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Coagulation, Urinalysis & body fluids > Normal Hemostasis > Flashcards

Normal Hemostasis Flashcards

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
Q

Vitamin K dependent factors

A

II, VII, IX, X

makes it possible for these factors to bind to calcium

26
Q

Intrinsic pathway

A

contact
XIIa + HMWK + PK
XIa + Ca2+
IXa + VIII + PL+ Ca2+ (intrinsic complex)

27
Q

Extrinsic pathway

A

vessel injury

TF+ VII + Ca2+ (extrinsic complex)

28
Q

Common pathway

A

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
Q

Fibrinolysis

A

when clot is no longer needed
enzymatic cleavage of fibrin to soluble fragments
fragments are then removed by macrophages

30
Q

Plasminogen (PLG)

A

as clotting begins, plasminogen binds to fibrin throughout the clot

31
Q

Plasminogen Activators

A

tissue plasminogen activator (tPA) & urokinase type plasminogen activator (uPA)
both activate plasminogen to plasmin

32
Q

Plasmin

A

initiates fibrinolysis

plasmin digests fibrin by hydrolysis - cleaves fibrin

33
Q

FDP/FSP

A

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
Q

Tissue factor pathway inhibitor (TFPI)

A

glycoprotein found on endothelial surfaces & serves as an anticoagulant by inhibiting factors VIIa & Xa (extrinsic & common pathway)

35
Q

Activated Protein C (!) & Protein S

A

proteins C & S are both Vit K dependent inhibitors, synthesized in the liver
together they inactivate factors Va & VIIIa (common pathway)

36
Q

Serine Protease Inhibitors

A

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
Q

Antithrombin III (AT)

A

binds & directly inactivates thrombin, & factors: IXa, Xa, XIa & XIIa, kallikrein, plasmin
MOST CLINICALLY SIGNIFICANT INHIBITOR
effect is enhanced 3-4x using heparin

38
Q

Alpha2-macroglobulin

A

inhibits kallikrein, plasmin, thrombin, Xa

39
Q

Alpha1-antitrypsin

A

inhibits factors XIa, thrombin, kallikrein, plasmin

40
Q

Heparin cofactor II (HCII)

A

inhibits thrombin

not as broad spectrum as AT

41
Q

CI-inhibitor

A

inhibitory of the esterase activity of Ci from the complement cascade
also inhibits F-XIIa (!)

42
Q

Protein Z

A

vit K dependent

enhances the inhibitory function against F-Xa

43
Q

Fibrinolytic activator

A

TPA- tissue plasminogen activator

Coagulation, Urinalysis & body fluids (4 decks)

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