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Block 7 week 4 > Coagulation - Freeman > Flashcards

Coagulation - Freeman Flashcards

1
Q

What does Factor V do in the coagulation cascade?

A
  1. activated factor V forms a complex with activated factor Xa
  2. this complex cleaves prothrombin into thrombin which forms fibrin - initiating platelet aggregation
  3. factor V is inactivated by activated Protein C
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2
Q

What is Factor V Leiden?

A

Factor V Leiden is a mutation at position 506 on the factor V gene. The mutation causes a Glutamic Acid residue to replace an Arganine residue. Position 506 is the place where factor V is normally cleaved into 2 fragments by activated Protein C. If factor V cannot be inactivated then there is increased risk for clotting.

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3
Q

Name some factors that can lead to vasoconstriction.

A
  1. compression due to obesity
  2. prior sites of a thrombus
  3. chemical factors such as nicotine and vasoconstriction agents
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4
Q

Name some modifiable risks for coagulation.

A
  1. obesity
  2. sedentary lifestyle
  3. travel
  4. pregnancy
  5. elective surgery - especiall ortho with its associated immobilization
  6. smoking
  7. prior DVT
  8. use of birth control pills
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5
Q

Name some un-modifiable risk factors for coagulation.

A
  1. Factor V Leiden
  2. prothrombin gene mutation
  3. malignancy
  4. emergent surgery
  5. chronic illnes
  6. Lupus anticoagulant
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6
Q

If you have a couple risk factors or have the Factor V Leiden mutation does that mean you will clot?

A

Not necessarily, you have to overwhelm the coagulation system. Even with the presence of risk factors it would take at least 4 risk factors at once to ensure abnormal clotting.

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7
Q

For acute thrombogenesis, why do patients require 7-10 full days of heparinization even with adequate coumadinization?

A

Coumadin basically causes vitamin K depletion which is required for the vitamin K dependent cofactors - factors II, VII, IX, X and protein C. The liver will continue to make these factors and some of them will already be carboxylated. These carboxylated factors will be inactivated according to their half lives but this takes time - so 7-10 days is needed for the Coumadin to work.

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8
Q

Can Coumadin be initiated at the same time as heparin?

A

Yes, because its effects will not be seen right away.

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9
Q

What is Lupus Anticoagulant?

A

LA is an acute phase reactant. If present then will see at time of an acute clot. It is called an anticoagulant because in vitro it caused a prolonged PTT but it is actually a procoagulant. If present then it is considered a risk factor for clotting.

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10
Q

What is recommended before making long-term therapeutic coumadin decisions when Lupus anticoagulant is present?

A

A repeat serology is recommended 3 months after an acute thrombotic event.

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11
Q

Describe the two types of Heparin induced thrombocytopenia.

A
  1. Type 1 - modest, transient decrease in platelets secondary to heparin induced platelet agglutination. Is self-limited, platelet counts can return to normal even while heparin is continued
  2. Type 2 - a drug induced, immune mediated response secondary to antibodies directed against Heparin-Platelet factor 4 complex that results in a 50% or greater drop in platelet counts. Severe thrombocytopenia with bleeding is rare.
  3. Type 2 is most common in the setting of major surgery where large volumes of heparin are required coronary artery bypass grafting.
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12
Q

How is Type II HIT diagnosed?

A

Measure radiolabeled 5-HT.

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13
Q

When should HIT be on the differential diagnosis?

A

Should be considered in all recently hospitalized patients returning with acute thrombosis within 1-2 weeks of their hospital stay. Clinically you will see thrombocytopenia and thrombosis. The thrombosis is treated with direct thrombin inhibitors.

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14
Q

Name some clinical characteristics of HIT.

A
  1. incidence is 10X greater than patients treated with unfractionated heparin than in those receiving LMWH
  2. incidence higher among surgical patients
  3. uncommon among pediatric, obstetrical, and hemodialysis patients
  4. thrombosis with declining platelets is seen in about 50% of patients with recent hospitalization
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15
Q

What are the direct thrombin inhibitors?

A
  1. Dabigatran
  2. Argatroban
  3. Ximelagatran
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16
Q

What drug can reverse the effects of too much Heparin?

A

Protamine Sulfate.

17
Q

What is the pathophysiology of DIC?

A

Widespread activation of the clotting cascade causing a consumption of clotting factors and platelets with resultant bleeding. The microvascular compromise secondary to thrombin formation results in tissue ischemia with result an end organ damage particularly of the liver and kidneys.

18
Q

What are some diseases or conditions that promote expression of tissue factor and thus promote DIC?

A
  1. gram pos or neg septicemia
  2. damaged cerebral tissue
  3. APL
  4. placental tissue from obstetric catastrophes
  5. snake venoms
  6. acute hemolytic transfusion reactions
  7. hypotension from any cause that results in endothelial cell damage
  8. massive tissue injuries such as trauma, burns and hypothermia
19
Q

Why does sepsis cause activation of coagulation?

A

Endotoxin, IL-1, TNF-a and other cytokines trigger the release of tissue factor and this causes activation of coagulation.

20
Q

What are the characteristic lab findings of DIC?

A
  1. prolonged PT/PTT or both
  2. thrombocytopenia
  3. decreased fibrinogen levels
  4. increased D-dimer
21
Q

What is the primary treatment for DIC?

