Acquired Coag Disorders

Question 1

Contrast acquired disorders of secondary hemostasis with the congenital ones.

Answer 1

• More common than inherited disorders
• Usually adults with no family history and no

personal history of bleeding disorders

• Multiple procoagulants tend to be deficient
• Typically seen in context of other disease

processes

Question 2

What type of vitamin is vit. k? Where do our bodies obtain vitamin K from? What is its role? Where does this take place? What is a drug that prevents it from doing this role?

Answer 2

• Fat-soluble vitamin
• 2 sources: – Dietary consumption – Bacterial synthesis in the GI tract
• Important for posttranslational modification

(gamma-carboxylation) of Factors II, VII, IX,

and X and anticoagulants Protein C and

Protein S – Occurs in the liver

Warfarin prevents vit. k from being able to recycle itself and thus it can’t perform more than one modification.

Question 3

What are the major mechanisms of vit. k deficiency? How quickly does this occur? Why? What lab features are there of deficiency? What are some treatments?

Answer 3

• Storage amounts in the liver are small
• Can lead to deficiency developing rapidly
• Major mechanisms of deficiency: – Fat malabsorption – Diffuse liver disease – Inadequate dietary intake
• Laboratory Features: – Prolonged PT – Normal PTT (will prolong later) – Normal TT and platelet count
• Treatment: – Correct the cause – Parenteral Vitamin K – FFP transfusion (4-6 hours; acute bleeding, surgery, etc)

Question 4

Describe hemorrhagic disease of the newborn including causes, clinical signs, things that make it worse and treatment.

Answer 4

• Low fetal reserves (poor placental transport)
• No GI flora
• Inefficient hepatic synthesis for first 3-4 months after

birth

• Breast milk is a poor source of Vitamin K
• Bleeding around umbilical cord stump, visceral bleeds,

CNS bleeds

• Exacerbated by maternal anticoagulant or

anticonvulsant medication use

• Treatment: preventative parental Vitamin K given after

delivery

Question 5

What is synthesized in the liver that is involved in coagulopathy of liver disease? What is cleared there? What other clinical manifestations are related to these? What is the result of all this?

Answer 5

Synthesis site of: – Procoagulants – Anticoagulants – Fibrinolytics – Antifibrinolytics

• Clearance site of: – Procoagulants – Fibrin degradation products – Plasminogen activator proteins
• Other clinical manifestations: – Vitamin K deficiency – Thrombocytopenia
• Therefore, liver disease yields a complex coagulopathy.

Question 6

Describe the timeline of coagulopathy of liver disease.

Answer 6

• Factor VII disappears first (half-life of 4-6

hours)  prolonged PT

• Factors V, II, IX, and X disappear next  prolonged aPTT
• Loss of fibrinogen abnormal thrombin time
• Thrombocytopenia
• Fibrin degradation products may appear
• Factor VIII usually remains normal

Question 7

What is DIC? Generally, waht causes it? What is the pathophysiology? What are the 4 most common specifici causes? What

Answer 7

Disseminated Intravascular Coagulation

• Thrombohemorrhagic disorder (acute, subacute, or
chronic) with excessive activation of the coagulation system
– Secondary disorder (not a primary condition)

• Initiating event: massive release of tissue factor,
thromboplastic substances, or widespread endothelial
injury – Most common causes: sepsis, major trauma, malignancy, and obstetric complications

• Consumption of platelets and coagulation factors  microangiopathic hemolytic anemia and tissue ischemia
• Activation of fibrinolytic mechanisms  bleeding

Question 8

What are the clinical manifestations? Describe/Name two specific patterns of clinical manifestations. How is it manifested if it is acute? Chronic? What must be done to treat it?

Answer 8

• Thrombi in brain, heart, lungs, kidneys,
adrenals, spleen, and liver – Microinfarcts that can be complicated by hemorrhage

• Meningococcemia  massive adrenal hemorrhages

(Waterhouse-Friderichsen syndrome)

• Sheehan postpartum pituitary necrosis
• In general, acute DIC  bleeding with chronic

DIC  thrombotic complications

• Must remove the inciting factor

Question 9

What lab findings are expected in DIC?

Answer 9

• Peripheral blood smear: schistocytes, thrombocytopenia

• Increased fibrin degradation products / D-
dimer

• Prolonged PT, aPTT, and TT
• Decreased fibrinogen