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The BIG Test > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

4 Steps Involved in Primary Hemostasis

A
  1. Adhesion of plts to damaged vascular wall
  2. Activation of plts
  3. Aggregation of plts
  4. Production of fibrin
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2
Q

What do each of the 4 steps of primary hemostasis require?

A

Adhesion requires VIII:vWF
Activation requires thrombin (Factor IIa)
Aggregation requires ADP and thromboxane A2
Production of fibrin requires all the pathways

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3
Q

What is the normal plt count?

Plts have an average life-span of _____ days.

A

150,000-400,000 cells/mL

8-12 days

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4
Q

Approx. ____% of the plt pool is sequestered in the spleen.

A

33%

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5
Q

When vascular endothelium is damaged and the subendothelium of the blood vessel is exposed, vWF anchors plts to the _____ layer of the _______.

A

Collagen

Subendothelium

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6
Q

vWF is synthesized and released by ________.

A

Endothelial cells

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7
Q

What is the most common inherited coagulation defect?

A

von Willebrand’s disease

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8
Q

____________ should be suspected in any patient with an increased bleeding time despite a normal plt count and normal clot retraction.

A

von Willebrand’s disease

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9
Q

What is the first line treatment for von Willebrand’s disease?

A

DDAVP - causes release of endogenous stores of vWF
Increased plt adhesion in 30 min that lasts for 4-6 hrs
SE in children = hyponatremia
*DDAVP causes thrombocytopenia in type 2B von Willebrand’s disease
Other options: cryoprecipitate, Factor 8

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10
Q

Cryoprecipitate contains which factors?

A

Factors 1, 8, 13

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11
Q

After plt activation by thrombin (Factor IIa), what 2 mediators are released?

A
  1. Thromboxane A2
  2. ADP

*These 2 mediators promote plt aggregation by uncovering fibrinogen receptors - fibrinogen (Factor I) attaches to its receptors and links the plts

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12
Q

The fibrinogen receptor is known as…

A

GPIIb/IIIa

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13
Q

Fibrinogen (Factor I) _______ plts.

A

Aggregates

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14
Q

How does aspirin work?

A

Renders cyclooxygenase I non-functional
Acetylation of cyclooxygenase
Prevents the conversion of arachidonic acid to thromboxane A2
WithOUT thromboxane A2 - plt aggregation is impaired
Persists for the life of the plt (8-12 days)

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15
Q

What is the rate-limiting enzyme in the conversion of arachidonic acid to thromboxane A2?

A

Cyclooxygenase

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16
Q

NSAIDs vs. Aspirin

A

Produce the same effects as aspirin BUT the depression of thromboxane A2 production is temporary (approx. 24-48 hrs) NOT permanent like aspirin (8-12 days)

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17
Q

How does clopidogrel (Plavix) work?

A

Anti-ADP agent

Persists for the life of the plt (8-12 days)

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18
Q

How does Eptifibatide and Abciximab work?

A

Anti-fibrinogen receptor (GPIIb/IIIa) drugs

Result - no linking of plts

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19
Q

What is the most common acquired blood clotting defect?

A

Inhibition of cyclooxygenase production by aspirin and NSAIDs
Most common cause of plt dysfunction

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20
Q

List the synonyms for clotting factors I, II, III, IV, VIII, XIII.

A 
I Fibrinogen
II Prothrombin
III Tissue factor
IV Calcium 
VIII:vWF von Willibrand's 
XIII Fibrin-stabilizing factor
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21
Q

All clotting factors are from the liver EXCEPT ____________.

A

3: vascular wall, traumatized cells
4: diet
8: vascular endothelial cells

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22
Q

Which clotting factors are Vit K dependent?

A

2, 7, 9, 10

Protein C, S

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23
Q

Explain the role of fibrin in blood coagulation.

A

After plts aggregate, fibrin is woven into plts and cross-linked
Cross-linking of fibrin strands requires Factor XIII
Now the clot is insoluble and stable!

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24
Q

Extrinsic Pathway

A

Damage outside of blood vessel
Release of thromboplastin/Factor 3/tissue factor
7 is activated
3a + 7a + 4 = 10 is activated

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25
Q

Intrinsic Pathway

A 
Exposure of blood to collagen
12 is activated 
11 is activated
9 is activated
9a + 8:Ca + 4 = 10 is activated
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26
Q

Final Common Pathway

A

10a + 5a + 4 = 2 is activated (prothrombin to thrombin)
Thrombin (2a) converts fibrinogen (1) to fibrin (1a)
In the presence of Factor 13, fibrin cross-linking occurs

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27
Q

What is the primary physiologic initiator of coagulation?

A

Thromboplastin

Factor 3

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28
Q

What helps position clotting factors on the surface of the plt so biochemical rxns can occur?

A

Calcium

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29
Q

Coumadin acts on the _________ and final common pathways.

Coumadin is assessed by _____ and _____.

A

Extrinsic

PT and INR

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30
Q

Heparin acts on the _________ and final common pathways.

Heparin is assessed by _______ and ______.

A

Intrinsic

PTT and ACT

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31
Q 
Hemophilia A 
What is it? 
Cause? 
Affects males or females? 
Is it common? 
Treatment?
A 
Factor 8:C deficiency 
Sex-linked recessive genetic disorder 
Carried by female, affects males 
2nd most commonly inherited coag disorder 
Tx - FFP, cryoprecipitate, 8 concentrate
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32
Q

Hemophilia B
What is it?
Treatment?

A

Christmas disease
Factor 9 deficiency
Tx - 9 concentrate

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33
Q

What is the most important clue to a clinically significant bleeding disorder in an otherwise healthy patient?

A

History

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34
Q

What is the most common reason for coagulopathy in patients receiving massive blood transfusions?

A

Lack of functioning plts

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35
Q

Plts in stored blood are nonfunctional after how many days?

A

1-2 days

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36
Q

Abnormalities of coagulation owing to dilution of what 2 factors may also be an issue other than lack of functioning plts in a patient who is receiving massive blood transfusions?

A
  1. Factor 5

2. Factor 8

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37
Q

What is the only acceptable clinical indication for transfusion of PRBCs?

A

To increase the oxygen carrying capacity of blood

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38
Q

What factors are present in FFP?

A

ALL factors EXCEPT plts

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39
Q

One unit of PRBCs will increase Hct by ____% or 1 g/dL.

A

3-4%

*1 mL/kg PRBCs will increase Hct 1%

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40
Q

One unit of plts will increase plt count by ________ mm3.

A

5,000-10,000/mm3

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41
Q

How does heparin work?

A

Heparin binds to ATIII

Increases the effectiveness of ATIII 1,000-10,000x

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42
Q

What is the purpose of antithrombin III?

A

Activated ATIII binds to Factor 2a (thrombin) and Factor 10a (to a lesser degree 9, 11, 12)
After binding, ATIII removes them from circulation
Anticoagulates the blood

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43
Q

Where is ATIII made?
ATIII strongly inhibits which 2 factors?
ATIII partially inhibits which 3 factors?
ATIII is a required cofactor for what?

A

Liver
Factors 2a, 10a (final common pathway)
Factors 9a, 11a, 12a (intrinsic pathway)
Heparin

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44
Q

Acquired ATIII deficiency states are found in patients with…

A

Cirrhosis of the liver

Nephrotic syndrome

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45
Q

What is the most common reason a patient is unresponsive to heparin?
What would you do to fix it?

A 
An ATIII deficiency 
Give FFP (includes all coag and anticoag factors made by the liver)
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46
Q

How does warfarin work?

A

Binds to the Vit K receptor in the liver
Inhibits production of the Vit K dependent clotting factors (2, 7, 9, 10)
*D/c 3-5 days pre-op

47
Q

How does protamine work?

A

Combines electrostatically/ionically with heparin
Protamine is positively charged (basic), heparin is negatively charged (acidic)
*Neutralization rxn

48
Q

What is an option if the patient has developed heparin-induced thrombocytopenia and you still need anticoagulation?

A

Direct thrombin inhibitors

Hirudin, Ximelgatran, Argatroban

49
Q 
Coagulation Tests - Normal Values 
Bleeding Time
Plt Count
PT
PTT
ACT
Fibrinogen
A 
Bleeding Time: 3-10 min
Plt Count: 150,000-400,000 cells/mL 
PT: 12-14 sec 
PTT: 25-35 sec 
ACT: 80-150 sec 
Fibrinogen: > 150 mg/dL
50
Q

Describe the clot-busting role of plasmin.

A

Plasminogen (inactive form of plasmin) is incorporated into a clot as the clot is formed
Tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA) convert plasminogen to plasmin
Plasmin breaks down fibrin

51
Q

Where is plasminogen synthesized?

52
Q

Facts about tPA

A

Incorporated into the forming clot
Produced by endothelial cells
Release is stimulated by thrombin and venous stasis

53
Q

What is the most widely used thrombolytic agent for intra-arterial infusion into the peripheral arterial system and grafts?

54
Q

How does aprotinin work?

A

Anti-fibrinolytic agent
Inhibits plasmin
Fibrin breakdown is slowed
Decrease intra-op blood loss

55
Q

How does epsilon aminocarproic acid (Amicar) and tranexamic acid work?

A

Displace plasmin from fibrin

Prevent the breakdown of fibrin

56
Q

What is the result of inhibiting plasmin?

