PLT Flashcards

(20 cards)

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

vwf acts on 1b (assisted by ristocetin), collagen acts on 1a, fibrinogen acts on 2b3a (assisted by ADP through P2Y12), that’s why when only ristocetin is added, the plt aggregation can’t happens due to defective 1b in case of bss

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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)

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