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Granular Leukocytes
Name and Number Characteristics Functions
Appearance
Neutrophils 60 – 70% of all 10-12 µm in diameter Phagocytosis: destruction of bacteria
WBCs Nucleus has 2-5 lobes with lysozyme, defensins (broad range of
connected by thin strands of antibiotic activity) and strong oxidants
chromatin
Cytoplasm has fine pale lilac
granules
Eosinophils 2-4% of all 10-12 µm in diameter Combats effects of histamine in allergic
WBCs Nucleus with 2 or 3 lobes reactions
Cytoplasm has large red Phagocytize Ag-Ab complex
orange granules Destroys certain parasitic worms
Basophils 0.5-1% of all 8-10 µm in diameter Liberate heparin, histamine, serotonin in
WBCs Nucleus has 2 lobes allergic reactions that intensify the
Large cytoplasmic granules overall response
appear deep blue purple
Agranular Leukocytes
Name and Number Characteristics Functions
Appearance
Lymphocytes (T 20-25% of all Small lymphocytes: 6-9µm in Mediate immune responses including
cells, B cells and WBCs diameter Ag-Ab reactions
natural killer cells) Large lymphocytes: 10-14mm B cells develop into plasma cells which
in diameter secrete Ab
Nucleus round or slightly T cells attack invading viruses, cancer
indented cells and transplanted tissue cells
Cytoplasm forms a rim around Natural killer cells attack a wide variety
the nucleus that looks sky blue; of infectious microbes and certain
the larger the cell, the more spontaneously arising tumor cells
cytoplasm is visible
Monocytes 3-8% of all 12-20 µm in diameter Phagocytosis (after transforming into
WBCs Nucleus is kidney shaped or fixed or wandering macrophages)
horseshoe shaped Monocytes migrate into the tissues,
Cytoplasm is blue gray and has enlarge, differentiate into
foamy appearance macrophages (fixed and wandering)
c. Platelets/ Thrombocytes
- 150,000-450,000/mm³
- 2-4µm in diameter; cell fragments live for 5-9 days
- contains many granules but no nucleus
- Forms platelet plugs in hemostasis, release chemicals which promote vascular spasm and
clotting
- aged and dead platelets are removed by fixed macrophages in the spleen and liver
WBC Physiology:
Entry of pathogens in the body >>> WBCs migrate to the affected areas by a process called EMIGRATION ( wbcs
roll in the endothelium, stick to it and squeeze between endothelial cells)
Lymhocytes: continually recirculate from blood to interstitial spaces of tissues to lymphatic tissues and back to
blood
: major types: a. T cells: attacks virus, fungi, transplanted cells, Ca cells, some bacteria
b. B cells: destroys bacteria and inactivates their toxins
c. Natural killer cells: attacks a wide variety of infectious microbes and some spontaneously
arising tumor cells
Granulocyte and monocyte: leave the bloodstream to fight infections and never return to it.
Neutrophils and macrophages: active in phagocytosis
: microbes and bacteria attract phagocytes by a phenomenon called CHEMOTAXIS
Neutrophils respond most quickly to tissue destruction by bacteria >>> after engulfing the bacteria >>> neutrophil
releases destructive chemicals: a. lysozyme: destroys bacteria
b. strong oxidants: similar to the household bleach; ex: H2O2, hypochlorite ion,
superoxide anion
: contains DEFENSINS: exhibit against a broad range of antibiotic activity against bacteria, fungi
Monocytes: take longer to reach site of infection but arrives in larger numbers
: enlarges and differentiates into wandering macrophages w/c clean up cellular debris and microbes
Eosinophils: enters tissue fluid; releases histaminase w/c combats effects of histamine
: phagocytizes Ag-Ab complexes; effective against some parasitic worms
Basophils: involved in inflammatory and allergic reactions
; leaves capillaries, enters tissues and develop into mast cells – liberate heparin, histamine, serotonin
: intensifies an inflammatory reaction and is involved in allergic reactions.
PLATELET FORMATION;
Hormone thrombopoietin >>> myeloid stem cells develop into megakaryocyte colony forming cells >>> develop into
precursor cells called MEGAKARYOBLASTS >>> megakaryocyte >>> platelets
HEMOSTASIS:
- sequence of responses that stops bleeding
- when blood vessels are damaged or ruptured, the hemostatic response must be quick and localized to the
region of damage and carefully controlled
3 Mechanisms:
1. Vascular spasm
- blood vessels are made of muscles >>> substances are released from the activated platelets
- reflexes are initiated by pain receptors
2. Platelet plug formation
a. Platelet Adhesion
- during an injury, platelets would go to the and stick to the parts of a damaged blood vessel
b. Platelet Release Reaction
- plts become activated and extends many projections that enable them to contact and interact with
each other
- they begin to liberate their contents: ADP- activates other plts
Serotonin- causes vasoconstriction
▪ contraction of smooth muscles
▪ decreased blood flow to the affected area
Thromboxane A2 (TXA2)- causes vasoconstriction
- also an aggregant
c. Platelet Aggregation
- makes other platelets sticky and adherent
- formation of a platelet plug which are initially loose and then is tightened by fibrin threads
3. Blood Clotting
- when blood forms a gel
- culminates in the formation of fibrin threads
- involves the clotting factors in the blood clotting cascade
BLOOD CLOTTING CASCADE (clotting factors and clotting cascade>>>refer to table and diagram)
CLOT RETRACTION
- consolidation or tightening of the fibrin clot
- fibrin threads attach to the damaged surfaces and gradually contract as the platelets pull on them
- as the clot retracts, it pulls the edges of the damages vessels together, decreasing the risk of further damage
- permanent repair of the blood vessel ensues
ROLE OF VITAMIN K
- required for the synthesis of factors II, VII, IX, X
- Normally produced by the bacteria in the large intestines
HEMOSTATIC CONTROL MECHANISM
1. Fibrinolytic System
o dissolves small inappropriate clots
o Fibrinolysis: dissolution of a clot
o Plasminogen: enzyme incorporated in a clot
: activated to plasmin or fibrinolysin by: thrombin
activated factor XII
tissue thromboplasminogen activator
: once formed, it can dissolve the clot by digesting Fibrin
: also inactivates Fibrinogen, Prothrombin, Factors V, VIII, XII
2. Prostacycline:
- From the endothelial cells and WBC’s
- opposes the action of thromboxane A2
- powerful inhibitor of platelet adhesion and release
3. Anticoagulants
a. Antithrombin:
- blocks the action of Factors XII, XI, X, IX, II
b. Heparin:
- produced by basophils and mast cells
- combines with antithrombin and increases its effectiveness in blocking thrombin
c. Activated Protein C
- inactivates Factors V, VIII which are factors not blocked by antithrombin
- enhances the activity of plasminogen activators
d. Warfarin (Coumadin):
- antagonist to Vit. K
- blocks the synthesis of Factors II, VII, IX, X
e. EDTA ( Ethylene Diamine Tetra Acetic acid)
f. CPD (Citrate Phosphate Dextrose)
- prevents clotting of donated blood by removing Calcium
g. Aspirin
- low doses inhibits vasoconstriction and platelet aggregation by blocking synthesis of TXA2
ABO AND Rh Blood Groups
- Agglutinogens/ Isoantigens: Antigens found on the surface of the RBC
HEMOLYTIC DISEASE OF THE NEWBORN (Erythroblastosis fetalis)