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4 Hemostasis and Related Disorders > 4.2 Secondary hemostasis and related bleeding disorders > Flashcards

4.2 Secondary hemostasis and related bleeding disorders Flashcards

1
Q

Anticoagulantion factors, list them (3)

A
  • Protein C and S
  • ATIII
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2
Q

Secondary hemostasis, main idea

A
  • Stabilization of weak platelet clot with thrombin (converts fibrinogen to fibrin for cross-linking)
  • thrombin formed by Coag cascade
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2
Q

Pt with long-term antibiotic therapy:

-what coagulation problem to be concerned about?

A
  • Vit K deficiency
  • long term abx can kill gut bacteria that produce Vit K
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3
Q

Pt with deep bleeding into muscles and joints–suspect what?

A

Suspect a coagulation disorder (Secondary hemostasis disorder)

-primary hemostasis usu presents with mucosal, skin bleeding instead

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4
Q

If Vit K cannot be absorbed in the gut, what else might not be absorbed?

A
  • fat-soluble vitamins: D,E,A,K
  • possible reason: lack of bile
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4
Q

Why does liver failure lead to hemostasis problems? (2 reasons)

-also, what lab test to follow effect of liver failure on coagulation

A

Secondary hemostasis is affected by liver failure:

  1. lack of coag factor production
  2. lack of epoxide reductase activation of Vit K

Lab test: PT

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5
Q

What does vWF do other than bind to SEC?

A
  • it stabilizes coag factor 8.
  • loss of vWF (VW disease) leads to increased PTT
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6
Q

Von Willebrand Disease

  • mech, etiology
  • labs (platelets, PT/PTT, coag factors)
  • Tx
A
  • genetic vWF deficiency
  • platelets cannot adhere to SEC. Decreased coagulation, skin and mucosal bleeding
  • labs:
  • platelets: normal
  • PT: normal
  • PTT: elevated (because vWF stabilizes F.8)
  • Ristocetin test: abnormal (test shows binding of vWF to GP1b)

-Tx: Desmopressin (ADH analog)–it increases vWF release from Weibel-Palade bodies in endothelial cells

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7
Q

Tissue factor pathway inhibitor

A

Inhibits F.7 at the start of the extrinsic tissue factor pathway

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9
Q

Disorders of Secondary Hemostasis

  • usual etiology
  • clinical presentation
A
  • usually Factor abnormalities
  • deep tissue bleeding into muscles and hemarthrosis
  • rebleeding after surgery (eg wisdom tooth extraction)
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10
Q

Epoxide reductase

A
  • enzyme that activates Vitamin K in liver.
  • coumadin inhibits this
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10
Q

Heparin vs Coumadin:

  • mechs
  • what lab test to monitor effect of each
A

Heparin:

  • activate ATIII, which inactivates thrombin and coag factors
  • use PTT

Coumadin:

  • inhibit epoxide reductase, which activates Vit.K
  • use PT
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11
Q

Disorders of Secondary hemostasis: -list them (7)

A
  1. Hemophilia A (F.8)
  2. Hemophila B (F.9)(Christmas disease)
  3. Coagulation Factor Inhibitor (Ab against coag factor)
  4. Von Willibrand Disease–vWF deficiency
  5. Vit K deficiency
  6. Liver failure:
    1) decreased production of coag factors
    2) decreased activation of Vit. K by epoxide reductase
  7. Large-volume transfusion
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12
Q

Pt with suspected hemophilia. You ask about family history of bleeding disorders but none. Is hemophilia still on your differential?

A

Yes. 30% of hemophilia A and B are de novo mutations.

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13
Q

Desmopressin

  • what does it tx other than diabetes insipidus
  • mech?
A
  • tx Von Willebrand disease
  • it increases vWF release from the Weidel-palade bodies of endothelial cells.
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14
Q

Hemorrhagic disease of the newborn

  • what is it
  • tx
A
  • Lack of GI colonization in newborns means little Vit K is produced.
  • Vit K injections are given to all newborns as prophylaxis
16
Q

Ristocetin test

A
  • observe binding of vWF to GP1b
  • Ristocetin induces this, inducing platelet adhesion/agglutination
  • Used to diagnose VW disease: if there is a vWF deficiency, the platelets do not agglutinate. (abnormal result)
17
Q

What is most common inherited coagulation disorder?

A

Von Willebrand Disease

18
Q

Coagulation Factor Inhibitor

  • what is this?
  • how to differentiate this from Hemophilia
A
  • Ab against coag factor (autoimmune).
  • F.8 most common, resembling Hemophilia A
  • how to differentiate: give F.8 to patient. If PTT is back to normal, then Hemophilia. If PTT still elevated, it is anti-F.8 Ab.
19
Q

Vit K deficiency

  • mech
  • where does intake of Vit K come from (2)
A
  • loss of activation of 2,7,9,10,C,S leads to coagulation problem
  • Remember, Vit K is made by gut bacteria in addition to being in leafy vegetables
20
Q

Vit K deficiency:

-what classic populations does this occur in (3)

A
  1. Newborns–lack of GI bacteria colonization that normally synthesize Vit K–Vit K injections are given to all newborns to prevent hemorrhagic disease of the newborn
  2. Long-term antibiotic therapy–can kill gut bacteria that synthesize Vit K
  3. Malabsorption–problem in fat-soluble vitamin absorption (eg no bile from bile duct obstruction). (problem absorbing all D,E,A,K vitamins)
22
Q

Coagulation cascade, draw it out

A
  1. left side: contact pathway–SEC, 12, 11, 9, 8. (measure with PTT)
  2. right side: Tissue factor pathway–Trauma + Tissue factor (thromboplastin), 7 (measure with PT)
  3. bottom: X, 5, 2, 1
22
Q

Hemophilia

-characteristic symptoms

A

-intramuscular bleeding, hemarthrosis

24
Q

ATIII

A
  • inhibits thrombin and coag factors
  • activated by Heparin
25
Q

Vitamin K:

  • what does it do
  • how to get it
  • what activates it
A
  • activates 2,7,9,10,C,S -proteins C and S are anticoags
  • 2,7,9,10 are coags
  • Vit K comes from leafy vegetables, and is also produced by gut bacteria -activated by epoxide reductase in liver (coumadin inhibits this)
26
Q

PT vs PTT

A
  • prothrombin time–measures extrinsic (TF) pathway
  • partial thromboplastin time–measures intrinsic (Contact) pathway
27
Q

Hemophilia

  • types
  • lab findings (platelet count, PT/PTT, coag factors)
  • Tx
A
  1. Hemophilia A (F.8)
    - lack of F.8
    - X-linked recessive, or de novo
  • labs:
  • platelet count: normal
  • PT normal
  • PTT elevated
  • Coags: lack of F.8

-Tx: give F.8

  1. Hemophilia B (F.9)–Christmas Disease
    - Just like Hemophilia A, except deficiency is F.9
28
Q

What’s the difference between classic symptoms of Primary hemostasis vs Secondary hemostasis

A

Primary: skin and mucosal bleeding

Secondary: deep tissue bleeding into muscles, joints, and rebleeding after surgery (eg wisdom tooth extraction)

29
Q

in addition to coag factors, what is needed to activate the coagulation cascade? (3)

A
  1. exposure to activating substance:
    1) subendothelial collagen (SEC)–contact pathway
    2) Tissue Factor (thromboplastin)–tissue factor pathway
  2. phospholipid surface of platelets
  3. calcium

4 Hemostasis and Related Disorders (5 decks)

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