#02: Blood I Continued/Blood II Flashcards
Forms of Hemoglobin
· There are 3 forms of hemoglobin. Oxyhemoglobin (when hemoglobin is maximally loaded with oxygen), deoxyhemoglobin (without oxygen) and carinohemoglobin (when hemoglobin is binded to oxygen).
Fetal Hemoglobin
· Fetal Hb is the main hemoglobin in the fetus during last 7 months of pregnancy. It is made up of 2 alpha chains and 2 gamma chains. Has a higher affinity for oxygen then regular hemoglobin. This is because the baby isn’t breathing in oxygen from the air but from the mother’s circulation, so a higher affinity is required.
Bohr Effect
· Bohr effect is when Hb binds to CO2 and H+. This interactions facilitates the release of O2 at the tissue.
Haldane Effect
· Haldane Effect is when deoxygenated blood Hb has a higher affinity for CO2 and protons then in oxygenated blood. Removes CO2/H+ from blood stream.
Anemia
Anemia is a disorder when there’s failure of the blood to oxygenate tissues.
Anemia Due To Insufficient # of RBCs
o Insufficient Number of RBCs
§ Hemorrhage, the result of blood loss.
§ Pernicious, a deficiency of vitamin B12. This vitamin is used to mature blood cells.
§ Aplastic, a disorder of the red bone marrow.
Anemia Due to Iron Deficiency
o Low Hb- Iron Deficient
§ If you have iron deficiency, oxygen can’t be grabbed, anemia.
§ Thalassemias, underproduction.
§ Sickle-cell anemia- point mutation.
Macrocytic Anemia
o Macrocytic anemia occurs when the average size of circulating erythrocytes is too large and spongy to be used. Deficiencies in both vitamin B12 and folic acid uptake result in the production of enlarged erythrocytes. Major concern for gastric bypass.
Microcytic Anemia
o Microcytic anemia is caused by iron deficiency. RBCs become smaller then should be. Most likely not making enough Hb.
Sickle Cell Anemia
o Sickle Cell Anemia is an autosomal recessive disorder that occurs when a person inherits two copies of the sickle-cell gene. Erythrocytes become sickle-shaped, making them unable to flow efficiently through the blood vessels to body tissues and more prone to destruction by rupture (hemolysis).
§ It results from a single amino acid mutation in the Hb-beta chain.
§ Hb “sticks” together in the deoxygenated state (RBC’s have so much Hb this clumping changes their shape to a C) and decreases Hb’s ability to bind O2 or move thru small vessels.
Carbon Monoxide Poisoning
o Carbon Monoxide can bind iron in hemoglobin, thus blocking its ability to bind O2.
§ Treatment is through putting someone in a hyperbaric chamber. Can supersaturate air with oxygen to compete with carbon monoxide to bind to Hb.
§ Cyanide poisoning works similarly to CO2 poisoning, but allosterically, binds somewhere other than the iron.
Erythropoesis
Erythropoesis is the process by which RBCs are formed.
Erythropoesis Through Life Stages
o In 1st and 2nd months, RBCs form in embryonic yolk sac.
o In 2nd to 5th months, RBCs form in liver and spleen.
In adults, RBCs form in red bone marrow, which are in various bones. (Vertebra, sternum, ribs, skull, scapula, pelvis)
What’s Required To Form RBC
o To form RBCs, it requires iron, vitamin B12, and folic acid.
Control of Erythropoiesis
o Control of Erythropoiesis
§ Hypoxia occurs as a result of low blood oxygen. It increases RBC production by increasing formation and release of erythropoietin (a glycoprotein hormone produced by the kidneys).
· Erythropoietin increases RBC production in two ways. Increase the production of proerythroblasts, and decreases the time required for erythrocyte maturation.
· Hypoxia increases erythropoietin release, which increases RBC production and the O2 carrying capacity of blood, which leads to eventual increase in blood O2, reversing hypoxia.
§ In cases of hyperxia, or too much blood oxygen or RBCs, erythropoietin levels are decreased.