Chapter 18: The Cardiovascular System: Blood PDF

THE CARDIOVASCULAR SYSTEM: BLOOD CHAPTER 18 18.1 – AN OVERVIEW OF BLOOD BLOOD IS CONNECTIVE TISSUE MADE OF RBC, WBC, AND PLATELETS (FORMED ELEMENTS) PLASMA – THE FLUID (MOSTLY WATER) SUSPENDS THE FORMED ELEMENTS TRANSPORTATION – NUTRIENTS, O2, HORMONES, WASTE, AND BYPRODUCTS DEFENSE – WBC TRAVEL TO...

THE CARDIOVASCULAR SYSTEM: BLOOD CHAPTER 18 18.1 – AN OVERVIEW OF BLOOD BLOOD IS CONNECTIVE TISSUE MADE OF RBC, WBC, AND PLATELETS (FORMED ELEMENTS) PLASMA – THE FLUID (MOSTLY WATER) SUSPENDS THE FORMED ELEMENTS TRANSPORTATION – NUTRIENTS, O2, HORMONES, WASTE, AND BYPRODUCTS DEFENSE – WBC TRAVEL TO PROTECT US AND PLATELETS TRAVEL TO WOUNDS FOR CLOTS HOMEOSTASIS – REGULATE BODY TEMP, WATER CONTENT, AND PH 18.1 – COMPOSITION OF BLOOD HEMATOCRIT – THE PERCENTAGE OF RBC IN BLOOD, 45% IS NORMAL BUFFY COAT – WBC AND PLATELETS BLOOD PLASMA - FLUID 18.1 – CHARACTERISTICS OF BLOOD BRIGHT RED JUST AFTER RECEIVING O2 AND DUSKY RED UNOXYGENATED VISCOSITY 5 TIMES THICKER THAN WATER DUE TO PLASMA PROTEINS AND FORMED ELEMENTS TEMP IS SLIGHTLY HIGHER THAN BODY TEMP DUE TO FRICTION – 100.4 PH IS ABOUT 7.4 – SLIGHTLY BASIC OR ALKALINE ABOUT 8% OF ADULT BODY WEIGHT – 5 L - 6 L MEN AND 4 L - 5 L WOMEN 18.1 – BLOOD PLASMA 92% WATER WITH LOTS OF SUBSTANCES, MOST ARE PROTEINS 7% ALBUMIN – MOST ABUNDANT PLASMA PROTEIN, MADE IN LIVER, TRANSPORTS FATTY ACIDS AND STEROID HORMONES, IT DRAWS IN WATER FROM TISSUE (54%) GLOBULINS – 2ND MOST COMMON, ALPHA AND BETA ARE MADE IN THE LIVER AND TRANSPORT LIPIDS AND FAT SOLUBLE VITAMINS, GAMMA ARE IMMUNOGLOBULINS FROM PLASMA CELLS (38%) FIBRINOGEN – LEAST COMMON, FROM THE LIVER AND ESSENTIAL FOR BLOOD CLOTTING (7%) FINAL 1% OF SOLUTES ARE ELECTROLYTES, GASES, NUTRIENTS, AND WASTES 18.2 – PRODUCTION OF THE FORMED ELEMENTS HEMOPOIESIS – PRODUCING RBC IN THE RED BONE MARROW (LIVER AND SPLEEN CAN GENERATE FORMED ELEMENTS IF NEEDED) HEMOPOIETIC STEM CELL (HEMOCYTOBLAST) – ALL FORMED ELEMENTS COME FROM THIS TYPE OF CELL, FORMS INTO 2 POSSIBLE TYPES OF CELLS LYMPHOID STEM CELL – BECOMES A LYMPHOCYTE FOR IMMUNITY, MATURES IN VARIOUS PLACES MYELOID STEM CELL – BECOMES ERYTHROCYTES, PLATELETS, GRANULAR LEUKOCYTE, OR MONOCYTES 18.2 – HEMOPOIETIC GROWTH FACTORS EPO – FROM THE KIDNEY DUE TO LOW O2 LEVELS, STIMULATES PRODUCTION OF RBC THROMBOPOIETIN – FROM LIVER AND KIDNEY, STIMULATES DEVELOPMENT OF PLATELETS CYTOKINES – LOCAL CELLULAR CHEMICALS THAT STIMULATE RESISTANCE TO DISEASE, 2 TYPES COLONY-STIMULATING FACTORS – STIMULATE DIFFERENTIATION OF MYELOBLASTS, OR INDUCES PRODUCTION OF MONOCYTES INTERLEUKINS – SIGNALING MOLECULE IN HEMOPOIESIS, DIFFERENTIATION AND MATURATION OF CELLS, PRODUCING IMMUNITY AND INFLAMMATION 18.2 – BONE MARROW BIOPSY – DIAGNOSTIC TEST TO DETECT FORMS OF ANEMIA AND/OR CANCER TRANSPLANT – REPLACE FAULTY BONE MARROW AND STEM CELLS WITH A HEALTHY MATCH. RADIATION AND/OR CHEMOTHERAPY IS FIRST USED TO DESTROY THE PATIENTS OWN MARROW BOTH REQUIRED A LARGE NEEDLE INTO THE ILIAC CREST, NOW BLOOD SAMPLE IS USUALLY SUFFICIENT 18.3 - ERYTHROCYTES COMMONLY CALLED RED BLOOD CELL (RBC), RETICULOCYTE BEFORE IT MATURES MOST COMMON FORMED ELEMENT, ABOUT 5 MILLION PER MICROLITER, ABOUT 25% OF TOTAL CELLS OF THE BODY CARRY O2 AWAY FROM THE LUNGS AND BRING SOME CO2 BACK TO LUNGS MATURES IN RED BONE MARROW, EXTRUDES NUCLEUS AND MOST ORGANELLES THEY RELY ON ANAEROBIC RESPIRATION AND DON’T SYNTHESIZE PROTEIN THEY HAVE A PLUMP BORDER AND A THIN CENTER, THEY ARE FLEXIBLE, AND THEY MOVE VERY SLOW IN A CAPILLARY 18.3 - ERYTHROCYTES WE PRODUCE ABOUT 2 MILLION PER SECOND, NEED GLUCOSE, LIPID, PROTEIN, AND OTHERS IRON – LESS THAN 20% CONSUMED IS ABSORBED, ANIMAL SOURCES ARE ABSORBED BETTER COPPER – HELPS TO ABSORB AND TRANSPORT IRON, NEEDED TO PRODUCE HEMOGLOBIN ZINC – FACILITATES THE SYNTHESIS OF THE HEME B VITAMINS – FOLATE AND B12 FACILITATE DNA SYNTHESIS RBC’S LIVE FOR ABOUT 120 DAYS AND ARE THEN EATEN BY MACROPHAGES, AA ARE RECYCLED TO FORM NEW RBC’S, IRON IS STORED OR RECYCLED, NON IRON PORTION EVENTUALLY URINATED OUT OR BECOMES BILE AND IS EXCRETED IN FECES 18.3 - HEMOGLOBIN A MOLECULE OF 4 FOLDED PROTEINS AND A HEME WHICH HAS AN IRON ION EACH IRON ION CAN HOLD 1 O2 MOLECULE THERE CAN BE 300 MILLION HEMOGLOBIN IN 1 RBC (1.2 BILLION O2 MOLECULES) WILL CARRY ABOUT 24% OF CO2 BACK TO THE LUNGS, 76% DISSOLVE IN PLASMA OR FORM BICARBONATE ION HEMOGLOBIN RARELY LEAVES ALL OF ITS O2 BEHIND INSUFFICIENT RBC IS ANEMIA, TO MANY RBC IS POLYCYTHEMIA (HIGH VISCOSITY) 18.3 PERCENT SATURATION – PERCENT OF HEMOGLOBIN SITES OCCUPIED BY O2, MEASURED BY A PULSE OXIMETER (NORMAL IS 95-100%) THE KIDNEYS HAVE RECEPTORS FOR O2 SATURATION SINCE THEY FILTER ABOUT 180 L/DAY IF O2 DECREASES THEN EPO PRODUCTION WILL INCREASE AND VICE VERSA PEOPLE LIVING AT HIGH ELEVATIONS NORMALLY HAVE A HIGHER HEMATOCRIT 18.3 – DISORDERS OF ERYTHROCYTES MORE THAN 400 TYPES OF ANEMIA IN 3 MAJOR GROUPINGS – BLOOD LOSS, POOR RBC PRODUCTION, OR EXCESSIVE RBC DESTRUCTION SICKLE CELL DISEASE – GENETIC DISORDER, ABNORMAL HEMOGLOBIN, DELIVERS LESS O2, AND ASSUMES A SICKLE SHAPE AT LOW O2 CONCENTRATIONS. SICKLED RBC CAN CLOG VESSELS MOST COMMON IS IRON DEFICIENCY ANEMIA VITAMIN DEFICIENCY – LOW B12 AND FOLATE – POOR DIET, DISEASES, PREGNANCY, EXCESSIVE ALCOHOL OR OTHER MEDS DISEASE MAY ALSO DESTROY OR INHIBIT RBC STEM CELLS OR RED MARROW 18.4 – LEUKOCYTES AND PLATELETS WHITE BLOOD CELL (WBC) – PROTECT AGAINST INVADING MICROORGANISMS AND CELLS