Hematology Exam 3 Flashcards
What are the two components of the blood and what do they consist of
Blood Plasma: Watery liquid containing dissolved substances
Formed Elements:
-Cells (red and white blood cells)
-Cell Fragments (platelets)
What is a heatocrit
Percentage of total blood volume occupied by RBCs
Function of Blood Components: Transportation, Protection, Blood Clotting
Transportation:
-Plasma -> nutrients, proteins, waste products
-RBCs -> carry O2 to tissues & CO2 from tissues
Protection:
-WBCs -> infection & cancer
Blood Clotting:
Platelets: blood clotting during blood loss
Where are all blood cells descended from?
Hematopoietic Stem Cells
-Undifferentiated cells that give rise to progenitor (precursor) of any of the blood cells
Erythropoiesis (RBCs Production)
-Erythropoietin (EPO hormone) activated erythrocytes (RBCs) production
-Proerythroblast divides several times forming erythroblast and begins synthesizing hemoglobin
-Reticulocyte form at end of development -> Nucleus ejected & center indented & maintain some mitochondria, ribosomes, ER
-Reticulocytes pass from red blood marrow into bloodstream by capillaries & develop into mature RBCs 1-2 day entering bloodstream
Overview erythropoiesis basic steps
Bone Marrow
Hematopoietic stem cell -> proerythroblast -> erythroblast -> reticulocyte
Blood
reticulocyte -> erythrocyte
Red Blood Cells: Hemoglobin, Globin, Heme, Fe2+
Lack nucleus and organelles
Regulates blood flow and pressure
Hemoglobin: O2 transporter
Globin: protein w/ two alpha & two beta chains
Heme: nonprotein pigment bound to each chain of globin
Fe2+: Center of heme ring binds one O2 -> 4 O2 per hemoglobin
O2 transport in RBCs
O2 bind to Iron ion at center of each heme ring
4 oxygen per metabolism
Reversible (O2 release in tissues)
CO2 transport in RBCs
CO2 is a waste product of metabolism
CO2 is carried mainly as bicarbonate ions in blood
Some CO2 remained dissolved in plasma
CO2 is released in lungs (breathed out)
CO2 + H2O <–CA–> H2CO3 <—> H+ + HCO3-
CA = carbonic anhydrase
Carbon Monoxide Poisoning: CO looks, symptoms, exposure
CO odorless, tasteless, colorless gas “silent killer”
Leading cause of accidental poisoning deaths in America
Symptoms: headache, nausea, fatigue
Prolong exposure can lead to brain damage & death
Mechanism of Carbon Monoxide Poisoning
-CO binds to Hb to form carboxyhemoglobin (HbCO)
-Prevents binding O2 to HB -> hypoxia
-HbCO can revert to HB but takes time (HbCO complex stable)
-Cells die and organs stop working
Recycling of Hemoglobin Components 1-7
1: Phagocytosis of ruptured RBSc by liver, spleen, red bone marrow
2: Globin and heme portions of Hb are split apart
3: Globin is broken down into amino acids (reused)
4: Iron from heme binds transferrin (membrane proteins)
5: Fe3+ detaches from transferrin & binds ferritin (iron storage protein) in muscle fibers, liver cells, macrophages of spleen & liver
6: Fe3+ reattaches to transferrin upon release or absorption
7: Fe3+ transferrin complex is transported to red bone marrow for hemoglobin synthesis, taken up by RBS precursors
Recycling of Hemoglobin Components 8-14
8: Erthropoiesis in red bone marrow generate RBSc enter circulation
9: Non-iron portion of heme is converted to biliverdin (green) then into bilirubin (yellow-orange)
10: Bilirubin enters blood and transported to the liver
11: Bilirubin is released by hepatocytes into bile
12: Bacteria convert bilirubin into urobilinogen in large intestine
13: Urobilinogen is absorbed back into blood, converted to urobilin, excreted in urine
14: Most urobilogen is eliminated from feces as stercobilin
Regulation of Erythropoiesis
Volume of circulating RBC remains constant because of regulation of RBC production
Negative Feedback -> Controlled condition is amount of O2 delivered to tissues
Control mechanism of erythrocyte production
Decrease RBC count
Reduced O2 levels in blood
Kidney releases erythropoietin
Erythropoietin stimulates
Red bone marrow
enhanced erythropeisis
More RBC
Increased O2 in blood
Blood Groups and Blood Types: what surface contains, categorized based on, major groups
-Surface of RBCs contain genetically determined assortment of antigens or agglutinogens
-Blood groups are categorized based on presence or absence of various antigens
-Two major blood groups are ABO and Rh
ABO Blood Group System and types
A: antigen A, 40%, B antibodies,
B: antigen B, 10%, A antibodies
AB: antigen A & B, 5%, none, universal recipient
O: none, 45%, Both A and B antibodies, universal donor
Blood plasma contains antibodies called ________ that reacts with the A or B antigens
agglutinins
Incompatible blood transfusion
Antibodies in recipient’s plasma binds to antigens on donated RBCs, causing agglutination and producing hemoolysis
