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PLE Pathology > Hemostasis and Related Disorders > Flashcards

Hemostasis and Related Disorders Flashcards

1
Q

End product of primary hemostasis

A

Platelet plug

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2
Q

End product of secondary hemostasis

A

Stabilize the weak platelet plug

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3
Q

Immediate response to endothelial damage

A

Transient vasoconstriction

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4
Q

Function of von Willebrand Factor

A

Binds to exposed collagen in damaged endothelium and the platelets then bind to the vWF

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5
Q

Platelets bind to vWF via what receptor

A

Gp1b

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6
Q

Source of von Willebrand factor

A 
Endothelial cell (majority)
platelet
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7
Q

Contents and location of Weibel palade body?

A

vWF and P selectin

found on endothelial cell

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8
Q

Binding of platelets to vWF causes degranulation which releases what substances and function

A 
ADP - causes expression of GpIIbIIIa necessary for aggregation
Thromboxane A2 (from platelet COX) - promotes platelet aggregation
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9
Q

Molecule which links platelets together

A

Fibrinogen

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10
Q

Thrombocytopenia usually presents with?

A

Mucosal bleeding (hemoptysis, skin, GI, hematuria) (intracranial if severe)

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11
Q

Autoimmune production of IgG against platelet antigens (like GpIIbIIIa)

A

Immune Thrombocytopenic Purpura

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12
Q

Most common cause of thrombocytopenia in children and adults

A

Immune Thrombocytopenic Purpura

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13
Q

Where are autoantibodies against platelets produced in ITP

A

Spleen

Spleen then destroyes these antibody tagged platelets

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14
Q

Lab findings in ITP

A

low platelet count
normal pt/ptt
increased megakaryocytes (compensation)

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15
Q

Initial Treatment for ITP

A

Corticosteroids, IVIG

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16
Q

How does IVIg work

A

Introduce immunoglobulin to body, spleen destroys that immunoglobulin instead of the autoimmune process

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17
Q

Pathologic formation of platelet microthrombi in small vessels

A

Microangiopathic Hemolytic Anemia

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18
Q

Pathophysiology of hemolytic anemia in Microangiopathic Hemolytic Anemia

A

If there is microthrombus, RBC passing through narrow vessel is damaged by the thrombus, yielding schistocytes.

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19
Q

What is a schistocyte

A

Damaged RBC, characteristic of hemolytic anemia

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20
Q

Two types of Microangiopathic Hemolytic Anemia and difference bet two

A

Thrombotic Thrombocytopenic Purpura - Hemolytic Uremic Syndrome

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21
Q

Enzyme decreased in TTP and function

A

ADAMSTS13 - degrades (prepares) vWF polymers to monomers for proper platelet adhesion,

if polymers remain, platelet excessively aggregates –> thrombus

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22
Q

Pathophysiology of Hemolytic Uremic Syndrome

A

Drugs or infection damage endothelium –> microthrombi –> shearing of RBC

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23
Q

Infection associated with HUS

A

E coli O 157:H7 - releases verotoxin

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24
Q

Clinical findings of TTP and HUS

A

Both - fever, hemolytic anemia, thrombocytopenia
TTP - CNS abnormality
HUS - Renal insufficiency

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25
Q

Treatment of TTP or HUS

A

Plasmapheresis, corticosteriois

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26
Q

Genetic Gp1b deficiency, leading to impaired platelet adhesion

A

Bernard Soulier Syndrome

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27
Q

Blood smear finding in Bernard Soulier syndrome?

A

Mild thrombocytopenia, enlarged platelets (immature, short lived platelets)

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28
Q

Genetic GpIIbIIIa deficiency

A

Glanzmann thrombastenia

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29
Q

End product of secondary hemostasis

A

Generation of thrombin which turns fibrinogen to fibrin, and fibrin is cross linked forming stable platelet plug

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30
Q

Clinical features of disorders of clotting factors

A

Deep tissue bleeding (muscles and joints), rebleeding after surgery

31
Q

PT vs PTT

A

PT - extrinsic and common pathway

PTT - intrinsic and common pathway

32
Q

Intrinsic, Extrinsic, and common pathwayas (factors only)

A

Intrinsic - 12 - 11 - 9 - 8 - 10
Extrinsic - 7 - 10
Common - 5 - 2 - 1

33
Q

What activates the intrinsic pathway?

A

Subendothelial collagen

34
Q

What activates the extrinsic pathway?

A

Tissue thromboplastin

35
Q

Heparin improves which clotting time?

A

PTT

36
Q

Coumadin improves which clotting time?

