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Pathology > Chapter 4 ( Hemostasis ) > Flashcards

Chapter 4 ( Hemostasis ) Flashcards

1
Q

In primary hemostasis , transient vasoconstriction of the blood vessel mediated by what ?

A

1- reflex neural stimulation

2- Endothelin released from endothelial cells

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2
Q

Von Willebrand factor function ? Source ?

A

Derived from the Webel-Palade bodies of endothelial cells and alpha-granules of platelets
Responsible for the platelet adhesion to vessel wall in primary hemostasis by binding :
1- exposed subendothelial collagen
2- GPIb receptor on the platelet

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3
Q

Mechanism of platelet degranulation in primary hemostasis ? Mediators released ?

A

Adhesion induces shape changes in the platelets and degranulation with release of these mediators :
1- ADP from platelet dense granules which promote exposure of GPIIb/IIIa receptor on the platelet
2- TXA2 which promotes platelet aggregation

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4
Q

Mechanism of platelet aggregation in primary hemostasis ?

A

By GBIIb/IIIa using fibrinogen as a linking molecule

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5
Q

Petechiae , purpura , ecchymosis sizes ?

A

Petechiae : 1-2 mm
Purpura : 3-10 mm
Ecchymosis : > 1 cm

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6
Q

Petechiae is a sign of ?

A

Thrombocytopenia and not usually seen with qualitative disorders

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7
Q

Bleeding time

A

2-7 mins

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8
Q

Mechanism of ITP ?

A

Autoimmune production of IgG ( produced by plasma cells of spleen )against platelet antigens

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9
Q

Lab findings of ITP ?

A

Decreased platelet count
Normal PT/PTT
Increased megakaryocytes on bone marrow biopsy

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10
Q

Mechanism of microangiopathic hemolytic anemia ?

A

Pathologic formation of platelet microthrombi in small blood vessels results in :
1- consumption of platelet
2- RBCs are sheared as they dross the microthrombi resulting in hemolytic anemia with Schistocytes

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11
Q

Microangiopathic hemolytic anemia is seen in which disease ?

A

TTP

HUS

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12
Q

Mechanism of TTP ?

A

Decrease of ADAMTS13 ( usually by an acquired autoantibody , which normally cleaves vWF multimers into smaller monomers for eventual degradation , large uncleaved multimers lead to abnormal platelet adhesion resulting in microthrombi

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13
Q

HUS mechanism ?

A

Endothelia damage by drugs or infection

Ex : children with E coli O157:H7 dysentery , E coli verotoxin damage endothelial cells

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14
Q

Clinical findings of TTP and HUS ?

A 
1- skin and mucosal bleeding 
2- MHA
3- Fever 
4- renal insufficiency 
5- CNS abnormalities
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15
Q

Lab findings of MHA ?

A 
Decreased platelet count 
Increased bleeding time 
Normal PT / PTT
Anemia with schistocytes 
Increased megakaryocytes on bone marrow biopsy
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16
Q

Bernard Soulier syndrome defect ? Findings ?

A

GPIb deficiency so platelet adhesion is impaired

Big platelets Sucked platelet number

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17
Q

Glanzmann thrombasthenia defect ?

A

GPIIb/IIIa deficiency resulting in impaired platelet aggregation

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18
Q

How aspirin decrease platelet aggregation ?

A

By inactivating cyclooxygenase leads to TXA2 deficiency

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19
Q

Mechanism of stabilization of the weak platelet plug in secondary hemostasis ?

A

Coagulation cascade generates Thrombin —> converts fibrinogen into fibrin —> fibrin is then cross-linked —> stable platelet fibrin thrombus

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20
Q

Activation of factors of coagulation cascade requires what ?

A

1- exposure to an activating substance :
Tissue thromboplastin activates factor Vll
Subendothelial collagen activates factor Xll
2- phospholipid surface of the platelet
3- calcium ( from platelet dense granules )

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21
Q

Lab findings in hemophilia A ?

A 
Increased PTT
Norma PT
Decreased factor Vlll
Normal platelet count 
Normal bleeding time
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22
Q

Hemophilia B ( Christmas disease ) defect ?

A

Factor lX deficiency

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23
Q

Coagulation factor inhibitor defect ? DD with hemophilia A ?

A

Acquired antibody against a coagulation factor , anti Factor Vlll is most common
PTT doesn’t correct upon mixing normal plasma with patient’s plasma ( contrary to hemophilia A )

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24
Q

Most common inherited coagulation disorder ?

A

Von Willebraand disease

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25
Q

Lab findings of Von Willebraand disease ?

A

Increased bleeding time
Increased PTT ( vWF normally stabilize factor Vlll )
Normal PT
Abnormal Ristocetin test

26
Q

Ristocetin action ?

A

Induces platelet agglutination by causin vWF to bind platelet GPlb

27
Q

Ttt of Von Willebraand disease

A

Desmopressin

Which increases vWF release from Weible Palade bodies of endothelial cells

28
Q

Enzyme that activate Vitamin K in the liver ?

