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Clin Med III - Heme/Onc > Coagulation Disorders > Flashcards

Coagulation Disorders Flashcards

1
Q

How is the body’s clotting system balanced?

A
  • Clotting factors (platelets, TF, etc)

- Anti-clotting factors (NO, protein C/S, etc)

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2
Q

What are examples of vessel bound clot INHIBITORS?

A
  • NO
  • Prostacyclin
  • Vascular endothelial ADPase
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3
Q

What are examples of vessel bound clot initiators?

A
  • TF
  • vWF
  • TXA2
  • Collagen
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4
Q

What does the cascade of soluble clotting factors consist of?

A

Intrinsic and extrinsic pathways leading to the common pathway

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5
Q

Which blood test evaluates the extrinsic pathway of clotting?

A

PT

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6
Q

Which blood test evaluates the intrinsic pathway of clotting?

A

aPTT

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7
Q

What is the MC inherited bleeding disorder?

A

von Willebrand disease

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8
Q

Describe vWF

A
  • Promotes adhesion and aggregation of platelets

- Carrier of Factor VIII

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9
Q

What breaks down ultra-large multimers of vWF?

A

ADAMTS13 enzyme

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10
Q

MC type of vWF disease?

A

Type 1

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11
Q

Describe Type 1 vWF disease

A
  • Autosomal co-dominant
  • MC type
  • Decreased quantity of vWF and FVIII activity (results in increased bleeding)
  • Tx: DDAVP (nasal spray or IV)
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12
Q

What patients normally have low levels of vWF and F VIII?

A

Type O blood

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13
Q

What type of vWF disease should NOT be treated with DDAVP?

A

Type 2b (excessively big multimers of vWF) - can worsen thrombocytopenia and precipitate abnormal clotting

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14
Q

Describe hemophilia A

A
  • Deficiency of F VIII

- X linked recessive (severe only in males)

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15
Q

Clinical presentation of hemophilia A

A

Easy bruising or bleeding (especially in male toddlers)

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16
Q

How to differentiate child abuse from hemophilia A?

A

Hemophilia A is NOT a/w fractures

17
Q

Treatment of hemophilia A

A

IV recombinant F VIII

prophylaxis also desirable

18
Q

Describe hemophilia B

A
  • Deficiency of F IX
  • X-linked recessive
  • Clinically identical to hemophilia A
19
Q

Treatment of hemophilia B

A

Recombinant F IX concentrate

20
Q

Describe F XI deficiency

A
  • Autosomal co-dominant

- MC in Jewish population

21
Q

Clinical presentation of F XI deficiency

A
  • Few are symptomatic
  • Most present in adulthood
  • Similiar symptoms to hemophilia (easy bruising and bleeding)
22
Q

Treatment of F XI deficiency

A

FFP

23
Q

Describe Vitamin K including its role in clotting

A
  • Fat soluble vitamin, absorbed through gut
  • Activation of many proteins including clotting factors II, VII, IX, X
  • Activation of anti-thrombotic proteins C and S
24
Q

Why can pathological bleeding/thrombosis occur in liver failure?

A

Liver is major homeostatic organ - dysfunction throws the hemostatic balance out of whack

25
Q

How to treat coagulopathy of liver disease?

A

FFP - then you can anticoagulate after if thrombosis is a significant problem

26
Q

Describe coagulopathy of kidney disease

A

Usually more mild than that of liver disease

27
Q

Treatment of coagulopathy of kidney disease

A

Restore renal function first! Then FFP/transfusion may help

28
Q

Clinical hallmark of DIC?

A

Diffuse bleeding frequently from mucosa/sites of previous surgery and organ failure d/t thromboses

29
Q

Lab findings characteristic of DIC

A
  • Microangiopathic Hemolytic Anemia

- Thrombocytopenia

30
Q

How to differentiate DIC from TTP?

A

PT and aPTT should be NORMAL in TTP (also fibrin degradation products)

31
Q

How to treat DIC?

A
  • First, address underlying cause
  • Next consider FFP
  • Use transfusions sparingly
  • Anticoag is risky
32
Q

What blood test monitors unfractionated heparin activity?

A

aPTT

33
Q

Describe hypercoaguable states in general

A
  • Pathologic thrombosis (particularly in venous structures)

- Excessive activation of soluble clotting factors

34
Q

What are the inherited hypercoaguable states?

A
  • Factor V Leiden

- Prothrombin gene mutation G20210A

35
Q

What is the MC inherited hypercoaguable state?

A

Factor V Leiden

36
Q

What does the Factor V Leiden mutation cause?

A

Resistance to the inhibitory effects of activated Protein C

37
Q

Situational risk factors for hypercoaguable states?

A
  • Surgery
  • Immobilization
  • Pregnancy
  • HRT
  • HIT
38
Q

Acquired risk factors for hypercoaguable states?

A
  • IBD
  • Portal HTN
  • Cancer and chemo
  • Nephrotic syndrome
  • Anti-phospholipid antibody syndrome (lupus anticoag)

Clin Med III - Heme/Onc (8 decks)

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