Haematology Flashcards

1
Q

If DVT is likely (Wells score 2 points or more)

A

Offer a proximal leg vein ultrasound scan with the result available within 4 hours if possible.

If the scan cannot be carried out within 4 hours of being requested, offer a D-dimer test, then interim therapeutic anticoagulation and a proximal leg vein ultrasound scan with the result available within 24 hours.

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2
Q

If DVT is unlikely (Wells score 1 point or less

A

offer a D-dimer test with the result available within 4 hours if possible. If the D-dimer result cannot be obtained within 4 hours, offer interim therapeutic anticoagulation while awaiting the result.
If the D-dimer test is positive, offer a proximal leg vein ultrasound scan with the result available within 4 hours.
If the result cannot be obtained within 4 hours, offer interim therapeutic anticoagulation and a proximal leg vein ultrasound scan with the result available within 24 hours.
If the D-dimer test is negative:
Stop interim therapeutic anticoagulation.
Consider an alternative diagnosis.

Advise the person that it is unlikely they have DVT, but they should be aware of the signs and symptoms of DVT and seek medical help if symptoms worsen or they experience chest pain or breathing difficulties.

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3
Q

If interim therapeutic anticoagulation is indicated:

A

Offer apixaban or rivaroxaban first-line, considering comorbidities, contraindications, the person’s preferences, and local protocols.
If apixaban or rivaroxaban are unsuitable, consider:
Low molecular weight heparin (LMWH) for at least 5 days, followed by dabigatran or edoxaban, or
LMWH alongside a vitamin K antagonist (warfarin) for at least 5 days.
Perform baseline blood tests, including full blood count, renal and hepatic function, prothrombin time (PT), and activated partial thromboplastin time (APTT).

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4
Q

Drug causes of pancytopaenia

A

cytotoxics
antibiotics: trimethoprim, chloramphenicol
anti-rheumatoid: gold, penicillamine
carbimazole*
anti-epileptics: carbamazepine
sulphonylureas: tolbutamide

*causes both agranulocytosis and pancytopaenia

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5
Q

G6PD deficiency mode of inheritence

A

X-linked recessive fashion

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6
Q

Summary of GDPD deficiency pathophysiology

A

NADPH is important for converting oxidizied glutathine back to it’s reduced form
reduced glutathine protects red blood cells from oxidative damage by oxidants such as superoxide anion (O2-) and hydrogen peroxide

↓ G6PD → ↓ reduced NADPH → ↓ reduced glutathione → increased red cell susceptibility to oxidative stress

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7
Q

Drugs causing haemolysis in G6PD deficiency

A

anti-malarials: primaquine
ciprofloxacin
sulph- group drugs: sulphonamides, sulphasalazine, sulfonylureas

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8
Q

Hodgkin’s lymphoma

A

malignant proliferation of lymphocytes characterised by the presence of the Reed-Sternberg cell.

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9
Q

Features of Hodgkin’s lymphoma

A

lymphadenopathy (75%)
most commonly in the neck (cervical/supraclavicular) > axillary > inguinal
usually painless, non-tender, asymmetrical
alcohol-induced lymph node pain is characteristic of Hodgkin’s lymphoma but is seen in less than 10% of patients
systemic - ‘B symptoms’ (25%)
weight loss
pruritus
night sweats
fever (Pel-Ebstein)
other possible presentations include a mediastinal mass
may be symptomatic (e.g. cough) or found incidentally on a chest x-ray

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10
Q

Immune (or idiopathic) thrombocytopenic purpura (ITP)

A

an immune-mediated reduction in the platelet count. Antibodies are directed against the glycoprotein IIb/IIIa or Ib-V-IX complex.

Children with ITP usually have an acute thrombocytopenia that may follow infection or vaccination. In contrast, adults tend to have a more chronic condition.

symptomatic patients may present with
petechiae, purpura
bleeding (e.g. epistaxis)
catastrophic bleeding (e.g. intracranial) is not a common presentation

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11
Q

Von Willebrand’s disease inheritence

A

majority of cases are inherited in an autosomal dominant fashion*

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12
Q

Role of von Willebrand factor

A

large glycoprotein which forms massive multimers up to 1,000,000 Da in size
promotes platelet adhesion to damaged endothelium
carrier molecule for factor VIII

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13
Q

Investigation results for von Willebrand disease

A

Investigation
prolonged bleeding time
APTT may be prolonged
factor VIII levels may be moderately reduced
defective platelet aggregation with ristocetin

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14
Q

Management of von Willebrand disease

A

tranexamic acid for mild bleeding
desmopressin (DDAVP): raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells
factor VIII concentrate

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15
Q

Post-thrombotic syndrome - symptoms/signs

A

painful, heavy calves
pruritus
swelling
varicose veins
venous ulceration

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