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Coagulation & Body Fluids > Normal Hemostasis > Flashcards

Normal Hemostasis Flashcards

1
Q

Hemostasis/Coagulation

A
  • processed involved when blood clots in response to an injury
  • interaction of blood vessels, platelets, coagulation factors, fibrinolysis
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2
Q

Hemostasis function

A
  • to keep blood within veins and arteries
  • prevent blood loss from injuries by formation of thrombi
  • re-establising blood flow during the healing process
  • maintain a complete balance between bleeding and clotting
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3
Q

3 Stages of Hemostasis

A
  1. Normal hemostasis
  2. Secondary hemostasis
  3. Fibrinolysis
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4
Q

Primary hemostasis

A
  • vasoconstriction upon injury of vessel to minimize blood loss
  • platelets accumulate/aggregate at site forming platelet plug
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5
Q

Secondary hemostasis

A
  • coagulation factors produce fibrin

- fibrin stabilizes fragile platelet plug (making it a clot)

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6
Q

Fibrinolysis

A

breakdown of fibrin to remove clot after healing of wound

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7
Q

Primary hemostasis involvement

A
  • blood clotting in response to vascular injury

- blood vessels and platelets involved

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8
Q

Structure of blood vessels

A
  • blood flows through central cavity (lumen)

- endothelial cells line lumen to protect vessel from injury

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9
Q

Activation of hemostasis

A
  • initiated by contraction of vessel
  • brings hemostatic components closer to vessel wall
  • damaged endothelial cells release factors that aid in hemostasis
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10
Q

Endothelial cells role in primary hemostasis

A
  • produce and secrete vWF (aids platelets)
  • produce tissue factor
  • expose collagen (secretes platelet activating factor)
  • release plasminogen activator inhibitor (inhibits fibrinolysis)
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11
Q

Platelet maturation

A

stem cell –> CFU-GEMM –> BFU Meg –> CFU Meg –> MK1 (megakaryoblast) –> MK2 (promegakaryocyte) –> MK3 (Megakaryocyte) –> platelets

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12
Q

MK1-MK3

A
  • undergoes endomitosis (DNA doubles, but no division occurs)
  • cell gets larger and larger
  • usually stop at 16N (DNA content)
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13
Q

Megakaryoblast (MK1)

A
  • 6-24 microns
  • scant basophilic cytoplasm
  • no visible granules
  • round nucleus
  • visible nucleoli
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14
Q

Promegakaryocyte (MK2)

A
  • nuclear division ends
  • cytoplasmic granule development begins
  • granules spread throughout
  • membrane demarcation begins (channel system)
  • multilobed nucleus
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15
Q

Megakaryocyte (M3)

A
  • cytoplasm becomes more purple
  • DMS finishes packaging platelets
  • proplatelets break off into circulation
  • large multilobed nucleus
  • no visible nucleoli
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16
Q

Mature megakaryocyte

A
  • all that’s left is nucleus when all proplatelets are released (metamegakaryocyte)
  • average platelet lifespan is 10 days
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17
Q

Platelet structure

A
  • peripheral zone: outermost zone
  • structural zone: microtubules, cytoskeletal network, microfilaments that provide support
  • organelle zone: mitochondria, glycogen particles, granules
  • membrane system: two systems of membranes
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18
Q

Platelets in Hemostasis

A
  • must be adequate in number and function

- normally don’t interact with other cells

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19
Q

Formation of Platelet Plug (Platelet action)

A
  • platelet adhesion
  • platelet activation
  • platelet shape change
  • platelet secretion of granules
  • platelet aggregation
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20
Q

Platelet adhesion

A
  • damaged vessel exposes blood flow to subendothelial connective tissue
  • connective tissue is composed of adhesive molecules
  • involves: vWF, platelet membrane receptor (GP1b), and collagen fibers
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21
Q

vWF

A
  • synthesized by endothelial cells and megakaryocytes
  • released into plasma and binds to GP1b receptor
  • forms a bridge connecting platelet to collagen fibers
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22
Q

collagen

A
  • adhesion of platelets promotes platelet spreading along vessel wall
  • platelet adhesion to wall activates platelets
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23
Q

