AJENG DIANTINI
CARDIOVASCULAR SYSTEM:
HEART (PUMP) BLOOD VESSELS (TRANSPORT) BLOOD HEART (PUMP) BLOOD VESSELS (TRANSPORT) BLOOD LYMPH LYMPH VESSEL CELLULAR ELEMENTS FLUID MATRIX = PLASMA
CIRCULATORY SYSTEM :
OXYGEN : LUNGS TO BODY TISSUES WASTE PRODUCT: BODY TISSUES TO KIDNEYS, LIVER, LUNGS, SWEAT GLANDS HORMONES, NUTRIENTS, ENZYMES THROUGHOUT THE BODY
REGULATES
BLOOD CLOTTING BODY TEMPERATURE ACID-BASE BALANCE (pH) AMOUNT OF WATER AND ELECTROLYTES IN BODY FLUIDS
PROTECTS
AGAINST HARMFUL MICROORGANISM & OTHER SUBSTANCES BY CONTRIBUTING WBC, PROTEINS, ANTIBODIES TO THE INFLAMMATORY AND IMMUNE RESPONSES
PROPERTIES OF BLOOD:
BLOOD VOLUME
VISCOSITY
COLOR
: OXYGENATED HB
pH
TEMPERATURE
: 38 C
COMPONENTS OF BLOOD
LIQUID PART
: PLASMA ( 55 %)
PLASMA
WATER: 90 % (DISSOLVING, TRANSPORTING NUTRIENTS) TO MAINTAIN THE NORMAL STATE OF HIDRATION SOLVENT FOR EXTRACELLULAR AND INTRACEL CHEMICAL REACTIONS CONTAIN MANY SOLUTES PLASMA PROTEINS: ALBUMINS , FIBRINOGEN, GLOBULINS
SYNTHESIZED IN LIVER WATER RETENTION IN BLOOD---- MAINTAIN
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
GLUCOSE
LIPIDS
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.
: 50 % THE VOLUME OF HUMAN BLOOD : 7 m IN DIAMETER 2 m THICK : LIKE A DISK, BICONCAVE PROVIDE
LARGER SURFACE DIFFUSION THAN A FLAT DISK.
RBC MATURE
Blood cells
HEMOGLOBIN
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
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, DIZZINESS CO2 (AUTOMOBILE EXHAUST FUME, CIGARETTE SMOKE) BINDS TO Hb 210 X FASTER THAN OXYGEN STABLE COMPOUND
2. 30 % CO2 REACTS WITH Hb CARBAMINOHEMOGLOBIN (HbCO2), WHICH IS CARRIED FROM TISSUE TO THE LUNGS AND THE CO2 IS EXCHANGED FOR O2
HAVE THIN, STRONG AND FLEXIBLE PLASMA MEMBRAN EASILY THROUGH SMALL BLOOD VESSEL
MOVE
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
IF PLASMA CONC. OF SOLUTE DECREASES BELOW NORMAL PLASMA BECOME HYPOTONIC THECELL SWELLS, BURSTS HEMOLYSIS
LIFE SPAN OF AN ERYTHROCYTES IS 80-120 DAYS, BECAUSE: IT HAS NO NUCLEUS UNABLE TO REPLACE THE ENZYME AND OTHER PROTEINS TO FUNCTION PROPERLY FRAGILE 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
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
WBC (GRANULOCYTES) ORYGINATE = ERYTHR, AND LEUKOPOIESIS ALSO OCCURS IN LYMPHOID TISSUES (LYMPH NODES, SPLEEN AND TONSILS)
BASIC CLASSIFICATIONS OF LEUCOCYTES: 1. GRANULOCYTES (POLYMORPHONUCLEAR LEUCOCYTES) 2. AGRANULOCYTES (MONONUCLEAR LEUCOCYTES) GRANULOCYTES
MOST NUMEROUS OF WBC, CONTAIN LARGE NUMBERS OF GRANULES IN THE CYTOPLASM THREE TYPES : NEUTROPHILS, EOSINOPHILS, BASOPHILS, WHEN STAINED BY WRIGHTS STAIN: NEUTROPHILS : LIGHT PINK BLUE BLACK EOSINOPHILS : RED RED ORANGE BASOPHILS : BLUE BLACK RED PURPLE
NEUTROPHILS
60 % 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
EOSINOPHILS
B-SHAPE NUCLEI PHAGOCYTES HAVE AMOEBOID MOVEMENT CONTAIN LYSOSOMAL ENZYMES AND PEROXIDASE INCREASES DURING ALLERGY ATTACKS, CERTAIN PARASITIC INFECTIONS, SOME AUTOIMMUNE DISEASES, CERTAIN TYPES OF CANCER. CONTAIN PLASMINOGEN WHICH HELPS DISSOLVE BLOOD CLOTS
BASOPHILS
LEAST NUMEROUS OF ALL GRANULOCYTES GRANUL 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
AGRANULOCYTES
MONOCYTES
MOBILE PHAGOCYTES, LARGEST BLOOD CELLS HAVE LARGE, FOLDED NUCLEI; GRANULES DEVELOP IN BONE MARROW, FROM MONOBLASTS ONCE IN TISSUE SPACES, MONOCYTES ENLARGED 5-10 X THEIR NORMAL SIZE AND BECOME PHAGOCYTIC MACROPHAGES MACROPHAG FORM THE RETICULOENDOTHELIAL SYSTEM, WHICH LINES THE VASCULAR PORTIONS OF THE LIVER, LUNGS, LYMPH NODES, THYMUS GLAND AND BONE MARROW MONOCYTES AND MACROPHAGES PRODUCE COLONY STIMULATING FACTOR (CSF) WHICH STIMULATE BONE MARROW TO PRODUCE MORE MONOCYTES AND NEUTROPHILS
LYMPHOCYTES
SMALL, 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
PLATELETS RELEASE : - GRANULES THAT CONTAIN SEROTONIN WHICH CONSTRICTS INJURED VESSELS AND RETARDS BLEEDING - ADP WHICH ATTRACTS MORE PLATELETS TO THE DAMAGED AREA
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
INHIBITION OF CLOTTING:
1.
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:
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.