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Chapter 18 A&P

QuestionAnswer
Functions of the blood (3) - Transport - Protection - Regulation
Transport function of the blood (6) - O2 - CO2 - nutrients - wastes - hormones - stem cells
Protection function of the blood (6) - Inflammation - reduce infection - destroy microorganisms - cancer cells - neutralize toxins - initiate clotting
Regulation function of the blood (3) - Fluid balance - stabilizes pH of ECF - temperature control
Hematology the study of blood
Components and General Properties of blood (2) - Adults have 4 to 6 L of blood - A liquid connective tissue consisting of cells and extracellular matrix
Plasma matrix of blood
Formed elements of blood and examples (4) - blood cells and cell fragments - red blood cells - white blood cells - platelets
Erythrocytes (3) - heaviest and settle first - 37% to 52% total volume - Hematocrit or PCV (packed cell volume)
White blood cells and plateles (2) - 1% total volume - Buffy coat
Plasma components and genral properties (3) - The remainder of volume - 47% to 63% - liquid portion of blood
Three categories of cells (formed elements) - Erythrocytes (RBC) - Platelets (Cell fragments from megakaryocyte in bone marrow) - Leukocytes (WBC)
Leukocyte types divided into two categories - Granulocytes (with granules) - Agranulocytes (without granules)
Granulocytes (3) - Neutrophils - Eosinophils - Basophils
Agranulocytes (2) - Lymphocytes - Monocytes
Serum (2) - remaining fluid when blood clots and solids are removed - identical to plasma except for the absence of fibrinogen
Three major categories of plasma proteins - Albumins - Globulins - Fibrinogen
Plasma proteins are formed by ... except ... liver immunoglobulins
Albumins (2) - smallest and most abundant - Contribute to viscosity and osmolarity
Globulins (2) - Provide immune system functions - Alpha, beta, and gamma globulins
Fibrinogen Precursor of fibrin threads (blood clot)
Nitrogenous compounds (2) - Free amino acids from dietary protein or tissue breakdown - Nitrogenous wastes (urea)
Nutrients in blood plasma (6) - glucose - vitamins - fats - cholesterol - phospholipids - minerals
Viscosity fluid resistance to flow (thickness)
Whole blood is ... times as viscous as water 4.5 to 5.5
Plasma is ... times as viscous as water 2.0
Osmolarity of blood concentration of dissolved particles that cannot pass through the blood vessel wall
If osmolarity of blood is too high blood absorbs too much water, increasing the blood pressure
If osmolarity of blood is too low too much water stays in tissue, blood pressure drops, and edema occurs
Optimum osmolarity is achieved by the body’s regulation of sodium ions, proteins, and red blood cells
Hypoproteinemia (4) - Deficiency of plasma proteins - Extreme starvation - Liver or kidney disease - Severe burns
Kwashiorkor (3) - Children with severe protein deficiency - thin arms and legs - swollen abdomen
Adult production of ... platelets, ... RBCs, and ... WBCs every day 400 billion 100-200 billion 10 billion
Hemopoiesis production of blood, especially its formed elements
Pluripotent stem cells (PPSC) Formerly called hemocytoblasts or hemopoietic stem cells
Colony‐forming unit specialized stem cells only producing one class of formed element of blood
Myeloid hemopoiesis blood formation in the bone marrow
Lymphoid hemopoiesis blood formation in the lymphatic organs (beyond infancy this only involves lymphocytes)
Two principal functions of erythrocytes (2) - Carry oxygen from lungs to cell tissues - Pick up CO2 from tissues and bring to lungs
Erythrocytes lack (2) - mitochondria - nucleus and DNA
Each hemoglobin molecule consist of (2) - four globins - four heme groups
globins and what it consist of for adult vs fetal (3) - Globins bind CO2 - Adult Hb has two alpha and two beta chains - Fetal Hb contains two alpha and two gamma chains
Heme groups Nonprotein moiety that binds O2 to ferrous ion (Fe) at its center
RBC count and hemoglobin concentration indicate amount of O2 blood can carry
Hematocrit (packed cell volume) (men vs women) (3) - percentage of whole blood volume composed of RBCs - Men 42% to 52% cells - women 37% to 48% cells
