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Perio and Path > Overview of Hemostasis and Thrombosis > Flashcards

Overview of Hemostasis and Thrombosis Flashcards

1
Q

Vascular injury leads to what to events that will both lead to the formation of a hemostatic plug?

A

Platelet activation and Coagulation activation

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2
Q

What are the 3 steps of platelet function?

A

adhesion -> Activation -> Aggregation

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3
Q

What are the 3 steps in coagulation?

A

Activation -> Thrombin Formation -> Fibrin formation, polymerization and Stabilization

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4
Q

What is Primary Hemostasis?

A

Platelet plug formation

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5
Q

What is secondary Hemostasis?

A

Fibrin Clot formation (coagulation cascade) Thrombin -> fibrin, with cross linking of fibrin by factor XIIIa

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6
Q

What is the Membrane receptor for Primary hemostasis?

A

Glycoprotein Ib

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7
Q

What is the adhesive protein for Primary hemostasis?

A

Von willebrand factor

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8
Q

What is the appropriate surface for primary hemostasis?

A

Subendothelial matrix

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9
Q

What are the regulators of Secondary Hemostasis?

A
  • serine protease inhibitors (antithrombin)
  • Protein C pathway (controls Va and VIIIa)
  • Fibrinolytic system (removes excess clot)
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10
Q

What are regulators of Primary Hemostasis?

A
  • NO
  • Prostacyclin (PGI2)
  • ADPase
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11
Q

How do Antithrombins ?

A

they basically bind to serine proteases and thrombin and inhibit their action. (SERPIN and HEPARIN both do this)

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12
Q

How does the Protein C system work as a regulator of Secondary hemostasis?

A

Activated Protein C plus protein S serve to inactivate factors Va and VIIIa.

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13
Q

What happen is there is a deficiency in Protein S or C?

A

Results in hypercoaguable states

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14
Q

______ is resistance to inactivation by Protein S and C.

A

Factor V leiden mutation

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15
Q

How does plasmin regulate secondary hemostasis?

A

Removes excess fibrin clot

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16
Q

What are the screening tests of Hemostasis?

A
  • Prothrombin time
  • International Normalized Ratio
  • Partial Thromboplastin time
  • Platelet count
  • Bleeding time
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17
Q

How does the Prothrombin time test work?

A
  • it screens for activtity of proteins in the EXTRINSIC pathway (Factors V, VII, II, X and fibrinogen)
  • Phospholipid and TF are added to patients plasma with Ca++
  • Time to form clot is noted (11-13 secs)
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18
Q

How does the Partial Thromboplastin time test work?

A

Screens for activity within the INTRINSIC pathway (Factors XII, XI, IX, VIII, X, V, II and fibrinogen)

  • Addition of negatively charged activator of factor XII to patient serum with Ca++
  • Clot is formed after 28-35 seconds
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19
Q

What are the Classifications of bleeding disorders?

A
  • Congenital vs. Acquired
  • Mild vs. Severe
  • Primary vs Secondary
  • Regulatory disorder
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20
Q

What are the clinical and lab findings of bleeding disorders of Primary Hemostasis?

A

Clinical:

  • Mucocutaneous bleeding
  • Excessive bleeding with trauma

Lab:

  • Prolonged BT/PFA-100
  • Thrombocytopenia
21
Q

What are the clinical and lab findings of bleeding disorders of Secondary hemostasis?

A

Clinical:

  • Soft tissue bleeding
  • Excessive bleeding with trauma

Lab:

  • Prolonged PT and PTT
  • Prolonged TT (Thrombin time)
22
Q

What are the clinical and lab findings of Regulatory bleeding disorders of hemostasis?

A

Clinical:

  • Soft tissue bleeding
  • Excessive bleeding with trauma

Lab:

  • Normal PT and PTT
  • Normal Bleeding time
  • Normal platelet count
23
Q

What are the 3 congenital Bleeding Disorders?

A
  • Von Willebrand disease
  • Factor VIII Deficiency
  • Factor IX deficiency
24
Q

Tell me about Von willebrand Disease…

A

Autosomal dominant disorder due to abnormalitles of vW factor.

  • Abnormalities may be quantitative or qualitative
  • Mucocutaneous bleeding (nose bleeds) is the dominant clinical manifestation
25
Q

What are the 3 classes of vWD?

A

Type 1 = Quantitative (Partial)
Type 2 = Qualitative
Type 3 = Quantitative (total)

26
Q

What are the clinical manifestations of vWD?

