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Year 3 OSCE > Miscellaneous Haematology > Flashcards

Miscellaneous Haematology Flashcards

1
Q

Antiphospholipid syndrome

A

Acquired disorder characterised by a hypercoaguable state

May be a primary disorder or secondary to SLE

Causes a paradoxical rise in APTT

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2
Q

Features of antiphospholipid syndrome

A

Venous or atrial thrombosis
Recurrent foetal loss
Livedo reticularis
Thrombocytopenia
Prolonged APTT
Pre eclampsia, pulmonary HTN

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3
Q

Antibodies associated with AP syndrome

A

Lupus anticoagulant
Anticardiolipin antibodies
Anti beta 2 glycoprotein I antibodies

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4
Q

Management of AP syndrome

A

Primary (no previous thrombi)- low dose aspirin

Secondary- lifelong warfarin with INR 2-3 (if continued add low dose aspirin and raise to 3-4)

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5
Q

Management of AP syndrome in pregnancy

A

Low dose aspirin when pregnancy confirmed
LMWH when foetal heart detected (stop at 34 weeks)

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6
Q

Non haemolytic febrile reaction

A

Fever, chills

Slow/stop the transfusion, paracetamol, monitor

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7
Q

Minor allergic reaction

A

Pruritus, urticaria

Temporarily stop the infusion, antihistamine, monitor

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8
Q

Anaphylaxis

A

Patients with IgA deficiency who have anti IgA antibodies

Hypotension, dyspnoea, wheezing, angioedema

Stop transfusion, IM adrenaline, ABC support

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9
Q

Acute haemolytic reaction

A

Fever, abdominal pain, hypotension, dark urine (3 hours post-transfusion)

ABO incompatible blood (human error). IgM destruction of RBC’s

Stop, send blood for Coombs test, repeat cross matching, supportive care

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10
Q

Transfusion associated circulatory overload

A

Pulmonary oedema, HTN

Slow transfusion, IV loop diuretics and oxygen

NB- The normal central venous pressure (normal = 0- 6 mmHg) is less consistent with fluid overload.

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11
Q

Transfusion related acute lung injury

A

Hypoxia, pulmonary infiltrates on CXR, fever, hypotension

Stop, oxygen and supportive care

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12
Q

Irradiated blood products

A

Depleted of T lymphocytes
Avoid transfusion associated graft versus host disease

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13
Q

Immune thrombocytopenia purpura

A

Immune mediated reduction in platelet count
Kids- often following an infection or vaccination
Adults- more chronic condition

Megakaryocytes in the bone marrow

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14
Q

ITP Features

A

Petechiae
Purpura
Bleeding
Catastrophic bleeding is rare
Type II hypersensitivity reaction

NB- can have anaemia alongside it (esp. if someone is bleeding)

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15
Q

Management of ITP

A

Emergency treatment: life-threatening or organ threatening bleeding: Platelet transfusion, IV methylprednisolone and intravenous immunoglobulin

Otherwise, PO steroids

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16
Q

Thrombotic thrombocytopenia purpura

A

ADAMST13
Platelet clots form in vessels leaving blood unable to clot so liable to bleed
Features
-fever
-fluctuating neuro signs (microemboli)
-microangiopathic haemolytic anaemia
-thrombocytopenia
-renal failure

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17
Q

Causes of TTP

A

Post infection (urinary, GI)
Pregnancy
Drugs- ciclosporin, OCP, penicillin
Tumours
SLE
HIV

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18
Q

Disseminated intravascular coagulation

A

Dysregulation of coagulation and fibrinolysis, leading to widespread clotting and resultant bleeding
TF released

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19
Q

Causes of DIC

A

Sepsis
Trauma
Obstetric complications eg. Amniotic fluid embolism or HELLP syndrome
Malignancy

NB- manage with FFP and cryoprecipitate

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20
Q

Typical blood picture of DIC

A

Decreased platelets
Decreased fibrinogen
Increased PT and APTT
Increased fibrinogen degradation products
Schistocytes due to microangiopathic haemolytic anaemia

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21
Q

Management of TTP

A

Plasma exchange
Steroids
Rituximab

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22
Q

Heparin induced thrombocytopenia

A

Antibodies developed against platelets in response to heparin

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23
Q

Features diagnosis and management of HIT

A

Antibodies activate a hypercoaguable state causing thrombosis and break down platelets causing thrombocytopenia (also hyperkalaemia)- A PROTHROMBITIC STATE

Diagnosis- HIT antibodies in blood

Management- switch to a different AC (eg. a direct thrombin inhibitor such as argatroban)

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24
Q

Acute graft versus host disease (GVHD)

A

Within 100 days of transplantation

Painful maculopapular rash (progress to toxic epidermal necrosis)
Jaundice
Watery or bloody diarrhoea
N and v
Culture negative fever

