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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
Chronic GVHD
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
26
Features of hereditary angioedema
Attacks preceded by painful macular rash Painless, non pruritic swelling of subcutaneous tissues May effect upper airway, skin, or abdominal organs
27
Management of hereditary angioedema
Acute- IV C1 inhibitor concentrate, FFP Prophylaxis- anabolic steroid (danazol)
28
Causes of hyposplenism
Splenctomy Sickle cell Coeliac disease Graves’ disease SLE amyloid
29
Lead poisoning features
Abdominal pain Peripheral neuropathy (mainly motor) Fatigue Constipation Blue limes on gum margin
30
Management of lead poisoning
Chelating agents DMSA EDTA Dimercapol D pencillamine
31
Management of neutropenic sepsis
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
Polycythaemia rubra Vera
Myeloproliferative disorder, often overproduction of RBC’s, neutrophils, platelets JAK2 mutation Older people
33
Features of PRV
Hyperviscosity, pruritus (after hot bath), Splenomegaly, haemorrhage, plethoric appearance, HTN, low ESR
34
Tests for PRV
FBC (raised cell numbers) JAK2 mutation Serum ferritin UE LFT
35
Differentiate true (primary or secondary) and relative polycythaemia
Red cell mass studies
36
PRV Management
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
Causes of Splenomegaly
Myelofibrosis Haematological malignancy Malaria Portal hypertension secondary to cirrhosis Haemolytic anaemia eg. hereditary spherocytosis Thalassaemia Rheumatoid arthritis (RA) EBV
38
Essential thrombocytosis
Myeloproliferative disorder which overlaps with CML, PRV, and Myelofibrosis
39
Features of thrombocytosis
Increased platelet count Thrombosis and haemorrhage seen Burning sensation in the hands JAK2 mutation
40
Management of thrombocytosis
Hydroxyurea Aspirin Interferon alpha
41
Administration of TXA
IV bolus followed by an infusion in cases of major haemorrhage
42
What is the most common inherited bleeding disorder?
VWD- autosomal dominant inheritance
43
Rouloux formation
Myeloma
44
Post thrombotic syndrome
Painful heavy calves Itching Swelling Varicose veins Venous ulceration Treat with compression stockings and elevated legs
45
Direct vs indirect Coomb's test
Direct- autoimmune haemolysis (spherocytes in haemolytic anaemia) Indirect- haemolytic disease of the newborn
46
Antiplatelet therapy and dental surgery
Antiplatelet therapy shouldn't not be changed
47
Indications for platelet transfusion in active bleeding
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
Indications for platelet transfusion if no active bleeding
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
Platelet levels to aim for prior to surgery/ invasive procedure
> 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
Cryoprecipitate
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
Acquired haemophilia
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
Drug induced thrombocytopenia
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
Blood loss in surgery
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
Amyloidosis
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
Porphyria cutanea tarda
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
Acute intermittent porphyria
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
Matching antigens in blood transfusions
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
Reticulocytes and chronic blood loss
In chronic blood loss, reticulocyte count would typically increase as the bone marrow produces more red blood cells.
59
Folate vs B12 anaemia
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
Warfarin and emergency surgery
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
Warfarin and emergency surgery
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
Differentiate true polycythaemia (ie. PRV) from secondary
The patient in this example has a normal SpO2 and EPO which suggest that the polycythaemia is not secondary in nature. T
63
Haemolysis and haptoglobins
low haptoglobins
64
One way to differentiate Myeloid and Lymphocytic leukaemia's
LL- usually raised lymphocytes ML- raised myeloid lineage cells eg. neutrophils and thrombocytes (platelets)

Year 3 OSCE (61 decks)

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