BLOOD “Sometimes the questions are complicated and the answers are simple.” ― Dr. Seuss

Functions of the blood Transportation Gases Nutrients Waste Hormones Regulation – pH, heat, fluid balance Protection – disease, blood loss

COMPONENTS FORMED ELEMENTS (LIVING) BUFFY COAT MATRIX (NOT LIVING) RED BLOOD CELLS (erythrocytes) BUFFY COAT LEUKOCYTES PLATELETS MATRIX (NOT LIVING) PLASMA RED CELLS ARE CONENCTIVE TISSUE, CARRY O2; SPIN BLOOD IN A TUBE AND YOU WILL SEE RED AT BOTTOM, THIN BUFFY COAT, AND SERUM AT TOP. CELLS ARE HEAVIER THAN SERA SO THEY SINK. RRBC – 45% OF BLOOD VOLUME = HEMATOCRIT LEVEL WBC & PLATELETS < 1% PLASMA= 55% 5-6 LITERS OF BLOOD IN A MALE Ph 7.35-7.45; TEMP 100.4 – SLIGHTLY WARMER THAN BODY

PLASMA 90% Water Nutrients, Salts (Electrolytes) Respiratory Gases Waste products Plasma Proteins (Most Abundant at 8%) HORMONES ALBUMIN CLOTTING FACTORS COMPLEMENT ALBUMIN IS A PLASMA PROTEIN

HOMEOSTASIS OF BLOOD LOW ALBUMIN= LIVER IS STIMULATED TO MAKE MORE PROTEIN CHANGE IN ACIDITY = LUNGS AND KIDNEYS WORK TO BALANCE IT PLASMA HELPS WITH HEAT DISTRIBUTION PLATELETS PREVENT BLOOD LOSS

RED BLOOD CELLS ANUCLEATE, NO MITOCHONDRIA FEW ORGANELLES FULL OF HEMOGLOBIN BICONCAVE DISK – INCREASES SURAFCE AREA FOR GAS EXCHANGE TRANSPORT OXYGEN/ CO2 4-6 MILLION CELLS /MM3 INCREASE CELLS = INCREASE THICKNES OF BLOOD LESS = THINNER & FLOWS EASILY 1 RBC HOLDS 250 MILLION HBG + 1 HBG HOLDS 4 O2= 1 BILLION MOLECULES OF O2 PER RBC

HEMOGLOBIN/ HEMATOCRIT HGB – MEASUREOF HEMOGLOBIN IN RBC MEN – 14 -17 G/ 100 ML WOMEN – 12 – 15 G/ 100 ML HCT – VOLUME % OF RBC IN WHOLE BLOOD MEN – 42 – 54% WOMEN – 36 -46% HINT: HCT IS 3 TIMES GREATER THAN HGB

LEUKOCYTES (WBC) 5,000 – 10,000/ MM3 COMPLETE CELL WITH NUCLEUS, ETC DIAPEDESIS – ABLE TO MOVE INTO AND OUT OF BLOOD VESSELS POSITIVE CHEMOTAXIS – ABILITY TO FIND AREAS OF TISSUE DAMAGE USE DIFFUSION GRADIENT WHEN BODY CALLS WBC TO TISSUE AREAS THAT ARE DAMAGED, THE BODY SPEEDS UP THEIR PRODUCTION (SPECIAL ORDER SUPPLY FROM THE FACTORY)

WBC GROUPS GRANULOCYTES AGRANULOCYTES NEUTROPHILS EOSINOPHILS BASOPHILS HISTAMINE HEPARIN AGRANULOCYTES LYMPHOCYTES MONOCYTES NEUTROPHILS – ACUTE INFECTION EOSINOPHILS – ALLERGIES AND PARASITIC INFECTIONS BASOPHILS – HISTAMINE CAUSES LEAKY VESSELS AND DRAWS OTHER WBC TO SITE OF INJURY LYMPHOCYTE – IN LYMPHATIC TISSUE MONOCYTES TRAVEL TO THE TISSUE AND BECOME MACROPHAGES

PLATELETS FRAGMENTS OF MEGAKARYOCYTES 150,000 – 450,000/ MM3 NEEDED IN THE CLOTTING CASCADE ACT LIKE SANDBAGS AT A BREAK IN THE LEVEE

HEMATOPOIESIS OCCURS IN RED BONE MARROW SKULL, PELVIS, RIBS, STERNUM AND PROXIMAL EPIPHYSIS OF LONG BONE HEMOCYTOBLAST (STEM CELL) STARTS OFF FROM THE MARROW BECOMES EITHER LYMPHOID OR MYELOID STEM CELL. CANNOT GROW, DIVIDE OR SYNTHESIZE PROTEINS = 120 DAY LIFE SPAN CAN’T ALTER PATH ONCE THEY START DOWN TO MYELOID OR LYMPHOID