Steroids

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25
Q

Chronic GVHD

A

100 days after transplantation
Can arise after cute disease or de novo

Scleroderma, vitiligo
Conjunctivitis, corneal ulcers, scleritis
Dysphagia, oral ulcers and lichenous changes
Obstructive or restrictive lung disease

IV steroids

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26
Q

Features of hereditary angioedema

A

Attacks preceded by painful macular rash
Painless, non pruritic swelling of subcutaneous tissues
May effect upper airway, skin, or abdominal organs

27
Q

Management of hereditary angioedema

A

Acute- IV C1 inhibitor concentrate, FFP
Prophylaxis- anabolic steroid (danazol)

28
Q

Causes of hyposplenism

A

Splenctomy
Sickle cell
Coeliac disease
Graves’ disease
SLE
amyloid

29
Q

Lead poisoning features

A

Abdominal pain
Peripheral neuropathy (mainly motor)
Fatigue
Constipation
Blue limes on gum margin

30
Q

Management of lead poisoning

A

Chelating agents

DMSA
EDTA
Dimercapol
D pencillamine

31
Q

Management of neutropenic sepsis

A

Don’t wait for bloods, start antibiotics
Piperacillin and taxaobactam

But in meningitis, if LP can be done in an hour, do that, then ABX

32
Q

Polycythaemia rubra Vera

A

Myeloproliferative disorder, often overproduction of RBC’s, neutrophils, platelets

JAK2 mutation

Older people

33
Q

Features of PRV

A

Hyperviscosity, pruritus (after hot bath), Splenomegaly, haemorrhage, plethoric appearance, HTN, low ESR

34
Q

Tests for PRV

A

FBC (raised cell numbers)
JAK2 mutation
Serum ferritin
UE LFT

35
Q

Differentiate true (primary or secondary) and relative polycythaemia

A

Red cell mass studies

36
Q

PRV Management

A

Aspirin
Regular venesection/ phlebotomy
Chemotherapy

NB- thrombotic events can be a cause of mortality and a proportion will progress to Myelofibrosis and acute leukaemia

37
Q

Causes of Splenomegaly

A

Myelofibrosis
Haematological malignancy
Malaria
Portal hypertension secondary to cirrhosis
Haemolytic anaemia eg. hereditary spherocytosis
Thalassaemia
Rheumatoid arthritis (RA)
EBV

38
Q

Essential thrombocytosis

A

Myeloproliferative disorder which overlaps with CML, PRV, and Myelofibrosis

39
Q

Features of thrombocytosis

A

Increased platelet count
Thrombosis and haemorrhage seen
Burning sensation in the hands
JAK2 mutation

40
Q

Management of thrombocytosis

A

Hydroxyurea
Aspirin
Interferon alpha

41
Q

Administration of TXA

A

IV bolus followed by an infusion in cases of major haemorrhage

42
Q

What is the most common inherited bleeding disorder?

A

VWD- autosomal dominant inheritance

43
Q

Rouloux formation

A

Myeloma

44
Q

Post thrombotic syndrome

A

Painful heavy calves
Itching
Swelling
Varicose veins
Venous ulceration

Treat with compression stockings and elevated legs

45
Q

Direct vs indirect Coomb’s test

A

Direct- autoimmune haemolysis (spherocytes in haemolytic anaemia)
Indirect- haemolytic disease of the newborn

46
Q

Antiplatelet therapy and dental surgery

A

Antiplatelet therapy shouldn’t not be changed

47
Q

Indications for platelet transfusion in active bleeding

A

Platelet count of <30 x 10 9 and clinically significant bleeding eg. haematemesis, melaena, prolonged epistaxis

Or platelet count of < 100 x 10 9 for patients with severe bleeding, or bleeding at critical sites, such as the CNS

NB- higher risk of bacterial contamination than other blood products

48
Q

Indications for platelet transfusion if no active bleeding

A

Platelet count of 10 x 10 9 except where platelet transfusion is contraindicated or there are alternative treatments for their condition

For example, do not perform platelet transfusion for any of the following conditions:
Chronic bone marrow failure
Autoimmune thrombocytopenia
Heparin-induced thrombocytopenia, or
Thrombotic thrombocytopenic purpura.

49
Q

Platelet levels to aim for prior to surgery/ invasive procedure

A

> 50×109/L for most patients
50-75×109/L if high risk of bleeding
100×109/L if surgery at critical site

NB- don’t get platelet level and Hb level confused

50
Q

Cryoprecipitate

A

Factor VIII
Fibrinogen
von Willebrand factor
Factor XIII

Blood product made from plasma
Usually transfused as 6 unit pool
Indications include massive haemorrhage and uncontrolled bleeding due to haemophilia

51
Q

Acquired haemophilia

A

Factor 8 acquired disorder. The elderly, pregnancy, malignancy and autoimmune conditions are associated with acquired haemophilia. Prolonged APTT is key to the diagnosis. Management involves steroids.

