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

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Presentation on theme: "BLOOD “Sometimes the questions are complicated and the answers are simple.” ― Dr. SeussDr. Seuss."— Presentation transcript:

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

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

3 COMPONENTS FORMED ELEMENTS (LIVING) RED BLOOD CELLS (erythrocytes) BUFFY COAT LEUKOCYTES PLATELETS MATRIX (NOT LIVING) PLASMA

4 90% Water Nutrients, Salts (Electrolytes) Respiratory Gases Waste products Plasma Proteins (Most Abundant at 8%) HORMONES ALBUMIN CLOTTING FACTORS COMPLEMENT

5 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

6 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

7 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

8 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

9 WBC GROUPS GRANULOCYTES NEUTROPHILS EOSINOPHILS BASOPHILS HISTAMINE HEPARIN AGRANULOCYTES LYMPHOCYTES MONOCYTES

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

11 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

12 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

13 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

14 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

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

16 #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

17 #2 VASCULAR SPASM ANCHORED PLATELETS SECRETE SEROTONIN CAUSING VASCULAR SPASM SPASM CONSTRICTS THE VESSEL WHICH DECREASES BLOOD LOSS

18 #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

19 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.

20 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

21 BLEEDING DISORDERS THROMBOCYTOPENIA – LOWERED LEVEL OF PLATELETS HEMOPHILIA – LACK OF A CLOTTING FACTOR LIVER FAILURE – LEADS TO INABILITY TO SYNTHESIZE ENOUGH CLOTTING FACTORS

22 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

23 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”

24 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

25 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

26 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

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

28 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

29 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

30 IMBALANCE OF RBC ANEMIA HEMOLYTIC –SICKLE CELL HEMORRHAGIC PERNICIOUS – VITAMIN B12 THALESSEMIA APLASTIC – BONE MARROW SUPPRESSION IRON DEFICIENCY POLYCYTHEMIA

31 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

32 CLOTTING DISORDERS HEMOPHILIA VON WILLEBRANDS DISEASE THROMBOCYTOPENIA DISSEMINATED INTRAVASCULAR COAGULATION

33 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


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