PLT Flashcards

1
Q

Why can splenectomy cause high PLT? (1)

A

Spleen normally sequester PLT, removal of spleen causes less PLT being removed, leading to high PLT

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2
Q

Why can aspirin prevent PLT aggregation? (2)

A

Inhibit COX, prevent formation of TXA2

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3
Q

Name 2 main players in PLT adhesion (2)

A

vWF & GPIb

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4
Q

Why in vWF disease, APTT will increase? (1) Is PLT decreasing in vWF disease? (1)

A

Factor 8 is vWF dependent & involved in APTT cascade
PLT usually normal in patient with vWF disease

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5
Q

Give 4 distinctive results to diagnose BSS (3) What exactly is BSS? (1) How about GT? (1)

A

Low PLT
Giant PLT
Normal ADP & Collegen & Epi, Abnormal Ristocetin (same for vWFD, reverse for GT)
CD42b- by flow cytometry (CD41/61- for GT)

BSS is GPIb (vWFR) deficiency
GT is GPIIb/IIIa (FIBR) deficiency

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6
Q

Why do some patients develop ITP? (1)

A

Viral infection

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7
Q

ADAMTS13 result is not available yet, how can you tell if the patient is having TTP or DIC? (1)

A

PT/APTT is abnormal in DIC but normal in TTP

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8
Q

HDFN has Antibody targeting RBC, is there a condition targeting PLT? (1)

A

anti-HPA1a
Also occur after transfusion

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9
Q

State 5 signs of TTP & HUS (5) Which sign is more common in TTP, HUS respectively? (2)

A

FATRN (Fever, Anaemia, Thrombocytopenia, Renal failure, Neurological symptoms)
Neurological symptoms in TTP
Renal failure in HUS

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10
Q

What are Storage pool deficiencies? (1)

A

PLT granule deficiency causing decreased release of ADP, ATP, calcium, and serotonin
ATP release can be measured by Lumi-aggregation

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11
Q

How can TTP be acquired? (1)

A

Anti-ADAMTS13

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12
Q

What is Hereditary hemorrhagic telangiectasia (HHT)? (2)

A

AD, Abnormal blood vessels leading to bleeding
Adolescence who have Nose bleed everyday
Can progress to stroke & HF

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13
Q

TXA2 stimulates PLT aggregation, what inhibits PLT aggregation? (1)

A

Prostacyclin from endothelial cell

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14
Q

You see agranular PLT in FR, what would you suspect? (1)

A

Gray’s syndrome (Alpha granule deficiency)

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15
Q

Instead of taking aspirin, the patient was prescribed clopidogrel/prasugrel as antiPLT, how to monitor its effect? (1)

A

irreversibly binding to P2Y12 (ADP R)
whole blood test using ADP as agonist
Report as % P2Y12 inhibition

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16
Q

The main use of platelet aggregometer, Lumi-aggregometer, VerifyNow, PFA-100 (4)

A

platelet aggregometer: BSS vs GT
Lumi-aggregometer: PLT granule deficiency
VerifyNow: monitor P2Y12 inhibitor like clopidogrel
PFA-100: Screening, collagen/EPI&raquo_space; collagen/ADP (If EPI+ADP- suspect aspirin)

17
Q

Which agonist gives a monophasic response? (1)

A

Collagen

18
Q

We give low dose Aspirin to elderly who is at risk of thrombosis, why?(1)

A

Aspirin is anti-pain and fever at high dose, and just anti-platelet at low dose

19
Q

Why steroid and montelukast are both effective in relieving asthma?

A

Steroid prevent AA formation so downstream leukotrienes are no produced. Montelukast act on leukotriene R so its bronchoconstriction effect is not expressed.

20
Q

Why COX2 inhibitor is desirable in pain killing? (3)

A

It prevents gastric ulcer, renal failure, thrombotic risk associated with steroid and non-selective NSAID