BLOOD

AJENG DIANTINI

CARDIOVASCULAR SYSTEM:HEART (PUMP)BLOOD VESSELS (TRANSPORT)BLOODCIRCULATORY SYSTEM :HEART (PUMP)BLOOD VESSELS (TRANSPORT)BLOODLYMPHLYMPH VESSELBLOOD = CONNECTIVE TISSUE :CELLULAR ELEMENTSFLUID MATRIX = PLASMA

FUNCTIONS OF THE BLOOD:TRANSPORTSOXYGEN : LUNGS TO BODY TISSUESWASTE PRODUCT: BODY TISSUES TO KIDNEYS, LIVER, LUNGS, SWEAT GLANDS HORMONES, NUTRIENTS, ENZYMES THROUGHOUT THE BODYREGULATESBLOOD CLOTTINGBODY TEMPERATUREACID-BASE BALANCE (pH) AMOUNT OF WATER AND ELECTROLYTES IN BODY FLUIDSPROTECTS AGAINST HARMFUL MICROORGANISM & OTHER SUBSTANCES BY CONTRIBUTING WBC, PROTEINS, ANTIBODIES TO THE INFLAMMATORY AND IMMUNE RESPONSES

PROPERTIES OF BLOOD:BLOOD VOLUME : ADULT 7-9 % OF TOTAL BODY WEIGHT OR 79 ml/kg OF TBW MAN : 5 6 L WOMAN : 4 5 L

VISCOSITY : 3.5 5.5 (WATER: 1.000 BLOODTHICKER,DENSER, MORE ADHESIVE THAN WATER; FLOWS 4-5 X MORE SLOWLY

SPECIFIC GRAVITY OR DENSITY: 1.045 1.065 (WATER: 1.000)

COLOR : OXYGENATED HB RED OXYGEN IS REMOVED BLUISH WBC, PLATELETSCLEAR PLASMA YELLOWISH

pH : SLIGHTLY ALKALINE, 7.35 7.45 ARTERIAL BLOOD IS MORE ALKALINE

TEMPERATURE : 38 C

COMPONENTS OF BLOOD

LIQUID PART : PLASMA ( 55 %)

SOLID PART (FORMED ELEMENTS) : (45 %)

RBC (ERYTHROCYTES), WBC (LEUCOCYTES), PLATELETS (THROMBOCYTES)

PLASMAWATER: 90 % (DISSOLVING, TRANSPORTING NUTRIENTS) TO MAINTAIN THE NORMAL STATE OF HIDRATION SOLVENT FOR EXTRACELLULAR AND INTRACEL CHEMICAL REACTIONS CONTAIN MANY SOLUTESPLASMA PROTEINS: ALBUMINS , FIBRINOGEN, GLOBULINSALBUMIN (60 %), SYNTHESIZED IN LIVER WATER RETENTION IN BLOOD---- MAINTAIN NORMAL BLOOD VOLUME AND PRESSURE CARRIER MOLECULE : HORMON

GLOBULINS (36 %):BASED ON STRUCTURE AND FUNCTION:, , GLOBULINS ARE PRODUCED BY LIVER. TRANSPORT LIPID (LDL, HDL)AND FAT SOLUBLE VITAMINS

GAMMA GLOBULINS = IMMUNOGLOBULINS: Ig A, Ig G, Ig M, IgD, and IgE FIBRINOGEN (4 %) :

BLOOD CLOTTING PLASMA ELECTROLYTES: Na + : OSMOTIC PRESSURE, FLUID MOVEMENTS, DETERMINE TOTAL VOLUME OF EXTRACELLULAR FLUID. ANOTHER : K+, Ca 2+, Mg 2+ ANIONS : Cl - , I -, PO4

NUTRIENTS AND WASTE PRODUCTS

GLUCOSE : THE MOST READILY AVAILABLE SOURCE OF ENERGY

AMINO ACIDS : BUILDING BLOCKS FOR PROTEIN SYNTHESIS

LIPIDS : FOUND IN THE FORM OF FOSFOLIPID, TRIGLYCERIDE, FFA, AND CHOLESTEROL IMPORTANT COMPONENTS OF NERVE CELLS, STEROID HORMONES, SOURCE OF FUEL

METABOLIC WASTE : LACTIC ACID

GASES AND BUFFERS

OXYGEN, NITROGEN, CARBON DIOXIDE.

CO 2 IS TRANSPORTED BY RBC AND PLASMA, IN THE DISSOLVED STATE AND IN THE FORM OF BICARBONATE ION (HCO3 -)

NITROGEN IS TRANSPORTED IN THE DISSOLVED STATE IN PLASMA.

