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Year 3 OSCE > Case 11- Anaemia > Flashcards

Case 11- Anaemia Flashcards

1
Q

General management of sickle cell anaemia

A

Avoid dehydration/ other triggers
Ensure vaccines up to date (flu and pneumococcal)
Antibiotic prophylaxis
Hydroxycarbamide- stimulates production of foetal Hb
Blood transfusion if severe anaemia
Exchange transfusion during acute crises
Bone marrow transplant can be curative

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2
Q

Signs and symptoms of anaemia

A

Fatigue, dyspnoea, faintness, palpitations, headache, tinnitus, angina, conjunctival pallor, SOB on exertion, atrophic glossitis, angular stomatitis, koilonychia, hair loss

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3
Q

Use osce stop when doing anaemia

A

L

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4
Q

Anaemia of chronic disease vs iron deficiency anaemia

A

Hb- low in both

Ferritin: low in iron deficiency , normal/high in ACD

Serum Iron: low in both

Transferrin saturation: low in both

Total iron binding capacity- high IDA, low AOCD

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5
Q

Blood film findings

A

Sickle cells
Schistocytes- microangiopathic haemolytic anaemia (HUS/ TTP)
Inclusion bodies- malaria
Spherocytes/ elliotocytes- hereditary spherocytosis/ elliptocytosis
Heinz bodies/bite and blister- G6PD deficiency
Prickle cells- autoimmune haemolytic anaemia
Acanthocytes- splenectomy/ ALD
Blast cells- leukaemia, haematological malignancy
Howell jolly bodies- post splenectomy and hyposplenism: sickle cell, coeliac disease, IBD
Tera drop poikilocytes- Myelofibrosis
Reticulocytes- haemolysis, haemorrhage
Target cells- have a ring of pallor. Liver disease, hyposplenism, thalassaemia

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6
Q

Aplastic anaemia

A

Pancytopenia and hypoplastic bone marrow
Peak incidence- 30 years

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7
Q

Causes of aplastic anaemia

A

Idiopathic
Congenital eg. Fanconi anaemia
Drugs- cytotoxic, chloramphenicol, sulphonamides, phenytoin, gold, benzene
Infection
Radiation

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8
Q

Autoimmune haemolytic anaemia

A

Divided into warm or cold depending on what temperature the antibodies cause haemolysis
Mostly idiopathic but can be secondary to infection, drugs, lymphoproliferative disorder
Characterised by a positive Coombs test (direct antiglobulin)

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9
Q

Warm autoimmune haemolytic anaemia (AHA)

A

IgG
Occurs in the spleen
Causes
-SLE
-neoplasia eg. Lymphoma, CLL
-methyldopa

Steroids, immunosuppression, splenectomy

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10
Q

Cold AIHA

A

IgM
Complement
Raynauds and acrocyanosis

Causes
-neoplasia (lymphoma)
-infection (mycoplasma, EBV)

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11
Q

Fanconi anaemia

A

Haem- aplastic anaemia, AML
Neuro abnormalities
MSK- short stature, radial abnormalities
Cafe au lair spots

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12
Q

Features of GPD6 deficiency

A

Haemolytic anaemia- neonatal jaundice
Gallstones
Splenomegaly
Heinz bodies and bite and blister cells seen on blood film

NB- difference with hereditary spherocytosis is the cells seen on a blood film

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13
Q

Diagnosing GPD6 deficiency

A

GPD6 enzyme assay 3 months after an acute episode of haemolysis

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14
Q

GPD6 haemolytic crisis precipitants

A

Infection
Beans
Drugs- anti malarials eg. Primaquine, cirpofloxacin, sulph drugs eg. Sulphonamides, sulfonylureas (glicazide), sulphasalazine

NB- Heinz bodies

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15
Q

Iron deficiency Anaemia investigations

A

FBC
Iron studies (serum ferritin low (but it’s an inflammatory protein so may be raised), TIBC high, transferrin saturation low)
Blood film- target cells, pencil poikilocytes, anisopoikilocytosis (red blood cells of different shapes and sizes)
Endoscopy- males and post menopausal females who present with iron deficiency anaemia (2 week wait for endoscopy)- urgent

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16
Q

Management of iron deficiency anaemia

A

Manage underlying cause
Iron rich diet- dark green leafy vegetables, meat, iron fortified bread
Oral ferrous sulphate- keep taking for 3 months after it has been corrected. SE’s include nausea, abdominal pain, constipation, diarrhoea, black stool

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17
Q

Paroxysmal nocturnal haemaglobinuria

A

Acquired disorder leading to haemolysis of any cells

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18
Q

Features and diagnosis of PNH

A

Haemolytic anaemia
Pancytopenia
Haemaglobinuria esp. in morning
Thrombosis eg. Budd chiari syndrome
Aplastic anaemia

Flow cytometry (CD59/ CD55)

19
Q

Management of PNH

A

Blood product replacement
Anticoagulation
Stem cell transplantation

20
Q

Causes of sideroblastic anaemia

A

Myelodysplasia
Alcohol
Lead
Anti TB medications

21
Q

Investigations for sideroblastic anaemia

A

FBC- microcytic anaemia
Iron studies- high ferritin, iron, transferrin saturation
Blood film- basophilic stippling of RBC’s
Bone marrow- Prussian blue staining will show ringed sideroblasts

22
Q

Sickle cell disease

A

Autosomal recessive haemolytic anaemia which predisposes to vasculo-occlusive crises

23
Q

Features of sickle cell disease

A

General- dactylitis, chronic haemolytic anameia (fatigue, pallor, weakness)

Vasculo-occlusive crises- bone, abdominal or chest pain. Ulcers and a vascular necrosis. Triggered by cold, dehydration, hypoxia, or infection.