Hemoglobin concentration of whole blood (men vs women) - Men 13 to 18 g/dL - Women 12 to 16 g/dL
RBC count (men vs women) - Men 4.6 to 6.2 million/μL - Women 4.2 to 5.4 million/μL
Erythropoiesis RBC production
How many RBCs are produced per second? 1 million
Erythropoiesis lifespan 120 days
how long does erythropoiesis take to develop 3 to 5 days
Erythrocyte Production (4 steps) 1) Hemopoietic stem cell 2) Colony forming unit (Erythrocyte CFU) 3) Precursor cells (Erythroblast and Reticulocyte) 4) Mature cells (erythrocyte)
Iron Metabolism ( first 4 steps) 1) Mix of Fe^2+ and Fe^3+ ingested 2) Stomach acid turns Fe^3+ to Fe^2+ 3)Fe2^+ binds to gastroferritin 4) Gastroferritin transports Fe^2 + to small intestine and releases it for absorption
Iron Metabolism (last 4 steps) 5) In blood plasma, Fe^2+ binds to transferrin 6) In liver, some transferrin releases Fe^2+ for storage 7) Fe2^+ binds to apoferritin to be stored as ferritin 8) Remaining transferrin is distributed to other organs
What does RBCs do in erythrocyte death and dispoal? RBCs rupture (hemolysis) in narrow channels of spleen and liver
What does macrophages in spleen do in erythrocyte death and dispoal? (2) - Digest membrane bits - Separate heme from globin
When macrophaes in spleen separate heme from globin what happens? (2) - Globins hydrolyzed into amino acids - Iron removed from heme
When iron is removed from heme what happens (4) 1) Heme pigment converted to biliverdin (green) 2) Biliverdin converted to bilirubin (yellow) 3) Released into blood plasma (kidneys—yellow urine) 4) Liver removes bilirubin and secretes into bile
When bilirubin is concentrated in gallbladder... (2) - released into small intestine - bacteria create urobilinogen (brown feces)
Polycythemia an excess of RBCs
types of polycythemia (2) - Primary polycythemia - Secondary polycythemia
Primary polycythemia Cancer of erythropoietic cell line in red bone marrow
Secondary polycythemia From dehydration, emphysema, high altitude, or physical conditioning
Dangers of polycythemia (2) - Increased blood volume, pressure, viscosity - Can lead to embolism, stroke, or heart failure
Causes of anemia (3) - Inadequate erythropoiesis or hemoglobin synthesis - Hemorrhagic anemias from bleeding - Hemolytic anemias from RBC destruction
Inadequate erythropoiesis or hemoglobin synthesis is caused by (5) - kidney failure and insufficient erythropoietin - iron-deficiency anemia - Pernicious anemia - Hypoplastic anemia - Aplastic anemia
Pernicious anemia autoimmune attack of stomach tissue leads to inadequate vitamin B12 absorption
Hypoplastic anemia slowing of erythropoiesis
Aplastic anemia complete cessation of erythropoiesis
RBC antigens called agglutinogens
Types of RBC antigens and how are they determined - Called antigen A and B - Determined by glycolipids on RBC surface
Antibodies called agglutinins
Agglutinins location and types - Found in plasma - Anti A and anti B
The ABO group and when does it appear - Antibodies (agglutinins); anti-A and anti-B - Appear 2 to 8 months after birth; max concentration by 10 years of age
Antibody-A or antibody-B (or both or neither) are found in plasma
Do you form antibodies against your antigens? no
The ABO group causes Agglutination
Agglutination Each antibody can attach to several foreign antigens on several different RBCs at the same time
The ABO group is responsible for mismatched transfusion reaction
Universal donor (3) - Type O: most common - Lacks RBC antigens - Donor's plasma may have both antibodies against recipient's RBCs ( Anti-A and Anti-B)
Universal recipient (2) - Type AB: rarest blood type - Lacks plasma antibodies; no Anti-A or Anti-B
Rh (C, D, E) agglutinogens discovered in rhesus monkey in 1940
Rh D is the most reactive
for Rh D, a pateint is considered blood type Rh+ if having D antigen (agglutinogens) on RBCs
Rh frequencies vary among ethnic groups
Which agglutinins are not normally present Anti-D
Anti-D agglutinins are formed in Rh- individuals exposed to Rh+ blood eg. Rh− woman with an Rh+ fetus or transfusion of Rh+ blood
Hemolytic disease of the newborn (HDN) can occur if Rh- mother has formed antibodies and is pregnant with second Rh+ child
