Exam 3: Circulatory System- Blood Part 2 Flashcards

1
Q

what do agranulocytes include?

A

monocytes and lymphocytes

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2
Q

monocytes

A

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

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3
Q

what do monocytes mature into in the connective tissue, CNS, and bone

A

connective tissue: macrophages
CNS: microglia
bone: osteoclasts

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4
Q

Monocytes as macrophages

A
  • 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)
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5
Q

lymphocytes and what they have roles in protecting against

A
20-40% leukocytes
protect against: 
-specific foreign antibodies
-abnormal/cancerous cells
-invading microorganisms 

play surveillance role in immunity

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6
Q

3 types of lymphocytes

A

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

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7
Q

thrombocytes (platelets)

A

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

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8
Q

hemostasis and the 3 stages

A

the process of halting bleeding

stages: vascular, platelet, coagulation

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9
Q

hemostasis: vascular stage

A
  • 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
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10
Q

hemostasis: platelet stage

A

within 15s after injury

  • damaged endothelium releases von Willibrand’s factor
  • promotes platelet adhesion
  • adhered platelets release ADP, PDGF, thromboxanes, thromboplastin, Ca
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11
Q

von willibrands factor

A

promotes binding of platelets to the damaged surface

makes the surface sticky, platelet adhesion

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12
Q

adhered platelets release (5 things)

A

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

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13
Q

what initiates blood clotting

A

thromboplastin (tissue factor)

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14
Q

hemostasis: coagulation

A

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

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15
Q

pathways in the initiation of clot formation

A

extrinsic and intrinsic but both share a common pathway to fibrin activation

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16
Q

extrinsic pathway

A

rapid, initiated by release of thromboplastin from damaged tissue
handles small actions like a scrape or papercut
may be enough

17
Q

intrinsic pathway

A

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

18
Q

clotting factor XII

A

Hageman’s factor, a serine protease

19
Q

clotting factor XI

A

plasma thromboplastin, antecedent serine protease

20
Q

clotting factor IX

A

christmas factor

serine protease

21
Q

clotting factor VII

A

stable factor; serine protease

22
Q

clotting factor XIII

A

fibrin stabilising factor; transglutaminase

23
Q

common pathway

A

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

24
Q

CF13

A

when activated it crosslinks individual fibrin strands to add strength to them
get stable mesh which is your fibrin clot

25
Q

intrinsic pathway in cascade

A

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)

26
Q

hemophilia

A

bleeding disease - do not clot properly - all involve intrinsic pathway

27
Q

hemophilia A

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

28
Q

hemophilia B

A
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
29
Q

hemophilia C

A

CF 11

equally seen in both sexes, on chromosome 4 - autosomal recessive not a sex linked trait

30
Q

fibrinolysis

A

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

31
Q

plasmin

A

breaks down the fibrin dissolving the clot