blood “sometimes the questions are complicated and the answers are simple.” ― dr. seussdr....
Post on 16-Dec-2015
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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)• RED BLOOD CELLS (erythrocytes)
BUFFY COAT• LEUKOCYTES
• PLATELETS
MATRIX (NOT LIVING)• PLASMA
PLASMA 90% Water Nutrients, Salts (Electrolytes) Respiratory Gases Waste products Plasma Proteins (Most Abundant at 8%)
• HORMONES
• ALBUMIN
• CLOTTING FACTORS
• COMPLEMENT
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
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
WBC GROUPS
GRANULOCYTES• NEUTROPHILS
• EOSINOPHILS
• BASOPHILS• HISTAMINE
• HEPARIN
AGRANULOCYTES• LYMPHOCYTES
• MONOCYTES
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
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
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
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
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
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
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• HEMOLYTIC –SICKLE CELL
• HEMORRHAGIC
• PERNICIOUS – VITAMIN B12
• THALESSEMIA
• APLASTIC – BONE MARROW SUPPRESSION
• IRON DEFICIENCY
POLYCYTHEMIA
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
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