1. BLOOD
“Sometimes the questions are complicated and the answers are simple.” ― Dr. 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) BUFFY COAT MATRIX (NOT LIVING)
RED BLOOD CELLS (erythrocytes)
BUFFY COAT
LEUKOCYTES
PLATELETS
MATRIX (NOT LIVING)
PLASMA
RED CELLS ARE CONENCTIVE TISSUE, CARRY O2;
SPIN BLOOD IN A TUBE AND YOU WILL SEE RED AT BOTTOM, THIN BUFFY COAT, AND SERUM AT TOP. CELLS ARE HEAVIER THAN SERA SO THEY SINK.
RRBC – 45% OF BLOOD VOLUME = HEMATOCRIT LEVEL
WBC & PLATELETS < 1%
PLASMA= 55%
5-6 LITERS OF BLOOD IN A MALE
Ph ; TEMP – SLIGHTLY WARMER THAN BODY

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

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
INCREASE CELLS = INCREASE THICKNES OF BLOOD
LESS = THINNER & FLOWS EASILY
1 RBC HOLDS 250 MILLION HBG + 1 HBG HOLDS 4 O2= 1 BILLION MOLECULES OF O2 PER RBC

7. HEMOGLOBIN/ HEMATOCRIT
HGB – MEASUREOF HEMOGLOBIN IN RBC
MEN – G/ 100 ML
WOMEN – 12 – 15 G/ 100 ML
HCT – VOLUME % OF RBC IN WHOLE BLOOD
MEN – 42 – 54%
WOMEN – %
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
WHEN BODY CALLS WBC TO TISSUE AREAS THAT ARE DAMAGED, THE BODY SPEEDS UP THEIR PRODUCTION (SPECIAL ORDER SUPPLY FROM THE FACTORY)

9. WBC GROUPS GRANULOCYTES AGRANULOCYTES NEUTROPHILS EOSINOPHILS
BASOPHILS
HISTAMINE
HEPARIN
AGRANULOCYTES
LYMPHOCYTES
MONOCYTES
NEUTROPHILS – ACUTE INFECTION
EOSINOPHILS – ALLERGIES AND PARASITIC INFECTIONS
BASOPHILS – HISTAMINE CAUSES LEAKY VESSELS AND DRAWS OTHER WBC TO SITE OF INJURY
LYMPHOCYTE – IN LYMPHATIC TISSUE
MONOCYTES TRAVEL TO THE TISSUE AND BECOME MACROPHAGES

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
CAN’T ALTER PATH ONCE THEY START DOWN TO MYELOID OR LYMPHOID

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
CONSTANCE BALANCE OF PRODUCTION AND BREAKDOWN, SO WE ALWAYS HAVE ENOUGH FUNCTIONAL RBCS
EPOIETIN WORKS ON HUMORAL NEGATIVE FEEDBACK

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
THE TRPPED RBCS FORM THE CLOT. CLOT BEGINS TO CONTRACT SQUEEZING OUT SERA & PULLING EDGES OF WOUND TOGETHER

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
VITAMIN k NEEDED BY LIVER CELLS TO MAKE CLOTTING FACTORS.
MAY NEED TO TRANSFUSE WITH RBC TO REPLACE 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
AGGLUTINATION CAN CAUSE CLOGIING OF THE SMALL VESSELS AROUND THE BODY.
OUR IMMUNE SYSTEM WILL BREAK THEM DOWN AND RID THEM FROM OUR BODY
TRANSFUSION REACTION – FEAR IS KIDNEY WILL BE CLOGGED BY THE HEME PORTION OF THE BROKEN CELLS CAUSING RENAL FAILURE; SX ALSO ARE FEVER, CHILLS, NAUSEA, VOMITING. TX IS TO FLUSH THE KIDNEYS TO PREVENT BLOCKAGE.

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
O HAS NO ANTIGEN SO IT CANT TRIGGER ANTIBODIES IN OTHERS = CAN GIVE TO ANYONE
AB HAS 2 SELF ANTIGEN AND NO ANTIBODIES SO IT CAN RECEIVE FROM ANYONE

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 POLYCYTHEMIA HEMOLYTIC –SICKLE CELL
HEMORRHAGIC
PERNICIOUS – VITAMIN B12
THALESSEMIA
APLASTIC – BONE MARROW SUPPRESSION
IRON DEFICIENCY
POLYCYTHEMIA
LOW RBC COUNT
LOW AMOUNT OF HBG IN RBC
ABNORMALLY SHAPED RBC RUPTURES EASILY
TOO MANY RBC = THICK BLOOD

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
PERNICIOUS ANEMIA BECOME THE STOMACH MUCOSA ATROPHIES WITH AGE.