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Flashcards in Hemostasis Deck (99)
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1
Q

what are the 3 parts to hemostasis?

A
  1. Primary hemostasis
  2. Secondary Hemostasis
  3. Anticoagulation
2
Q

What is the main Factor in Hemostasis?

A

platelet

3
Q

what is part 1 of hemostais and what if the main objective

A

Primary hemostasis

Platelet plug

4
Q

what is part 2 of hemostasis and what if the main objective

A

Secondary Hemostasis

Fibrin production

5
Q

what is part 3 of hemostasis and what if the main objective

A

Anticoagulation

break down clot

6
Q

Steps in primary Hemostasis:

what are the 3 steps in primary hemostasis?

A
  1. Adhesion
  2. Activatiion
  3. Aggregation

ALL A’s

7
Q

Steps in primary Hemostasis:

How is Adhesion accomplished?

A

Adhesion of platelets to damaged vascular wall

8
Q

Steps in primary Hemostasis:

Adhesion of the platelets requires what hemostasis factor

A

vWF (VIII)

9
Q

Steps in primary Hemostasis:

how is activation accomplished?

A

activation of platelets requires thrombin (factor IIa)

10
Q

Steps in primary Hemostasis:

how is aggregation accomplished?

A

aggregation of platelets requires ADP and thromboxane A2

11
Q

Steps in primary Hemostasis:

again the main ingrediant to all hemostasis is what?

A

the platelet

12
Q

Steps in primary Hemostasis:

what is required for adhesion

A

vWF

13
Q

Steps in primary Hemostasis:

what is required for activation?

A

thrombin (IIa)

14
Q

Steps in primary Hemostasis:

what is required for aggregation

A

ADP

Thromboxane A2

15
Q

Adhesion of Platelets:

what is platelets life span

A

8-12 days

16
Q

Adhesion of Platelets:

normal platelet count

A

150,000-400,000 cells/mL

17
Q

Adhesion of Platelets:

Approx 33% of platelets are sequestered where?

A

Spleen

18
Q

Adhesion of Platelets:

what factor Adheres platelets to the collogen layer of the subendothelium?

A

vWF

19
Q

Adhesion of Platelets:

vWF is synthesized and reeased from where?

A

endothelial cells

20
Q

Adhesion of Platelets:

the illistration show vWF anchoring platelets to the wall of a damaged blood vessel.

this is the adhesion aspect of the primary hemostasis

A
21
Q

Adhesion of Platelets:

Magnified look at how vWF anchors platelets

A
22
Q

Adhesion Disorders:

what is the most common inherited coagulation defect

A

von Willebrands disease

23
Q

Adhesion Disorders:

what is the 1st line treatment for von Willebrands disease

A

D-amino-D-arginine vasopressin (desmopressin, DDAVP)

24
Q

Adhesion Disorders:

how does DDAVP work

A

causes release of endogenous stores of vWF

25
Q

Adhesion Disorders:

what is the dose of DDAVP

A

0.3 mcg/kg IV over 10-20 min

26
Q

Adhesion Disorders:

with DDAVP administration platelet adhesion is increased within how long

A

30 min

27
Q

Adhesion Disorders:

DDAVP can cause what in type 2B von WIllebrands disease

A

thrombocytopenia

28
Q

Adhesion Disorders:

vWF can be increased by giveing DDAVP as well as what other 2 drugs?

A

Cryoprecipitate

Purified factor VIII

29
Q

Adhesion Disorders:

Cyo cantains what coag factors

A

I

VIII

XIII

(1,8,13)

30
Q

Adhesion Disorders:

if a pt does not respond to DDAVP what should be given next

A

cryo

31
Q

Adhesion Disorders:

again what are 3 treatments for von Willebrands disease

A

DDAVP

Cryo

Purified Factor VIII

32
Q

What is the 2nd step of PRIMARY hemostasis?

A

Activation

33
Q

Activation of Platelets:

what is the mechanism in which a platelet becomes activated?

A

Thrombin (IIa) combines w/ thrombin receptor on the platelet surface

a process ensues and the platelete changes shape and releases mediators

The main 2 mediators are Thromboxane A2 and ADP

(these will later promote aggregation)

34
Q

Activation of Platelets:

what is the most important molecule in teh activation of platelets

A

Thrombin

35
Q

Activation of Platelets:

what are the 2 mediators released from platelet activation

A

ADP

Thromboxane A2

36
Q

Activation of Platelets:

what do Thromboxane A2 and ADP do?

A

uncover Fibrinagen (I) receptors (more secefic GPIIb/IIIa)

37
Q

Activation of Platelets:

see the picture as a reference. Note the shape change and the release of mediators

A
38
Q

Activation of Platelets:

what is the precurser to Thrombin?