A
  1. treat the underlying condition - treat bacterial infection with broad spectrum, empiric antibiotics until microbe can be identified
  2. supportive care, including maintaining platelets at greater than 100,000 and maintaing fibrinogen at greater than 100.
22
Q

What kinds of conditions can lead to hypocoagulative states and bleeding?

A
  1. trauma
  2. infections
  3. drugs
  4. disorders of the coagulation system such as platelets and congenital or acquired factor disorders - platelet disorders are common but not often associated with clinically relevant bleeding
  5. disorders of organ systems such as liver failure, renal failure, CABG surgery, myeloproliferative syndromes
23
Q

What are some drugs that can cause bleeding?

A
  1. GP IIb/IIIa inhibitors such as Plavix
  2. COX I inhibitors such as aspirin
  3. Heparin
  4. Coumarins
  5. ginko and ginseng
24
Q

Renal failure can lead to acquired platelet dysfunction. What is one of the treatments for this condition?

A

DDAVP or Desmopressin. This drug works by limiting the amount of water excreted by the kidney and it also causes release of vWF from Weibel Palade bodies. vWF binds to platelets and also increases the half life of Factor VIII.

25
Q

What conditions cause prolonged PT?

A
  1. use of Coumadin
  2. Liver disease due to decreased synthesis of vit. K dependent factors
  3. malnutrition - due to inability to make protein factors
26
Q

What conditions cause prolonged PTT?

A
  1. presence of Lupus anticoagulant and acquired factor inhibitors
  2. vWF
  3. Factor VIII/IX deficiency or inhibitor use
  4. use of Heparin
27
Q

What is a mixing study used for?

A

A mixing study is used to evaluate a prolonged PTT. You add the patient’s plasma to test plasma and see if the prolonged PTT is normalized. If there is correction then this means the patient has a factor deficiency and you perform a factor assay. If there is no correction then test for Lupus anticoagulant. If LA is not present then there may be inhibitor present. Do a factor assay to see which factor is decreased and do an inhibitor assay for that specific factor.

28
Q

What is Von Willebrand disease?

A

It is a Factor VIII deficiency that can be inherited (autosomal dominant) or can be acquired.

29
Q

How many types of inherited Von Willebrand disease are there?

A
  1. Type 1 - quantitative deficiency
  2. Type 2 - qualitative deficiency
  3. Type 3 - total deficiency
30
Q

What causes acquired von Willebrand disease?

A
  1. lymphoproliferative disorders
  2. monoclonal gammopathies
  3. myeloproliferative disorders - especially Essential thrombocytosis
  4. mechanical - Heyde’s Syndrome
31
Q

What is unique about factor VIII?

A

It can be thought of as two distinct molecules.

  1. Factor VIII vWF - platelet adhesion to sites of vascular injury and the subendothelial matrix
  2. Factor VIII hemophilia - a procoagulant
32
Q

What are some characteristics of von Willebrand disease?

A
  1. autosomal dominant if caused by a mutation
  2. clinically will see mucosal ‘oozing’ after surgery or trauma
  3. if there is greater than 20% activity of vWF then the disease is mild, if there is between 10-20% activity then the disease is moderate and if there is less than 10% activity then the disease is severe
33
Q

What are some characteristics of Hemophilia?

A
  1. X -linked inheritance
  2. clinically - spontaneous hemarthroses
  3. two types - A and B, type B is also called factor IX disease and Christmas disease
34
Q

How is von Willebrand disease treated?

A
  1. IV DDAVP for mild cases with bleeding
  2. nasal spray DDAVP for children that experience mild playground injuries or women with heavy menses
  3. Factor VII replacement
35
Q

What is Heyde’s syndrome?

A

A syndrome caused by aortic valve stenosis resulting in GI bleeding at sites of colonic angiodysplasia with exaggeration of bleeding secondary to mechanical destruction of ultra-large von Willebrand factor molecules (acquired von Willebrands). This from Dr. Freeman’s notes. Wikipedia says that it is a syndrome characterized by aortic valve stenosis and GI bleeding. The bleeding is caused by induction of von Willebrand disease Type IIa by mechanical destruction.

36
Q

Describe acquired TTP.

A

A disease caused when auto-antibodies are formed against ADAMTS-13, a metalloproteinase involved in the normal processing of vWF.

37
Q

What symptoms/signs are associated with acquired TTP?

A
  1. fever
  2. renal insufficiency
  3. microangiopathic hemolytic anemia
  4. thrombocytopenia
  5. neurological symptoms - hallucinations, AMS etc.
  6. mostly affects adults, the above ‘pentad’ of symptoms is indicative of TTP clinically but all the symptoms do not necessarily manifest
38
Q

What lab abnormalities are associated with TTP?

A
  1. anemia/thrombocytopenia
  2. increased LDH
  3. slightly increased serum creatinine
  4. schostocytes in peripheral smear
39
Q

What are some causes of acquired TTP and what percentage of cases are associated with this cause?

A
  1. E. coli 0:157
  2. idiopathic - 40%
  3. autoimmune diseases/infections/cancer - 27%
  4. drug associated (i.e. quinine) - 6%
  5. bloody diarrhea prodrome - 8%
  6. pregnancy/postpartum - 7%
  7. hematopoietic cell transplantation - 6%

Block 7 week 4 (6 decks)

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