A

PT

37
Q

Disease with factor 8 deficiency, x linked recessive but can arise de novo from mutation

A

Hemophilia A

38
Q

Disease with factor 9 deficiency

A

Hemophilia B, Christmas Disease

39
Q

Acquired antibody against clotting factors? What is most common?

A

Clotting factor inhibitor

Anti - Factor 8

40
Q

Utility of mixing study and logic behind it

A

Mix normal plasma with patient plasma
If hemophilia - PTT improves (clotting factors of normal plams)
IF clotting factor inhibitor - PTT still deranged (antibody attacks new cloting factors)

41
Q

Most common inherited coagulation disorder

A

Von Willebrand disease (vWF deficiency)

42
Q

Ristocetin test is used for what disease

A

Von Willebrand disease

43
Q

Von Willebrand factor helps in stabilizing what clotting factor

A

Factor 8

44
Q

Treatment for von willebrand disease

A

Desmopressin (*increase vWF release from weibel palade bodies)

45
Q

Vitamin K does which step in the Vit K dependent factors

A

Gamma carboxylation

46
Q

What enzyme activates Vitamin K and in what organ

A

Epoxide reductase - liver

47
Q

Pathology of heparin induced thrombocytopenia

A

Heparin binds to platelet factor 4, which leads to IgG mediated platelet destruction, , then fragments activate other platelets leading to thrombosis

48
Q

Pathologic activation of coagulation cascade

A

Disseminated Intravascular coagulation

49
Q

Clinical features of DIC

A

Ischemia and infarction from coagultion

Mucosal bleeding from consumption of platelets and factors

50
Q

What reptile when bites can cause DIC

A

Rattlesnake

51
Q

Product from splitting of cross linked fibrin during fibrinolysis

A

D-dimer

This is why used for screening DIC, pulmo embo

52
Q

What converts plasminogen to plasmin

A

tissue Plasminogen Activator

53
Q

Functions of plasmin

A
  1. breaks fibrin
  2. breaks fibrinogen
  3. breaks clotting factors
  4. prevents platelet aggregation
54
Q

What molecule inactivates plasmin?

Where is it produced?

A

Alpha 2 anti-plasmin

Liver

55
Q

This blocks activation of plasminogen, which can be used for treating disorders of fibrinolysis

A

Aminocaproic acid

56
Q

Features of a thrombus which differentiates it from postmortem clot

A
  1. Lines of Zahn

2. Attached to vessel wall

57
Q

What are Lines of Zahn

A

Layer of alternating blood cells and fibrin found in thrombosis

58
Q

What is Virchow’s Triad

A

Hypercoagulable state
Stasis/Turbulence
Endothelial Cell Damage

59
Q

Deficiency of which vitamins can lead to homocystenuria?

A

Folate and B12

60
Q

Characterized by vessel thrombosis,mental retardation long slender fingers, and lens dislocation from elevated homocysteine levels

A

Cystathionine beta synthase deficiency

61
Q

Protein C and Protein S function?

A

Inactivate Factor 5 and 8

62
Q

Pathophysiology of Warfarin skin necrosis

A

Protein c AND s are destroyed before vitamin K is, so less anticoagulant means more thrombosis in the skin, hence name

63
Q

What is Factor V Leiden

A

Mutated form of Factor V with no cleavage site for protein C and S

64
Q

Most common inherited cause of hypercoagulable state

A

Factor V Leiden

65
Q

Inherited point mutation in prothrombin

A

Prothrombin 20210A

66
Q

Decreased protective effect of heparin like molecules on endothelium

A

Antithrombin III deficiency

antithrombin prevents excessive clotting

67
Q

Effect of estrogen on coagulation factors

A

Increased coagulation factor production –> increased thrombosis

68
Q

Feature of atherosclerotic embolus

A

Cholesterol clefts in embolus

69
Q

Bends and Chokes are associated with?

A 
Decompression sickness (Nitrogen embolism)
Muscle and joint pain; respiratory distress
70
Q

Chronic form of decompression sickness associated with multifocal ischemic necrosis of bone

A

Caisson disease

71
Q

Sustance in amniotic fluid which triggers coagulation cascade and may lead to DIC

A

Tissue Thromboplastin

72
Q

Histologic findings in amniotic fluid embolus

A

Squamous cells and keratin debris

73
Q

Gross appearance of pulmonary infarction

A

Hemorrhagic wedge shaped infarct

74
Q

Complication of reorganization of chronic pulmonary embolus

A

Pulmonary Hypertension

PLE Pathology (10 decks)

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