BLOOD Flashcards
Alkilosis
Blood pH above 7.45
Acidosis
Blood pH below 7.35
% body weight composition of blood
8%
Plasma
Non-living fluid matrix
Formed elements
Living Blood “Cells”
Erythrocytes
Red Blood Cells
Leukocytes
White Blood Cells
Dissolved solutes in blood
Nutrients, gases, hormones, wastes, proteins, and inorganic ions
Platelets
Thrombocytes, cell fragments
Plasma proteins most abundant solutes
Albumin, globulin, fibrinogen
Albumin
Osmotic balance and buffers pH
Globulins
Immune response & lipid transport
Fibrinogen
Blood Clotting
Leukocytes make up _____% of total blood volume
<1% (Close to 0.1%)
Leukocytosis
WBC Count > 11,000/uL
Diapedesis
Process of WBC’s passing through capillary walls into surrounding tissue
Granulocytes
Visible cytoplasmic granules (Neutrophils, eosinophils, basophils)
Agranulocytes
No visible cytoplasmic granules (Lymphocytes & Monocytes)
Buffy coat
Leukocytes & Platelets
Neutrophils
-Polymorphonuclear leukocytes
-Very phagocytic
Eosinophils
-Lysozyme-like granules
-Allergies, asthma, and general immune response
Lymphocytes
-Mainly in lymphocyte tissue
-T Lymphocytes (Against virus-infected cell & tumor cells)
B Lymphocytes (Antibody producing cells)
Monocytes
-Leave circulation to enter tissue
-Actively phagocytic cells
-Activates lymphocytes
Spectrin
Plasma membrane protein of erythrocytes
Basophils
Granules contain histamine (inflammatory chemical)
Platelets
-Cytoplasmic fragments of megakaryocytes
-Act in clotting process
Myeloid Stem cell fate
All other cell types
Lymphoid stem cell fate
B & T Lymphocytes
Thrombopoietin
Regulator for formation of platelets
Lifespan of erythrocyres
100-120 days
Hematopoietic Stem Cells
Stem cells giving rise to blood cells
Carbamino hemoglobin
CO2 binding to hemoglobin
Percent hemoglobin composition in erythrocytes
97%
Hematopoietic stem ells
Stem cells that give rise to all formed elements of blood
Hematocrit
Packed cell volume
Hematocrit levels in men & women
-47% ± 5 for males
-42% ± 5 for females
Formula for hematocrit
Volume of RBC/Volume of total blood
Causes/Signs of high hematocrit
-Dehydration
-Polycythemia Vera: Disease of bone marrow forming too many RBC’s
-Lung/Heart Disease: Low oxygen triggering too much RBC production
Cause of blue horse shoe crab blood
Copper acting as heme instead of iron
Too much erythrpoiesis
Increased blood viscosity
Too little erythropoiesis
Tissue Hypoxia
Erythropoietin
Hormone released by kidneys that directly stimulates erythropoiesis
Affect of testosterone
Increased erythropoiesis causing high RBC count in males
Bodies response to hypoxia
Kidneys release erythropoietin causing growth of red bone marrow and an increase in RBC count which allows blood to carry more O2
Impact of kidney failure & dialysis on blood
No production of EPO from kidneys causing an increase count in RBCs
Causes of hypoxia
-Decreased RBC number
-Insufficient hemoglobin per RBC
-Reduced availability of O2
Reasons for having an increased risk of stroke while at high altitude
Low environmental oxygen levels causing tissue hypoxia which leads to overproduction of RBC’s causing increase in blood viscosity
Effects of EPO
-Rapid maturation of committed marrow cells
-Increased circulating reticulocyte count in 1-2 days
Fate of erythrocytes as they age
Degredation due to a loss of spectrin and end up in the spleen to be englufed by macrophages
Fate of heme during RBC destrction
Degraded into liver bilirubin. Liver will secrete this bilirubin to serve the production of bile which aids in lipid digestion. Bilirubin will event degrade into a pigment that we excrete in feces. Iron is salvaged for reuse.
Fate of globin in RBC destruction
Metabolized into amino acids that are released for recirculation and re-uptaken by cells for protein synthesis
Cause of renal anemia
Lack of EPO often due to renal disease
Cause of aplastic anemia
Destruction or inhibition of red marrow. Often treated with transfusions or transplanted stem cells.
Cause of hemolytic anemias
Premature RBC lysis causes by hemoglobin abnormalities, incompatible transfusions, or infections
Thalassemia
-Typically meditteranean ancestry
-One faulty or missing globin chain causing thin and delicate RBCs.
Sickle Cell anemia
-One amino acid wrong in globin beta chain of hemoglobin causing crescent shaped RBCs when blood has low O2.
-RBC’s can rupture easily and can block capillaries and small vessels
Malaria in sickle cell anemia
Parasite is unable to mature giving immune properties to host
Polycethemia Vera
“True” increased RBC Count
-Bone marrow cancer can create excess RBC’s causing an increase in blood viscosity
Secondary polycythemia
-Less O2 available causing an increase production in EPO leading to increased RBC count
-Leads to a lower plasma volume
-Used in blood doping
Hemostasis
-Series of reactions for stoppage of bleeding
-Requires clotting factors & substances released by platelets and injured tissues
Three steps of hemostasis
- Vascular spasm
- Platelet plug formation
- Coagulation
Vasoconstriction
Paracrine molecule signaling for the constriction of blood vessels. Secretion of these signals is promoted by the breaking of vessels & endothelial cells
Plug formation
Activated platelets form a temporary platelet plug that is made by sticking of platelets to collagen fibers by von Willebrand factor.
Signals that promote platelet accumulation
-ADP
-Serotonin and thromboxane A2
-Ca2+
Impact of platelet interaction with collagen
Activation of platelet synthesis
Properties of coagulation
Must remain local as surrounding cells must prevent accumulation of clotting
Intrinsic coagulation
Triggered by factors within the blood/blood vessel
Extrinsic coagulation
Triggered by factors outside the blood/blood vessel
Contact activation or intrinsic pathway
Triggered by negatively charged surfaces
-Activated platelets
-Collagen
Tissue factors or extrinisc pathway
Triggered by exposure to tissue factor or factor III-Significantly faster due to less reactions being needed
Three phases of coagulation
- Prothrombin activator formation
- Prothrombin converted to enzyme thrombin
- Thrombin catalyzes fibrinogen–> fibrin
Role of platelet-derived growth factor
Division of smooth muscle cells and fibroblasts to rebuild blood vessel outer walls
Role of vascular endothelial growth factor
Restores endothelial lining
Fibrinolysis
-Removes unneeded clots after healing
-Begins within 2 days and continues for several days
Plasmin
Fibrin digesting enzyme
-Produced by activated plasminogen
-Trapped during clot formation causing a negative feedback loop
Thrombus
Blood clot
Embolus
Unattached mass that travels in the bloodstream
Thrombocytopenia
Deficient number of circulating platelets
-Platelet count <50,000/uL
-Treated with transfusion of concentrated platelets
-Petechiae appear due to spontaneous wide spread hemorrhage
Reasons for an inability to synthesize procoagulants
-Impaired liver function
-Caused by vitamin K deficiency, hepatitis, and cirrhosis
Hemophilia A
Factor VIII deficiency (77% of all cases)
Hemophilia B
Factor IX deficiency
Hemophilia C
Mild type; factor XI deficiency
Disseminated intravascular coagulation
Widespread clotting of an intact vessel combined with severe bleeding
Causes of disseminated intravascular coagulation
Usually pregnancy complications or incompatible blood transfusions that result in adverse reactions
Reason for aspirin to not be instructed before surgery
Acetylsalicylic acid acts as an anti-thrombotic drug preventing the activation of thromboxane and prostaglandin. Therefore, no possible plug formation to stop bleeding in intrinsic pathways
Life Span of Platelets
10 days
Area of blood cell formation in bone marrow
Axial skeleton, girdles, and proximal epiphysis of humerus and femur.
Reason to give children vitamin K shots
In order to have the means necessary to form clots an infant may not otherwise be able to heal
