BLOOD
“Sometimes the questions
are complicated and the
answers are simple.”
― Dr. Seuss
Functions of the blood

Transportation

Regulation – pH, heat, fluid balance
Protection – disease, blood loss

• Gases
• Nutrients
• Waste
• Hormones
COMPONENTS

FORMED ELEMENTS (LIVING)

BUFFY COAT

MATRIX (NOT LIVING)
• RED BLOOD CELLS (erythrocytes)
• LEUKOCYTES
• PLATELETS
• 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

HCT – VOLUME % OF RBC IN WHOLE
BLOOD
• MEN – 14 -17 G/ 100 ML
• WOMEN – 12 – 15 G/ 100 ML
• 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 NEWBORNGIVE 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

POLYCYTHEMIA
• HEMOLYTIC –SICKLE CELL
• HEMORRHAGIC
• PERNICIOUS – VITAMIN B12
• THALESSEMIA
• APLASTIC – BONE MARROW SUPPRESSION
• IRON DEFICIENCY
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