Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clotting is my Passion > Exam 1 I am tired and sad and running out of hope > Flashcards

Exam 1 I am tired and sad and running out of hope Flashcards

1
Q

Define Hemostasis

A

Stopping blood flow with a fine balance between bleeding and clotting

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

What parameters are involved in hemostasis?

A

Vacular, platelets, fibrin clot formation - coagulation cascade, control (inhibitory systems), fibrinolysis

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

Procoagulant - what are things that participate in coagulation?

A

Platelets, vWF, coagulation factors, collagen

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

What does a deficiency in procoagulants result in?

A

BLEEDING
(except XII, Ia, PK, HMWK dysfunction)

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

Anticoagulant - what are things that participate in the regulation or inhibition of coagulation?

A

Antithrombin, Protein C, Protein S, HC II, Protein Z/ZPI, TFPI

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

What is the function of antithrombin?

A

Inactivates IIa, Xa, (IXa, XIa, XIIa, plasmin)

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

What is the function of Protein C?

A

Inactivates thrombin and thrombomodulin

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

What activates Protein C?

A

Thrombin and thrombomodulin

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

What is the function of Protein S?

A

In its free form, it is a Protein C cofactor

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

What is the function of HCII?

A

It neutralizes IIa (thrombin)

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

What is the function of TFPI?

A

Inhibits TF3/VIIa complex

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

What does a deficiency in anticoagulants result in?

A

THROMBOSIS

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

Profibrinolytic - what are things that participate in fibrinolysis?

A

Plasminogen (to plasmin), tPA, Factor XIIa, Kallikren, Urokinase

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

What is the function of Plasminogen (to plasmin)?

A

Lyses fibrin and fibrinogen and inactivates Va, VIIIa, and XIIa

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

What is the function of tPA?

A

Catalyzes the conversion of plasminogen to plasmin

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

What is the function of kallikren?

A

Formation and release of bradykinin

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

What is the function of urokinase?

A

Enzyme that converts plasminogen to plasmin

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

What does a deficiency in profibrinolytics result in?

A

THROMBOSIS

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

Antifibrinolytic - what are things that participate in the regulation or inhibition of fibrinolysis?

A

PAI-1 & 2, Alpha-2 Antiplasmin, Alpha-2 Macroglobulin, TAFI, Factor XIa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the function of PAI-1 & 2?

A

Neutralize tPA

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

What is the function of Alpha-2 Antiplasmin?

A

Binds plasmin

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

What is the function of Alpha-2 Macroglobulin?

A

Binds plasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the function of TAFI?

A

Alters the fibrin clot so that it is less recognizable by plasmin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the function of XIa?

A

Enhances TAFI production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What does a deficiency in antifibrinolytics result in?

A

BLEEDING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the difference between FDP and D-Dimer?

A

D-Dimer is a specific FDP only present upon the degradation of a cross linked fibrin.

Factor 13 has stabilized the clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

FDP stands for what? What are FDPs?

A

Fibrinogen Degradation Products

Fragments X, Y, D, and E are FDPs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are primary fibrinolysis intermediates?

A

X and Y

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are primary fibrinolysis end products?

A

D and E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

T/F: FDPs can act as coagulation inhibitors by attaching to fibrin monomer and preventing polymerization and clot formation

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Function of anticoagulants?

A

Inhibit the coagulation cascade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What anticoagulants are we concerned with?

A

Coumadin/Warfarin

Heparin

Direct Thrombin Inhibitors

Direct Xa inhibitors

33
Q

Mechanism of Coumadin/Warfarin

A

Keeps Vitamin K in storage form

Stops Vitamin K dependent factors (II, VII, IX, and X)

34
Q

Mechanism of Heparin

A

Increase inhibitory effect of AT which creates an irreversible complex with IIa, IXa, Xa, XIa, XIIa, and plasmin

35
Q

Mechanism of Direct Thrombin Inhibitors

A

Neutralizes thrombin by binding to the active site and extending fibrin bound thrombin

36
Q

Mechanism of Direct Xa inhibitors

A

Inhibits Factor Xa (no AT requires)

37
Q

Function of Anti-Platelets

A

Prevents platelet aggregation

38
Q

What drug that we are concerned with is an anti-platelet?