Anti- D antibodies can cross placenta
Prevention of Hemolytic disease of the Newborn RhoGAM given to pregnant Rh− women so she will not form anti-D antibodies
WBC are the ... abundant formed element least ( 5,000 to 10,000 WBCs/uL)
WBC protect against infectious microorganisms and other pathogens
WBC have a ..., nucleus Conspicuous/visible
WBCs spend only a few hours in the bloodstream before migrating to connective tissue
WBCs retain their organelles for protein synthesis
All WBCs have lysosomes called nonspecific (azurophilic) granules
Granulocytes (some WBCs) have specific granules that contain enzymes and other chemicals employed in defense against pathogens
Types of leukocytes (2) - Granulocytes (contain granules - Arganulocytes (Lack prominent granules)
Types of Granulocytes (3) - Neutrophils ( 60% to 70%) - Eosinophils (2% to 4%) - Basophils (less than 1%)
Neutrophils (3) - barley visible; three to five lobed nucleus - aggressively antibacterial - Neutrophilia
Neutrophilia rise in number of neutrophils in response to bacterial infection
Eosinophils (4) - Large rosy-orange granules; bilobed nucleus - increased numbers in parasitic infections, collagen diseases, allergies, diseases of spleen and CNS - phagocytosis of antigen - Release enzymes to destroy large parasites
Basophils (4) - Large, abundant, violet granules - increased numbers in allergies - secrete histamine (vasodilator) - secrete Heparin (anticoagulant)
vasodilator speeds flow of blood to an injured area
anticoagulant promotes the mobility of other WBCs in the area
Types of Agranulocytes (2) - Lymphocytes (25% to 33%) - Monocytes (3% to 8%)
Lymphocytes (3) - Variable amounts of bluish cytoplasm (scanty to abundant) -Ovoid/round, uniform dark violet nucleus - increased numbers in diverse infections and immune responses
Monocytes (3) - Usually largest WBC - Ovoid, kidney-, or horseshoe-shaped nucleus - increased numbers in chronic infections and inflammation
Lymphocytes functions (4) - Destroy cells - "Present" antigens to activate other immune cells - Coordinate actions of other immune cells - Secrete antibodies and provide immune memory
Monocytes fucntions (3) - Leave bloodstream and transform into macrophages - Phagocytize pathogens and debris - "Present" antigens to activate other immune cells - antigen-presenting cells (APCs)
Leukopenia low WBC count: below 5,000 WBCs/μL
Cause and Effects of Leukopenia Causes: Radiation, poisons, infectious disease Effects: elevated risk of infection
Leukocytosis high WBC count: above 10,000 WBCs/μL
Cause and Differential WBC count of Leukocytosis Causes: infection, allergy, disease Differential WBC count: identifies what percentage of the total WBC count consist of each type of leukocyte
Leukemia cancer of hemopoietic tissue usually producing a very high number of circulating leukocytes
Myeloid leukemia uncontrolled granulocyte production
Lymphoid leukemia uncontrolled lymphocyte or monocyte production
Acute leukemia appears suddenly, progresses rapidly, death within months
Chronic leukemia undetected for months, survival time 3 years
Effetcs of leukemia (3) - normal cell percentages disrupted - impaired clotting - opportunistic infections
Values of a complete blood count (5) - Hematocrit - Hemoglobin concentration - Total count for RBCs, reticulocytes, WBCs, and platelets - Differential WBC count - RBC size and hemoglobin concentration per RBC
Hemostasis (3) - The cessation/ending of bleeding - Stopping fatal leaks - Hemorrhage
Hemorrhage excessive bleeding
Three hemostatic mechanisms - Vascular spasm - Platelet plug formation - Blood clotting (coagulation)
Platelets small fragments of megakaryocyte cells
Platelet contains a complex internal structure and an open canalicular system
Normal platelet count 130,000 to 400,000 platelets/μL
Platelet functions (6) - secrete vasocontrictors= reduce blood loss - form platelet plugs - secrete procoagulants/clotting factors - attract neutrophils and monocytes to inflammation - phagocytize/destroy bacteria - growth factors = repair blood vessels
Vascular spasm - prompt constriction of a broken vessel - most immediate protection agaisnt blood loss
