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HemOnc > Pathology Part 2- Bleeding Disorders > Flashcards

Pathology Part 2- Bleeding Disorders Flashcards

1
Q

What are 3 main causes of bleeding abnormalities?

A
  1. Derangement of coagulation proteins
  2. Abnormalities in blood vessel walls
  3. Platelet deficiency or dysfunction
    - CAN BE ANY COMBO
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2
Q

When do you see large ecchymoses and/or hematomas with bleeding into GI tract, urinary tract, or joints?

A

When there’s an abnormality in clotting factors

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3
Q

What is the initial presentation of abnormality in clotting factors?

A

Males bleed lots after circumcision

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4
Q

What factors is vitamin K required for?

A

2, 7, 9, 10, protein S, protein C

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5
Q

What can cause Vit. K deficiency?

A

Nutritional or iatrogenic (WARFARIN)

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6
Q

4 screening tests for Vit. K Deficiency?

A
  1. Bleeding time- don’t do this, it’s barbaric
  2. Platelet count (decreased)
  3. PT- EXTRINSIC
  4. PTT- INTRINSIC
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7
Q

What makes vWF?

A

ENDOTHELIAL CELLS

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8
Q

What does vWF do?

A

Facilitate platelet adhesion to subendothelial collagen

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9
Q

What indicates the presence of vWF?

A

Ristocetin (these dudes bind to platelets and activate vWF on surface and WHAM BAM PLATELET AGGREGATION

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10
Q

What receptor does vWF bind to on platelets?

A

GP Ib

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11
Q

What happens to you if you have VW disease?

A
  • BLEED

- Mucous membranes (versus clotting deficiency which is more joints), wounds, periods, ect.

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12
Q

3 types of vWF, tell me bout em?

A

1: Heterozygote: NOT ENOUGH, mild-mod bleeding, most common
2. Heterozygote: DEFECTIVE, mild-mod bleeding
3. Homozygous: NONE, severe bleeding

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13
Q

If you have hemophilia A, what are you missing and how did you get it?

A

FACTOR 8

-X-Linked (boys more often affected)

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14
Q

If you have hemophilia B, what are you missing and how did you get it?

A 
FACTOR 9 (CHRISTMAS DISEASE...HOHOHO)
-X-linked
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15
Q

Are the symptoms the same for hemophilia A and B

A

YES

  • Spontaneous hemorrhages (into joints)
  • NO petechiae and ecchymoses (usually absent)
  • Hemorrhage after trauma or operation
  • Normal bleeding time and platelet counts
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16
Q

In hemophilia A and B, whats the deal with the PT and PTT?

A

PTT is LOOOOONG (but corrects with mixing study when you give the blood the FACTOR IT NEEDS 8 or 9)
PT is NORMAL

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17
Q

What is a secondary complication of many diseases causing activation of the coagulation system, then fibrin thrombi produces throughout microcirculation, then activation of the fibrinolytic system?

A

DIC

18
Q

What does DIC consume?

A

Platelets, coagulation factors, and fibrinogen

-Initial clotting, but eventual bleeding as you use up all the factors

19
Q

What are 5 things DIC is associated with?

A
  1. Infection and Sepsis
  2. Bleeding
  3. Childbirth (for the momma)
  4. Massive inflammation or organ failure
  5. Malignancies (acute promyelocytic leukemia)
20
Q

How do you treat DIC?

A

Give em fibrinogen (cryoprecipitate)

-Treat underlying condition

21
Q

What is a condition where you get small skin petechiae and purpura, with normal lab values (bleeding time, coag times, platelet count)?

A

Non-thrombocytopenic purpura

22
Q

What else is on a ddx for non-thrombocytopenic purpura?

A
  1. Infectious diseases
  2. Drug reactions
  3. Collagen disorders
  4. Henoch-Schoenlein Purpura
  5. Hereditary hemorrhagic telangiectasia
23
Q

What can be caused by

  1. Inadequate production (via megakaryocytes in BM)
  2. Increased peripheral destruction (immune mediated)
  3. Splenic sequestration (primary or secondary)
  4. Hemodilution
A

THROMBOCYTOPENIA

24
Q

What causes neonatal or post-transfusion purpura?

A

Development of antibodies agaisnt platelet antigens

25
Q

What antibody is thought to be responsible for post-transfusional thrombocytopenia?

A

Anti-PL (A1)

-An Ag negative patient gets exposed to PL(A1) from allogeneic platelet transfusion

26
Q

What is it called when platelets get opsonized by patient’s anti-platelet Ig?

A

Idiopathic thrombocytopenic purpura

27
Q

What removes the platelets in ITP?

A

SPLENIC MACROPHAGES

28
Q

Who do you see ITP a lot in?

A

Women of reproductive age or in association with myeloid or lymphoid malignancy

29
Q

What is given for ITP?

A

IV immunoglobulin or steroids

30
Q

What causes microangiopathic hemolytic anemia?

A

You get fibrin formation in peripheral blood vessels that shears and dismembers the RBCs as they flow by creating RBC fragments/Schistosomes

31
Q

Whats the triad for HUS?

A
  1. Hemolytic anemia
  2. Thrombocytopenia
  3. Renal failure
    * NO NEURO SYMPTOMS
32
Q

What can cause HUS?

A

SHIGA TOXIN –> E.Coli O157:H7
(WHY IS SHE SAYING SUGAR LIKE THAT!?)
or idiopathic

33
Q

What is the pentad (ooo fancy) for TTP?

A
  1. Fever
  2. Hemolytic anemia
  3. Renal failure
  4. Transient neurologic defects
  5. Thrombocytopenia
    FAT RN
34
Q

What causes TTP?

A

Autoantibodies to ADAMTS13- this cleaves vWF…. if it doesn’t work, you get big giant vWF chunks floating around that shear the RBCs as they are trying to FLOW

35
Q

True or False: TTP is hematologic emergency

A

TRUE, HOLY CRAP get outta bed and get to the hospital like 5 minutes ago

36
Q

What is done for TTP?

A

PLASMAPHERESIS to remove those stupid immune complexes and then give donor plasma that has ADAMTS-13 so you can have happy tiny vWF

37
Q

What is deficient in Bernard- Soulier Syndrome?

A

GP Ib/V/IX

  • You get a defective adhesion of platelets to subendothelial collagen (vWF-GP Ib)
  • AUTOSOMAL RECESSIVE
38
Q

What is defeicient in Glanzmann Thrombasthenia?

A

Fibrinogen receptor IIb/IIIa

  • Defective platelet aggregation (with ADP, Collagen, Epi, or Thrombin)
  • AUTOSOMAL RECESSIVE
39
Q

What are the congenital qualitative disorders of defective platelet function?

A

Disorders of platelet secretion

  • Normal aggregation with ADP or collagen, but impariment of responses by secretion of prostaglandins or release of ADP
  • STORAGE POOL DISEASES
40
Q

How is it more commona to get defective platelets?

A

ACQUIRED DEFECTS

41
Q

What are the 2 acquired defects for platelet function mentioned?

A
  1. NSAIDS- Suppress cyclooxygenase and block prostaglandin/thromboxane production
  2. Uremia: Via end stage renal failure

HemOnc (8 decks)

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