RED BLOOD CELLS (ERYTHROCYTES

RBC : 50 % THE VOLUME OF HUMAN BLOOD

MEASURE : 7 m IN DIAMETER 2 m THICK

SHAPE : LIKE A DISK, BICONCAVE PROVIDE LARGER SURFACE AREA FOR GAS DIFFUSION THAN A FLAT DISK.

RBC MATURE: NO LONGER HAS A NUCLEUS OR MANY ORGANELLES (MITOCHONDRIA) RELY ON ITS STORE OF ALREADY PRODUCED PROTEINS, ENZYMES AND RNA.

Erythrocytes (Red Blood Cells)

Blood cells

HEMOGLOBIN

Hb IS AN OXYGEN CARRYING GLOBULAR PROTEIN

Hb CONSIST OF : 5 % HEME (IRON CONTAINING PIGMENT) COLOR 95 % GLOBIN (PP PROTEIN)

MAN HAVE MORE Hb THAN FEMALE FIGURE 18.3: Hb HAS 4 PP CHAIN (2 & 2 ), ATTACHED TO IT ARE HEME GROUP, WHICH ARE ATTACHED TO IRON GROUP (BINDING SITE FOR OXYGEN), IRON ATOM OXYGEN CARRYING SUBSTANCE.

FUNCTION: COMBINE WITH OXYGEN AND RELEASE IT TO BODY TISSUE.CARRIES CO2 FROM TISSUES TO LUNGS MAINTAIN A STABLE ACID BASE BALANCE IN THE BLOOD.

OXYHEMOGLOBIN RED COLOR BLUISH COLOR REDUCED Hb.FETAL HEMOGLOBIN (HbF)---- HAS GREATER AFFINITY FOR OXYGEN

Structure of Hemoglobin

TRANSPORT OF OXYGEN IN BLOOD

MAJOR ROLE OF ERYTHROCYTE

MORE O2 IN BLOOD THAN THERE IS IN THE TISSUE HbO2 DIFFUSE INTO THE CELLS

SOME TOXIC AGENTS (INCECTICIDES, SULFUR DIOXIDE) BINDS TO Hb MORE READILY THAN OXYGEN DOES PREVENT Hb FROM CARRYING OXYGEN EFFECTIVELY.

LACK OF OXYGEN NUMBNESS, DIZZINESSCO2 (AUTOMOBILE EXHAUST FUME, CIGARETTE SMOKE) BINDS TO Hb 210 X FASTER THAN OXYGEN STABLE COMPOUND

TRANSPORT OF CARBONDIOXIDE IN BLOOD

ERYTHROCYTE CARRYING OXYGEN FROM LUNGS TO BODY TISSUES AND CARRYING CO2 FROM THE TISSUES TO THE LUNGS.

CO2 IS MORE SOLUBLE IN WATER THAN 02 IS

IN BLOOD CO2 IS TRANSPORTED IN 3 WAYS:60 % CO2 REACTS WITH WATER:

CO2 + H2O ====== H2CO3

H2CO3 IS CONVERTED QUICKLY:

H2CO3 ========= HCO3 + H+

CARBONIC ACID IN BLOOD IS VERY SMALL AND THE REACTION HAPPEN IN RBC . H2CO3 MOVES OUT THE RBC AND IS CARRIED IN THE PLASMA POSITIVE CHARGE IN RBC. FOR EQUILIBRIUM AND HOMEOSTASIS, CHLORIDE IONS MOVE INTO RBC.

2. 30 % CO2 REACTS WITH Hb CARBA- MINOHEMOGLOBIN (HbCO2), WHICH IS CARRIED FROM TISSUE TO THE LUNGS AND THE CO2 IS EXCHANGED FOR O2

3. 10 % CO2 IS DISSOLVED IN THE PLASMA AND RBC AS MOLECULAR CO2

ERYTHROCYTE MEMBRANES AND SOLUTE CONCENTRATIONHAVE THIN, STRONG AND FLEXIBLE PLASMA MEMBRAN MOVE EASILY THROUGH SMALL BLOOD VESSEL THE MEMBRANE IS PERMEABLE TO WATER, O2, CO2 , GLUCOSE, UREA, ETC BUT IMPERMEABLE TO Hb, LARGE PROTEIN.

CONC. IN THE PLASMA IS ISOTONIC TO THE FLUID INSIDE ERYTHROCYTE CONSTANT OSMOTIC PRESSURE ON BOTH SIDES OF PLASMA MEMBRANE NORMAL CELL SHAPE.

