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Heme Week 3 > Coagulation disorders - Primary hemostasis > Flashcards

Coagulation disorders - Primary hemostasis Flashcards

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1
Q

This is the initial response to vascular injury

A

Vasoconstriction

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2
Q

Vasoconstriction has this effect on the rate of blood loss

A

Slows

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3
Q

What is primary hemostasis?

A

Endothelium is activated to secrete vWF
Platelets adhere, activate, aggregate

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4
Q

What is secondary hemostasis?

A

Fibrin clot forms to enmesh platelet aggregate

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5
Q

What is tertiary hemostasis?

A

Clot limitation and dissolution

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6
Q

Is this primary, secondary, or tertiary hemostasis:
Endothelium is activated to secrete vWF
Platelets adhere, activate, aggregate

A

Primary

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7
Q

Is this primary, secondary, or tertiary hemostasis:
Fibrin clot forms to enmesh platelet aggregate

A

Secondary

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8
Q

Is this primary, secondary, or tertiary hemostasis:
Clot limitation and dissolution

A

Tertiary

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9
Q

Patients with this type of hematology issue may present with:
Palpable purpura
Ecchymoses

A

Intrinsic vascular disorders

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10
Q

Patients with this type of hematology issue may present with:
Mucosal bleeding (epistaxis, GI, menstrual)

A

Platelet defects or deficiency

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11
Q

Patients with this type of hematology issue may present with:
Small cutaneous bleeds (petechiae, purpura)

A

Platelet defects or deficiency

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12
Q

Patients with this type of hematology issue may present with:
Soft tissue bleeds (intramuscular, etc)

A

Coagulation defects

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13
Q

Patients with this type of hematology issue may present with:
Joint bleeds (hemarthrosis)

A

Coagulation defects

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14
Q

Patients with this type of hematology issue may present with:
Venous thrombosis

A

Hypercoagulability - tends to be due to platelet/coagulation factors

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15
Q

Patients with this type of hematology issue may present with:
Arterial thrombosis

A

Hypercoagulability - tends to be due to endothelial disorders

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16
Q

This molecule in platelet granules stabilizes clots

A

Factor XIII

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17
Q

This molecule in platelet granules activates platelets

A

ADP

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18
Q

This molecule in platelet granules activates platelets and induces vasoconstriction

A

thromboxane A2

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19
Q

This molecule in platelet granules is a substrate for many coag factor reactions

A

Membrane phospholipids

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20
Q

This molecule in platelet granules binds collagen

A

Glycoproteins

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21
Q

Platelets adhere to exposed collagen, and this is mediated by this binding to von Willebrand Factor

A

Glycoprotein-1b

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22
Q

Platelets adhere to exposed collagen, and this is mediated by glycoprotein-1Bb binding to this