A
  • epistaxis
  • Ecchymoses
  • mucosal bleeding
  • Bleeding with trauma or surgery
  • Symptoms often improve post -adolescence
27
Q

What are the Lab features of vWD?

A 
BT/PFA-100 = prolonged
PTT = usually prolonged
VIII = decrease to normal
vWF :ag: = Decreased to normal
vWF :Rcof: = Decreased to normal
28
Q

What is the Tx for vWD?

A
  • Desmopressin
  • Antifibrinolytic agents
  • Factor VIII concentrates
  • Cryoprecipitate
29
Q

Tell me about Hemophilia A…..

A

The most serious bleeding disorder…

  • X linked recessive disorder caused by deficiency of factor VII.
  • symptoms start in early childhood.
30
Q

What are the clinical manifestations of Hemophilia A?

A
  • Hemarthosis
  • soft tissue bleeding
  • Excessive bleeding with trauma
  • intramuscular hematomas
  • intracerebral hemorrhage
  • bleeding into other tissues.
31
Q

What are the Lab features of Hemophilia A?

A 
BT/PFA-100 = Normal
PTT = prolonged
VIII = decrease 
vWF :ag: = normal
vWF :Rcof: =  normal
Factor IX = normal
32
Q

What are the 3 classes of Hemophilia A?

A

Severe = 5% Factor VIII

33
Q

What is the Tx for Hemophilia A?

A
  • Factor VIII concentrates

- Inhibitors of Fibrinolysis

34
Q

Tell me about Hemophilia B…..

A

Sex linked recessive disorder caused by deficiency in factor IX.
* Clinical and lab manifestations are similar to deficiency of factor VIII. Can also be mild moderate or severe.

35
Q

What are the 3 classes of platelet disorders?

A

Quantitive
Qualitative
Combined

36
Q

What is the mechanism of Thrombocytopenia?

A
  • Decreased platelet production (Quantitative)
  • Increased destruction of platelets
  • sequestration
  • Congenital vs aquired
37
Q

How is Thrombocytopenia evaluated?

A
  • Peripheral blood smear
  • bone marrow examination
  • platelet antibody determination
  • Clinical history
38
Q

Tell me about Acute/Childhood Immune Thrombocytopenic purport (ITP)….

A
  • Viral prodrome common
  • sudden onset
  • severe thrombocytopenia
  • Frequently undergoes remission
  • M:F = 1:1
39
Q

Tell me about Chronic/adult Immune Thrombocytopenic purport (ITP)….

A
  • No antecedent infection
  • Gradual onset
  • Moderate Thrombocytopenia
  • Infrequent remission
  • More common in females.
40
Q

What is the Pathophysiology of ITP?

A

Autoantibodies directed at the platelet membrane antigens (GPIb/IX and IIb/IIIa are common targets)

*increased IgG bound to the platelet surface promotes increased sequestration/destruction by the reticuloendothelial system.

41
Q

What are the clinical manifestations of ITP?

A
  • Petechial hemorrhages
  • Ecchymoses (brusing)
  • Bleeding with trauma or surgery
42
Q

What bone marrow and blood findings would you expect with ITP?

A
  • Megakaryocyte normal to increased

- No Microangiopathic changes on blood smear review.

43
Q

What is the treatment for ITP?

A
  • Corticosteroids
  • Intravenous immunoglobulin
  • Immunosuppression
  • Splenectomy
44
Q

What is Thrombotic Thrombocytopenia Purpura TTP?

A

An acute disorder characterized by intravascular platelet activation with formation of platelet rich micro thrombi throughout circulation. *can be inherited or acquired

45
Q

What causes TTP?

A

a deficiency of ADAMS 13, a metalloprotienase that usually degrades very high molecular weight vWF.

46
Q

What is DIC?

A

Unregulated widespread intravascular activation of the hemostatic system.

47
Q

When does DIC occur?

A
  • Infections
  • Tissue Injury (trauma, burn, surgery)
  • Obstetrical complications
  • Certain malignancies
48
Q

What are the clinical manifestations of DIC?

A 
- bleeding from multiple sites
 Thromboembolic problems 
- Hypotension and shock
- respiratory dysfunction
- Hepatic dysfunction
- Renal dysfunction
- CNS dysfunction
49
Q

What is the Tx for DIC?

A
  • remove/reverse the intuiting stimulus
    Supportive therapy with transfusions of blood products:
  • FFP: coagulation and regulatory proteins
  • Cryoprecipitates: fibrinogen, VIII, vWF
  • Platelets

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