A

prothrombin II

once activated becomes IIa Aka thrombin

39
Q

what is the 3rd step in primary hemostasis?

A

Aggregation of platelets

40
Q

Aggregation of Platelets:

what is teh main molecule that is responsiable for aggregations platelets?

A

Fibrinogen (I)

41
Q

Aggregation of Platelets:

___ and ____ uncover the fibrinogen recetors on the actvated platelets

A

TXA2

ADP

42
Q

Aggregation of Platelets:

once the receptors are uncovered fibrinogen atteches to it’s receptors and links platets to what?

A

other platelets

43
Q

Aggregation of Platelets:

at this point when the fibrinogen is adhearing platelets to other platelets the developing clot in water soluble and firable and it is termed what 3 things

A

Platelet plug

white thrombus

white clot

44
Q

Aggregation of Platelets:

check out the picture

A
45
Q

Aggregation Disorders:

with aspirin the acetylation of platelet cyclooxygenase persist for how long?

A

the life of the platelet 8-12 days

46
Q

Aggregation Disorders:

what is the rate limiting enzyme in the conversion of arachidonic acid to TXA2

A

cyclooxygenase (COX)

47
Q

Aggregation Disorders:

without _____ platelete aggregation in impaired

A

TXA2 (thromboxane A2)

48
Q

Aggregation Disorders:

NSAIDs such as ketorolac and ibuprofen produce the same effects as aspirin, but the depressin of Thromboxane A2 production by platlets if temporary. How long is it for

A

24-48 hours

49
Q

Aggregation Disorders:

How does Clopidogrel (plavix) work to cause coagulation

A

anti ADP agent

works the life of platelet

50
Q

Aggregation Disorders:

what antiplatelet medication increases cAMP in platelets and thus prevents aggrigation?

A

Dipyridamole (persantine)

also is classified as a PDE-I inhibitor

51
Q

Aggregation Disorders:

What receptors do Anti-fibrinogen receptor drugs work on

A

GPIIb/IIIa

52
Q

Aggregation Disorders:

how do anti-fibrinogen receptor drugs work?

A

the “cap” and block the fibrinigen receptor, thus preventing fibrinogen from attaching and linking platelets together.

53
Q

Aggregation Disorders:

what are 3 anti-fibrinogen receptor drugs in use

A
  • Eptifibatide (integrilin)
  • Abciximab (ReoPro)
  • Tirofiban (aggrastat)
54
Q

what is the second part of hemostasis? not primary hemostasis but hemostasis in general?

A

secondary hemostasis

55
Q

What is the main goal of 2ndary hemostasis?

A

Production of fibrin

56
Q

Secondary hemostasis:

fibrin production involves what?

A

all of the clotting factors

57
Q

Secondary hemostasis:

name the cloting factors

A
  1. Fibrinogen
  2. prothrombin
  3. tissue factor
  4. calcium
  5. Proacceleration
  6. NONE
  7. proconvertin
  8. vWF & Antihemophiliac factor
  9. christmas factor
  10. stuart-prower factor
  11. Plasmin thromboplastin antecedent
  12. Hagamen factor
  13. Fibrin stabilizing factor
58
Q

Secondary hemostasis:

what are the vit K dependent factors

A

2

7

9

10

C

S

59
Q

Secondary hemostasis:

what is Factor I (fibrinogen) once activated (Ia) called

A

Fibrin

60
Q

Secondary hemostasis:

After platelets aggregate ___ is woven into platelets and cross-linked.

A

Fibrin

61
Q

Secondary hemostasis:

the cross linked fibrin is _____ in water

A

Insoluble in water

62
Q

Secondary hemostasis:

After platlets aggregate, fibrin is woven into platelets and cross linked, the crosslinked fibrin is insoluble in water. thus the fibrin clot is now stable. The clot is now called what 2 things

A

red thrombus

red clot

63
Q

Secondary hemostasis:

cross linking of fibrin strands requires what factor

A

XIIIa

Fibrin stabilizing factor

64
Q

Secondary hemostasis:

the final steps in fibrin prouction involve what pathways

A

Intrinsic

Extrinsic

Final common

65
Q

Secondary hemostasis:

heres a picture

A
66
Q

Secondary hemostasis:

here is a colored picture

A
67
Q

Secondary hemostasis:

what type of bond stabilizes the fibrin network

A

Covalent

68
Q

Secondary hemostasis:

so we learned about cryo earlier now why is cryo an important drug for coagulation?