A

von Willebrand Factor

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23
Q

This is a receptor on platelets that binds vWF, mediating platelet adherence

A

GP-1b

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24
Q

GP-1b on platelets binds to vWF, which binds to this

A

Exposed collagen

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25
This is produced by endothelium and platelets, and forms a bridge between platelets and collagen
vWF
26
Platelets adhere to ECM via this complex
vWF-GP1b
27
ADP is involved in this part of primary hemostasis
Platelet activation
28
This compound activates platelets, which undergo shape change and surface molecule conformational change
ADP
29
ADP activates platelet shape change, and the platelet "sticky ends" have a high density of this
Glycoprotein 2b/3a
30
GP-2b/3a on platelets binds this, to form connecting bridge between platelets
Fibrinogen
31
This molecule binds fibrinogen to form connecting bridge between platelets
GP-2b/3a
32
This agonist enhances GP1b-vWF binding
Ristocetin
33
Ristocetin is a platelet aggregation agonist that enhances binding of this
GP1b-vWF
34
ADP, epinephrine and collagen enhance platelet aggregation via this receptor
GP-2b/3a
35
This test of platelet function involves a standardized small incision, and time to stop bleeding is measured
Bleeding time
36
How do platelet aggregation studies work?
Agonists (ADP, arachidonic acid, ristocetin) given Specimen turbidity is measured
37
Factor VIII is stabilized when bound to this
vWF
38
Factor VIII activity is usually normal in disorders with this type bleeding
Platelet-type
39
von Willebrand disease produces this type bleeding
Platelet-type
40
Bernard-Soulier disease produces this type bleeding
Platelet-type
41
Glanzmann Thrombasthenia produces this type bleeding
Platelet-type
42
Immune thrombocytopenic purpura produces this type bleeding
Platelet-type
43
Nose bleed is this type of bleeding
Platelet-type
44
Excessive mucosal bleeding after the dentist is this type of bleeding
Platelet-type
45
Heavy menstrual bleeding (menorrhagia) is this type bleeding
Platelet-type
46
This is the most common type of von Willebrand disease
Type 1
47
Type 1 von Willebrand disease has this inheritance pattern
Autosomal dominant
48
This type of von Willebrand disease has decreased vWF with normal function
Type 1
49
This type of von Willebrand disease has normal vWF activity (Ag:Activity ratio = 1)
Type 1
50
This type of von Willebrand disease involves decreased multimers, and may have abnormal multimeric assays
Type 2
51
This is a rare subtype of von Willebrand disease, that is many different disorders with qualitative vWF defects
Type 2
52
These types of von Willebrand disease may have prolonged ristocetin aggregation
Types 2 and 3
53
This type of von Willebrand disease is a complete absence of vWF antigen
Type 3
54
Type 3 von Willebrand disease has this inheritance pattern
Autosomal recessive
55
This type of von Willebrand disease will have PTT prolonged due to destabilized Factor VIII
Type 3
56
Type 3 von Willebrand disease results in prolonged PTT due to this
Destabilized Factor VIII
57
In Type 3 von Willebrand disease, this lab test is abnormal due to destabilized Factor VIII
Prolonged PTT
58
Patients with this condition may have mucosal bleeding, purpura, heavy menses, and post-surgical or post-trauma bleeding
von Willebrand disease
59
This may be used as treatment for von Willebrand disease, for pre-procedural use or during bleeding event
ddAVP produces release of endothelial vWF multimers
60
ddAVP can treat these conditions
von Willebrand disease Bernard-Soulier syndrome Disorders of primary hemostasis
61
ddAVP can treat von Willebrand disease, because it produces release of this
Endothelial vWF multimers
62
This is an autosomal recessive platelet disorder due to GP1b complex defect
Bernard-Soulier syndrome
63
Bernard-Soulier syndrome has this inheritance pattern
Autosomal recessive
64
Bernard-Soulier syndrome is due to a defect in this
GP1b
65
Morphology of this disorder of primary hemostasis will show large platelets
Bernard-Soulier syndrome
66
What is the morphology seen in Bernard-Soulier syndrome?
Large platelets
67
What are the levels of platelets in Bernard-Soulier syndrome?
Thrombocytopenia range: 20k to almost normal
68
Diagnosis of this can be confirmed with flow cytometry for GP1b deficiency
Bernard-Soulier syndrome
69
This is the treatment for Bernard-Soulier syndrome
ddAVP or antifibrinolytics for mild bleeding Platelet transfusion for severe
70
This is an autosomal recessive platelet disorder due to defective GP2b/3a
Glanzmann thrombasthenia
71
Glanzmann thrombasthenia has this inheritance pattern
Autosomal recessive
72
Glanzmann thrombasthenia is due to a defect in this
GP2b/3a
73
Glanzmann thrombasthenia is a defect in GP2b/3a, resulting in decreased platelet binding of this
Fibrinogen
74
What are the levels of platelets in Glanzmann thrombasthenia?
Normal
75
This disorder of primary hemostasis has very high bleeding time
Glanzmann thrombasthenia
76
What is the morphology seen in Glanzmann thrombasthenia?
Normal
77
This disorder of primary hemostasis has decreased levels of ADP, epinephrine, collagen, and arachidonic acid
Glanzmann thrombasthenia Levels are normal in Bernard-Soulier syndrome and vWD
78
Platelet aggregation in this condition is decreased with Ristocetin agonist but partially preserved
Glanzmann thrombasthenia
79
This condition is an acquired autoimmune destruction of platelets
Immune thrombocytopenic purpura (ITP)
80
This is the most common acquired thrombocytopenia in adults or children
Immune thrombocytopenic purpura (ITP)
81
Patients with Immune thrombocytopenic purpura (ITP) often have antibodies against this
GP2b/3a
82
What results in thrombocytopenia in Immune thrombocytopenic purpura (ITP)?
Splenic consumption
83
Immune thrombocytopenic purpura (ITP) at this age is usually an acute disease that follows viral infection or immunization
Childhood
84
Immune thrombocytopenic purpura (ITP) at this age is usually a chronic disease
Adult
85
Immune thrombocytopenic purpura (ITP) is an acquired autoimmune destruction of these
Platelets
86
Patients with this condition will have very low platelet count with normal RBC and WBC morphology Present with petechiae, purpura, menorrhagia, GI/mucosal bleeding
Immune thrombocytopenic purpura (ITP)
87
a patient with very low platelet count but normal RBC/WBC morphology likely has this condition
Immune thrombocytopenic purpura (ITP)
88
What is the treatment for adult Immune thrombocytopenic purpura (ITP)?
Steroids, IVIG, Rituximab Splenectomy
89
This condition is antibody induced platelet activation and aggregation
Heparin induced thrombocytopenia
90
Heparin forms complexes with these, of platelet alpha granules
PF4 (platelet factor 4)
91
In Heparin induced thrombocytopenia, antibodies form against this complex
Heparin-PF4 (platelet factor 4)
92
During Heparin induced thrombocytopenia, PF4 binds these on platelet surface
GAGs
93
In Heparin induced thrombocytopenia, heparin displaces GAGs on platelet surface to form this
PF4-heparin complex
94
In Heparin induced thrombocytopenia, antibodies form against PF4-heparin complex, and this activates adjacent platelets
Fc portion
95
What effects does heparin have on platelet levels?
Decreases (>50% decline) Heparin induced thrombocytopenia
96
Thrombocytopenia and thrombosis after exposure to a certain drug in a recent clinical setting, are likely due to this
Heparin induced thrombocytopenia

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