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STEP Pathology > deck_4988687 > Flashcards

deck_4988687 Flashcards

1
Q

Which one of the following drugs does not increase the risk of bleeding?1. Aspirin2. Clopidogrel3. Ibuprofen4. Acetaminophen

A

4.

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2
Q

A 25 year female is evaluated by you for easy bruisability. She has no h/o epistaxis or menorrhagia. Has a brother who also has easy bruising, no other family with bleeding tendency. She has her wisdom teeth extracted with no bleeding two months ago. On exam you note a high arched palate, and she is double jointed. Her Platelet count, FVIII level, vonwillebrand ag, vonwillebrand activity, PT and PTT are normal. Her likely diagnosis is:a. Von Willebrand’s diseaseb. ITPc. Hemophilia Ad. Likely non hematologic cause such as a collagen disorder.

A

D.

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3
Q

Workup of a bleeding patient begins with what?

A

personal history of bleeding and family history

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4
Q

Which of the following is NOT a sign of bleeding?1.Purpura2.Petechiae3.Ecchymoses4.Hemarthrosis (bleeding into joints)5.Gangrene

A

5.

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5
Q

What are some collagen disorders with bleeding?

A

-ehlers danlos-osteogenesis imperfecta

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6
Q

What are some possible causes of thrombocytopenia?

A

-decreased production-increased destruction-increased sequestration-other

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7
Q

What are some causes of decreased production of platelets?

A

-aplastic anemia-chemo/drugs (alcohol too)-nutritional deficiency (B12, B6, Folic acid)-congenital bone marrow failure (Falconi, Wiskott-Aldrich)-chloramphenicol

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8
Q

What are some causes of increased destruction of platelets (thrombocytopenia)?

A
  • immune mediated (hep C, HIV, drug induced)- cross reactivity of antibodies to another virus (H. pylori and clymdia common). Since viruses trigger it, removal of the virus can be a good treatment)- heparin-induced thrombocytopenia (F4 antibodies formed)- DIC, TTP
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9
Q

What is once thing that is released when platelets aggregate?

A

platelet phospholipid (PF3), on which the clot begins to form

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10
Q

Dental bleeding, menorrhagia, and tonsillar bleeding indicate what?

A

problems with platelets or vMF

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11
Q

Post operative bleeding, spontaneous hematomas, or joint bleeding indicate what?

A

problems with the clotting system/factors

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12
Q

T or F. Factor XII deficiency does not cause any bleeding

A

T. And can on some occasions actually lead to thrombosis

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13
Q

What is MPV on a CBC?

A

mean platelet volume- sometimes slightly larger platelet sizes even with lower numbers is enough to form a clot

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14
Q

What should you consider if platelet counts are low?

A
  • bone marrow examination- platelet antibodies- screening for DIC
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15
Q

What should you consider if platelet counts are normal after looking at a smear?

A
  • platelet aggregation studies with agonists such as ADP, adrenaline, collagen, and ristocetin (PFA (platelet closing time)-100)-other special platelet studies, e.g. adhesion studies, nucleotide pool measurement- vMF assay/ FVIII assay
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16
Q

What would a prolonged closing time indicate?

A

a defect in platelet function or vMF diseasenormal 120-130 (runs a stream of platelets through a tube and aggregation closes it off)

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17
Q

What things could cause a normal PTT and a long PT?

A

-liver disease-warfarin-vitamin K deficiency-low Factor VII/defect

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18
Q

What things could cause a long PTT and a normal PT?

A

-Heparin-Lupus anticoagulant (APS)-Low VIII, IX, XI, or XII-Low HMWK/prekallikrein-DIC

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19
Q

What things could cause a long PT and a long PTT?

A

-liver disease-warfarin at high levels -vitamin deficiency-low factor V or X-low fibrinogen/prothrombin-citrate effect due to high HCT (artifact due to citrate being to high)

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20
Q

What is a normal bleeding time?

A

1-6 min

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21
Q

What is a normal PTT?normal PT?

A

25-35 sec11-15 sec

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22
Q

What should you do if PT or PTT is abnormal?

A

first make sure its not an artifact and repeat testing

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23
Q

What is PT or PTT is still abnormal?

A

review history and if still confused do a mixing study- add normal plasma and see if it corrects. If you have a factor deficiency when you do the mixing study, you see a correction. If you have a coagulation inhibitor (antibodies to something in the clotting system), it will not correct

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24
Q

What should you do if you do the mixing study and it corrects?

A

clotting factor assays to id deficiency and a clinical correlation to determine whether deficiency is congenital or acquired

25
Q

What should you do if you do the mixing study and it doesn’t correct?