IF PLASMA CONC. OF SOLUTE INCREASES ABOVE NORMAL PLASMA BECOME HYPERTONIC THE CELL SHRINKS, OR CRENATES.

IF PLASMA CONC. OF SOLUTE DECREASES BELOW NORMAL PLASMA BECOME HYPOTONIC THECELL SWELLS, BURSTS HEMOLYSIS

DESTRUCTION AND REMOVAL OF ERYTHROCYTESLIFE SPAN OF AN ERYTHROCYTES IS 80-120 DAYS, BECAUSE:IT HAS NO NUCLEUSUNABLE TO REPLACE THE ENZYME AND OTHER PROTEINS TO FUNCTION PROPERLYFRAGILE ERYTHR. PASS THROUGH THE NARROW CAPILLARIES (SINUSOIDS) OF THE SPLEEN, LIVER AND OTHER PARTS OR RES, THEIR LEAKY MEMBRANES RUPTURE AND THE CELLULAR REMNANTS ARE ENGULF BY MACROPHAGE.MACROPHAG DIGEST THE Hb INTO SMALLER AMINO ACIDS THE HEME PORTION IS CONVERTED INTO BILIVERDIN AND THEN INTO BILIRUBIN WHICH BINDS TO PLASMA ALBUMIN AND IS TRANSPORTED TO THE LIVER.WITHIN THE LIVER, BILIRUBIN IS BOUND TO GLUCURONIC ACID AND IS SECRETED IN BILE.

LIVER IS FAULTY JAUNDICE THE IRON PORTION OF HEME IS BOUND TO PROTEIN AND STORED IN BONE MARROW AS FERRITIN.

Iron cycle

Metabolism of Bilirubin released by heme breakdown

WHITE BLOOD CELLS (LEUCOCYTES)

SCAVENGER THAT DESTROY MICROORGANISM

REMOVE FOREIGN MOLECULE

REMOVE DEBRIS FROM DEAD OR INJURED TISSUE CELLS

SLIGHT LARGER TO MUCH LARGER THAN ERYT

HAVE NUCLEI, AND THE CELLS ARE ABLE TO MOVE INDEPENDENTLY AND PASS THROUGH BLOOD VESSEL WALLS INTO THE TISSUES

ABLE TO PRODUCE ENERGY

THEY CAN SYNTHESIZE PROTEIN AND ARE ABLE TO PRODUCE mRNA IN THE NUCLEI

ADULTS : 4000 11000/mm3

PRODUCTION OF WBC (LEUKOPOIESIS)WBC (GRANULOCYTES) ORYGINATE = ERYTHR, AND LEUKOPOIESIS ALSO OCCURS IN LYMPHOID TISSUES (LYMPH NODES, SPLEEN AND TONSILS)

BASIC CLASSIFICATIONS OF LEUCOCYTES:GRANULOCYTES (POLYMORPHONUCLEAR LEUCOCYTES)2. AGRANULOCYTES (MONONUCLEAR LEUCOCYTES)

GRANULOCYTESMOST NUMEROUS OF WBC, CONTAIN LARGE NUMBERS OF GRANULES IN THE CYTOPLASMTHREE TYPES : NEUTROPHILS, EOSINOPHILS, BASOPHILS, WHEN STAINED BY WRIGHTS STAIN:NEUTROPHILS : LIGHT PINK BLUE BLACKEOSINOPHILS : RED RED ORANGEBASOPHILS : BLUE BLACK RED PURPLE

NEUTROPHILS60 % FROM GRANULOCYTES

PHAGOCYTES THAT ENGULF AND DESTROY MICROORGANISM AND OTHER FOREIGN MATERIAL

GRANULES INSIDE THE CYTOPLASM : ENZYME (LYSOZYME) THAT DIGEST AND DESTROY THE INTRUDERS.

NEUTROPHIL MAY BE DESTROYED AS THEIR GRANULES ARE DEPLETED

DEAD MICROORGANISM AND NEUTROPHILS MAKE UP THE THICK, WHITISH FLUID PUS

SPESIFIC CHEMICALS RELEASED AT THE SITE OF INFECTION CHEMOTAXIS PROCESS

NEUTROPHIL (AND LEUCOCYTES) ARE ABLE TO DEFORM, ELONGATE AND SQUEEZE INTO THE PORES OF CAPILLARY WALLS DIAPEDESIS

EOSINOPHILSB-SHAPE NUCLEIPHAGOCYTES HAVE AMOEBOID MOVEMENTCONTAIN LYSOSOMAL ENZYMES AND PEROXIDASEINCREASES DURING ALLERGY ATTACKS, CERTAIN PARASITIC INFECTIONS, SOME AUTOIMMUNE DISEASES, CERTAIN TYPES OF CANCER.CONTAIN PLASMINOGEN WHICH HELPS DISSOLVE BLOOD CLOTS