A

Epoxide reductase

29
Q

Effect of liver failure on coagulation is followed by ?

A

PT

30
Q

Causes of DIC ? Their mechanisms ?

A

1- obstetric complications : Tissue thromboplastin in amniotic fluid activates coagulation
2- sepsis : Endotoxins and cytokine ( TNF , IL1 ) induce endothelial cells to make tissue factor
3- adenocarcinoma : Mucin activates coagulation
4- acute promyelocytic leukemia : primary granules activates coagulation
5- rattlesnake bite : venom activates coagulation

31
Q

Lab findings of DIC ?

A 
Decreased platelets 
Increased PT /PTT
Decreased fibrinogen 
Microangiopathic anemia 
Elevated D dimer
32
Q

The best screening for DIC ?

A

Elevated D dimer

33
Q

Source of D dimer ?

A

Splitting of cross linked fibrin , not from splitting of fibrinogen

34
Q

Mechanism of heparin induced thrombocytopenia ?

A

Heparin can form a complex with a molecule on the surface of platelets called platelet factor 4 to which the patient’s immune system form an IgG autoantibodies leading to consumption of the platelets by spleen , fragments of destroyed platelets may activate the remaining platelets to form thrombi

35
Q

Functions of plasmin ?

A

1- cleaves fibrin and serum fibrinogen
2- destroys coagulation factor
3- blocks platelets aggregation

36
Q

Enzymes that inactivates plasmin ?

A

Alpha2-antiplasmin

37
Q

Causes of abnormal increase in fibrinolysis ? Their mechanisms ?

A

1- radical prostatectomy : release Urokinase that activates plasmin
2- cirrhosis of liver : reduces the production of alpha2-antiplasmin

38
Q

Lab findings of increased fibrinolysis ?

A

Increased PT / PTT
Increased bleeding time
Normal platelet count
Normal D dimer

39
Q

Ttt of increased fibrinolysis ?

A

Aminocaproic acid : blocks activation of plasminogen

40
Q

Features that distinguish thrombus from postmortum clot ?

A

1- lines of Zahn

2- attachment to vessel wall

41
Q

Causes for disruption of normal blood flow ?

A

Immobilization
Cardiac wall dysfunction
Aneurysm

42
Q

Role of endothelia cells in preventing thrombosis ?

A 
1- block exposure of subendothelial collagen and underlying tissue factor 
2- produces Prostacyclin PGI2 and NO
3- secrete heparin-like molecules 
4- secrete tissue plasminogen activator 
5- secrete thrombomodulin
43
Q

Function of thrombomodulin ?

A

Redirects thrombin to activate protein C

44
Q

Causes of endothelia cells damage ?

A

Atherosclerosis
Thrombosis
Homocysteinemia

45
Q

Protein C and S functions ?

A

Inactivates factors V , Vlll

46
Q

Mode of inheritance of protein C and S deficiency ?

A

Autosomal dominant

47
Q

Factor V Leiden ?

A

Mutated form of factor V , that lacks the cleavage site for deactivation by protein C and S

48
Q

Most common inherited cause of hypercoagulable state ?

A

Factor V Leiden

49
Q

Prothrombin 20210A ?

A

Inherited point mutation in prothrombin that results in increased gene expression

50
Q

Anti-thrombin lll deficiency mechanism ?

A

Decrease the protective effect of heparin like molecules produced by the endothelium —> increase risk of thrombosis

51
Q

Key diagnostic feature of Anti-thrombin lll deficiency ?

A

PTT doesn’t rise with standard heparin dosing

52
Q

Ttt of anti-thrombin lll deficiency ?

A

High doses of heparin to activate the limited anti-thrombin lll , coumadin is then given to maintain an anticoagualble state

53
Q

Mechanism of oral contraceptives in causing hypercoagulable state ?

A

Estrogen induces increased production of coagulation factors

54
Q

Characteristic of atherosclerotic embolus ?

A

Presence of cholesterol clefts in the embolus

55
Q

Fat embolus clinical features ?

A

Dyspnea

Petechiae on the skin overlying the chest

56
Q

Decompression sickness clinical features ?

A 
Joint and muscle pain ( bends ) 
Respiratory symptoms ( chokes )
57
Q

Chronic form of decompression sickness ( gas embolus ) ? Characteristic ?

A

Caisson disease

Multifocal ischemic necrosis of bones

58
Q

Amniotic fluid embolus clinical features ? Characteristic ?

A

Dyspnea
Neurologic symptoms
DIC
Presence of Squamous cell and keratin debris from fetal skin in embolus

59
Q

Why pulmonary embolism is most often silent ?

A

Dual blood supply of the lung

The embolus is usually small

60
Q

Gross examination of pulmonary embolism ?

A

Hemorrhagic wedge shaped infarct

61
Q

Cause of death in pulmonary embolism ?

A

Electromechanical dissociation

Pathology (18 decks)

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