A
  • Factor (I) Fibrinogen (Ia) fibrin- causes crosslinking
  • VIII vWF- promotes platelet adhesion
  • XIII Fibrin stabilizing factor- forms covalent bond at cross-linked areas stabilizing the fibrin clot
69
Q

Secondary hemostasis: Coagulation Cascade

what factors are in the extrinsic pathway?

A

III- Thromboplastin or tissue factor

VII- proconvertin

70
Q

Secondary hemostasis: Coagulation Cascade

where does damage occur is the extrinsic pathway is activated

A

outside the cell

71
Q

Secondary hemostasis: Coagulation Cascade

what factors are in the intrinsic pathway?

A

XII- hagamen

XI- Plasma thromboplastin

IX- christmas

VIII- vWF

72
Q

Secondary hemostasis: Coagulation Cascade

the ending factors in both the intrinsic and extrinsic pathways combine with what factor to go to factor 10 in the common fina pathway

A

IV calcium

73
Q

Secondary hemostasis: Coagulation Cascade

what factors are in the final common pathway

A

X

V

II

I

XIII

74
Q

Secondary hemostasis: Coagulation Cascade

what factors are Ca++ dependent factors

A

2,7,9,10

same as Vit K dependent factors

75
Q

Secondary hemostasis: Coagulation Cascade

what drug works on the extrinsic pathway?

what labs monitor it?

A

Coumadin

PT/INR

76
Q

Secondary hemostasis: Coagulation Cascade

what drug works on the intrinsic pathway? what labs monitor it?

A

Heparin

PTT

ACT

77
Q

Secondary hemostasis: Coagulation Cascade

my drawing of the pathway

A
78
Q

Secondary hemostasis: Coagulation Cascade

what pathway does cryo mostly work on and why?

A

Common final pathway

b/c it has factors 1,8,13 and 1 and 13 are both in the final pathway

79
Q

Secondary hemostasis: Coagulation Cascade

Valley’s picture

A
80
Q

Congenital Disorders of Coagulation:

hemophilia A affects what factor

A

VIII:C deficiency

81
Q

Congenital Disorders of Coagulation:

treatment for Hemophilia A

A

FFP and Cryo (both have VIII

Factor VIII concentration

82
Q

Congenital Disorders of Coagulation:

What factor deficiency causes hemphilia B

A

AKA Christmas disease

IX

83
Q

Congenital Disorders of Coagulation:

treatment of Hemophilia B Christmas disease

A

Heat treated concentration of factor IX

84
Q

Anticoagulation:

how does antithrombin work

A

Activated antithrombin binds to thrombin (IIa) and factor Xa greatly

By attaching to these clotting factors esp thrombin and Xa antithrombin effectivly removes them from circulation

thus anticoagulating blood

85
Q

Anticoagulation:

what drug works by increasing the effectivness of antithrombin by 1,000 fold or more?

A

heparin

86
Q

Anticoagulation:

besides IIa and Xa what other factors does antitrhombin work on

A

IX
XIa

XIIa

87
Q

Anticoagulation:

Antithrombin is made in the liver and neutralizes the final pathway by what factors? and the intrinsic pathway by what factors?

A

Common IIa and Xa

Intrinsic XIIa, XIa, and IX

88
Q

Anticoagulation:

what is a required cofactor for heparin to work

A

antithrombin

89
Q

Anticoagulation:

aquired anithrombin def states are found in what type of patients

A

cirrhosis of liver

Nephrotic syndrome

90
Q

Anticoagulation:

what is the most common reason a pt is unresponsive to heparin

A

antithrombin def

91
Q

Anticoagulation:

if someone is unresponsive to heparin what would u give them and why?

A

FFP

it comtains all coagulation and anticoagulation factors produced by the liver

92
Q

Anticoagulation:

heparin block what pathway(s)

A

Intrinsic and common

93
Q

Anticoagulation:

protamine reverses the effects of heparin how?

A

neutralization

94
Q

Anticoagulation: fibrinolysis

what breaks down fibrin

A

Plasmin

95
Q

Anticoagulation: fibrinolysis

what is converted into plasmin to break down fibrin

A

Plasminogen

96
Q

Anticoagulation: fibrinolysis

after plasminogen is converted into plasmin and plasmin starts to breakdown fibrin, what are the fibrin degradation products refered to as

A

Fibrin split products

97
Q

DIC:

what are the most common precipitating factors in the surgical pt

A

Shock

Ischemia

and infection

98
Q

DIC:

what happens to lab values

Platelets

Fibrinogen

Prothrombin

Factors V, VIII, XIII

Fibrin split products

A

Platelets- decreased

Fibrinogen- decreased

Prothrombin- decreased

Factors V, VIII, XIII- decreased

Fibrin split products- Increased

99
Q

Memory master pages

A

IA8a-e

IB13

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