A

think inhibitor- further testing is needed

26
Q

What happens in antiphospholipid syndrome?

A

antibodies against platelet phospholipids prevent clotting (increased PTT) yet the antibodies attack the endothelium leading to a hyper-coagulable state and a thrombophilia

27
Q

What deficiency would be suggested by delayed (6-9 hrs) bleeding?

A

XIII deficiency- common after dental extractions

28
Q

What happens in May-Heggin anomaly?

A

you make larger but less platelets leading to a thrombocytopenia (Bernard Soulier is similar)

29
Q

What happens in gestational thrombocytopenia?

A

In 2-3rd trimester of pregnancy, placenta expands and platelets are essentially diluted out so a thrombocytopenia exists even though number and function is good

30
Q

What effect does iron deficiency have on platelets?

A

leads to thrombocytosis usually

31
Q

What happens in heparin-induced thrombocytopenia?

A

antibodies against factor IV are formed in the presence of heparin which paradoxically ACTIVATE platelets (so clots can form!!), clump them, and then clear them from circulation

32
Q

What is thrombotic microangiopathy (things like TTP, HUS, aHUS)?

A

platelets are activated (complement mediated (aHUS), or toxin induced) and cleared (so again, these are paradoxic in the sense that platelets are activated and micro thrombi can form even though they are cleared leading to a thrombocytopenia)

33
Q

What is DIC?

A

micro-thrombi found yet platelets are reduced-paradoxic

34
Q

What is vMF type 2B?

A

vMF is so excitable and sticks to platelets and sucks them out of circulation leading to thrombocytopenia

35
Q

What happens in hemophagocytosis?

A

macrophages become activated following infection (CMV common) and digest active elements of the blood including platelets leading to thrombocytopenia

36
Q

How does uremia cause platelet dysfunction (but not decreased numbers)?

A

when urea is high it ametifies the receptors on platelets and denature them

37
Q

T or F. In MDS platelets are abnormal functionally

A

T. In MPN they are defective too even though a thrombocytosis exists

38
Q

If you look on a bone marrow smear and see large platelets with high MPV it indicates what?

A

since young platelets are large and accounting for this, this indicates a consumptive processbone marrow exam is usually not indicated

39
Q

What causes immune thrombocytopenia (ITP)?

A

Not clear- combo of B and T cell mediated antibodies and they bind platelets and are taken up by the RES

40
Q

What should you do if you get an abnormal platelet closing time?

A

order a platelet aggregation study

41
Q

If you have a normal platelet count but an abnormal bleeding time, what should you think of?

A
  • aspirin- uremia- VMF disease
42
Q

What does PTT gauge?

A

XII, XI, IX, and VIII defects

43
Q

If your mixing study does not correct (aka inhibitor) and you’re not bleeding, what is most likely?

A

lupus anticoagulant (APS)- other factor inhibitor drugs

44
Q

If your mixing study does not correct and you’re bleeding/bruising, what is most likely?

A

factor VIII inhibitor

45
Q

What is the most common bleeding disorder?

A

vMF disease. then hemo A, then B

46
Q

What population is factor XI deficiency common in?

A

Ashkenawi Jew

47
Q

How can you distinguish factor VIII deficiency and vMF disease?

A

vMF is AR and Hemo A is X-linkedboth have prolonged PTT and low FVIII levels vMF has a prolonged bleeding timeonly FVIII defic has normal vMF levels

48
Q

Where is vMF disease bleeding common?

A

mucosal bleeding

49
Q

Where is FVIII bleeding common?

A

hemarthrosis and hematoma

50
Q

How is Hemo A treated?

A

DDAVP for mild- increases vMF and VIII (not effective for IX)severe- factor concentrate, not cryoprecipitate

51
Q

How is Hemo B treated?

A

factor concentrates

52
Q

What is Rosenthal’s disease?

A

FXI deficiency

53
Q

How is Rosenthal’s treated?

A

no FXI concentrate available, so FFP (fresh frozen plasma) is used

54
Q

How is vMF disease treated?

A

-factor VIII concentrate-DDAVP

55
Q

How is lupus anticoagulant testing done?

A

dilute russel viper venom test (DRWT)- activates antibodies

56
Q

Coagulopathy of liver disease causes what?

A

causes thrombophilia and bleeding in the same settingcauses thrombocytopenia, decreased production of clotting factors, increased fibrinolytic activity, dysfibrinogenemia, vitamin K deficiencybut it activates FVIII too!!

57
Q

Which factors are affected by liver disease?

A

V, VII, and X

58
Q

Which factors are affected by vitamin K deficiency?

A

VII and X

59
Q

Which factors are affected by DIC?

A

V, VII, VIII, and X

STEP Pathology (80 decks)

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