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Cardiopulmonary Exam 1 > White's Hemostasis Lecture > Flashcards

White's Hemostasis Lecture Flashcards

1
Q

Hemostasis refers to

A

formation of a barrier to blood

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2
Q

Three types of barriers to blood

A

hemostatic plug, blood clot or thrombus

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3
Q

Primary hemostasis

A

1) primary hemostasis – primary plug – platelet aggregation

creates a physical plug causing vasoconstriction to reduce blood flow

platelets interact with broken vessel + each other to form primary hemostatic plug

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4
Q

Secondary Hemostasis

A

fibrin is deposited on the platelets, making the plug even more insoluble

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5
Q

Third stage of hemostasis

A

fibrinolysis, removal of clot

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6
Q

coagulation factors

A

soluble blood proteins that form fibrin

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7
Q

Fibrin clot: the goal

A

involves converting fibriogen into fibrin

fibrinogen is the largest of the plasma protein, constitutes about 4% of blood plasma proteins

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8
Q

another name for circulating inactive coagulation factors

A

zymogens

these can be activated by proteolysis

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9
Q

what is a zymogen

A

an inactive protein/enzyme that is activated by site specific proteolysis

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10
Q

In the liver, enzymes with “pre” and “pro” areas ndicate what

A

pre - for secretion; an area that is cleaved to permit secretion
pro- to keep inactivated; an area that is kept to maintain inactivation

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11
Q

when acted on by the final protein, ________, fibrinogen is converted to fibrin

A

thrombin

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12
Q

Named factors vs unnamed factors

A 
Factor 1 (F1): fibrinogen
F2: prothrombin
F3: Tissue factor 
F4-F8 unnamed 
F9: Christmas factor 
F10-F11 unnamed 
F12 Contact Factor 
F13 Plasma transglutaminase
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13
Q

What three things happen after a tissue injury to prevent blood loss?

A

1) vasoconstriction
2) Collagen exposure activates platelets producing a primary hemostatic plug
3) Tissue factors lead to the overlaying of fibrin to produce a fibrin clot.

the “fibrin clot” is composed of fibrin and platelet aggregation

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14
Q

Prothrombin is activated to thrombin by a

A 
serine protease (prothrombinase)
serine residues are in the active site then
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15
Q

Thrombin as serine protease

A

thrombin cuts fibrinogen at ARG-GLY sites

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16
Q

fibrinogen: how it gets activated to fibrin

A

fibrinogen has 3 domains (D–E–D), 3 subunits (alpha, beta, gamma), and 2 sites for cleaving, A and B (superior/inferior to alpha subunit)

the Alpha subunit can subsequently fit into the gamma site of another fibrinogen’s gamma site: this is the cross linking effect.

alpha (E domain, A site) fits into the gamma (D domain) site, creating a

while cleavage of A peptide uncovers sites in the E domain that are complementary to the D domain

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17
Q

what is the “basic” interaction allowing fibrin to aggregate?

A

E domains (A sites) interact with D domains on adjacent fibrin (gamma subunit) over and over,

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18
Q

in addition to the A site (E Domain) gamma (D domain) interaction, what other site does thrombin cleave?

A

the B sites: thenceforth B sites interact to form a 3 dimensional wall

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19
Q

“soft clot”

A

this is when fibrinogen’s D and E domains interact, and the B sites interact to form the three dimensional wall

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20
Q

E–D domain interactions use ___ bonds in _______ formation

A

H bonds in soft clot formation

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21
Q

Hard Clot Formation

A

Use covalent bonds between NH2 of glutamine and NH3 of lysin

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22
Q

What bonds form the hard clot?

A

NH2 of glutamine and NH3 of lysine, catalyzed by transglutaminase (Factor XIIIa)

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23
Q

FXIII —> FXIIIa via

A

thrombin, which activates transglutaminase

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24
Q

Prothrombin’s post-translational modification is

A

important for clot localization

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25
Q

How is protrhombin modified?

A

a glutamic acids gets an additional carboxyl group that adds a -2 charge to an R group on amino acid = gamma carboxyglutamate.

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26
Q

What is protrhombin’s post-translational modification called

A

gamma-carboxyglutamate

glutamic acid on prothrombin receives a corboxylic acid group that has a -2 charge

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27
Q

Why is the additional charged group added to glutamic acid on prothrombin important?

A

Damaged tissue rexposes calcium (+2 charge) at the site of injury, so carboxyglutamine can bind it perfectly with the -2 charge added.

in turn Calcium binds platelets which have exploded uncovering negatively charged phospholipids as they invert

28
Q

Platelet phospholipids

A

invert after binding to exposed collagen

negative charge on inverted phospholipids binds calcium which is also stabilized by the carboxyglutamate in the thrombin

29
Q

Vitamin K

A

caryboxylation of prothrombin requires vK

30
Q

4 enzyme involved in carboxylation of glutamic acid in prothrombin

A

Vitamin K Hydroquinone–> oxidized to Vitamin K epoxide by Carboxylase (activated by VKH)–> reduced to VKH by Epoxide Reductase

warfarin and Dicoumerol: competitive inhibitors of epoxide reductase.

