The BIG Test > Hemostasis > Flashcards

Hemostasis Flashcards

(114 cards)

Study These 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

33%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

vWF is synthesized and released by ________.

A

Endothelial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the most common inherited coagulation defect?

A

von Willebrand’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cryoprecipitate contains which factors?

A

Factors 1, 8, 13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The fibrinogen receptor is known as…

A

GPIIb/IIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Fibrinogen (Factor I) _______ plts.

A

Aggregates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

Cyclooxygenase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does clopidogrel (Plavix) work?

A

Anti-ADP agent

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does Eptifibatide and Abciximab work?

A

Anti-fibrinogen receptor (GPIIb/IIIa) drugs

Result - no linking of plts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

All clotting factors are from the liver EXCEPT ____________.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which clotting factors are Vit K dependent?

A

2, 7, 9, 10

Protein C, S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Intrinsic Pathway
``` Exposure of blood to collagen 12 is activated 11 is activated 9 is activated 9a + 8:Ca + 4 = 10 is activated ```
26
Final Common Pathway
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
27
What is the primary physiologic initiator of coagulation?
Thromboplastin | Factor 3
28
What helps position clotting factors on the surface of the plt so biochemical rxns can occur?
Calcium
29
Coumadin acts on the _________ and final common pathways. | Coumadin is assessed by _____ and _____.
Extrinsic | PT and INR
30
Heparin acts on the _________ and final common pathways. | Heparin is assessed by _______ and ______.
Intrinsic | PTT and ACT
31
``` Hemophilia A What is it? Cause? Affects males or females? Is it common? Treatment? ```
``` 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 ```
32
Hemophilia B What is it? Treatment?
Christmas disease Factor 9 deficiency Tx - 9 concentrate
33
What is the most important clue to a clinically significant bleeding disorder in an otherwise healthy patient?
History
34
What is the most common reason for coagulopathy in patients receiving massive blood transfusions?
Lack of functioning plts
35
Plts in stored blood are nonfunctional after how many days?
1-2 days
36
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?
1. Factor 5 | 2. Factor 8
37
What is the only acceptable clinical indication for transfusion of PRBCs?
To increase the oxygen carrying capacity of blood
38
What factors are present in FFP?
ALL factors EXCEPT plts
39
One unit of PRBCs will increase Hct by ____% or 1 g/dL.
3-4% | *1 mL/kg PRBCs will increase Hct 1%
40
One unit of plts will increase plt count by ________ mm3.
5,000-10,000/mm3
41
How does heparin work?
Heparin binds to ATIII | Increases the effectiveness of ATIII 1,000-10,000x
42
What is the purpose of antithrombin III?
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
43
Where is ATIII made? ATIII strongly inhibits which 2 factors? ATIII partially inhibits which 3 factors? ATIII is a required cofactor for what?
Liver Factors 2a, 10a (final common pathway) Factors 9a, 11a, 12a (intrinsic pathway) Heparin
44
Acquired ATIII deficiency states are found in patients with...
Cirrhosis of the liver | Nephrotic syndrome
45
What is the most common reason a patient is unresponsive to heparin? What would you do to fix it?
``` An ATIII deficiency Give FFP (includes all coag and anticoag factors made by the liver) ```
46
How does warfarin work?
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
How does protamine work?
Combines electrostatically/ionically with heparin Protamine is positively charged (basic), heparin is negatively charged (acidic) *Neutralization rxn
48
What is an option if the patient has developed heparin-induced thrombocytopenia and you still need anticoagulation?
Direct thrombin inhibitors | Hirudin, Ximelgatran, Argatroban
49
``` Coagulation Tests - Normal Values Bleeding Time Plt Count PT PTT ACT Fibrinogen ```
``` 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
Describe the clot-busting role of plasmin.
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
Where is plasminogen synthesized?
Liver
52
Facts about tPA
Incorporated into the forming clot Produced by endothelial cells Release is stimulated by thrombin and venous stasis
53
What is the most widely used thrombolytic agent for intra-arterial infusion into the peripheral arterial system and grafts?
Urokinase
54
How does aprotinin work?
Anti-fibrinolytic agent Inhibits plasmin Fibrin breakdown is slowed Decrease intra-op blood loss
55
How does epsilon aminocarproic acid (Amicar) and tranexamic acid work?
Displace plasmin from fibrin | Prevent the breakdown of fibrin
56
What is the result of inhibiting plasmin?
Fibrin that is formed breaks down slowly | So bleeding is decreased
57
What are the risks of aprotinin?
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
Name 4 commonly encountered problems associated with abnormal hemostasis.
1. DIC 2. Liver disease 3. Renal disease - uremia 4. Multiple transfusions
59
Disseminated Intravascular Coagulation (DIC) Describe. Diagnosis?
Manifestation of an underlying disease process No lab test for DIC Lab tests reflect consumption of clotting factors + enhanced fibrinolysis
60
What OB emergencies are associated with DIC?
Abruptio placentae | Amniotic fluid embolism
61
What are the most common precipitating factors for acute DIC in surgical patients?
Shock Ischemia Infection
62
Lab Abnormalities in DIC