WITH MUTATED DNA, THEY CLEAN UP DEBRIS PLATELETS REPAIR DAMAGED BLOOD VESSELS AND PROVIDE GROWTH FACTORS FOR HEALING AND REPAIR 18.4 – CHARACTERISTICS OF LEUKOCYTES LARGER AND FEWER THAN RBC, COMPLETE CELLS WITH NUCLEUS AND ORGANELLES MANY TYPES OF WBC WITH A MUCH SHORTER LIFE SPAN THEY CAN LEAVE THE VESSELS THROUGH DIAPEDESIS THEY MAY CONTINUE TO MOVE LIKE AN AMOEBA OR TAKE UP A FIXED POSITION THEY ARE ATTRACTED TO CERTAIN CHEMICALS (CHEMOTAXIS) RELEASED BY CELLS 18.4 - CLASSIFICATION GRANULAR LEUKOCYTES – ABUNDANT GRANULES IN THE CYTOPLASM (NEUTROPHILS, EOSINOPHILS, AND BASOPHILS), PRODUCED IN RED BONE MARROW, LIFESPAN OF HOURS TO DAYS, AND HAS A NUCLEUS WITH MULTIPLE LOBES AGRANULAR LEUKOCYTES – MANY FEWER GRANULES (MONOCYTES WHICH BECOME MACROPHAGES AND LYMPHOCYTES FROM THE LYMPHOID STEM CELL LINE) 18.4 - GRANULAR NEUTROPHILS – MOST COMMON, 50-70% OF ALL LEUKOCYTES, RAPID RESPONDERS TO SITE OF INFECTION, EFFICIENT PHAGOCYTES, GOOD AGAINST BACTERIA, THEY CONTAIN LYSOZYME AND DEFENSINS TO BREAKDOWN MEMBRANES AND WALLS EOSINOPHILS – 2-4% OF LEUKOCYTES, GRANULES INCLUDE ANTIHISTAMINE, MOLECULES TO FIGHT PARASITIC WORMS, CAPABLE OF PHAGOCYTOSIS ESPECIALLY IF ANTIBODIES ARE BOUND TO THE TARGET BASOPHILS – LEAST COMMON, SLIGHTLY SMALLER, THEY INTENSIFY THE INFLAMMATORY RESPONSE (MAST CELLS DO THAT TOO), GRANULES RELEASE HISTAMINE AND HEPARIN (OPPOSES CLOTTING) 18.4 – AGRANULAR LEUKOCYTES LYMPHOCYTES – ONLY FORMED ELEMENTS FROM LYMPHOID STEM CELLS, SECOND MOST COMMON LEUKOCYTE, ESSENTIAL IN IMMUNE RESPONSE, 3 TYPES NATURAL KILLER – GENERAL NONSPECIFIC IMMUNITY AGAINST FOREIGN CELLS OR BODY CELLS THAT DON’T EXPRESS “SELF” PROTEINS B AND T CELLS – SPECIFIC IMMUNITY, B CELLS LEAD TO PLASMA CELLS AND ANTIBODY, THEY BOTH HAVE MEMORY CELLS AFTER EXPOSURE THAT LAST FOR YEARS MONOCYTES – FROM MYELOID STEM CELLS, LARGE SIZE, BECOME MACROPHAGES AS THEY LEAVE CIRCULATION, THEY RELEASE CHEMICALS TO ATTRACT OTHER LEUKOCYTES, LOTS ARE FOUND NEAR VIRAL AND FUNGAL INFECTIONS, TB, AND LEUKEMIA 18.4 - LIFECYCLE HOURS TO DAYS PRODUCED IN BONE MARROW FULLY CAPABLE OF MITOSIS WHICH LETS US MAINTAIN IMMUNITY FOR LIFE 18.4 – DISORDERS OF LEUKOCYTES LEUKOPENIA – TOO FEW LEUKOCYTES ARE PRODUCED, UNABLE TO FIGHT OF DISEASE LEUKOCYTOSIS – TOO MANY LEUKOCYTES, BUT MOST ARE NONFUNCTIONAL, INCREASED RISK FOR DISEASE LEUKEMIA – CANCER INVOLVING AN ABUNDANCE OF LEUKOCYTES WHICH DO NOT FUNCTION PROPERLY. CHRONIC – MATURE LEUKOCYTES FAIL TO DIE, ACUTE – OVERPRODUCTION OF YOUNG IMMATURE LEUKOCYTES LYMPHOMA – CANCER OF MASSES OF MALIGNANT T AND B CELLS COLLECT IN LYMPH NODES, SPLEEN, LIVER, AND OTHER TISSUES. LEUKOCYTES DON’T FUNCTION PROPERLY, VULNERABLE TO INFECTION 18.4 - PLATELETS A FRAGMENT OF THE CYTOPLASM OF A CELL IN A PLASMA MEMBRANE (MEGAKARYOCYTE) MEGAKARYOCYTES RELEASE 2000-3000 PLATELETS DURING A LIFESPAN AND ARE THEN CONSUMED BY MACROPHAGES PLATELETS ARE SMALL AND NUMEROUS, 33% STORED IN SPLEEN FOR FUTURE RELEASE STOP BLOOD FLOW FOLLOWING DAMAGE TO A VESSEL, SECRETE GROWTH FACTOR FOR REPAIR THROMBOCYTOSIS – TOO MANY PLATELETS, UNWANTED CLOTS THROMBOCYTOPENIA – TOO FEW PLATELETS, POOR CLOTTING, EXCESSIVE BLEEDING 18.5 - HEMOSTASIS VASCULAR SPASM – IN RESPONSE TO A VESSEL SEVERED OR PUNCTURED, TRIGGERED BY ENDOTHELINS (LOCAL CHEMICALS) PLATELETS PLUG – PLATELETS STICK TO ENDOTHELIUM AND COLLAGEN, THEY CLUMP AND RELEASE ADP (HELP PLATELETS ADHERE), SEROTONIN (MAINTAIN VASOCONSTRICTION), PROSTAGLANDINS, AND PHOSPHOLIPIDS (MAINTAIN VASOCONSTRICTION AND ACTIVATE CLOTTING CHEMICALS) COAGULATION – FORMATION OF A BLOOD CLOT OF A MESH OF FIBRIN 18.5 - COAGULATION EXTRINSIC PATHWAY – NORMALLY TRIGGERED BY TRAUMA, QUICKER AND MORE DIRECT INTRINSIC PATHWAY – TRIGGERED BY INTERNAL DAMAGE TO VESSEL WALL, LONGER AND MORE COMPLEX, COMPLETED IN A FEW MINUTES COMMON PATHWAY – THE OVERLAP IN EVENTS OF EXTRINSIC AND INTRINSIC, BEGINS WITH FACTOR 10 (STUART-PROWER FACTOR), THEN PROTHROMBIN CONVERTS TO THROMBIN WHICH CONVERTS FIBRINOGEN INTO FIBRIN 12 KNOWN CLOTTING FACTORS SECRETED PRIMARILY BY LIVER AND PLATELETS VITAMIN K REQUIRED BY LIVER FOR MANY CLOTTING FACTORS 18.5 CONTRACTILE PROTEINS PULL THE EDGES OF THE CLOT TOGETHER FIBRINOLYSIS – GRADUAL DEGRADATION OF THE CLOT BY PLASMIN, BRADYKININ IS RELEASED TO COUNTERACT THE SEROTONIN AND PROSTAGLANDIN ANTICOAGULANT – OPPOSES COAGULATION, ANTITHROMBIN AND HEPARIN OPPOSE CONVERSION OF PROTHROMBIN 18.5 – DISORDERS OF CLOTTING HEMOPHILIA – DEFICIENCY OF A CLOTTING FACTOR THROMBOPHILIA – TENDENCY TO FORM THROMBOSIS, GENETIC OR ACQUIRED (LUPUS, IMMUNE REACTION TO HEPARIN, SICKLE CELL DISEASE, PREGNANCY AND OBESITY) A THROMBUS THAT BREAKS FREE IS CALLED AN EMBOLUS AND IF IT GETS TRAPPED IT CAN BECOME AN EMBOLISM ASPIRIN INHIBITS THE AGGREGATION OF PLATELETS, BUT IT INCREASES RISK OF ULCERS 18.6 – BLOOD TYPING RBC WITH FOREIGN ANTIGENS WILL TRIGGER AN IMMUNE RESPONSE, ANTIBODIES CAUSE RBC TO CLUMP TOGETHER (AGGLUTINATION), CLUMPS BLOCK VESSELS, HEMOGLOBIN IS RELEASED AND OVERWHELMS THE KIDNEYS CAUSING FAILURE ABO GROUP – ABSENCE OR PRESENCE OF A AND B ANTIGENS, GENETICALLY DETERMINED, ANTIBODY IS PREFORMED RH GROUP – ABSENCE OR PRESENCE OF A SECOND RBC ANTIGEN, ANTIBODY IS PRODUCED AFTER EXPOSURE TO THE ANTIGEN LIKE AN RH- MOTHER AND A RH+ BABY 18.6 DONORS AND RECEIVERS SHOULD MATCH IN AN IDEAL SITUATION UNIVERSAL DONOR – O-, STILL SOME COMPLICATIONS THAT SHOULD BE OVERCOME UNIVERSAL RECIPIENT – AB+, STILL SOME COMPLICATIONS THAT SHOULD BE OVERCOME