31
Q

Coumadin

A

warfarin, competitive inhibitor of Epoxide Reductase: prevents Vk from activating enzyme responsible for carboxylating glutamic acid in prothrombin

32
Q

Dicoumerol

A

competitive inhibitor of epoxide reductase

33
Q

warfarin facts

A

active ingredient in rat poison, patients have to be watched carefully

WARF = “Wisconsin Alumni Research Fund” patented by university of wisconsin.

34
Q

Clotting cascade of _______

A

serine proteases, contain serine residue in active site of proteases

exist as zymogens- inactive enzymes made by proteolytic cleavage

35
Q

Intrinsic PW

A

workhorse of the clotting cascade, does not requires a protein outside of the blood to be activated

36
Q

Extrinsic PW

A

the “SPARK” to get the clotting cascade going

37
Q

Intrinsic PW factors

A

12, 11, 9, and 8:, all activated. Importantly,

(F8/F9)a

38
Q
  1. Intrinsic PW begins with ______ being activated by ______
A

contact factor (12) being activated by active form of pre-kalikrein (Kalikrein), a protease

XII (surface activation) —> XIIa

39
Q
  1. Intrinsic PW’s second step is activation of ______ by —-
A

XI by Calcium-bound XIIa

40
Q
  1. Intrinsic PW’s third step is activation of ____ by ____
A

IX by XIa+PF3+Calcium—> IXa

PF3 is the inverted phospholipid on the platelet that binds calcium

41
Q
  1. Intrinsic PWs fourth step is the formation of
A

IXa - VIIIa complex

Thrombin activates VIII

42
Q

Start of Common PW begins with

A

(IX–VIII) = Tenase

Tenase activate X —> Xa in the presence of PF3 and Calcium

Xa combines with FVa to form PROTHROMBINASE

V is activated by thrombin

43
Q

Which factor is common to intrinsic and extrinsic?

A

X

44
Q

what two factors are activated during the intrinsic PW

A

VIII and V

45
Q

Prothrombinase

A

Va+Xa

46
Q

Xa–Va activate

A

This is the prothrombinase that activates thrombin

47
Q

Hemophilia is deficiency in what factors

A

Type A is VIII deficiency and Type B is IX deficiency

48
Q

Amplification Cascade

A

a handful of XII causes a massive clotting cascade signal, each factor is increased at each stop of the clotting cascade

49
Q

Extrinsic Pathway

A

Activated by a component not normally in the blood, factor III (tissue factor)

Tissue factor activates VII

50
Q

How EX PW begins

A

factor III activates factor VII
VIIa combine with another factor III to form a complex

VIIa-TF complex

The rest is the common PW

Vlla+TF complex activate X—Xa while thrombin activates V to Va

Va+Xa form Prothrombinase

Prothrombinase activates prothrombin –> thrombin

thrombin continues cascade

51
Q

Common PW is just

A

Factor X to the fibrin clot formation

52
Q

How is thrombin active if thrombin is actively produced?

A

~ 1% of FVII circulates as FVIIa, but does not contact damaged tissue

After damage, VII and XIII tissue factor combine to form complex that activates FX

Platelets release FVa, released from platelets
forms FXa–FVa complex (prothrombinase comlex) which gets things going

53
Q

Why is Extrinsic important outside of its own contributions to the clotting cascade? How does it relate to the intrinsic PW?

A

It sets the intrinsic in motion by setting VII into motion (VIIa)

54
Q

Vitamin K Dependent Factors: 3 factors that aren’t glutamic acid that require vitamin K activated carboxylation

A

X, IX, VII

55
Q

Positive Feedback Mechanism for clotting factors

A

Thrombin, XIa, Xa, VIIa

56
Q

Partial THromboplastin Time

A

PTT

Clotting time from Factor XII to fibrin clot –» intrinsic pathway, reference is 35 sec

57
Q

Prothrombine Time

A

PT

Clotting time from factor VII to fibrin clot —> extrinsic and common pathwayas

reference time = 10 - 12 sec

58
Q

Clotting in vivo requires a

A

TF: tissue factor, initiating component (FIII)

59
Q

So what is REALLY be tested for in vivo?

A

VIIa-TF complex, which activates FIX

FIX combines with activated VIII to activate FX, which combines with thrombin-activated V
to activate prothrombin –> thrombin

IXa –VIII (Tenase)

60
Q

Regulation I: How fibrin is turned off

A

thrombin binds it and inactivates it

Thrombin can cut FVIIIA to inactivate form FVIIIi
Thrombin can cut Xa to Xi
Thrombin can cut Va to Vi

hrombin can cut prothrombin to create an inactive form

61
Q

Regulation II: How Thrombin works to this end

A

combines with a protein called Thrombomodulin to create TTM complex

this cleaves a protein called Protein C into active protein Ca

Protein Ca and others inactive FVa and FVIIIa which decreases thrombin

62
Q

Anticlotters: preventing clotting

A

warfarin and dicoumerol

63
Q

Protects platelet integrity

A

aspirin

64
Q

Heparin

A

activates antithrombin III by binding to thrombin and Xa, which it inactivates

65
Q

TPA

A

tissue plasminogen factor

percursor to plasmin, dissolves clot
fibrinolysis

first genetically engineered human protein to be approved for use in humans, given to remove clot, aslo after stroke if given early

Cardiopulmonary Exam 1 (21 decks)

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