52
Q

Drug induced thrombocytopenia

A

quinine
abciximab
NSAIDs
diuretics: furosemide
antibiotics: penicillins, sulphonamides, rifampicin
anticonvulsants: carbamazepine, valproate
heparin

NB- if not one of these drugs and an isolated thrombocytopenia in a well person, think ITP

53
Q

Blood loss in surgery

A

Unlikely- Group and save
Hysterectomy (simple), appendicectomy, thyroidectomy, elective lower segment caesarean section, laparoscopic cholecystectomy

Likely- Cross-match 2 units
Salpingectomy for ruptured ectopic pregnancy, total hip replacement

Definite- Cross-match 4-6 units
Total gastrectomy, oophorectomy, oesophagectomy, Elective AAA repair, cystectomy, hepatectomy

54
Q

Amyloidosis

A

amyloidosis is a term which describes the extracellular deposition of an insoluble fibrillar protein termed amyloid
amyloid is derived from many different precursor proteins
in addition to the fibrillar component, amyloid also contains a non-fibrillary protein called amyloid-P component, derived from the acute phase protein serum amyloid P
other non-fibrillary components include apolipoprotein E and heparan sulphate proteoglycans
the accumulation of amyloid fibrils leads to tissue/organ dysfunction

Classification
systemic or localized

Diagnosis
Congo red staining: apple-green birefringence
serum amyloid precursor (SAP) scan
biopsy of skin, rectal mucosa, or abdominal fat

55
Q

Porphyria cutanea tarda

A

Porphyria cutanea tarda is the most common hepatic porphyria. It is due to an inherited defect in uroporphyrinogen decarboxylase or caused by hepatocyte damage e.g. alcohol, hepatitis C, oestrogen.

Features
classically presents with photosensitive rash with blistering and skin fragility on the face and dorsal aspect of hands (most common feature)
hypertrichosis
hyperpigmentation

Investigations
urine: elevated uroporphyrinogen and pink fluorescence of urine under Wood’s lamp
serum iron ferritin level is used to guide therapy

Management
chloroquine
venesection (preferred if iron ferritin is above 600 ng/ml)

56
Q

Acute intermittent porphyria

A

Acute intermittent porphyria (AIP) is a rare autosomal dominant condition caused by a defect in porphobilinogen deaminase, an enzyme involved in the biosynthesis of haem. The results in the toxic accumulation of delta aminolaevulinic acid and porphobilinogen. It characteristically presents with abdominal and neuropsychiatric symptoms in 20-40-year-olds. AIP is more common in females (5:1)

The classical presentation is a combination of abdominal, neurological and psychiatric symptoms:
abdominal: abdominal pain, vomiting
neurological: motor neuropathy
psychiatric: e.g. depression
hypertension and tachycardia common

Diagnosis
classically urine turns deep red on standing
raised urinary porphobilinogen (elevated between attacks and to a greater extent during acute attacks)
assay of red cells for porphobilinogen deaminase
raised serum levels of delta aminolaevulinic acid and porphobilinogen

Management
avoiding triggers
acute attacks
IV haematin/haem arginate
IV glucose should be used if haematin/haem arginate is not immediately available

57
Q

Matching antigens in blood transfusions

A

HLA-DR, specifically HLA-DRB3/4/5, is the most important set of antigens to match.

B and A antigens are the next most important.

C and DQ are less important.

58
Q

Reticulocytes and chronic blood loss

A

In chronic blood loss, reticulocyte count would typically increase as the bone marrow produces more red blood cells.

59
Q

Folate vs B12 anaemia

A

Folate deficiency is a cause of macrocytic anaemia however it does not cause neurological symptoms such as peripheral neuropathy or confusion- B12/pernicious anaemia.

60
Q

Warfarin and emergency surgery

A

If surgery can wait for 6-8 hours - give 5 mg vitamin K IV

If surgery can’t wait - 25-50 units/kg four-factor prothrombin complex

61
Q

Warfarin and emergency surgery

A

If surgery can wait for 6-8 hours - give 5 mg vitamin K IV

If surgery can’t wait - 25-50 units/kg four-factor prothrombin complex

62
Q

Differentiate true polycythaemia (ie. PRV) from secondary

A

The patient in this example has a normal SpO2 and EPO which suggest that the polycythaemia is not secondary in nature. T

63
Q

Haemolysis and haptoglobins

A

low haptoglobins

64
Q

One way to differentiate Myeloid and Lymphocytic leukaemia’s

A

LL- usually raised lymphocytes
ML- raised myeloid lineage cells eg. neutrophils and thrombocytes (platelets)

Year 3 OSCE (61 decks)

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