Platelets & bleeding disorders flashcards
18 high-yield MRCP Part 1 cards from the Intellect Medicos Haematology & Oncology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
Study these 18 cards Save progress — free account
-
What is first-line treatment for immune thrombocytopenia (ITP) when treatment is needed?
Show answer
Corticosteroids (e.g. prednisolone); IVIG when a rapid platelet rise is needed.
Why? ITP is caused by autoantibodies against platelet glycoproteins (GPIIb/IIIa, GPIb/IX); steroids and IVIG reduce platelet destruction.
-
What is the urgent first-line treatment of thrombotic thrombocytopenic purpura (TTP)?
Show answer
Plasma exchange plus corticosteroids (with caplacizumab and rituximab).
Why? Plasma exchange removes the anti-ADAMTS13 antibodies and replaces the enzyme, stopping vWF-driven microthrombi.
-
Which blood test confirms TTP?
Show answer
ADAMTS13 activity assay — activity below 10%.
Why? ADAMTS13 normally cleaves ultra-large vWF multimers; without it, platelets clump in small vessels.
-
What is the mechanism of caplacizumab in TTP?
Show answer
An anti-von Willebrand factor nanobody that stops vWF binding to platelets.
Why? It halts platelet microthrombus formation while plasma exchange and immunosuppression take effect.
-
In DIC with bleeding, which blood product is given when fibrinogen is below 1.5 g/L?
Show answer
Cryoprecipitate.
Why? Cryoprecipitate is a concentrated source of fibrinogen (plus FVIII, FXIII and vWF).
-
A patient with type 1 von Willebrand disease needs a dental extraction. What is the usual haemostatic cover?
Show answer
Desmopressin (DDAVP) before the procedure plus tranexamic acid.
Why? DDAVP releases stored vWF and factor VIII from endothelial Weibel–Palade bodies; type 1 is a partial deficiency, so it responds well.
-
Haemophilia A is deficiency of ______ and haemophilia B (Christmas disease) of ______; both are inherited as X-linked recessive disorders.
Show answer
factor VIII; factor IX
Why? Both prolong the APTT with a normal PT and platelet count; haemarthroses are typical.
-
Haemophilia A is deficiency of factor VIII and haemophilia B (Christmas disease) of factor IX; both are inherited as ______ disorders.
Show answer
X-linked recessive
Why? Both prolong the APTT with a normal PT and platelet count; haemarthroses are typical.
-
How does emicizumab work in haemophilia A?
Show answer
A bispecific monoclonal antibody that bridges activated factor IX and factor X, mimicking factor VIII.
Why? It replaces the missing cofactor function and still works when factor VIII inhibitors are present; it is given subcutaneously as prophylaxis.
-
What is the mechanism of action of tranexamic acid?
Show answer
Antifibrinolytic: it binds plasminogen and blocks its conversion to plasmin.
Why? Less plasmin means clots are broken down more slowly — useful in heavy menstrual bleeding, dental bleeding, epistaxis and trauma.
-
Giant platelets plus abnormal ristocetin-induced aggregation that does NOT correct with normal plasma suggest which disorder?
Show answer
Bernard–Soulier syndrome (GPIb-IX-V deficiency).
Why? Platelets lack the receptor for vWF, so they cannot adhere — adding normal plasma (vWF) does not help.
-
How do eltrombopag and romiplostim raise the platelet count in ITP?
Show answer
They are thrombopoietin (TPO) receptor agonists that stimulate megakaryocytes to produce more platelets.
Why? They are second-line options for persistent or chronic ITP; eltrombopag is oral and romiplostim is a weekly subcutaneous injection.
-
Which subtype of von Willebrand disease causes thrombocytopenia, and why?
Show answer
Type 2B — the abnormal vWF has increased affinity for platelet GPIb, so platelets bind it and are cleared.
Why? This gain-of-function vWF binds platelets spontaneously; the complexes are removed, lowering both the platelet count and large vWF multimers.
-
A man with haemophilia A stops responding to factor VIII infusions. Which assay detects and quantifies the cause?
Show answer
Bethesda assay (measures factor VIII inhibitor titre).
Why? Some patients develop neutralising alloantibodies (inhibitors) to infused factor VIII; the Bethesda assay measures their strength.
-
Is desmopressin (DDAVP) useful in haemophilia B?
Show answer
No — DDAVP releases stored factor VIII and vWF, not factor IX. Haemophilia B is treated with factor IX concentrate.
Why? Desmopressin acts on endothelial stores (Weibel–Palade bodies), so it only helps mild haemophilia A and type 1 vWD.
-
NICE platelet transfusion thresholds: prophylactic transfusion if platelets are below ______ × 10⁹/L (reversible marrow failure, no bleeding); transfuse for clinically significant bleeding if below 30 × 10⁹/L.
Show answer
10
Why? Thresholds balance bleeding risk against the risks of transfusion (platelets carry the highest bacterial contamination risk).
-
NICE platelet transfusion thresholds: prophylactic transfusion if platelets are below 10 × 10⁹/L (reversible marrow failure, no bleeding); transfuse for clinically significant bleeding if below ______ × 10⁹/L.
Show answer
30
Why? Thresholds balance bleeding risk against the risks of transfusion (platelets carry the highest bacterial contamination risk).
-
What is the targeted treatment for atypical (complement-mediated) haemolytic uraemic syndrome?
Show answer
A terminal complement C5 inhibitor — eculizumab (or ravulizumab).
Why? Atypical HUS is driven by uncontrolled alternative-pathway complement activation (e.g. factor H, factor I or MCP mutations); blocking C5 stops the thrombotic microangiopathy.