Decreased: plts, Factors 1, 2, 5, 8, 13 Increased: fibrin degradation (split) products
63
What is the most common cause of an isolated high PT?
Liver disease
64
How does liver disease affect coagulation? | What is the Tx?
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
How does uremia affect coagulation? | What is the Tx?
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
Are plt transfusions helpful in uremia?
NO, they are ineffective | The transfused plts rapidly become abnormal
67
What are the issues associated with massive blood transfusions?
Deficiencies of plts, Factors 5 and 8
68
Diffuse bleeding during massive transfusion is generally caused by...
Thrombocytopenia
69
What is the best test of primary hemostasis or plt function?
Bleeding time
70
What antiplatelet agent prevents ADP-induced plt aggregation?
Ticlopidine | *D/c 14 days prior to surgery
71
Post-op bleeding with continued oozing from wounds and catheter sites suggests what disorder?
DIC
72
What is DDAVP?
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
What is the onset time of heparin?
< 1 min
74
What 3 problems can administration of protamine cause?
1. Systemic hypotension 2. Pulmonary HTN 3. Allergic rxns * Adverse events are d/t histamine release
75
What is the max recommended dose of Protamine?
50 mg within 10 min | *Rapid injection may cause histamine relase - facial flushing, bronchoconstriction, tachycardia, hypotension
76
What is the protamine dose?
1 mg of protamine for every 100 units of heparin predicted to still be circulating
77
What are the 3 antidotes of warfarin?
1. Vit K 2. Fresh whole blood 3. FFP
78
When should the last dose of LMWH be given prior to surgery ?
12 hrs before the procedure | *Restart 12 hrs after the procedure
79
Neuraxial interventions should be delayed ___ hrs after a dose of LMWH.
10-12
80
If a neuraxial cath is in place and a dose of heparin/LMWH is given, how long should you wait before removing the cath?
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
Erthropoietin Where is it made? What stimulates the release? What does it do?
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
What is the normal life span of a RBC?
120 days
83
Where dose the breakdown of Hgb occur? What are the breakdown products?
Liver Iron + porphyrin *Porphyrin is converted to bilirubin
84
What globin chains does normal Hemoglobin A have?
2 beta globin chains | 2 alpha globin chains
85
What is the most important determinant of blood viscosity?
Hematocrit
86
What clotting factor is not a plasma protein?
Factor 4 calcium
87
What is the function of Protein C?
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
What abnormality would be found with several days of aspirin therapy?
Prolonged bleeding time
89
What are 5 compensatory mechanisms to increase oxygen delivery in chronic anemia?
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
Aplastic anemia is due to what? | What is the most common cause?
Lack of functioning bone marrow | Cancer chemotherapeutic drugs
91
Megaloblastic anemia aka pernicious anemia develops when their is a deficiency of what?
Lack of either Vit B12 OR folic acid RBCs fail to mature RBCs are large and immature
92
What kind of RBCs result in iron deficiency anemia?
Hypochromic | Microcytic
93
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?
``` 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
What is the hereditary defect in thalassemia?
Impaired synthesis of the... Alpha globin strands - alpha-thalassemia Beta globin strands - beta-thalassemia
95
What is the principle sign seen in thalassemia?
Anemia
96
What disease results from a mutation on each of the beta-globin strands of Hemoglobin A?
Has a valine instead of glutamate at the 6th position Hemoglobin S results Sickle cell anemia
97
What does it mean with the patient has sickle cell trait?
Heterozygous (HbA 60% and HbS 40%) Sickling rarely occurs *10% of black Americans
98
What hematocrits are seen in patients with sickle cell anemia?
18-30% > 70% of total hemoglobin is HbS *0.5% of black Americans
99
What is the problem of HbS?
When partial pressure of O2 is low and HbS releases O2, HbS molecules attach to each other and form aggregates - sickle shape
100
What 3 ways does HbS differ from HbA?
HbS has a... 1. Lower affinity for O2 (P50 = 31 mmHg) 2. Less soluble in aqueous solution 3. Polymerizes and precipitates upon deoxygenation
101
At what PO2 does sickling being?
PO2 < 50 mmHg
102
What is the lifespan of RBCs in a patient with sickle cell anemia?
10-15 days
103
How do you prevent sickling?
Keep the patient warm and hydrated Supplement with oxygen Maintain a high CO Avoid stasis - vasoconstriction, tourniquets, pressure
104
What is the goal of partial exchange transfusion in a patient with sickle cell disease?
Increase the normal Hgb to 50% and achieve a Hct of 35-40%
105
What are the most abundant factors in FFP?
Factor 5 and 8
106
Must FFP be ABO compatible?
Yes
107
Which factor has the shortest 1/2 life?
Factor 7 | 4-6 hrs
108
Does FFP or cryoprecipitate have more fibrinogen in it?
Cryoprecipitate
109
Virchow's Triad
1. Endothelial injury 2. Stasis or turbulent blood flow 3. Hypercoagulability
110
What is thrombin time (TT)?
Evaluates the ability of thrombin to convert fibrinogen to fibrin Normal TT 9-11 sec
111
Does plt count measure plt function?
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
Spontaneous bleeding occurs when plt count falls below...
20,000 per mL
113
What 3 herbals can cause anemia?
1. Garlic 2. Ginseng 3. Ginkgo * D/c 2 weeks prior to surgery
114
``` Which is of greatest cause for concern? Increased PT Increased PTT Increased bleeding time Increased ACT ```
Increased bleeding time
The BIG Test
flashcards
Decks in class (21)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions