Transcript Homeostasis Defense Against Blood Loss

Unit III: Homeostasis
Defense Against Blood Loss
Chapter 17
pp. 586-593
Leukocytes (WBCs)
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5,000 to 10,000 WBCs/L
Conspicuous nucleus
Travel in blood before migrating to connective tissue
Protect against pathogens
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
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
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)
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
CSFs
Platelets
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
Hemostasis
• All 3 pathways involve platelets
Hemostasis
Vascular Spasm
Knife blade
• Prompt constriction of the broken vessel
Blood vessel injury
Vascular
spasm
• Stimuli
– pain receptors
– smooth muscle injury
– platelets release serotonin (vasoconstrictor)
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
Release of chemicals
PDGF, Ca ,
• thromboxane A2 (an eicosanoid) Plasma in (ADP,
platelet factors)
2+
vessel lumen
Platelet
aggregation
Platelet
adhesion to
damaged
vessel
Endothelium
Basal
lamina
Vessel
wall
Contracted smooth
Platelet plug
muscle cells
may form
Interstitial
Cut edge of
fluid
vessel wall
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
Coagulation Pathways
Common Pathway
Extrinsic
Pathway
Intrinsic
Pathway
Factor X
Tissue factor
complex
Factor X
activator
Prothrombinase
Prothrombin
Thrombin
Factor
VII
Fibrin
Fibrinogen
Factor
XI
Factor III
Factor XII
Tissue
damage
Contracted smooth
muscle cells
Factors
IX, VIII
• 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
• Reaction Cascade
• Clot retraction occurs within 30 minutes
• growth factor secreted by platelets
Reaction cascade (time)
Fate of Blood Clots
Factor
XII
Factor
XI
Factor
IX
Factor
VIII
Factor
X
Prothrombin
activator
Thrombin
Fibrin
• Fibrinolysis (dissolution of a clot)
– Plasminogen  plasmin, a fibrin-dissolving enzyme (clot buster)
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
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
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
Anticoagulants
•Salts, heparin
•Coumarin
•Vitamin K deficiency
–Needed for synthesis of clotting factors
•Aspirin
–Suppresses formation of thromboxane A2
•Medicinal leeches