A

Fibrin that is formed breaks down slowly

So bleeding is decreased

57
Q

What are the risks of aprotinin?

A

Increases the risk of perioperative MI
May exacerbate renal dysfunction
May cause a primary allergic rxn after the first dose
May cause a severe anaphylaxis after a second dose or greater dose

58
Q

Name 4 commonly encountered problems associated with abnormal hemostasis.

A
  1. DIC
  2. Liver disease
  3. Renal disease - uremia
  4. Multiple transfusions
59
Q

Disseminated Intravascular Coagulation (DIC)
Describe.
Diagnosis?

A

Manifestation of an underlying disease process
No lab test for DIC
Lab tests reflect consumption of clotting factors + enhanced fibrinolysis

60
Q

What OB emergencies are associated with DIC?

A

Abruptio placentae

Amniotic fluid embolism

61
Q

What are the most common precipitating factors for acute DIC in surgical patients?

A

Shock
Ischemia
Infection

62
Q

Lab Abnormalities in DIC

A

Decreased: plts, Factors 1, 2, 5, 8, 13
Increased: fibrin degradation (split) products

63
Q

What is the most common cause of an isolated high PT?

A

Liver disease

64
Q

How does liver disease affect coagulation?

What is the Tx?

A

Thrombocytopenia from hypersplenism
Increase lytic activity d/t poor clearance of tPA
Plt dysfunction from elevated fibrin split products
Synthesis of ALL coag factors is decreased (except Factor 8)
Tx - replace clotting factors with FFP, cryoprecipitate, and Vit K

65
Q

How does uremia affect coagulation?

What is the Tx?

A

Plt dysfunction - impaired adherence and synthesis of thromboxane A2 and ADP
Fibrinogen and other clotting factors are decreased
Fibrinolytic system is impaired
Tx - dialysis, elevation of Hct, cryoprecipitate, DDAVP

66
Q

Are plt transfusions helpful in uremia?

A

NO, they are ineffective

The transfused plts rapidly become abnormal

67
Q

What are the issues associated with massive blood transfusions?

A

Deficiencies of plts, Factors 5 and 8

68
Q

Diffuse bleeding during massive transfusion is generally caused by…

A

Thrombocytopenia

69
Q

What is the best test of primary hemostasis or plt function?

A

Bleeding time

70
Q

What antiplatelet agent prevents ADP-induced plt aggregation?

A

Ticlopidine

*D/c 14 days prior to surgery

71
Q

Post-op bleeding with continued oozing from wounds and catheter sites suggests what disorder?

72
Q

What is DDAVP?

A

Analogue of ADH
Used as a substitute for ADH to concentrate the urine
Used to treat von Willebrand’s (Type 1) - stimulates the release of existing vWF from endothelial cells

73
Q

What is the onset time of heparin?

74
Q

What 3 problems can administration of protamine cause?

A
  1. Systemic hypotension
  2. Pulmonary HTN
  3. Allergic rxns
    * Adverse events are d/t histamine release
75
Q

What is the max recommended dose of Protamine?

A

50 mg within 10 min

*Rapid injection may cause histamine relase - facial flushing, bronchoconstriction, tachycardia, hypotension

76
Q

What is the protamine dose?

A

1 mg of protamine for every 100 units of heparin predicted to still be circulating

77
Q

What are the 3 antidotes of warfarin?

A
  1. Vit K
  2. Fresh whole blood
  3. FFP
78
Q

When should the last dose of LMWH be given prior to surgery ?

A

12 hrs before the procedure

*Restart 12 hrs after the procedure

79
Q

Neuraxial interventions should be delayed ___ hrs after a dose of LMWH.

80
Q

If a neuraxial cath is in place and a dose of heparin/LMWH is given, how long should you wait before removing the cath?

A

Heparin - 2-4 hrs WITH a normal PTT or ACT (wait 1 hr after removal b4 redosing)
LMWH - 10-12 hrs (wait 2 hrs after removal b4 redosing)

81
Q

Erthropoietin
Where is it made?
What stimulates the release?
What does it do?

A

Kidneys make 90%, liver makes 10%
Released in response to hypoxia
Stimulates bone marrow to produce and release RBCs
*At high altitudes, inspired PO2 and PaO2 are low - erthropoietin is stimulated

82
Q

What is the normal life span of a RBC?

83
Q

Where dose the breakdown of Hgb occur? What are the breakdown products?

A

Liver
Iron + porphyrin
*Porphyrin is converted to bilirubin

84
Q

What globin chains does normal Hemoglobin A have?

A

2 beta globin chains

2 alpha globin chains

85
Q

What is the most important determinant of blood viscosity?

A

Hematocrit

86
Q

What clotting factor is not a plasma protein?

A

Factor 4 calcium

87
Q

What is the function of Protein C?

A

Vit K dependent anticoagulant
Thrombin (2a) activates protein C
Protein C then promotes fibrinolysis by… Promoting release of tPA from endothelial cells
Destroying plasminogen activator inhibitor
Cleaves Factors 5a and 7a

88
Q

What abnormality would be found with several days of aspirin therapy?

A

Prolonged bleeding time

89
Q

What are 5 compensatory mechanisms to increase oxygen delivery in chronic anemia?

A
  1. Increased CO
  2. Increased 2,3 DPG levels
  3. Increased P50 (right shift)
  4. Increased dissolved O2
  5. Decreased blood viscosity - increased flow
90
Q

Aplastic anemia is due to what?

What is the most common cause?

A

Lack of functioning bone marrow

Cancer chemotherapeutic drugs

91
Q

Megaloblastic anemia aka pernicious anemia develops when their is a deficiency of what?

A

Lack of either Vit B12 OR folic acid
RBCs fail to mature
RBCs are large and immature

92
Q

What kind of RBCs result in iron deficiency anemia?

A

Hypochromic

Microcytic

93
Q

Deficiency in glucose-6-phosphate dehydrogenase (G6PDH).
What is the most common clinical manifestation of this disorder?
What % of the black population?
What 2 drugs should be avoided?

A 
Chronic hemolytic anemia 
1% of the black population 
1. Nitropursside
2. Prilocaine 
*Vulnerable to cyanide toxicity 
Also: Aspirin, PCN, Stretomycin, Sulfonamides, Quinidine, Doxorubicin, Methylene blue *May trigger a hemolytic crisis 5 days after administration
94
Q

What is the hereditary defect in thalassemia?

A

Impaired synthesis of the…
Alpha globin strands - alpha-thalassemia
Beta globin strands - beta-thalassemia

95
Q

What is the principle sign seen in thalassemia?

96
Q

What disease results from a mutation on each of the beta-globin strands of Hemoglobin A?

A

Has a valine instead of glutamate at the 6th position
Hemoglobin S results
Sickle cell anemia

97
Q

What does it mean with the patient has sickle cell trait?

A

Heterozygous (HbA 60% and HbS 40%)
Sickling rarely occurs
*10% of black Americans

98
Q

What hematocrits are seen in patients with sickle cell anemia?

A

18-30%
> 70% of total hemoglobin is HbS
*0.5% of black Americans

99
Q

What is the problem of HbS?

A

When partial pressure of O2 is low and HbS releases O2, HbS molecules attach to each other and form aggregates - sickle shape

100
Q

What 3 ways does HbS differ from HbA?

A

HbS has a…

  1. Lower affinity for O2 (P50 = 31 mmHg)
  2. Less soluble in aqueous solution
  3. Polymerizes and precipitates upon deoxygenation
101
Q

At what PO2 does sickling being?

A

PO2 < 50 mmHg

102
Q

What is the lifespan of RBCs in a patient with sickle cell anemia?

A

10-15 days

103
Q

How do you prevent sickling?

A

Keep the patient warm and hydrated
Supplement with oxygen
Maintain a high CO
Avoid stasis - vasoconstriction, tourniquets, pressure

104
Q

What is the goal of partial exchange transfusion in a patient with sickle cell disease?

A

Increase the normal Hgb to 50% and achieve a Hct of 35-40%

105
Q

What are the most abundant factors in FFP?

A

Factor 5 and 8

106
Q

Must FFP be ABO compatible?

107
Q

Which factor has the shortest 1/2 life?

A

Factor 7

4-6 hrs

108
Q

Does FFP or cryoprecipitate have more fibrinogen in it?

A

Cryoprecipitate

109
Q

Virchow’s Triad

A
  1. Endothelial injury
  2. Stasis or turbulent blood flow
  3. Hypercoagulability
110
Q

What is thrombin time (TT)?

A

Evaluates the ability of thrombin to convert fibrinogen to fibrin
Normal TT 9-11 sec

111
Q

Does plt count measure plt function?

A

NO - bleeding time measures quality and quantity of plts

*Bleeding time is NOT a reliable test of clotting - BUT it is the best test of plt function

112
Q

Spontaneous bleeding occurs when plt count falls below…

A

20,000 per mL

113
Q

What 3 herbals can cause anemia?

A
  1. Garlic
  2. Ginseng
  3. Ginkgo
    * D/c 2 weeks prior to surgery
114
Q 
Which is of greatest cause for concern? 
Increased PT 
Increased PTT
Increased bleeding time
Increased ACT
A

Increased bleeding time

The BIG Test (21 decks)

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