BASOPHILSLEAST NUMEROUS OF ALL GRANULOCYTESGRANUL CONTAIN HEPARIN, HISTAMINE, SLOW REACTING SUBSTANCE-A (SRS-A).SRS-A PRODUCE SOME OF THE ALLERGIC SYMPTOMS AS BRONCHIAL CONSTRICTION.PLAY IMPORTANT ROLE IN PROVIDING IMMUNITY AGAINST PARASITES

AGRANULOCYTESMONOCYTES : 5 % OF LEUCOCYTESLYMPHOCYTES : 30 % OF LEUCOCYTES

MONOCYTES

MOBILE PHAGOCYTES, LARGEST BLOOD CELLSHAVE LARGE, FOLDED NUCLEI; GRANULESDEVELOP IN BONE MARROW, FROM MONOBLASTSONCE IN TISSUE SPACES, MONOCYTES ENLARGED 5-10 X THEIR NORMAL SIZE AND BECOME PHAGOCYTIC MACROPHAGESMACROPHAG FORM THE RETICULOENDOTHELIAL SYSTEM, WHICH LINES THE VASCULAR PORTIONS OF THE LIVER, LUNGS, LYMPH NODES, THYMUS GLAND AND BONE MARROWMONOCYTES AND MACROPHAGES PRODUCE COLONY STIMULATING FACTOR (CSF) WHICH STIMULATE BONE MARROW TO PRODUCE MORE MONOCYTES AND NEUTROPHILS

LYMPHOCYTESSMALL, MONONUCLEAR, LARGE ROUND NUCLEUS THAT OCCUPIES MOST OF THE CELL

THEIR NAME COME FROM LYMPH, THE FLUID THAT TRANSPORTS THEM

ORIGINATE FROM HEMOCYTOBLASTS OF BONE MARROW, INVADE LYMPHOID TISSUES WHERE THEY ESTABLISH COLONIES.

MOST LYMPHOCYTES ARE FOUND IN LYMPH NODES, SPLEEN, THYMUS GLAND, TONSILS, ADENOIDS AND LYMPHOID TISSUE OF GIT

ABLE TO RE-ENTER THE CIRCULATORY SYSTEM

SOME LYMPHOCYTES LIVE FOR YEARS, RECIRCULATING BETWEEN BLOOD AND LYMPHOIDS ORGANS.

LYMPHOCYTES ARE NOT PHAGOCYTES

2 TYPES : B CELLS AND T CELLS - BOTH REGULATE CELLULAR IMMUNE RESPONSE - SECRETE CHEMICALS THAT DESTROY BACTERIA, POISONS, VIRUSES, TISSUE AND CHEMICAL DEBRIS - WHEN B CELLS ACTIVATED, THEY ENLARGE AND BECOME PLASMA CELLS

PLATELETS (THROMBOCYTES)DISK-SHAPED, ONE-QUARTER THE SIZE OF ERYTHROCYTES

START THE INTRICATE PROCESS OF BLOOD CLOTTING

MUCH MORE NUMEROUS THAN LEUCOCYTES, AVERAGING ABOUT 350,000/ M3

LACK NUCLEI, INCAPABLE OF CELL DIVISION

LIFE SPAN 7-8 DAYS

NOT ACTUALLY BLOOD CELLS BUT ARE CELLULAR FRAGMENTS OF MEGAKARYOCYTES

PLATELETS ADHERE TO EACH OTHER AND TO THE COLLAGEN IN CONNECTIVE TISSUE

WHEN BLOOD VESSEL IS INJURED (CAPILLARIES RUPTURE MANY TIMES A DAY), PLATELETS MOVE TO THE SITE, BEGIN TO CLUMP TOGETHER, ATTACHING THEMSELVES TO THE DAMAGED AREA

PLATELETS RELEASE : - GRANULES THAT CONTAIN SEROTONIN WHICH CONSTRICTS INJURED VESSELS AND RETARDS BLEEDING - ADP WHICH ATTRACTS MORE PLATELETS TO THE DAMAGED AREA

HEMOSTASIS : THE PREVENTION OF BLOOD LOSS

HEMOSTATIC MECHANISM CONSISTS OF:1. CONSTRICTION OF BLOOD VESSELS 2. THE CLUMPING TOGETHER (AGREGATION) OF PLATELETS 3. BLOOD CLOTTING