A

Aspirin

39
Q

Mechanism of Aspirin

A

Inhibits cyclooxygenase to reduce TXA2 production (which stimulates activation of new platelets and increases aggregation)

40
Q

Mechanism of thrombolytics (Fibrin specific or fibrin non-specific)

A

Dissolves the clot

41
Q

What is the type of disorder, defect, and laboratory results we would see in Von Willebrands (Type 1)

A

Disorder: Adhesion

Defect: vWF deficiency (all multimers)

Tests:
PFA = INC
PT = normal
APTT = INC (d/t DEC VIII_
PLT Aggregation = abnormal Ristocetin (will correct with addition of NP)

42
Q

What is the type of disorder, defect, and laboratory results we would see in Bernard-Soulier

A

Disorder: Adhesion

Defect: Lack of Gp1b

Tests:
PFA = INC
PLT = DEC
Large PLT
PLT Aggregation = abnormal Ristocetin

43
Q

What is the type of disorder, defect, and laboratory results we would see in Glanzmann’s

A

Disorder: Aggregation

Defect: Lack GPIIb and GPIIIa

Tests:
PFA = INC
PT = normal
APTT = normal
PLT count = normal
PLT aggregation = normal ONLY w/Ristocetin

44
Q

What is the type of disorder, defect, and laboratory results we would see in Delta Storage Pool

A

Disorder: Release

Defect: Lack of dense granules

Tests:
Hypo or granular plts

45
Q

What is the type of disorder, defect, and laboratory results we would see in Gray Platelet

A

Disorder: Release

Defect: Marked DEC in platelet alpha granules

Tests:
Hypo or granular plts

46
Q

What is the type of disorder, defect, and laboratory results we would see in ITP

A

Disorder: Thrombocytopenia

Defect: Spontaneous – adults/AIDS; kids/immunization

Tests:
PFA = INC
PLT count = LOW <20,000
Large plt (variable)
BM = megakaryocyte hyperplasia
Deficient clot retraction

47
Q

What is the type of disorder, defect, and laboratory results we would see in TTP

A

Disorder: Thrombocytopenia

Defect: Autoantibody against ADAMTS13, vWF cannot break apart

Tests:
- Hemolytic anemia with schistocytes
- Thrombocytopenia/hemorrhage
- Fluctuating neurological dysfunction
- Fever
- Progressive renal disease

48
Q

What is the type of disorder, defect, and laboratory results we would see in HUS

A

Disorder: Thrombocytopenia

Defect: Resembles TTP with NO neurologic symptoms. Plts are sequestered in kidney

Tests:
- MAHA
- thrombocytopenia
- acute renal failure (RBCs, protein, and casts in urine)

49
Q

What is the type of disorder, defect, and laboratory results we would see in HELLP

A

Disorder: Thrombocytopenia

Defect: Release of TXA2. Microvascular endothelial damage. Vascular lesions. Intravascular plt activation

Tests:
- Hemolysis: hgb/hct, LDH, bili, Hapt, schisto
- PLT count = LOW <200,000
- Hepatic dysfunction (AST >42, ALT >24, LDH >164)

50
Q

What is the type of disorder, defect, and laboratory results we would see in drug induced thrombocytopenia

A

Disorder: thrombocytopenia

Defect: Antibody complex attaches to platelet

Tests:
- Plt count LOW
- Test for the presence of heparin-induced ab in the patient plasma (use a plt aggregometer; if ab is present, plts will aggregate)

51
Q

What is the site of formation of the coagulation factors?

