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(J2) RBCs and Bleeding Disorders > Secondary (Clotting Factors) Hemostatic Disorders > Flashcards

Secondary (Clotting Factors) Hemostatic Disorders Flashcards

1
Q

What are common symptoms of secondary hemostatic (coagulation factor) disorders?

A
  • hemarthrosis
  • traumatic ecchymosis/hematoma
  • prolonged bleeding from laceration (ie. surgery)
  • GI/urinary tract bleeding
  • petechiae typically not seen
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2
Q

What is the most common inherited coagulation disorder?

A

von Willebrand disease

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3
Q

How does vitamin K related to hemostasis?

A

Vitamin K is required for production of factors II, VII, IX, X and proteins C and S

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4
Q

How does liver failure relate to hemostasis?

A

Many of the coagulation factors are made in the liver and may be deficient in severe liver failure

-liver is also responsible for activating vitamin K, meaning no vitamin K-dependent coagulation factors

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5
Q

How is the effect of liver failure on coagulation followed?

A

PT, shows changes earlier from liver failure than other measures

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6
Q

What is hemophilia A?

A
  • deficiency in factor VIII (hemophilia “A-ight/8”)
  • X-linked recessive
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7
Q

What lab findings would be expected in hemophilia A?

A
  • elevated PTT (FVIII is in the intrinsic pathway)
  • normal PT
  • normal platelets
  • normal bleeding time
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8
Q

What is the classical presentation of hemophilia A?

A

-male

*symptoms vary with severity of disease*

-hemarthrosis (very indicative of hemophilia)

-muslce hemorrhages (very indicative of hemophilia)

-petechiae absent

  • traumatic ecchymosis/hematoma
  • prolonged bleeding from laceration (ie. surgery)
  • GI/urinary tract bleeding
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9
Q

What is the treatment for hemophilia A?

A

recombinant FVIII

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10
Q

What test confirms hemophilia A?

A

Performance of PTT with patients plasma and with plasma lacking factor VIII identifies if it is factor VIII and not a different intrinsic pathway factor that is deficient.

PTT does not correct in hemophilia A,

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11
Q

What is hemophilia B?

A

-hemostatic disorder caused by a deficiency in factor IX

-X-linked recessive

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12
Q

What lab findings would be expected in hemophilia B?

A
  • elevated PTT (FIX is in the intrinsic pathway)
  • normal PT
  • normal platelets
  • normal bleeding time
  • indisthinguishable from hemophilia A without assay of coagulation factor levels
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13
Q

What is the classical presentation of hemophilia B?

A
  • male
  • clinically indistinguishable from hemophilia A

*symptoms vary with severity of disease*

  • hemarthrosis (very indicative of hemophilia)
  • muslce hemorrhages (very indicative of hemophilia)
  • petechiae absent
  • traumatic ecchymosis/hematoma
  • prolonged bleeding from laceration (ie. surgery)
  • GI/urinary tract bleeding
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14
Q

What is the treatment for hemophilia B?

A

recombinant FIX

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15
Q

What is acquired hemophilia?

A
  • coagulation disorder caused autoimmune Abs against coagulation factors
  • FVIII is the most common
  • they mimic deficiency in cooresponding coagulation factor
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16
Q

How is hemophilia destinguished from acquired hemophilia?

A

Mixing study

  • patients serum is mixed with serum containing all coagulation factors, PT/PPT is performed again
  • if PT/PTT corrects it is hemophilia (Ab blocks coagulation factor in added serum)
17
Q

What is von Willebrand disease?

A

-inherited hemostatic disorder caused by a deficiency von Willebrand factor

18
Q

What lab findings would be expected in von Willebrand disease?

A
  • increased bleeding time (platelet adhesion affected)
  • elevated PTT (decreased half-life of FVIII due to lack of vWF)
  • normal PT
  • normal platelets
19
Q

What is the mechanism of von Willebrand disease?

A
  • vWB binds exposed subendothelial collagen
  • platelet GPIb binds vWB during adhesion
  • decreased vWF -> impaired platelet adhesion
  • vWF also stabilizes FVIII
  • decreased vWF -> decreased FVIII
20
Q

What is the classical presentation of von Willebrand disease?

A
  • mucosal and skin bleeding similiar to in platelet dysfuctions (*unusual since platelets are normal)
  • no hemarthrosis (*despite elevated PTT/impacted FVIII)
21
Q

What is the Ristocetin test?

A

-normally, ristocetin causes vWF to bind platelet GFIb -> agglutination of platelets

-if vWF is lacking, when ristocetin is added to blood agglutination will not occur

22
Q

What is the treatment for von Willebrand disease?

A

-desmopression (increased vWB release from Weibel-Palade bodies of endothelium)

23
Q

What is disseminated intravascular coagulation (DIC)?

What occurs with DIC?

A
  • pathologic activation of coagulation cascade and fibrinolysis
  • almost always secondary to some other disease processes
  • consumes coagulation factors and platelets
  • microthrombi -> ischemia/infarct and microagniopathic hemolysis
  • bleeding from mucosal surfaces
24
Q

What lab findings would be expected in DIC?

A
  • decreased platelet count (used up)
  • increased PT/PTT (coagulation factors used up)
  • decreased fibriongen
  • microangiopathic hemolytic anemia
  • **elevated D-dimer (product of split cross-linked fibrin) (best screening test)
25
Q

What are possible causes of DIC?

A
  • tissue thromboplastin in amniotic fluid (pregnant women)
  • sepsis (E. coli and N. meningitidis endotoxin)
  • adenocarinoma (mucin)
  • acute promyelocytic leukemia (excessive primary granules)
  • rattlesnake venmon
26
Q

What is the most common cause of DIC?

A

-pregnancy complicaitons

(J2) RBCs and Bleeding Disorders (10 decks)

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