Platelet activation

A
  • morphological and functional change of platelets

- secretion of granules, formation of aggregates

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24
Q

Platelet agonist

A
  • agent that induces platelet activation
  • some generated by platelets, others by cells/molecules at site of injury
  • binds to specific receptor on platelet
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25
Q

Platelet derived agonists

A

ADP
Serotonin
Platelet activating factor
Thromboxan A2 (TXA2)

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26
Q

Non-platelet derived agonists

A

Collagen
Thrombin**
Epinephrine

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27
Q

Platelet shape change

A
  • triggered by adhesion to collagen via vWF
  • discs –> spheres with projections (pseudopods)
  • allows greater chance of contact, become sticky
28
Q

Platelet secretion of granules

A

alpha and dense granules released into surrounding area

29
Q

Alpha granules

A
  • thrombospondin: promotes plt to plt interaction
  • vWF: platelet adhesion
  • Platelet-derived growth factor: promotes smooth muscle growth
30
Q

Dense granules

A
  • ADP: promotes platelet aggregation
  • Calcium: regulates platelet activation/aggregation
  • serotonin: promotes vasoconstriction
31
Q

Platelet aggregation

A
  • attachment of platelets to one another
  • 10-20 secs after vessel injury
  • platelets arrive and become activated by TXA2, ADP, etc
  • platelets become sticky and clump together = aggregation
  • platelets also secrete granules
32
Q

Platelet plug

A
  • primary hemostatic plug
  • clumping acts as a plug to stop bleeding
  • fragile and easily dislodged
  • anchored to vessel wall by secondary hemostasis
33
Q

Secondary hemostasis

A
  • reinforcement of platelet plug with stable fibrin clot

- initiation of coagulation cascade (ending in fibrin formation)

34
Q

Hemostatic reactions

A
  • occurs in a cascade/waterfall-like manor
  • zymogens (inactive factors) are sequentially activated
  • end result if fibrin clot
35
Q

Coagulation factors

A
  • proteins, most are made in the liver
  • normally present in plasma as zymogens
  • factor deficiencies produce bleeding tendency disorders
  • Fibrinogen group, Prothrombin group and Contact group
36
Q

Fibrinogen group

A
  • I, V, VIII, XIII
  • consumed during coagulation process
  • present in plasma, absent in serum
37
Q

Prothrombin group

A
  • II, VII, IX, X
  • consumed during coagulation process (except II)
  • Vitamin K dependent (so they can bind Ca2+)
38
Q

Contact group

A
  • XI, XII, Prekalikrein (PK), High molecular weight kininogen
  • not consumed during coagulation
  • requires contact with a surface for activation
39
Q

The Coagulation cascade

A
  • initiation occurs either via the intrinsic (contact) pathway or via the extrinsic (tissue factor) pathway
  • converge to a single pathway (common pathway)
  • single, tissue factor pathway in vivo
  • intrinsic pathway necessary for large amount of fibrin
40
Q

Extrinsic pathway

A
  • tissue factor (thromboplastin) is exposed when vessel is injured and it initiates the pathway
  • tissue factor complexes with factor VII to start pathway
  • continues until clot is formed (end of common pathway)
41
Q

Intrinsic pathway

A
  • substances normally present in circulation
  • exposure to collagen, subendothelium activates factor XII and XI (contact group)
  • continues until clot is formed once activated
42
Q

Common pathway

A
  • convergence of intrinsic and extrinsic pathways
  • starts with initiation of factor X by either pathway
  • factor X activates prothrombin (II) to thrombin (IIa)
  • thrombin cleaves fibrinogen (I) to make fibrin strands AND activates factor XIII
  • factor XIII links and stabilizes fibrin strands
43
Q

Fibrinolysis

A
  • slow process of breaking down fibrin when clot is no longer needed
  • enzymatic cleavage into soluble fragments
  • initiated upon fibrin formation (so we don’t overly clot)
  • gradually dissolves clot as tissue repair occurs
44
Q

