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EXAM #2 mlt 126
MLT 126: HEMATOLOGY AND COAGULATION
| Question | Answer |
|---|---|
| Describe the major characteristics of a mature erythrocyte | it is made up of Hgb, which is important for gas exchange. when the membrane becomes rigid around the end of cell death (120), macrophages are triggered to phagocytize the old cell |
| This pigment is synthesized during RBC maturation and is responsible for the gas exchange abilities of RBCs? | Heme |
| Define Hematopoiesis | production of RBCs based on HSC differentiation that later evolves into the maturation of erythrocytes |
| What glycoprotein hormone triggers a negative feedback loop of RBC production during hypoxia? | EPO |
| Where is EPO produced and what development is it most essential in stimulating? | kidneys; fetal development |
| What part of hemoglobin is actually responsible for transporting oxygen to tissues and carbon dioxide out of tissues? | Heme |
| What triggers the phagocytosis of old RBCs? | The lessened flexibility of their cell membranes |
| What differentiates Relative polycythemia to primary and secondary polycythemia? | It is not caused by an increase of EPO secretion; rather, dehydration creates an inflated increase in RBCs |
| True or False: The abnormal production of tissue is a result of excessive EPO secretion. This is known as Secondary Polycythemia | False. Secondary=severe tissue hypoxia, while Primary=neoplasm/abnormal tissue production |
| Describe EPO and its major role in erythropoiesis | EPO is a glycoprotein hormone produced by the kidneys that is responsible to changing committed erythroid progenitor cells into proerythroblasts |
| What is the relationship between EPO and tissue hypoxia? Does it affect platelet production? | An excessive decrease in oxygen triggers the secretion of EPO, forming a negative feedback loop. Once RBC volume is getting closer to a state of equilibrium, the EPO levels will decrease. EPO can encourage megakaryocytes production during excessive bleeds |
| What CFU has EPO receptors that, when bound, cause them to form into unipotential rubriblasts? | CFU-E |
| True or False: CFU-B is formed by EPO receptors, but is not actively proliferating | true |
| Describe what a Pronormoblast is. | - N:C ratio of 10:1 (few cytoplasm) - fine chromatin in the nucleus and some nucleoli can be found (or none) - only in bone marrow - has a basophilic cytoplasm |
| Describe what a Prorubicyte's characteristics are | - 12-17micrometres - nucleoli can be present here, but eventually disappear - coarse chromatin forms due to decrease in RNA transcription/protein synth - deeper blue cytoplasm - N:C ratio of 6:1 |
| What stages of erythropoiesis have basophilic cytoplasms and why? | Pronormoblast/Rubriblast/Erythroblast and Basophilic Normoblast/Prorubricyte; they have high amounts of protein and RNA activity |
| What causes the pink and blue hues of a Polychromic Normoblast to appear grey? | This is the stage where Hemoglobin production begins |
| What makes the nucleus of a Orthochromic Normoblast different than its previous precursor cells? | It is situated by the end of the cell membrane to prepare for expulsion; it is also the last erythroid precursor cell to contain a nucleus |
| Why is the cytoplasm of a reticulocyte polychromic? | There are still remnants of RNA in the cytoplasm; awaiting to get catabolized |
| What three processes are necessary in order for reticulocytes to evolve into erythocytes in peripheral circulation? | - RNA catabolization - ribosomes will dissolve - hemoglobin will occupy the cell fully |
| Where does Hgb begin to synthesis, and when does it begin to appear | synth-basopchromic/prorubricyte visible=polychromic/rubricyte |
| Describe how porphyrin forms into heme | after protoporphyrinogen gets converted into protoporphyrin, 4 ferrous (Fe2+) ions combine with protoporphyrin to form heme |
| What form of iron can cross the cell membrane to form heme in the mitochondria? | ferrous iron (Fe2+) |
| What organelle instructs the synthesis of Hgb? | Mitochondria |