Cause and Effects of vascular spasm Cause: pain receptors, smooth muscle injury and platelets release serotonin (vasoconstrictor) Effects: prompt constriction of a broken vessel and provides time for other two clotting pathways
Pain receptors of vascular spasm some directly innervate blood vessels to constrict
Prompt constriction of a broken vessel in vascular spasm (2) - Pain receptors - short duration (minutes) - Smooth muscle injury - longer duration
For platelet plug formation, intact vessels have a smooth endothelium coated with prostacyclin—a platelet repellant
For platelet plug formation, broken vessels exposes collagen
For platelet plug formation, platelet pseudopods stick to damaged vessel and other platelets
For platelet plug formation, pseudopods contract a platelet plug
For platelet plug formation, platelets degranulate releasing a variety of substances
For platelet plug formation, serotonin is a vasoconstrictor
For platelet plug formation, ADP attracts and degranulates more platelets
For platelet plug formation, Thromboxane A2, an eicosanoid... promotes platelet aggregation, degranulation, and vasoconstriction
For platelet plug formation, positive feedback cycle is active until break in small vessel is sealed
Coagulation (clotting) last and most effective defense against bleeding
Coagulation converts plasma protein fibrinogen into insoluble fibrin threads to form framework of clot
Procoagulants (clotting factors) (2) - usually produced by the liver - Are present in plasma
Extrinsic pathway Factors released by damaged tissues begin cascade (outside blood)
Intrinsic pathway Factors found in blood begin cascade (platelet degranulation)
Extrinsic pathway steps (4) 1) Tissue Damage 2) Tissue Factor (TF) 3) VIIa by Ca 4) TF + VIIa by Ca
Intrinsic pathway steps (6) 1) Collagen exposed 2) XIIa 3) XIa 4) IXa by Ca 5) VIIIa by Ca/PF 6) IXa + VIIIa by Ca/PF
Common pathway where intrinsic and extrinic pathways converge
Common pathway steps (7) 1) Xa 2) Va Ca/PF 3) Prothrombin activates Thrombin with Ca/Prothrombinase 4) Fibrinogen 5) Fibrin 6) Cross linked fibrin 7) thrombin also activates XII
Clot retraction occurs within 30 minutes
Platelet-derived growth factor secreted by (2) - platelets and endothelial cells - Mitotic stimulant for fibroblasts and smooth muscle to multiply and repair damaged vessel
Fibrinolysis dissolution of a clot
Factor XII speeds up formation of kallikrein enzyme
Kallikrein converts plasminogen into plasmin, a fibrin-dissolving enzyme that breaks up the clot
Prevention of platelet repulsion Platelets do not adhere to prostacyclin-coated endothelium
Prevention of thrombin dilution By rapidly flowing blood
Prevention of natural anticoagulants (2) - Heparin (from basophils and mast cells) interferes with formation of prothrombin activator – Antithrombin (from liver) deactivates thrombin before it can act on fibrinogen
Deficiency of any clotting factor can shut down the coagulation cascade
Hemophilia family of hereditary diseases characterized by deficiencies of one factor or another
Sex-linked recessive (on X chromosome) (2) - Hemophilia A missing factor VIII (83% of cases) - Hemophilia B missing factor IX (15% of cases)
Hemophilia C missing factor XI (autosomal)
Thrombosis abnormal clotting in unbroken vessel
Thrombus clot
Pulmonary embolism clot may break free, travel from veins to lungs
Embolus anything that can travel in the blood and block blood vessels
Infarction (tissue death) may occur if clot blocks blood supply to an organ (MI or stroke)
What is required for formation of clotting factors Vitamin K
What are the types of vitamin K antagonists - Coumarin - warfarin (Coumadin) - heparin
Aspirin suppresses thromboxane A2
Other anticoagulants discovered in animal research (2) - Medicinal leeches used since 1884 (hirudin) - Snake venom from vipers (arvin)
Dissolving clots that have already formed (3) - strepokinase - Tissue plasminogen activator - Hementin
Streptokinase enzyme made by streptococci bacteria
Tissue plasminogen activator (TPA) works faster, is more specific, and now made by transgenic bacteria
Hementin produced by giant Amazon leech
Created by: JessicaKim1230
 

 



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