Plasminogen (PLG)

A
  • circulates as inactive molecule
  • binds to fibrin throughout clot
  • activated to plasmin by tissue plasminogen activator (tPA) and urokinase type plasminogen activator (uPA)
45
Q

Plasmin (PLN)

A
  • initiates fibrinolysis

- digests fibrin by hydrolysis

46
Q

FDP/FSP

A
  • fibrin degradation products/fibrin split products
  • fragments formed as fibrin is broken down
  • cleared by the liver
  • detection is diagnostic for hemostatic disorders
  • plasmin splits fibrin to X and Y fragments (early FDPs)
  • Y fragment is split into D and E fragments (late FDPs)
  • fragments exert antithrombin effect (prevents clotting)
47
Q

Regulators of coagulation

A

regulated by activators and inhibitors

48
Q

Regulation of Secondary Hemostasis

A
  • limit the amount of fibrin clot formed to prevent ischemia

- localize clot formation to site of injury to prevent widespread thrombosis

49
Q

Secondary Hemostasis inhibitors

A 
Tissue factor pathway inhibitor (TFPI)
Activated Protein C and Protein S
Antithrombin III (AT)
Alpha2-macroglobulin
Alpha1-antitrypsin
Heparin cofactor II (HCII)
C1-inhibitor
Protein Z (PZ)
ZPI
50
Q

Tissue factor pathway inhibitor (TFPI)

A
  • glycoprotein on endothelial cell surfaces

- inhibits factor VIIa and Xa

51
Q

Activated Protein C and Protein S

A
  • C is major inhibitor in coagulation pathway
  • Vitamin K dependent inhibitors
  • synthesized in the liver
  • inhibit Va and VIIIa
52
Q

Serine Protease Inhibitors (serpins)

A
  • inhibit by trapping enzyme with serpin so it loses activity
  • Antithrombin III (AT), Alpha2-macroglobulin, Alpha1-antitrypsin, Heparin cofactor II (HCII)
53
Q

Antithrombin III (AT)

A
  • most clinically relevant serine protease inhibitor
  • enhanced by heparin (heparin won’t work without it)
  • synthesized by the liver and endothelial cells
  • inhibits thrombin, factors IXa, Xa, XIa, XIIa, kallikrein and plasmin
54
Q

Alpha2-macroglobulin

A

inhibits kallikrein, plasmin, thrombin, factor Xa

55
Q

Alpha1-antitrypsin

A

inhibits factor XIa, thrombin, kallikrein, plasmin

56
Q

Heparin cofactor II (HCII)

A

inhibits thrombin

57
Q

C1-inhibitor

A
  • inhibits esterase activity of C1 from complement cascade
  • inhibits contact system proteases (XIIa, IXa, kallikrein, PLN)
  • main inhibitor of XIIa
58
Q

Protein Z (PZ)

A
  • Vitamin K dependent protein

- enhances inhibitory function of ZPI against factor Xa

59
Q

ZPI

A
  • plasma serpin that inhibits factor Xa

- PZ-dependent

60
Q

Fibrinolytic activator

A
  • Tissue plasminogen activator (TPA)
  • produced by endothelial cells
  • aids in regulation of fibrinolysis
  • clot-busting drug
61
Q

Fibrinolytic inhibitors

A

Plasminogen activator inhibitor 1 and 2 (PAI-1 and PAI-2)
Thrombin activated fibrinolysis (TAFI)
Alpha 2 - antiplasmin inhibitor
Alpha 2 - macroglobulin

62
Q

Plasminogen activator inhibitor 1 and 2 (PAI-1 and PAI-2)

A

inhibits tPA and uPA

63
Q

Thrombin activated fibrionolysis (TAFI)

A

suppresses plasminogen binding to fibrin

64
Q

Alpha 2 - antiplasmin inhibitor

A

inhibits plasmin

65
Q

Alpha 2 - macroglobulin

A

inhibits plasmin

Coagulation & Body Fluids (3 decks)

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