Exam 3: Circulatory System- Blood Part 2 Flashcards
what do agranulocytes include?
monocytes and lymphocytes
monocytes
2-8% of leukocytes
have high amounts of lysosomes
precursor to non-lobed (mononucleated) phagocytes
can activate and attract defense cells to the damaged area
what do monocytes mature into in the connective tissue, CNS, and bone
connective tissue: macrophages
CNS: microglia
bone: osteoclasts
Monocytes as macrophages
- secrete neutrophil and monocyte chemotactic factors
- additional secretions attract fibroblasts to regions of injury
- function in activation of lymphocytes in specific immunity (B and T cells)
lymphocytes and what they have roles in protecting against
20-40% leukocytes protect against: -specific foreign antibodies -abnormal/cancerous cells -invading microorganisms
play surveillance role in immunity
3 types of lymphocytes
T lymphocytes: protect against foreign cells presenting specific markers/antigens
B cells: produc antibodies against specific antigens
NK cells: surveillance of abnormal cells; important in detecting cancer
thrombocytes (platelets)
nonnucleated cell fragments
originate from fragmentation of giant cell, megakaryocyte
involved in clot formation
secrete chemicals that attract platelets and initiate clotting factors
contain filaments that contract blood vessel walls to minimize damaged area
when no damage they do NOT stick to eachother
hemostasis and the 3 stages
the process of halting bleeding
stages: vascular, platelet, coagulation
hemostasis: vascular stage
- begins right after damage, can last up to 30 minutes
- damage triggers localized sympathetic response - vasoconstriction slows bleeding
- damages endothelium secrete chemicals attracting platelets
- exposed basement membrane attracts platelets
hemostasis: platelet stage
within 15s after injury
- damaged endothelium releases von Willibrand’s factor
- promotes platelet adhesion
- adhered platelets release ADP, PDGF, thromboxanes, thromboplastin, Ca
von willibrands factor
promotes binding of platelets to the damaged surface
makes the surface sticky, platelet adhesion
adhered platelets release (5 things)
ADP: attracts platelets
PDGF: promotes repair of vessel
Thromboxane: stimulates vessel spasms - vasoconstriction
Thromboplastin (tissue factor): clotting factor 3; initiates blood clotting!!
Ca: required for clotting factor cascade
what initiates blood clotting
thromboplastin (tissue factor)
hemostasis: coagulation
30s to minutes after injury
ends with conversion of serum protein fibrinogen converting to fibrin by thrombin
fibrin forms a network of fibers that traps blood cells and platelets to form clot/thrombus
initiation of clot formation is in 2 pathways
pathways in the initiation of clot formation
extrinsic and intrinsic but both share a common pathway to fibrin activation
extrinsic pathway
rapid, initiated by release of thromboplastin from damaged tissue
handles small actions like a scrape or papercut
may be enough
intrinsic pathway
initiated by clotting factors coming in contact with exposed collagen in blood vessel walls
takes 5-10 min to begin
takes over for more serious or internal bleeding
clotting factor XII
Hageman’s factor, a serine protease
clotting factor XI
plasma thromboplastin, antecedent serine protease
clotting factor IX
christmas factor
serine protease
clotting factor VII
stable factor; serine protease
clotting factor XIII
fibrin stabilising factor; transglutaminase
common pathway
starts when you activate CF 10
in presence of platelets, Calcium and CF 5 turn inactive thrombin into active thrombin
thrombin activates fibrinogen into fibrin to get polymerization and CF13
CF13
when activated it crosslinks individual fibrin strands to add strength to them
get stable mesh which is your fibrin clot
intrinsic pathway in cascade
surface contact, damaged cells; collagen and CF12 activated (Hageman’s factor)
CF 11 thromboplastin comes in to start cascade
CF 10 can feedback and activate CF 11 to keep going
CF 11 activates CF 9 (christmas factor) which activates CF 8(antihemophilia factor)
hemophilia
bleeding disease - do not clot properly - all involve intrinsic pathway
hemophilia A
CF 8 - at final step to activate common pathway
on x chromosome, if someone deficient in CF 8 they will not initiate common factor through intrinsic pathway
hemophilia B
CF 9 (christmas factor) on x chromosome see more in men than women bc women have opportunity to be heterozygous, men do not, only have one x
hemophilia C
CF 11
equally seen in both sexes, on chromosome 4 - autosomal recessive not a sex linked trait
fibrinolysis
as repair continues, clot needs to be dissolved
thrombin and tissue plasminogen activator, released from endothelium, activates plasmin
slow activation of plasmin to allow healing
plasmin
breaks down the fibrin dissolving the clot