranulation (release of antimicrobial cytotoxic molecules from secretory vesicles called granules) activates the clotting cascade (clotting plasma protein system from systemic inflammatory response) 3. Tissue factor & platelets activate clotting cascade: secondary hemostasis; forms fibrin clots • Tissue factor and platelets activate clotting cascade: then we have fibrinogen converting to fibrin, which is the end product of that clotting system which forms a proper clot – secondary hemostasis (more permanent one) = fibrin clot 4. Clot retraction & fibrinolysis (dissolution): • Fibrinolysis: the breakdown of that clot via breakdown of fibrin and fibrin is the basis of that clot • Excessive bleeding: can be d/t  o Factor deficiency: can have this if we have a deficiency in any of those factors which are in the clotting cascade (14 factors that play a role in getting to that end point of fibrin development); deficiency in any of those  excessive bleeding