| What causes the formation of sideroblasts? | If there is a decreased about of globin formation due to excess in iron storage, then there will be less porphyrin to form via ferrous iron chelation. this causes iron to aggregate onto the mitochondria and around the nucleus |
| What molecule regulates oxygen affinity in the Luebring-Rapaport pathway? How does it function? | 2-3 DPG phosphates. Responsible for binding with heme |
| Describe the positive feedback loop between Deoxygenated Hgb and oxygen. | When deoxygenated Hgb first binds with an oxygen molecule, its alpha chain alters to allow more oxygen to bind to the second alpha chain. This is alignment of alpha chains is maximizes oxygen intake because the 2,3 DPG is expelled from the beta chains |
| What is the primary way that we transport Co2? | Bicarbonate ions goes into plasma, where it gets brought to the lungs and expelled via respiration, while Cl- moves into the RBC, causing the Chloric shift |
| Which method of CO2 transport would cause a shift to the right? | Direct CO2 transport; the formation of carbaminohemoglobin and salt bridges decreases oxygen affinity in tissues |
| What role does plasma play in CO2 transport? | It can either dissolve CO2 or move it to the lungs (where it gets expelled) after the Chloric shift occurs (HCO3- out, CL- in ) |
| What is the normal composition of Hgb in a normal adult? | Mainly HgbA1, then a little bit of HgbA2 and 2% HgbF |
| What globin chain is associated with fetal development? | Gamma |
| Cyanosis is a Hgb disorder associated with.... | excessive population of sulfhemoglobin, which can then combine with CO and denature the Hgb. this creates precipitated Hgb in the form of Heinz bodies |
| What kind of iron is unable to bind to oxygen? What kind of pathway is necessary to prevent this spontaneous accumulation? | Ferric (Fe3+); Methemoglobin reductase pathway converts methemoglobin back to hemoglobin (Fe3+ to Fe2+) |
| What is the most common way we analyze for abnormal Hgb populations? | Hgb electrophoresis; separation based on charge |
| Why would Kleihauer-Betke test be performed? | To assess Hgb F status in maternal blood |
| Asymptomatic cyanosis is often a result of | Hgb M Disease |
| What causes Hemolytic Anemias to occur, and which is the most common? | Enzymatic deficiency; Pyruvate kinase, which affects ATP generation in the Embden-Meyerhof pathway |
| Define Deformability | the ability of RBCs to contort their flexible membrane to travel through blood vessels |
| Which enzyme would cause Hgb to be more susceptible to denaturation (as a result of poor globin integrity)? | Glucose-6-Dehydrogenease |
| What pathway is responsible for generating ATP from breaking down glucose? What would deficiencies look like in vivo vs in vitro? | Embden-Meyerhof; vivo=premature cell dreath, vitro=non-viable RBCs for blood transfusions |
| What pathways is responsible for converting NADH to NADHP to ultimately produce glutathione to prevent Hgb oxidation? | Oxidase/Hexose Monophosphate Shunt |
| If the shunt is defective, what will occur? | Glucose doesn't convert enough glutathione, leaving the Hgb to denaturate and create Heinz bodies |
| What pathway is responsible for converting methemoglobin back to hemoglobin/converting ferric iron to functional, ferrous iron? | Methemoglobin reductase |
| How does Extravascular Hemolysis occur? | RBC membrane swells due to water intake, trapping it in the splenic sieve. this triggers macrophages to perform phagocytosis and the low pH promotes oxidation. |
| After phagocytosis, how is Hgb broken down? | iron: transferrin brings it back to bone marrow to get recycled globin: brought to liver, gets broken down in to amino acids porphyrin: broken down into CO and bilirubin that gets excreted as bile (after conjugation) |
| How does Hgb end up getting excreted in urine? | Mechanical/traumatic damage causes Hgb to get released into bloodstream. If haptoglobin cannot bind to enough Hgb, it'll get excreted in urine |
| What cell variation would have a high RDW | Anisocytosis |
| A defect in nuclear maturation can cause | Macrocyclic production |
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innazukaa
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