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COMLEX 2 > Platelet Disorders > Flashcards

Platelet Disorders Flashcards

1
Q

Bernard-Soulier syndrome platelet count

A

-/decrease

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2
Q

Bernard-Soulier syndrome bleeding time

A

increase

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3
Q

defect in platelet plug formation ->

A

increase bleeding time

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4
Q

platelet abnormalities ->

A

micro hemorrhage: mucus membrane bleeding, epistaxis, petechiae, purpura, increase bleeding time, possibly decreased platelet count

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5
Q

Bernard-Soulier syndrome mechanism

A

defect in platelet plug formation

large platelets

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6
Q

Bernard-soulier syndrome comments

A

decrease GpIb -> defect in platelet-to-vWF adhesion

abnormal ristocetin test that does not correct with mixing studies

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7
Q

Glanzman thrombasthenia platelet count

A

–

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8
Q

Glanzmann thrombasthenia bleeding time

A

increase

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9
Q

Glanzmann thrombasthenia mechanism

A

defect in platelet intern αIIb ß3 (GpIIb/IIIa) -> defect in platelet-to-platelet aggregation, and therefore platelet plug formation

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10
Q

Glanzmann thrombasthenia labs

A

blood smear shows no platelet clumping

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11
Q

HUS platelet count

A

decrease

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12
Q

HUS bleeding time

A

increase

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13
Q

HUS characterized by

A

thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure

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14
Q

HUS presentation

A

typical HUS seen in children, accompanied by diarrhea and commonly caused by Shira-like toxin of EHEC
HUS in adults does not present with diarrhea; EHEC infection not required

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15
Q

immune thrombocytopenia platelet count

A

decrease

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16
Q

immune thrombocytopenia bleeding time

A

increase

17
Q

immune thrombocytopenia mechanism

A

anti-GpIIb/IIIa antibodies -> splenic macrophage consumption of platelet-antibody complex
may be primary or secondary to autoimmune disorder, viral illness, malignancy, or drug reaction

18
Q

immune thrombocytopenia labs

A

increase megakaryocytic on bone marrow biopsy

19
Q

immune thrombocytopenia treatment

A

steroids, IVIG

rituximab or splenectomy for refractory ITP

20
Q

TTP platelet count

A

decrease

21
Q

TTP bleeding time

A

increase

22
Q

TTP mechanism

A

inhibition or deficiency of ADAMTS 13 (vWF metalloprotease) -> decrease degradation of vWF multimers

23
Q

TTP pathogenesis

A

increase large vWF multimers -> increase platelet adhesion -> increase platelet aggregation and thrombosis

24
Q

TTP labs

A

schistocytes, increase LDH, normal coagulation parameters

25
Q

TTP symptoms

A

FAT RN

pentad of Fever, microangiopathic hemolytic Anemia, Thrombocytopenia, Renal failure, Neurologic symptoms

26
Q

TTP treatment

A

plasmapheresis, steroids

27
Q

von willebrand disease platelet count

A

normal

28
Q

vWD bleeding time

A

increase

29
Q

vWD PT

A

normal

30
Q

vWD PTT

A

normal or increased

31
Q

vWD mechanism

A

intrinsic pathway coagulation defect: decrease vWF -> increase PTT (vWF acts to carry/protect factor VIII)
defect in platelet plug formation: decrease vWF -> defect in platelet-to-vWF adhesion
autosomal dominant

32
Q

vWD treatment

A

desmopressin, which releases vWF stored in endothelium

33
Q

DIC platelet count

A

decrease

34
Q

DIC bleeding time

A

increase

35
Q

DIC PT

A

increase

36
Q

DIC PTT

A

increase

37
Q

DIC mechanism

A

widespread activation of clotting -> deficiency in clotting factors -> bleeding state

38
Q

causes of DIC

A

Sepsis (gram negative), Trauma, Obstetric complications, acute Pancreatitis, Malignancy, Nephrotic syndrome, Transfusion
(STOP Making New Thrombi)

39
Q

DIC labs

A

schistocytes, increase fibrin degradation products (D-Dimers), decrease fibrinogen, decreas factors V and VIII

COMLEX 2 (37 decks)

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