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Module 5: GI > Hemostasis II > Flashcards

Hemostasis II Flashcards

1
Q

What are weibel palade bodies?

A

vessicular bodies released by endothelial cells after damage to a vessel wall

  • they include von Willibrand Factor as well as P-selectin

–> will activate both clotting and margination of PMNs

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2
Q

What are the 4 steps of Primary Hemostasis?

A
  • *1. Transient constriction of damaged vessel**
  • mediated by reflex neural stimulation and endothelin released from endothelial cells
  • *2. Platelet adhesion to surface of disrupted vessel**
  • vWF (released by endothelial cells and platelets) binds exposed subendothelial collagen
  • platelets bind vWF using GPIb receptor
  • *3. Platelet degranulation**
  • adhesion induces shape change and degranulation
  • ADP (dense granules) promotes exposure of GPIIb/IIIa receptor on platelets
  • TXA2 promotes platelet aggregation
  • *4. Platelet Aggregation**
  • Platelets aggregate via GpIIb/IIIa using fibrinogen as linking molecule
  • results in platelet plug
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3
Q

What are symptoms of primary hemostasis disorders?

A

Primary hemostasis disorders are caused by either thrombocytopenia or non-functional thrombocytes

Results in:

Petechiae*, purpura, ecchymoses

Easy Bruising

Mucosal bleeding

*Petechiae are sign of thrombocytopenia and are not usually seen with qualitative disorders

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4
Q

What causes TTP?

A

Decreased ADAMTS13

  • ADAMTS13 normally cleaves vWF mlutimers into smaller monomers for evenutal degredation
  • leaving uncleaved, multimers leads to abnormal platelet adhesion, resulting in microthrombi
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5
Q

What are clinical findings of TTP and HUS?

A

Skin and mucosal bleeding (platelets consumed in platelet microthrombi)

** Microangiopathic hemolytic anemia** (platelet microthrombi shear RBCs in kidney and CNS)

Fever

renal insufficiency (predominant in HUS)

CNS abnormalities (predominant in TTP)

Thrombocytopenia

Increased bleeding time

Normal PT/PTT

Anemia with schistocytes

Increased megakaryocytes on BM biopsy

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6
Q

What is Bernard-Soulier syndrome?

A

Genetic GPIb deficiency: platelet adhesion is impaired

  • Mild thrombocytopenia with enlarged plateletes (Big Suckers = Bernard-Soulier)
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7
Q

What is Glanzmann thromblasthenia?

A

Genetic GIIb/IIIa deficency: platelet aggregation impaired (no primary hemostasis)

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8
Q

How does aspirin affect bleeding time?

A

Aspirin irreversibly inactivates COX1/2

  • Results in a lack of TXA2, which then impairs platelet aggregation (TXA2 is chemical messenger to bring in other platelets)
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9
Q

What is the process of secondary hemostasis?

A
  • Coagulation cascade produces thrombin
  • thrombin cleaves fibrinogen into fibrin, which is then cleaved and cross-linked

–> end product is: a stable Platelet-fibrin thrombus

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10
Q

What is necessary for the activation of the coagulation factors?

A
  1. Exposure to an activating substance
  2. Phospholipid surface (platelets)
  3. Calcium
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11
Q

What does the PT and PTT measure, respectively?

A

PT = extrinsic
(You do PT outside)

PTT = intrinsic

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12
Q

What is hemophilia A?

A

Genetic Factor VIII deficiency

  • X-linked recessive; predominanty affects males
  • Can arise form new mutation without family history!
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13
Q

What are signs and symptoms of hemophilia A?

A

Deep tissue, joint and post-surgical bleeding

Increased PTT, Normal PT

Decreased Factor VIII

Normal platelet count and bleeding time

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14
Q

What is hemophilia B?

A

Genetic Factor IX deficiency (Christmas factor deficiency)

  • Resembles hemophilia A, except Factor IX levels are decreasd instead of Factor VIII
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15
Q

What is the most common coagulation factor inhibitor?

A

Anti-factor VIII

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16
Q

What are signs and symptoms of vWF deficiency?

A

Note: most common type is autosomal dominant with decreased vWF

Decreased ability for platelets to adhese to damaged vessel using GPIb

- Mild mucosal and skin bleeding

- Increased bleeding time

  • Increased PTT (need vWF to stabilized factor VIII), normal PT

- Abnormal ristocetin test

17
Q

What is treatment for vWF deficiency?

A

Desmopressin

  • Increases release of vWF from Weibel-Palade bodies of endothelial cells
18
Q

Vitamin K deficiency affects what coagulation factors?

A

II (thrombin), VII, IX, and X

(Vit. K required to gamma-carboxylate these factors)

19
Q

How does Vitamin K deficiency occur?

A

Vitamin K is produced by bacteria in our gut

Deficiencies occur in:
Newborns
Long-term antibiotic therapy
Malabsorption

20
Q

Why does liver failure result in bleeding disorders?

A

Decreased production of coagulation factors

Decreased activation of vitamin K by epoxide reductase (therefore, no activation of II, VII, IX, and X)

Effect of liver failure on coagulation is followed using PT (Factor VII has shortest half-life)

21
Q

What is HIT?

A

Heparin Induced Thrombocytopenia

  • Platelet destruction that arises secondary to heparin therapy
  • Heparin forms complex with Platelet Factor 4
    Patient then develops IgG antibodies to this complex resutling in destruction of platelets
  • Fragments of destroyed platelets may activate remaining platelets, leading to thrombosis
22
Q

How is HIT treated?

A

Stop Heparin and a different anticoagulant (NOT coumadin = these patients are at increased risk of coumadin skin necrosis)

23
Q

What is DIC?

A

Disseminated Intravascular Coagulation

- Pathologic activation of coagulation cascade

- Widespread microthrombi result in ischemia and infarction

- Consumption of platelets and factors results in bleeding, especially from IV sites and mucosal surface (mouth, lung, GI tract, kidneys, etc)

  • *Almost always secondary to another disease process:**
  • Obstetric complication (amniotic fluid)
  • Sepsis
  • Adenocarcinoma
  • Acute promyelocytic leukemia (by release of Auer rods)
  • Rattlesnake bite
24
Q

What are the laboratory findings of DIC?

A

Decreased platelet count

Increased PT/PTT

Decreased fibrinogen

Microangiopathic hemolytic anemia

Elevated fibrin split products (D-dimer)

Module 5: GI (19 decks)

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