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27 Cards in this Set
- Front
- Back
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arvin
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cool and strong
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blood is a connective tissue
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kugj
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how many erythrocytes are in the blood per microliter
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several million,
platlets are several hundred thousand |
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5 types of leukocytes
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neutrophils (50-70% of total leukocytes)
lymphocytes monocytes eosinophils basophils |
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normal hematocrit levels
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40-50% in males
35-45% in females |
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what types of hematocrit levels do you see in polycythemia
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extremely high
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buffy coat
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thin layer of leukocytes and platlets just above the hematocrit. normally occupies 1% of blood
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plasma vs serum definitions
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plasma - liquid phase of unclotted blood
serum - liquid phase the remains after the blood is allowed to clot serum = plasma - clotting factors |
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blood smear stains
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Romanovsky stains such as Wright's or Giemsa
methylene blue - nuclei ribos and basophil granules purple azure dyes - azurophilic granules (lysosomes) reddish purple Eosin - specific granules of eosinophils red, and RBC salmon pink |
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how do RBC's convert CO2 to bicarbonate
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carbonic anhydrase (makes HCO3- bicarbonate), the bicarbonate once made then leaves the RBC
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what does the shape of the RBC do in terms of function?
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it increases SA for gas exchange
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Reticulocytes
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still contain a few residual polysomes, certain stains can cause them to clump together and form a dark staining network(reticulum)
they account for ~1% of circulating RBC's increased reticulocytes indicated increased RBC production and possible clinical importance(like hemolytic anemia) |
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RBC
lifespan cytoskeleton spectrin, ankryin, band 4.1, actin, glycophorin, band3 |
lifespan - 120 days, when they loose flexibility they are destroyed by the spleen (also bone marrow and liver)
cytoskeleton - spectrin lattice ( spectrin tetramers, actin ankyrin band 4.1) just beneath plasma mem is bound to integral mem proteins - glycophorin and band 3 |
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what is poikilocytosis
what are the three types of poikilocytes |
abnormalitites in RBC shape
abnormally shaped RBC = poikilocyte spherocytes elliptocytes drepanocytes(sickle cell) |
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hereditary sphereocytosis
hereditary elliptocytosis |
-defect that interfere with anchoring of the cytoskeleton to plasma mem
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defect in erythrocyte size
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anisocytosis
macrocytes - abnormally large (folate and vitamin b12 defic) microcytes - abnormally small (iron) |
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hyperchromic
hypochromic RBC's |
hyperchromic - mass amoutn hemoglibun, rare
hypochromic - decreased hemoglobin |
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anemia
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decreased O2 carrying capacity by blood
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platlets (thrombocytes)
size structure |
2-3 micrometers(rbc is 7.5)
has a hyalomere (clear outter) and a granulomere(basophilic inner) |
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what granules does the granulomere contain?
DEAL |
delta granules - Ca and Serotonin, also ATP and ADP
alpha - larger/more numerous, have PGDF(platlet-derived growth factor) - von Willebrand Factor - thrombospondin - thromboplastin (converts prothrombin to thrombin) -fibrinogen Lambda granules - lysosomes(clot reabsorption) |
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what do these things do
vWF thrombospondin thromboplastin PDGF serotonin Ca |
von Willebrand factor - released by damaged epithelial cells it binds collagen in the basement membrane, platlets then have vWF receptors which allows them to adhere to the damaged site
thrombospondin - adhesion thromboplastin - clotting (prothrombin->thrombin) PGDF - platlet derived growth factor, vessel repair, strongly mitogenic serotonin - platlet aggregation and vasoconstriction Ca - promotes secretion of alpha and delta platlet granules, after about an hour the clot retraction happens and it is needed to activate Myosin-ligh-chain-kinase inorder for the platlets to contract |
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von Willebrands disease
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deficiency of vWF, most common bleeding disorder
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Bernard-Soulier disease
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defic of platler receptor for vWF
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glanzmann's thrombasthenia
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defic of platlet receptor for fibrinogen , doesnt allow aggregation and crosslinking of platlets
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what is happens when a blood vessel is damaged?
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1)platlets adhere to exposed vWF basment membrane
2)platlets aggregate and crosslink using fibrinogen 3) adherent platlets are activated and release Ca, and cleave arachidonic acid via cox to TXA2, TXA2 Ca and serotonin promote further aggregation 4) Vasoconstriction by serotonin and TXA2 5)blood coagulation, meshwork of FIBRIN stabalizes platlet plug and forms a 2o hemostatic plug 6)clot retraction after ~ 1hr, Ca required to activate MLCK 7)Clot resorption - TPA lyse and lysosomal enz resorb 8) vessel repair via PDGF(mitogenic) |
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what two types of membrane bound tubules does the granulomere of platlets have?
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open canilicular system - invag of plasmlemma
dense tubular system - stores Ca not continuous w/plasmalemma |
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regulation of platlet activation
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normally collagen and lamanin are not exposed (these would acitvate)
healthy endothelia produce PGI2 which inhibits platlet aggregation and thrombomodulin which inhibits blood clotting |
