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Phys Exam 3: Ch 32
Red Blood cells
| Question | Answer |
|---|---|
| What are the contents of a RBC, and what are the fxns of its components? | Cytoplasm contains: (1) Hb - carries 4 O2 molecules per molecule Hb; (2) Carbonic anhydrase, to form bicarb, to cary CO2 from tissues to lungs |
| What is the concentration of RBCs? | 4.5-5.2x10^6 RBC/mm^3 |
| Where are RBCs produced before birth? | Mostly liver, but also spleen & lymph nodes |
| Where are RBCs produced after birth? | Bone marrow; before age 5: marrow of all bones; In adults: marrow of axial bones (skull, ribs, sternum, pelvis), and only the proximal ends of long bones |
| What is the average life span of RBCs? | 100-120 days |
| Calculate the production rate of RBCs | (5x10^6/mm^3)/120 days = 1.5x10^8/min per day |
| Lay out the RBC family tree | Hematopoietic stem cell --> committed stem cell --> erythroblast --> erythrocyte |
| What is the fxn of erythropoietin (EPO)? | EPO is a "differentiation enhancer": is required for differentiation into proerythroblasts (CFU-E) |
| What is an Hematopoietic stem cell (HSC)? | uncommitted stem cells; basis of all blood cells |
| What are colony-forming unit-erythrocytes (CFU-E)? | A committed stem cell |
| What is an erythroblast? | cell fills w/Hb; nucleus condenses |
| What is a reticulocyte? | some organelles remain, cell leave marrow by diapedesis into capillaries |
| What can the reticulocyte count be used to measure? | Usedas index to rate of RBC formation |
| What is an erythrocyte? | Mature RBC |
| What stimulates differentiation of HSCs? | Response to decreased O2 levels, the juxtaglomerular cells of the kidneys secrete EPO |
| What stimulates secretion of EPO? | Secreted in response to lower O2 delivery to the juxtaglomerular cells of the kidney; due to hemorrhage, anemia, high altitude, cardiac failure |
| Discuss injection of EPO | To increase [RBC] and O2 delivery to tissues - in severe anemia, after chemo, or to enhance athletic performance |
| How can an elevated hematocrit cause blood vessel blockage? | Elevated hematocrit + dehydration increases viscosity --> blockage |
| What structures are missing from an RBC? | Nucleus, mitochondria, and ER |
| How is ATP produced in RBCs? | Anaerobic glycolysis |
| Describe recycling of Hb after RBCs burst | After cells burst in the spleen, the resident macrophages phagocytize Hb; Kupffer cells in the liver also do this |
| Where to worn-out RBCs burst? | Spleen, mostly |
| Review RBC life cycle image | |
| Describe disposal of Hb | Globin is broken into AAs; Iron is transported on transferrin to tissues and stored on ferritin; Heme group is converted to bilirubin and secreted into bile, bile is secreted into the intestine |
| Where is iron stored? | Mostly in liver, also pancreas, heart |
| Discuss how the body prevents the toxic bilirubin from depositing in the brain | Bilirubin deposits in the brain are toxic, some is converted to urobilin in the intestine, reabsorbed, and excreted |
| What causes jaundice? | Heme converted to bilirubin is not all going into bile, instead into blood |
| Discuss Hemochromatosis | Excess Fe absorption and storage |
| What causes Hemochromatosis | Genetic, excess Fe intake, deficiency of hepcidin (a protein that blocks Fe transport across the gut); Fe is excreted only by epithelial shedding and menstruation; Free ion catalyses formation of free radicals and is toxic |
| What are the sx of Hemochromatosis? | Cirrhosis of the liver, diabetes, cardiomyopathy, arthritis, joint pain |
| How do you detect Hemochromatosis? | Serum ferritin levels, MRI |
| What is the tx for Hemochromatosis? | Phlebotomy (removal of a volume of blood), chelating agents (binds Fe from diet), and long term nutritional therapy |
| What is Anemia? | A Hb deficiency in the blood |
| What is Iron Deficiency Anemia? | Low Fe absorption; intestinal Fe absorption is normally very slow |
| What is Hemorrhagic Anemia? | Excess blood loss |
| How is diabetes caused by Hemochromatosis? | Fe is stored in pancreas, causing destruction of Beta cells by free radicals |
| How is cardiomyopathy caused by Hemochromatosis? | Fe is stored in heart tissue, causing destruction of myocytes by free radicals |
| What is Pernicious Anemia? | Vitamin B12 deficiency |
| What is Aplastic Anemia? | Bone marrow deficiency |
| What is Sickle Cell Anemia? | Abnormal Hb |
| What is Hemolytic Anemia? | Destruction of RBCs |
| What causes Iron Deficiency Anemia? | Most common cause in US is hemorrhage (menstruation, GI bleeding due to ulcer, polyp, tumor); Most common cause world-widen is parasitic infection (schistosomiasis, hookworm, amoeba; is Urinary and GI type of anemia |
| What is the most common Anemia? | Iron Deficiency Anemia |
| What are the sx of Iron Deficiency Anemia? | small RBCs w/reduced Hb content (microcytic, hypochromic) |
| What causes Aplastic Anemia? | Damage to bone marrow by chemicals, radiation, infection, autoimmune disease; 50% of cases have unknown cause |
| What is/are the population(s) most affected by Aplastic Anemia? | teens (autoimmune) and the elderly (accumulated damage, unknown causes) |
| What is the most common cause of death due to Aplastic Anemia? | Radiation exposure |
| What are the tx of Aplastic Anemia? | Immunosuppressive theray, stem cell transplant |
| What causes the vitamin B12 deficiency of Pernicious Anemia? | Autoimmune destruction of parietal cells of the stomach that produce Intrinsic Factor |
| What are the sx of Pernicious Anemia? | Enlarged, fragile, and fewer RBCs (megaloblastic); demyelination and neuropathy, paresthesia, ataxia, depression, paralysis |
| Describe Intrinsic Factor | A glycoprotein secreted by the parietal cells of the stomach, binds to to vitamin B12 in food, blocks digestion of B12, binds to intestinal cells and enables absorption of B12 |
| Describe the fxn of vitamin B12 | regenerates folate, another B12 enzyme is essential for myelin production |
| Tx of B12 deficiency | vitamins, injection of B12 |
| Why is folate important? | required for thymine production & DNA synthesis |
| Describe Sickle Cell Anemia | 1 AA change in Hb sequence produces HbS; in conditions of low O2 (exercise, exertion) HbS forms long crystals inside the RBCs; these rigid RBCs jam in the capillaries, esp in joints |
| What does Sickle Cell Anemia cause? | Ischemia, more crystal formation, pain, enlarged spleen, kidney damage, infarctions, strokes |
| Why does Sickle Cell Anemia still around? | Malaria parasite cannot reproduce in RBCs w/HbS, so a heterozygote has a survival advantage |
| Describe how Malaria causes Hemolytic Anemia | Parasite lives w/in liver cells & RBCs; after asexual multiplication the host cell is lysed and the progeny infects other cells, cell lysis releases histamine causing shock; decreased [RBC] causes anemia |
| What are some causes of Hemolytic anemia? | Malaria, Rh disease, Some venoms (ex: rattlesnakes), some drugs (usually as part of an immune response) |
| How does Rh disease cause Hemolytic anemia? | Abs from Rh- mom develop agains Rh factor in blood of Rh+ baby; these ABs cause agglutination and lysis of RBCs |
| What drugs can cause Hemolytic anemia? | penicillin, L-dopa, quinine |
Created by:
hclark86
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