1. Unit III: Homeostasis Defense Against Blood Loss
Chapter 17 pp

2. Leukocytes (WBCs) 5,000 to 10,000 WBCs/L Conspicuous nucleus
Travel in blood before migrating to connective tissue
Protect against pathogens

3. Leukocyte Descriptions
Granulocytes
neutrophils (60-70%) - fine granules; 3 to 5 lobed nucleus
 in bacterial infections
eosinophils (2-4%) - large rosy granules; bilobed nucleus
 in parasitic infections or allergies
basophils (<1%) - large, violet granules
 in chicken pox, sinusitis, diabetes
Histamine and heparin

4. Leukocyte Descriptions
Agranulocytes
lymphocytes (25-33%) - round, uniform dark violet nucleus
 in diverse infections and immune responses
monocytes (3-8%)
largest WBC; ovoid, kidney-, or horseshoe- shaped nucleus
 in viral infections and inflammation

5. Leukopoiesis Leukocyte life cycle multipotent stem cells  CFU’s
myeloblasts – form neutrophils, eosinophils, basophils
monoblasts - form monocytes
lymphoblasts - form 3 types of lymphocytes
Colony-stimulating factors (CSF)
WBCs provide long-term immunity (weeks-decades)

6. Abnormal Leukocyte Counts
Leukopenia - low WBC count (<5000/L)
causes: radiation, poisons, infectious disease
effects: elevated risk of infection
Leukocytosis = high WBC count (>10,000/L)
causes: infection, allergy and disease
differential count - distinguishes % of each cell type
Leukemia = cancer of hemopoietic tissue
myeloid and lymphoid - uncontrolled WBC production
acute and chronic - death in months or  3 years
effects – deficiency of competent formed elements; impaired clotting

7. Platelets Normal Count - 130,000 to 400,000 platelets/L Functions:
CSFs
Progenitor Cell
Multipotent
Stem cell
Megakaryocytes
Platelets
Normal Count - 130,000 to 400,000 platelets/L
Functions:
vasoconstrictors
platelet plugs
secrete clotting factors
initiate formation of clot-dissolving enzyme
phagocytize bacteria; chemically attract neutrophils and monocytes to sites of inflammation
secrete growth factors

8. All 3 pathways involve platelets
Hemostasis
All 3 pathways involve platelets

9. Hemostasis Vascular Spasm
Knife blade
Blood vessel injury
Vascular
spasm
Prompt constriction of the broken vessel
Stimuli
pain receptors
smooth muscle injury
platelets release serotonin (vasoconstrictor) .

10. Hemostasis Platelet Plug Formation
broken vessel exposes collagen
platelet pseudopods
contract and draw walls of vessel together  platelet plug
degranulation
serotonin (vasoconstrictor)
ADP attracts and degranulates more platelets
thromboxane A2 (an eicosanoid)
Platelet
adhesion to
damaged
vessel
aggregation
Endothelium
Platelet plug
may form
Cut edge of
vessel wall
Contracted smooth
muscle cells
Vessel
wall
Basal
lamina
Release of chemicals
(ADP, PDGF, Ca2+,
platelet factors)
Plasma in
vessel lumen
Interstitial
fluid

11. Hemostasis Coagulation
“Clotting”
conversion of plasma protein fibrinogen into insoluble fibrin threads to form framework of clot
Extrinsic mechanism
factors released by damaged tissues
Intrinsic mechanism
factors found in blood (platelet degranulation)
Procoagulants (clotting factors)
activate one factor and it will activate the next to form a reaction cascade

12. Coagulation Pathways Extrinsic mechanism initiated by Factor III
Common Pathway
Factor X
Fibrin
Thrombin
Fibrinogen
Prothrombinase
Prothrombin
Tissue factor
complex
Factor
VII
Factor III
Tissue
damage
activator
Factors
IX, VIII XI
Factor XII
Contracted smooth
muscle cells
Intrinsic
Extrinsic mechanism
initiated by Factor III
fewer steps
15 seconds formation
Intrinsic mechanism
initiated by factor XII
cascade to factor XI to IX to VIII to X
3-6 minutes formation
Calcium required for either pathway

13. Fate of Blood Clots Reaction Cascade
Factor
XII
Factor XI
Factor IX
Reaction Cascade
Clot retraction occurs within 30 minutes
growth factor secreted by platelets
Fibrinolysis (dissolution of a clot)
Plasminogen  plasmin, a fibrin-dissolving enzyme (clot buster)
Factor
VIII
Reaction cascade (time)
Factor X
Prothrombin
activator
Thrombin
Fibrin

14. Prevention of Inappropriate Clotting
Platelet repulsion
Thrombin dilution
by rapidly flowing blood
Natural anticoagulants
heparin (from basophils and mast cells) interferes with formation of prothrombin activator
antithrombin (from liver) deactivates thrombin before it can act on fibrinogen

15. Hemophilia Genetic lack of any clotting factor
Sex-linked recessive (on X chromosome)
hemophilia A missing factor VIII (83% of cases)
hemophilia B missing factor IX (15% of cases)
note: hemophilia C missing factor XI (autosomal)
Physical exertion causes bleeding
hematomas
transfusion of plasma or purified clotting factors

16. Coagulation Disorders
Thrombosis - abnormal clotting in unbroken vessel
most likely to occur in leg veins of inactive people
Embolism - clot traveling in a vessel
pulmonary embolism - clot may break free, travel from veins to lungs
Infarction may occur if clot blocks blood supply to an organ (MI or stroke)
650,000 Americans die annually of thromboembolism

17. Anticoagulants Salts, heparin Coumarin Vitamin K deficiency
Needed for synthesis of clotting factors
Aspirin
Suppresses formation of thromboxane A2
Medicinal leeches