CH. 19 - BLOOD
I. INTRODUCTION
A. FUNCTIONS
1. TRANSPORTATION
a. Gases
b. Nutrients
c. Wastes
d. Hormones
2. MAINTENANCE of HOMEOSTASIS
a. Temperature
b. Fluid & electrolyte levels
3. PROTECTION
a. Immunity - disease
b. Clots
B. CONNECTIVE TISSUE
1. 2 Components
a. FORMED ELEMENTS - cells, fragments
b. PLASMA - fluid
2. 4-6 liters in body
3. 8% of body weight
4. pH 7.35-7.45
C. COMPOSITION - KNOW Fig. 19.1, p. 648
II. PLASMA - 55% of blood (Tab. 19.1, p. 649), pale straw yellow
- 91% H2O, 9% dissolved/colloid
- Remove FIBRIN (clots) = SERUM
A. PROTEINS
1. ALBUMIN (58%) - Osmotic pressure, buffer
2. GLOBULINS (38%) - Transport, immun. (Ab) & complement
3. FIBRINOGEN (4%) - Clotting
B. IONS - Na+, K+, etc.
C. NUTRIENTS - glucose, A.A., etc.
D. N2 WASTE - Urea, creatinine, etc.
E. GASES - O2, CO2,
F. HORMONES & ENZYMES - regulation
III. FORMED ELEMENTS - 45% of blood (Tab. 19.2, p. 650) (Fig. 19.7, p. 657)
- HEMATOCRIT (FIG. 19.16, p. 668)
- 95% RBC, 5% WBC (LEUKOCYTES) + PLATELETS
A. HEMATOPOIESIS - F.E. production (Fig. 19.2, p. 651)
1. Stem cells - produce all formed elements
2. Embryo - all over
3. Newborn - bone marrow
4. Adult - axial red marrow
B. ERYTHROCYTES (RBC)
1. Biconcave disks, enucleated, 110-120 day lifespan
2. Contain ATP, lipids, carbonic anhydrase & mostly . . .
3. HEMOGLOBIN a. Heme - contains Fe, O2 transport
b. Globin - protein, CO2 transport
c. Fe - 4 g in body, 2/3 in Hgb
d. O2 + Hgb Û OXYHEMOGLOBIN, reversible
e. CO2 + Hgb Û CARBAMINO-Hgb, reversible
f. CO + Hgb è CARBOXY-Hgb, IRREVERSIBLE !
(use hyperbaric chamber to force O2 in)
4. RBC Life History (Fig. 19.5, p. 655)
a. 2.5 X 106 RBC destroyed/produced per second !
b. ERYTHROPOIESIS - stim. by ERYTHROPOIETIN
c. RBC breakdown (Fig. 19.6, p. 656)
Hgb i. Globin è A.A. è proteins
ii. Fe è recycled/stored
iii. Heme è BILIRUBIN è Bile (Yellow)
d. JAUNDICE = HYPERBILIRUBINEMIA
i. Yellow skin & sclera
ii. Indicates possible liver damage
iii. U.V. light helps cure in newborns
C. LEUKOCYTES - WBC’s (Fig. 19.8, p. 659)
- Nucleated, defense, scavenge è Pus
- Motile, amoeboid, chemotactic
- DIAPEDESIS - move through vessel walls
GRANULOCYTES - granules which stain, 3
1. NEUTROPHILS - v. small granules
- small phagocytes
- 60-70% of WBC
- 1st line of defense, é means infection
- Polymorphonuclear, 2-5 lobed nuclei
2. EOSINOPHILS - red granules
- 1-4% of WBC
- fxn in allergic rxns/inflamm. & worm parasites
- reduces histamines è êinflammation
3. BASOPHILS - purple granules
- < 1% of WBC
- allergic rxns/inflammation
- release histamines è éinflammation
- release HEPARIN èinhibits clotting
AGRANULOCYTES - few granules, 2, can live for decades
4. LYMPHOCYTES - almost all nucleus, round
- 20-30% of WBC
- Immunity/antibody production. . . Ch. 22
- many types . . . later
5. MONOCYTES - largest WBC
- 2-8% of WBC
- é in Monos = chronic infection
- blood è tissues è MACROPHAGE, eat debris
D. PLATELETS = THROMBOCYTES
1. Enucleated, cell fragments
2. Clotting
IV. HEMOSTASIS - stop bleeding
A. 3 TYPES
1. VASCULAR SPASM - smooth muscle contraction
- Immediate but temporary
2. PLATELET PLUG - minor damage/tear (Fig. 19.9, p. 660)
- triggered by collagen contact
3. COAGULATION/CLOT (Fig. 19.11, p. 662 – KNOW!)
- “cascade”, 3 major stages
***NOTE: - Vitamin K required for many factors’ production
-
a. Stage 1: Activated FACTOR X
Factor V, Ca 2+--->ê
ê
b. Stage 2: PROTHROMBINASE
ê FACTOR XIII
PROTHROMBIN------->THROMBIN---------->ê
+ Ca2+ ê Activated FACTOR XIII
ê ê
c. Stage 3: FIBRINOGEN------->FIBRIN-------->CLOT
+ Platelets
B. CAUSES - 2
1. EXTRINSIC - triggered by chem. OUTSIDE vessel
a. TISSUE FACTOR (THROMBOPLASTIN)
b. in C.T. & epithelial tissue
2. INTRINSIC - triggered by chem. INSIDE damaged vessel (collagen)
a. FACTOR XII activated
b. also platelet activation
C. REGULATION - Anticoagulants: ê thrombin act.è no clot
1. HEPARIN & ANTITHROMBIN – produced naturally
2. ASPIRIN - treat heart disease
D. CLOT RETRACTION - fibrin retracts, pulls wound together
E. CLOT DISSOLUTION = FIBRINOLYSIS (Fig. 19.12, p. 664)
1. PLASMIN dissolves fibrin as wound heals
F. THROMBUS - clot in vessels
G. EMBOLUS - clot breaks free
V. BLOOD GROUPING - (lab)
A. TRANSFUSION - é blood volume & O2 carrying after loss
1. Before 1901, 1 in 20 successful, hit & miss
B. ABO Types (Fig. 19.13, 19.14, p. 665)
1.Phenotype Antigen Antibody
A A anti-B
B B anti-A
AB A & B neither
O neither anti-A & B
2. O - “Universal donor”
í ê î Problem: If O given to AB,
A ê B won’t agglut. occur? A little,
î ê í but diluted, not usually serious
AB - “Universal recipient”
C. Rh - 1940 in rhesus monkey
1. Rh+ have Rh antigen (18 different types) - 85%
2. Rh- have NO Rh antigen - 15%
3. PROBLEM: Rh- female has Rh+ baby (Fig. 19.15, p. 667)
a. If some Rh+ bloodè Rh- motherè
Stim antibody production against Rh+ cells = IgG
IgG can cross placentaè attack baby’s RBC
= ERYTHROBLASTOSIS FETALIS
b. Usually no problem 1st pregnancy, problem in next
4. SOLUTION - give RhoGAM right after birth
a. RhoGAM binds to any fetal RBC that may have entered
mother’s circulation.
D. DIAGNOSTIC BLOOD TESTS - in lab
E. Know clinical impacts notes & blood disorders (p. 669)