Normal Hemostasis Flashcards

(43 cards)

1
Q

Hemostasis

A

coagulation or hemostasis is the process involved when blood clots in reponse to an injury

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2
Q

3 stages of normal coagulation

A
  1. primary hemostasis
  2. secondary hemostatsis
  3. fibrinolysis
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3
Q

Primary hemostasis

A

injury-> damaged vessels initiate hemostasis:

contraction of vessels: minimizes blood flow to wound area & brings platelets & coag factors closer to vessel wall

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4
Q

Megakaryoblast MK1

A
6-24 microns
scant basophilic cytoplasm
no visible granules
round nucleus
visible nucleoli
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5
Q

Promegakaryocyte MK2

A

cytoplasmic granule development begin
membrane demarcation begins
nucleus lobulated
no visible nucleus

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6
Q

Megakaryocyte MK3

A

cytoplasmic RNA (blue) disappear so it is more purple
proplatelets-groups of platelets break off into circulation
granular cytoplasm
large, multilobed nucleus

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7
Q

Mature Megakaryocyte

A

after proplatelets have been released

all that is left is the nucleus, which is phagocytized by macrophages & broken down

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8
Q

Platelet Structure

A

peripheral zone: phospholipid layer w/ protein
structural zone: microtubules etc
organelle zone: granules & organelles
membrane systems

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9
Q

Formation of Platelet plug involves:

A
platelet adhesion
platelet activation
platelet shape change
platelet secretion of granules
platelet aggregation
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10
Q

Platelet Adhesion

A
damaged vessels exposes flowing blood to subendothelial connective tissue that is composed of adhesive molecules
3 components:
1. vWF -links platelet to subendothelial
2. platelet membrane receptorGPlb
3. collagen fibers
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11
Q

Platelet adhesion: vWF

A

synthesized by endothelial cells & megakaryocytes
absorbed onto the surface of the platelet bound to its receptor GPlb
becomes a bridge connecting the platelet to the collagen fibers

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12
Q

Platelet Activation

A

leads to :
shape change, secretion of granules into surrounding tissue, formation of aggregates
only activated plts are able to proceed w/ formation of plug

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13
Q

Platelet Agonists

A

an agent that induces plt activation
each agonist binds to the plt surface at its specific receptor site
ADP, serotonin, platelet activating factor, TXA2
collagen, thrombin (!), epinephrine

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14
Q

Platelet shape change

A

adhesion of platelets to collagen fibers via vWF triggers shape change:
pseudopods, become extremely sticky

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15
Q

Platelet secretion

A

release of granules into surrounding area

granules: alpha & dense granules

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16
Q

Alpha granules

A

thrombospondin- promotes plt to plt interaction
vWF- plt adhesion
plt-derived growth factor (PDGF) -promotes smooth muscle growth

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17
Q

Dense granules

A

ADP- promotes plt aggregation
Calcium- regulates plt activation/aggregation
Serotonin-promotes vasoconstriction

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18
Q

Platelet Aggregation

A

attachment of plt to one another

activation leads to secretion of substances stored in granules - ADP etc

19
Q

Platelet plug

A

primary hemostatic plug
fragile & easily dislodged
plug is stabilized to vessel wall via 2ndary hemostasis

20
Q

Secondary Hemostasis

A

rapid reinforcement of plt. plug w/ fibrin clot

requires coagulation factors

21
Q

Coagulation factors

A

inactive coag factors - zymogens

almost all are made in the liver & are proteins

22
Q

classification of coag factors

A
  1. fibrinogen group
  2. prothrombin group
  3. contact group
23
Q

Fibrinogen group

A
includes factors:
I (fibrinogen)
V - heat liable
VIII
XIII
all factors are consumed during process of coag
present in plasma & absent in serum
24
Q

Prothrombin Group

A
includes factors:
II (prothrombin)
VII
IX
X
factors are not consumed during coag (except II)
Vit K dependent!
25
Vitamin K dependent factors
II, VII, IX, X | makes it possible for these factors to bind to calcium
26
Intrinsic pathway
contact XIIa + HMWK + PK XIa + Ca2+ IXa + VIII + PL+ Ca2+ (intrinsic complex)
27
Extrinsic pathway
vessel injury | TF+ VII + Ca2+ (extrinsic complex)
28
Common pathway
X Xa + V + PL + Ca2+ = prothrombin complex prothrombin (II) is then converted to thrombin (IIa) via above complex thrombin then converts fibrinogen (I)->fibrin & XIII-> XIIIa forms crossliked fibrin
29
Fibrinolysis
when clot is no longer needed enzymatic cleavage of fibrin to soluble fragments fragments are then removed by macrophages
30
Plasminogen (PLG)
as clotting begins, plasminogen binds to fibrin throughout the clot
31
Plasminogen Activators
tissue plasminogen activator (tPA) & urokinase type plasminogen activator (uPA) both activate plasminogen to plasmin
32
Plasmin
initiates fibrinolysis | plasmin digests fibrin by hydrolysis - cleaves fibrin
33
FDP/FSP
fibrin degradation or split products fragments from fibrinolysis that are rapidly cleared from circulation by the liver consists of : X,Y,D, E these fragments exert an antithrombin effect
34
Tissue factor pathway inhibitor (TFPI)
glycoprotein found on endothelial surfaces & serves as an anticoagulant by inhibiting factors VIIa & Xa (extrinsic & common pathway)
35
Activated Protein C (!) & Protein S
proteins C & S are both Vit K dependent inhibitors, synthesized in the liver together they inactivate factors Va & VIIIa (common pathway)
36
Serine Protease Inhibitors
known as serpins inhibit target by trapping the enzyme w/ the serpin & resulting in loss of activity Antithrombin III (AT), ALpha2-macroglobulin, alpha1-antitrypsin, Heparin cofactor II,
37
Antithrombin III (AT)
binds & directly inactivates thrombin, & factors: IXa, Xa, XIa & XIIa, kallikrein, plasmin MOST CLINICALLY SIGNIFICANT INHIBITOR effect is enhanced 3-4x using heparin
38
Alpha2-macroglobulin
inhibits kallikrein, plasmin, thrombin, Xa
39
Alpha1-antitrypsin
inhibits factors XIa, thrombin, kallikrein, plasmin
40
Heparin cofactor II (HCII)
inhibits thrombin | not as broad spectrum as AT
41
CI-inhibitor
inhibitory of the esterase activity of Ci from the complement cascade also inhibits F-XIIa (!)
42
Protein Z
vit K dependent | enhances the inhibitory function against F-Xa
43
Fibrinolytic activator
TPA- tissue plasminogen activator