Hemostasis And Thrombosis Flashcards

(54 cards)

1
Q

Primary Hemostasis

A

Platelets Plug Formation

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

Secondary Hemostasis

A

Fibrin Clot formation

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

Primary Hemostasis membrane receptor

A

Glycoproteins Ib

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

Primary Hemostasis adhesive protein

A

VWf

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

Primary Hemostasis appropriate surface

A

Subendothelial matrix

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

Platelets activation secretion

A

Alpha granules and dense bodies

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

Platelets activation of GP _____receptor

A

IIb/IIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Platelet activation _____ reorganization and ______ change

A

Phospholipid

Shape change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Platelet shape change important, why?

A

From rounded discs to flat plates increases surface area

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

Formation of fibrin clot with crosslinking of ________

A

Fibrin monomers by factor XIIIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Regulation of Primary Hemostasis (platelets )

A

NO
PGI2
ADPase

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

Regulation of Secondary Hemostasis (Coag Pathway)

A

Serine protease (antithrombin)
Protein C pathway
Fibrinolytic system

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

Fibrinolytic systems

A

Removes excess clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Protein c pathway controls

A

Va and Viiia

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

Serpins

A

Anti thrombin-serine protease inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Activated protein C plus _____ serve to inactive factors _____ and _____

A

Protein

Va
VIIIa

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

Protein C or S deficiencies result in

A

Hypercoagulable states

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

Plans in

A

Removes excess fibrin clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Screening test of Hemostasis

A
Prothrombin Time
Internal normalized ratio
Partial thromboplastin time
Platelet count
Bleeding time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Prothrombin Time

A

Screens for activity of Proteins in the extrinsic pathway

Phospholipid and tissue factor are added to plasama with Ca

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

Extrinsic pathway proteins

A

Factors V VII II X and fibrinogen

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

Partial Thromboplastin Time

A

Screams for activity within the intrinsic pathway

Negatively charged activator of factor XII to serum together with Ca

Clot formation after 28-35 seconds

23
Q

PTT is used to monitor

24
Q

INR is used to monitor

25
Clinical manifestation of primary Hemostasis disorders
Muccocutaenous bleeding Petechial Excessive bleeding with trauma
26
Lab findings of primary Hemostasis disorders
Prolonged BT/PFA-100 | Thrombocytopenia
27
Clinical manifestations of secondary Hemostasis disorders
Soft tissue bleeding | Excessive bleeding with trauma
28
Lab findings of secondary Hemostasis disorders
Prolonged PT and PTT | Prolonged TT
29
Clinical manifestation of regulatory disorders associated with bleeding
Soft tissue bleeding | Excessive bleeding with trauma
30
Lab manifestations of regulatory disorders of Hemostasis
Normal PT and PTT Normal Bleeding Normal platelet count
31
Congenital Bleeding disorders (3)
Von Willebrand Disease Favor VIII deficiency Factor IX deficiency
32
Von Willebrand Disease
AD Mucocutaenous bleeding is the dominant clinical manifestation
33
Classification of vWD
Type 1: quantitative partial Type 2: Qualitative Type Quantitive total
34
Clinical manifestations of vWD
``` Epistaxis Ecchymoses Mucosal bleeding Bleeding with trauma or surgery Symptoms often improve post adolescence ```
35
Treatment of vWD
``` Desmopressin Antifibrinolytic agents Factor VIII concentrates Cryoprecipitate Recombinant factor VIII ```
36
Hemophilia A
X linked recessive disorder | Deficiency of factory VIII
37
Hemophilia lab features all normal except
Factor VIII decreased PTT prolonged
38
Hemophilia A Classification
Severe <1% viii Moderate Mild>5% VIII
39
Hemophilia B
Sex linked Recessive Factor IX deficiency
40
Hemophilia A: Therapy
Factor VIII concentrates Recombinant Factor Inhibitors of fibrinolysis
41
Hemophilia B: therapy
Factor IX concentrates Recombinant Factor IX Inhibitors of fibrinolysis
42
Mechanisms of thrombocytopenia
Decreased platelet production Increased destruction Sequestration Congenital versus acquired
43
Acute Childhood ITP
``` Viral prod Rome common Sudden onset Sever thrombocytopenia Spontaneous remission M:F 1:1 ```
44
Chronic adult ITP
``` No antecedent infection Gradual onset Moderate thrombocytopenia Infrequent spontaneous remission More common in females ```
45
ITP autoantibodies direct at
Platelet membrane antigens Increased IgG bound to the platelet surface promotes increased sequestration/destruction by the reticuloendothelial system
46
ITP clinical features
Petechial hemorrhages Gingival bleeding Ecchymoses Bleeding with trauma or surgery
47
ITP bone marrow and blood findings
Megakaryocytes normal to increased No microangipathic changes on blood smear review
48
ITP therapy
Corticosteroids Intravenous immunoglobulin Immunosuppressive Splenectomy
49
TTP Thrombocytopenic Purpura
Acute disorders characterized by intravascular platetl activation with formation of platelet rich microthrombi throughout the circulation
50
TTP due to
deficiency of ADAMTS 13 a metalloporetinase that normally degrades very high molecular weight Can be inherited or acquired
51
Disseminated Intravascular coagulation DIC
Unregulated widespread intravascular activation of the Hemostatic system
52
DIC clinical setting
Infection Tissue injury Obstetrical complications Certain malingancies
53
DIC clinical manifestation
``` Bleeding from multiple sites Thromboembolic problems Hypotension and shock Respiratory dysfunction Hepatic dysfunction Real dysfunction CNS dysfunction ```
54
DIC therapy
Remove/Re the initiating stimulus Supportive therapy with transfusion of blood products FFP- Coagulation and regulatory proteins Cryoprecipatesis- Fibrinogen VIII vWF Platelets- Platelets