Rh blood group: discovery, Rh+, Rh-
First discovered in blood of Rhesus monkey
Rh positive: RBCs contain Rh antigen
Rh negative: RBCs do not contain Rh antigen
Normally plasma does not contain antibodies against Rh antigen
What happens if Rh- gets Rh+ blood
Rh- gets Rh+ blood, immunosystem make Rh antibodies that remain in blood
If second transfusion w/ Rh+, formed Rh- antibodies will cause agglutination & hemolysis of donated RBCs
Neutrophils: location and function
Granular leukocyte (visible granular)
Location:
Circulation; some in tissue
Function:
Phagocytosis of bacteria
Basophils: location and function
Granular leukocyte (visible granular)
Location:
Circulation
Function:
Release histamine -> promotes inflammation in allergic reactions
Release heparin -> coagulation
Eosinophils: location and function
Granular leukocyte (visible granular)
Location:
In blood and mucosal surfaces
Function:
Kill parasites
Inflammatory response
Monocytes: location and function
Agranular leukocytes
Location:
Circulation (short time as phagocytes)
Function:
Phagocytes: migrate into tissues & organs, develop as macrophages
Macrophages: engulf cellular debris and microbes
Lymphocytes: location and function
Agranular leukocytes (not visible leukocytes)
Location:
Lymphoid tissues (lymphoid nodes, thymus, spleen)
Function:
B lymphocytes (beta) - destroy bacteria, generate -> antibody production plasma cell
T lymphocytes (T) - Attack viruses, fungi, transplanted cells, cancer cells, some bacteria
Natural Killer (NK) - Attack infectious microbes, spontaneously arising tumor cells
Mast Cells
In most tissues
Release, histamine, heparin, and proteases during inflammation
Three aspects of stop bleeding in hemostasis
Quick, localized, controlled
What are the three mechanisms to stop blood loss
-Blood vessel spasm
-Platelet Plug Formation
-Blood Coagulation or clotting (form fibrin threads)
What stimulates platelets production
thrombopoietin
platelets are cell fragments
Platelets functions
-store and release chemicals that promote blood clotting
-form platelet plug
-7-10 day life span
-removed by macrophages (in spleen or liver)
Platelets have alpha and dense granule content released during platelet activation what are they
Alpha
-Fibrinogen
-van Willebrand factor
-Factor V and VIII
-Fibronectin
-Thrombin
Dense granule
-Ca+, ADP, ATP
-histamine
-serotonin
-epinephrine
Hemostasis Vascular Spasm
-Damage to blood vessels activates contraction of smooth muscle
-Cause damage to smooth muscle, platelet factors, pain receptor
-Reduced blood loss for several minutes to hours
Hemostasis Platelet Plug Formation
-Three stages
-Surface Receptors
-Stored components are released from platelet
-Activation of platelet aggregation
Platelet Plug Formation stage 1
Platelet Adhesion
-Platelets contact and stick to damaged blood vessel
-Collagen fibers and van Willebrand factors exposed to blood
Platelet Plug Formation stage 2
Platelet Activation
-Platelet release the content of granules
-Agents induce change in shape, proteins, metabolism (activation)
-Platelet extend projection and release vesicle content
Platelet Plug Formation stage 3
Platelet Aggregation
-Gathering of platelets
-Recruited by ADP, TXA2, Thrombin
-Form platelet plug (fibrin threads tighten plug)
Formation of fibrin plug
-Fibrous protein involved in formation of hemostatic plug
-Covers platelet plug forming a loose fibrin thread
-Molecules are crosslinked between lysine and glutamine by factor 13
(factor 13 -> make more stable, disulfide bonds)
Blood Coagulation importance
*Form hemostatic plug
-activation of plasma coagulation proteins (clots)
-Are proteases
-Factors form thrombin and fibrin
-Enzymatic reactions
Coagulation pathways: extrinsic
Quick
-Tissue Factor leaks into the blood from damaged cells
-TF with Ca2+ activates factor X
-Factor X with factor V & Ca2+ form prothrombinase
Coagulation pathways: intrinsic
Slow
-Direct contact with blood
-Exposed collagen fibers and phospholipids activate clotting factor XII
–Factor XII with Ca2+ activates factor IX then others
–Factor X, V, and Ca2+ form prothrombinase
Coagulation pathways: common pathway
Begins when prothrombinase formed
-prothrombinase and Ca2+ catalyze conversion of prothrombin into thrombin
Fibrinolytic System (deletion of blood clots)
Elimination of fibrin plug
-system breaks down fibrin clot to fibrin degradation products
–Plasminogen dissolves clot at site of damage once damage is repaired
–Plasmin dissolves small inappropriate clots
–Restores obstructed circulation
Three thrombin functions
-Bind to Ca2+ and converts fibrinogen to fibrin
-activates factor XIII crosslinks, stabilizes, strengthens fibrin threads (final plug)
-Activates factor V and platelets