HEMOSTASIS IS A SPECIFIC TYPE OF HOMEOSTASIS THAT PREVENT BLOOD LOSS

VASOCONSTRICTIVE PHASE:

THE VESSEL WALL CONSTRICTS IN ORDER TO NARROW THE OPENING OF THE VESSEL AND SLOW THE FLOW OF THE BLOOD

THIS VASOCONSTRICTION IS DUE TO : - CONTRACTION OF THE SMOOTH MUSCLE OF THE VESSEL WALL - THE RELEASE OF THE VASOCONSTRICTOR CHEMICALS FROM PLATELETS

CONSTRICTION OF CAPILLARIES IS DUE TO VASCULAR COMPRESSION CAUSED BY THE PRESSURE OF LOST BLOOD THAT ACCUMULATES IN SURROUNDING TISSUES.

INJURED BLOOD VESSELS MAY CONTINUE TO CONSTRICT FOR 20 MIN OR MORE

PLATELETS PHASE

PLATELETS WILL SWELL AND ADHERE TO THE COLLAGEN IN ADJACENT CONNECTIVE TISSUES. THIS ATTACHMENT STIMULATES VASOCONSTRICTION.

PLATELETS HAVE BECOME VERY STICKY, SO THAT AS MORE AND MORE OF THEM MOVE INTO THE INJURED AREA, THEY STICK TOGETHER CLOG SMALL OPENING IN THE VESSEL OF WITH A PLATELETS PLUG.

THE PROCESS IS CALLED PLATELETS AGGREGATION.

IT STOPS HUNDREDS OF SMALL HEMORRHAGES EVERY DAY AND IT TRIGGERS THE BLOOD CLOTTING MECHANISM

BASIC MECHANISM OF BLOOD CLOTTING(COAGULATION PHASE)THE BASIC CLOTTING MECHANISM INVOLVES THE FOLLOWING EVENTS:1. AIDED BY A PLASMA GLOBULIN CALLED ANTIHEMOPHILIC FACTOR (AHF), BLOOD PLATELETS DISINTEGRATE AND RELEASE THE ENZYME THROMBOPLASTINOGENASE AND PLATELETS FACTOR 3.2. THROMBOPLASTINOGENASE COMBINE WITH AHF TO CONVERT THE PLASMA GLOBULIN THROMBOPLASTINOGEN INTO THE ENZYME THROMBOPLASTIN3. THROMBOPLASTIN COMBINES WITH CALCIUM IONS TO CONVERT THE INACTIVE PLASMA PROTEIN PROTHROMBIN INTO THE ACTIVE ENZYME THROMBIN.

4. THROMBIN ACTS AS A CATALYST TO CONVERT THE SOLUBLE PLASMA PROTEIN FIBRINOGEN INTO THE INSOLUBLE, STRINGY PLASMA PROTEIN FIBRIN.

INHIBITION OF CLOTTING:

SMOOTHNESS OF THE INNER WALLS NORMALLY PREVENTS ACTIVATION OF THE INTRINSIC CLOTTING MECHANISM

2. A THIN LAYER OF NEGATIVELY CHARGED PROTEIN MOLECULES ATTACHED TO THE INNER WALL, REPELS THE CLOTTING FACTORS, PREVENTING THE INITIATION OF CLOTTING INJURY TO A BLOOD VESSEL REMOVES BOTH OF THESE SAFEGUARDS.

ANTICOAGULANT:HEPARIN AND ANTI THROMBINANTICOAGULANT DRUGS: STREPTOKINASE : ACTIVATE PLASMINOGEN TO SPEED FIBRINO- LYSIS GENETICALLY ENGINEERED (RECOMBINANT TISSUE PLASMINOGEN ACTIVATOR (rt-PA) IS EFFECTIVE IN DISSOLVING INTRAVASCULAR BLOOD CLOTS WHEN DELIVERED DIRECTLY THROUGH A CLOTTED AREA THROUGH A CATHETER. DICUMAROL : RESEMBLES VITAMIN K FIBRINOLYSIS (CLOT DESTRUCTION)IF BLOOD CLOTS ARE NOT REMOVED PROMPLY, THE BLOOD VESSEL WILL BECOME CLOGGED.

PLASMINOGEN IS ACTIVATED INTO AN ENZYME CALLED PLASMIN. THE PLASMIN DIGESTS THE THREADS OF FIBRIN BY MAKING THEM SOLUBLE AND BREAKING THEM INTO SMALL FRAGMENTS. THE FRAGMENTS ARE REMOVED FROM THE BLOODSTREAM BY PHAGOCYTIC WBC AND MACROPHAGES.

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