A

Liver

52
Q

List the Vitamin K dependent factors

A

II, VII, IX, and X

53
Q

Factor I

A

Fibrinogen

Clot formation

54
Q

Factor II

A

Prothrombin

Activation of factors I, V, VII, VIII, XI, XIII, Protein C, and platelets

55
Q

Factor III

A

Tissue factor III

Cofactor of VIIa

56
Q

Factor IV

A

Calcium

Role in binding of phospholipid coagulation factors

57
Q

Factor V

A

Labile Factor

Cofactor of X – prothrombinase complex

58
Q

Factor VII

A

Proconvertin

Enables factors IX and X

59
Q

Factor VIII

A

von Willebrand Factor Complex

Cofactor of IX complex

60
Q

Factor IX

A

Christmas Factor

Forms the complex with VIII; Enables factor X

61
Q

Factor X

A

Stuart-Prower Factor

Forms the prothrombinase complex together with Factor V, which will activate Factor II

62
Q

Factor XI

A

Activates factor IX

63
Q

Factor XII

A

Hageman Factor

Enables factors XI, VII, and Prekallikrein

64
Q

Factor XIII

A

Fibrin Stabilizing Factor

Creates cross-links between fibrin monomers

65
Q

How does Waldenstrom’s macroglobulinemia and multiple myeloma can cause bleeding tendencies?

A

Igs coating platelets and collagen fibers

66
Q

How does the following vascular disorder effect coagulation: hereditary hemorrhagic telangiectasia

A
  • Vessel walls are reduced to single layer of EC and inadequate support structures resulting in fragile vessels
  • Telangiectasias: Dilated superficial vessels that will blanche (lose color with pressure, unlike petechiae
  • Bleeding
67
Q

How does the following vascular disorder effect coagulation: Ehlers-Danlos Syndrome

A
  • Indian rubber man (hypermobile joints and stretchy skin)
  • Collagen disorder: Issues with adhesion
68
Q

How does the following vascular disorder effect coagulation: Allergic and drug-induced purpura

A
  • Autoimmune vacular injury
  • Drug causes development of antibody to vessel walls
69
Q

How does the following vascular disorder effect coagulation: Henoch-schonlein purpura

A
  • Usually a child following upper respiratory infection
  • IgA deposits in vessels: Rash, abdominal pain, joint pain, proteinuria/hematuria. Small % advance to renal disease
70
Q

How does the following vascular disorder effect coagulation: Scurvy

A
  • Vitamin C deficiency
  • Decreased synthesis of collagen results in weakened capillary walls
71
Q

How does the following vascular disorder effect coagulation: Senile Purpura

A
  • Elderly
  • Usually forearms and back of hands
  • Loss of collagen and subcutaneous fat/elastic fibers to support for small blood vessels
72
Q

Common agonist or aggregating agent of von willebrands

A

Ristocetin - corrects with NP

73
Q

Common agonist or aggregating agent of bernard soulier

A

Ristocetin

74
Q

Common agonist or aggregating agent of Glanzmann’s Thrombasthenia

A

All abnormal except ristocetin

75
Q

Common agonist or aggregating agent of Delta storage pool disease

A

ADP

76
Q

Common agonist or aggregating agent of Gray platelet

A

ADP

77
Q

Common agonist or aggregating agent of Aspirin or NSAID therapy

A

Arachidonic acid curve = more sensitive

78
Q

von Willebrand factor activity– Ristocetin co-factor (vWF: RCo) – Ristocetin Induced Platelet Agglutination

A

Uses patient PRP - patient’s own platelets and plasma

Normal with all agents except Ristocetin

Add NP and it will correct for VWD

79
Q

von Willebrand factor activity– Ristocetin co-factor (vWF: RCo) – Ristocetin Cofactor (vWF:Rco)

A

Uses patient’s plasma and donor or lyophilized platelets

Measures the ability of patient’s plasma cWF to agglutinate donor platelets in the presence of Ristocetin

Clotting is my Passion (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions