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