CONTINUED RBC DIVIDES MANY TIME, ACCUMULATES HGB; WHEN GETS ENOUGH HGB, CELL EJECTS NUCLEUS & ORGANELLES, COLLAPSES ON SELF = BI-CONCAVE IMMATURE RBC IS A RETICULOCYTE TAKES 3-5 DAYS UNTIL A MATURE RBC PRODUCTION RATE CONTROLLED BY ERYTHROPOIETIN (KIDNEY) IN RESPONSE TO O2 LEVELS IN BLOOD. E-POIETIN STIMULATES BONE MARROW CONSTANCE BALANCE OF PRODUCTION AND BREAKDOWN, SO WE ALWAYS HAVE ENOUGH FUNCTIONAL RBCS EPOIETIN WORKS ON HUMORAL NEGATIVE FEEDBACK

CONTINUED AS THEY AGE, RBC BECOMES RIGID AND BREAKS APART ELIMINATED BY MACROPHAGES IN THE SPLEEN , LIVER AND OTHER TISSUES GLOBIN &IRON IS RECYCLED HEME IS BROKEN DOWN AND EXCRETED BY LIVER

LEUKOCYTE AND PLATELET FORMATION COLONY STIMULATING FACTORS AND INTERLEUKIN INCREASE LEUKOCYTE PRODUCTION IN THE MARROW THROMBOPOIETIN INCREASES RATE OF PLATELET FORMATION BONE MARROW BIOPSY ASPIRATES MARROW FROM STERNUM OR ILIUM FOR EXAMINATION REGARDING DISEASES

HEMOSTASIS - CLOTTING PLATELET PLUG FORMATION VASCULAR SPASMS COAGULATION/ CLOTTING FIBROUS TISSUE FORMATION GROWS INTO THE CLOT AND PERMANENTLY CLOSE THE DAMAGE IN THE VESSEL

#1-PLATELET PLUG FORMATION PLATELETS DO NOT STICK TO SMOOTH SURFACES COLLAGEN FIBER EXPOSURE CAUSES PLATELETS TO BECOME STICKY AND ADHERE TO DAMAGED AREA SECRETE CHEMICALS THAT ATTRACT MORE AND MORE PLATELETS UNTIL A PLUG IS FORMED

#2 VASCULAR SPASM ANCHORED PLATELETS SECRETE SEROTONIN CAUSING VASCULAR SPASM SPASM CONSTRICTS THE VESSEL WHICH DECREASES BLOOD LOSS

#3 COAGULATION INJURED TISSUE RELEASES (TF) TISSUE FACTOR PF3 (ON PLATELET), TF, VITAMIN K, CALCIUM, & CLOTTING FACTORS MAKE PROTHROMBINASE PROTHROMBINASE CONVERTS PROTHROMBIN INTO THROMBIN THROMBIN ALTERS FIBRINOGEN TO FIBRIN WHICH FORMS THE MESH TO TRAP RBCS THE TRPPED RBCS FORM THE CLOT. CLOT BEGINS TO CONTRACT SQUEEZING OUT SERA & PULLING EDGES OF WOUND TOGETHER

CLOTTING USUALLY TAKES 3-6 MINUTES ONCE CLOTTING HAS STARTED, THE TRIGGERING FACTORS ARE INACTIVATED TO PREVENT WIDESPREAD CLOTTING IN BODY PRESSURE SPEEDS UP CLOTTING BY RELEASING LOCAL TISSUE FACTORS ENDOTHELIUM GROWS AND CLOT IS MACROPHAGED, SCAR REMAINS.

UNDESIRABLE CLOTTING THROMBUS – STABLE CLOT IN A VESSEL EMBOLUS – MOVING CLOT IN A VESSEL FACTORS THAT ENCOURAGE CLOTTING: SEVERE BURNS PHYSICAL BLOWS ACCUMULATION OF FATTY MATERIAL SLOW FLOWING BLOOD BLOOD POOLING

BLEEDING DISORDERS THROMBOCYTOPENIA – LOWERED LEVEL OF PLATELETS HEMOPHILIA – LACK OF A CLOTTING FACTOR LIVER FAILURE – LEADS TO INABILITY TO SYNTHESIZE ENOUGH CLOTTING FACTORS VITAMIN k NEEDED BY LIVER CELLS TO MAKE CLOTTING FACTORS. MAY NEED TO TRANSFUSE WITH RBC TO REPLACE CLOTTING FACTORS

HUMAN BLOOD GROUPS ANTIGEN – SOMETHING OUR BODY RECOGNIZES AS FOREIGN “NOT ME” WE RECOGNIZE OUR OWN AS “ME” GIVING “NOT ME” TO “ME” CAUSES OUR BODY TO BUILD ANTIBODIES TO “NOT ME”; WHEN SEE “NOT ME”, THE ANTIBODIES BIND WITH THEM AND CLUMP (AGGLUTINATE) 30 COMMON RBC ANTIGENS AGGLUTINATION CAN CAUSE CLOGIING OF THE SMALL VESSELS AROUND THE BODY. OUR IMMUNE SYSTEM WILL BREAK THEM DOWN AND RID THEM FROM OUR BODY TRANSFUSION REACTION – FEAR IS KIDNEY WILL BE CLOGGED BY THE HEME PORTION OF THE BROKEN CELLS CAUSING RENAL FAILURE; SX ALSO ARE FEVER, CHILLS, NAUSEA, VOMITING. TX IS TO FLUSH THE KIDNEYS TO PREVENT BLOCKAGE.