Aplastic crisis- parvovirus B19 (pancytopenia)

Sequestration crises- pooling of blood in liver, spleen causing organomegaly (but spleen may also be atrophied due to repeated splenic infarcts)

24
Q

Treatment of a sickle cell crisis

A

analgesia e.g. opiates
rehydrate
oxygen
consider antibiotics if evidence of infection

blood transfusion
-indications include: severe or symptomatic anaemia, pregnancy, pre-operative
-does not rapidly reduce the percentage of Hb S containing cells

exchange transfusion
-indications include: acute vaso-occlusive crisis (stroke, acute chest syndrome, multiorgan failure, splenic sequestration crisis
-rapidly reduces the percentage of Hb S containing cells

25
Q

Investigations for sickle cell anaemia

A

Usually picked up with the newborn heel prick test
FBC- anaemia, LFT, UE, blood film (sickle shaped RBC’s, Howell jolly bodies)
Haemaglobin electrophoresis (definitive diagnosis)

26
Q

Features of Thalassaemia

A

Haemolytic anameia (RBC’s are fragile and breakdown easily)
Microcytic anaemia, fatigue, pallor, jaundice, gallstones, Splenomegaly, poor growth and development, pronounced forehead and malar eminences

27
Q

Investigations for Thalassaemia

A

FBC (microcytic anaemia), blood film
Haemoglobin electrophoresis

28
Q

Alpha Thalassaemia

A

Blood transfusions
Splenectomy
Bone marrow transplant may be curative

29
Q

Beta Thalassaemia major

A

Failure to thrive
Regular transfusions
Splenectomy
Bone marrow transplant may be curative

30
Q

Iron overload in Thalassaemia

A

As a result of faulty RBC’s, recurrent transfusions, increased iron absorption in response to the anameia
Patients have serum ferritin checked regularly
Management involves limiting transfusions and iron chelation

31
Q

Features of iron overload

A

Like haemachromatosis;

Fatigue, cirrhosis, infertility, impotence, heart failure, arthritis, diabetes, osteoporosis, joint pain

Desferrioxamine may help

32
Q

B12 deficiency

A

Anaemia symptoms eg. Breathlessness
Peripheral neuropathy with numbness or Parasthesia
Mood or cognitive changes
Visual changes
Loss of vibration sense or proprioception
Subacute spinal cord degeneration

33
Q

Investigations for B12 deficiency

A

FBC, blood film
Serum B12
Intrinsic factor antibody (gold standard)

34
Q

Investigating haemolytic anaemia

A

Urinalysis- haemaglobinuria
FBC, UE, LFT, serum bilirubin, LDH, blood film
Coombs test (autoimmune)
Hb electrophoresis
Osmotic fragility testing
Enzyme assays

35
Q

What is hereditary spherocytosis

A

Most commonly hereditary haemolytic anaemia in people on Northern European descent
Autosomal dominant
Sphere shaped RBC
Spleen destroys RBC’s- get Splenomegaly over time

36
Q

Presentation of HS

A

Failure to thrive, jaundice, gallstones
Splenomegaly, aplastic crisis precipitated by parvovirus infection
Degree of haemolysis variable

37
Q

Diagnosis and Management of HS

A

Acute haemolytic crisis- supportive, transfusion

Long term treatment- folate replacement, splenectomy

Diagnosis- EMA binding, cryohaemolysis test, electrolysis may also be used

38
Q

G6PD deficiency vs HS

A

Male vs male/female
African and Mediterranean vs Northern European
Intravascular vs extra vascular haemolysis (hence splenomegaly and possible splenectomy)
Heinz bodies in G6PD

39
Q

High reticulocyte count in sickle cell anaemia

A

Possible due to haemolytic crisis or acute sequestration

NB- low reticulocytes- think parvovirus

40
Q

Sequestration crisis

A

sickling within organs such as the spleen or lungs causes pooling of blood with worsening of the anaemia
associated with an increased reticulocyte count

41
Q

Aplastic crisis

A

caused by infection with parvovirus
sudden fall in haemoglobin
bone marrow suppression causes a reduced reticulocyte count

42
Q

Blood film for hyposplenism/splenectomy

A

Acanthocytes (S/H)
Howell jolly (S/H)
Target cells (H)

43
Q

Beta thalassaemia trait

A

Beta-thalassaemia trait is an autosomal recessive condition characterised by a mild hypochromic, microcytic anaemia. It is usually asymptomatic

Features
mild hypochromic, microcytic anaemia - microcytosis is characteristically disproportionate to the anaemia
HbA2 raised (> 3.5%)

Year 3 OSCE (61 decks)

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