ABO BLOOD GROUPS TYPE A HAS “A” ANTIGEN TYPE B HAS “B’ ANTIGEN TYPE O HAS NEITHER ANTIGEN TYPE AB HAS BOTH A AND B ANTIGEN THE ANTIGEN CAUSES RECOGNITION OF “SELF” ANTIBODIES ARE BUILT TO “NOT SELF”

CONTINUED “A” ANTIGEN HAS “NOT B” ANTIBODIES “B” ANTIGEN HAS “NOT A” ANTIBODIES “O” HAS NO ANTIGEN; HAS BOTH “NOT A & NOT B” ANTIBODIES SO IS THE UNIVERSAL DONOR BUT CAN ONLY RECEIVE ‘O’ “AB” HAS BOTH ANTIGEN THEREFORE HAS NO ANTIBODIES; IS THE UNIVERSAL RECIPIENT, CAN ONLY GIVE TO AB O HAS NO ANTIGEN SO IT CANT TRIGGER ANTIBODIES IN OTHERS = CAN GIVE TO ANYONE AB HAS 2 SELF ANTIGEN AND NO ANTIBODIES SO IT CAN RECEIVE FROM ANYONE

RH GROUPS RH ANTIGENS ARE DETERMINED AT BIRTH POSITIVE MEANS YOU HAVE THE ANTIGEN, NEGATIVE MEANS YOU DON’T TRANSFUSE RH- WITH RH+ BLOOD CAUSES ANTIBODIES TO BE BUILT ANTIBODIES WILL LYSE RBC ON SECOND CONTACT HEMOLYTIC DISEASE OF THE NEWBORN- GIVE RHOGAM TO PREVENT ANTIBODIES

BLOOD TYPING TEST BLOOD BY MIXING IT WITH ANTI A OR ANTI B SERUM AND WATCH FOR AGGLUTINATION SAME IS DONE FOR RH FACTOR CROSS MATCHING USES THE PATIENTS BLOOD AND THE DONOR BLOOD TO ASSESS FOR AGGLUTINATION

WHOLE BLOOD TRANSFUSIONS TREAT MASSIVE HEMORRHAGE REPLACES LOSS EXCHANGE BLOOD FOR HEMOLYTIC DISEASE OF THE NEWBORN

USING BLOOD COMPONENTS HEMAPHARESIS- REMOVE BLOOD, SPIN OUT NEEDED ELEMENTS, & RETURN REMAINDER OF CELLS ANS PLASMA TO PERSON PLASMAPHARESIS – REMOVE BLOOD, SPIN IT AND RETURN THE FORMED ELEMENTS

USE OF PLASMA REPLACES BLOOD VOLUME TO PREVENT SHOCK – NO RED CELLSSO DO NOT NEED TO TYPE IT ALBUMIN 5% OR 25% FFP = FRESH FROZEN PLASMA CRYOPRECIPITATE – FACTOR 8 & FIBRINOGEN GAMMA GLOBULIN

IMBALANCE OF RBC ANEMIA POLYCYTHEMIA HEMOLYTIC –SICKLE CELL HEMORRHAGIC PERNICIOUS – VITAMIN B12 THALESSEMIA APLASTIC – BONE MARROW SUPPRESSION IRON DEFICIENCY POLYCYTHEMIA LOW RBC COUNT LOW AMOUNT OF HBG IN RBC ABNORMALLY SHAPED RBC RUPTURES EASILY TOO MANY RBC = THICK BLOOD

IMBALANCE WITH WBC LEUKOPENIA- LOWERED WBC COUNT IN BLOOD NEUTROPENIA – LOWERED NEUTROPHIL COUNT LEUKOCYTOSIS – MORE THAN 11,000/ MM3 LEUKEMIA – LARGE NUMBER OF IMMATURE WBC SENT FROM MARROW

CLOTTING DISORDERS HEMOPHILIA VON WILLEBRANDS DISEASE THROMBOCYTOPENIA DISSEMINATED INTRAVASCULAR COAGULATION

DEVELOPMENTAL FETAL HEMOGLOBIN CARRIES MORE OXYGEN THAN AFTER BORN IF RBC ARE BROKEN DOWN FASTER THAN INFANTS IMMATURE LIVER CAN HANDLE, JAUNDICE OCCURS AS WE AGE, CLOTS, LEUKEMIAS AND ANEMIAS INCREASE IN FREQUENCY PERNICIOUS ANEMIA BECOME THE STOMACH MUCOSA ATROPHIES WITH AGE.