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2a high tier > Haematology > Flashcards

Haematology Flashcards

1
Q

What is the general clinical presentation of anaemia?

A

Non-specific symptoms:
- Fatigue, headaches, faintness, dyspnoea, breathlessness, angina, anorexia, intermittent claudification, palpitations

Signs:

  • May be absent
  • Pallor, tachycardia, systolic flow murmur, cardiac failure
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2
Q

What is the aetiology of microcytic anaemia?

A
  • iron deficiency anaemia
  • anaemia of chronic disease
  • thalassaemia
  • lead poisoning
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3
Q

What is the aetiology of iron deficiency anaemia?

A
  • blood loss (GI bleeding, menorrhagia, hookworm)
  • poor diet
  • increased demands (e.g. during growth and pregnancy)
  • malabsorption (poor intake, coeliac disease)
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4
Q

What is the pathophysiology of iron deficiency anaemia?

A

Less iron is available for haem synthesis therefore less haemoglobin is made, leading to smaller RBCs

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5
Q

What are the risk factors of iron deficiency anaemia?

A
  • undeveloped countries
  • high vegetable intake
  • premature infants
  • delayed introduction of mixed feeding in infants
  • hookworm infection
  • coeliac disease
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6
Q

What is the clinical presentation of iron deficiency anaemia?

A
  • general anaemia symptoms
  • brittle nails and hair
  • spoon-shaped nails
  • atrophy of papillae on tongue
  • ulceration of the corner of the mouth
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7
Q

What are the differential diagnoses of iron deficiency anaemia?

A
  • thalassaemia
  • sideroblastic anaemia
  • anaemia of chronic disease
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8
Q

How is iron deficiency anaemia diagnosed?

A
  • blood count and film (small, pale RBCs and variation in RBC shape and size)
  • low serum ferritin
  • low serum iron
  • low reticulocyte count
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9
Q

How is iron deficiency anaemia managed?

A
  • find and treat cause
  • oral iron (e.g. ferrous sulphate)
  • parenteral iron (e.g. IV iron in extreme causes)
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10
Q

What is the pathophysiology of anaemia of chronic disease?

A
  • decreased release of iron from the bone marrow to developing erythroblasts
  • inadequate erythropoietin response to anaemia
  • decreased RBC survival
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11
Q

What is the main risk factor of anaemia of chronic disease?

A

Having a chronic disease

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12
Q

How is anaemia of chronic disease diagnosed?

A
  • low serum iron and total iron-binding capacity
  • normal or raised serum ferritin
  • blood count and film (RBCs are normal/ microcytic and pale)
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13
Q

How is anaemia of chronic disease managed?

A
  • treat underlying cause

- give erythropoietin to raise haemoglobin level

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14
Q

What is the aetiology of normocytic anaemia?

A
  • acute blood loss
  • anaemia of chronic disease
  • endocrine disorders (e.g. hypopituitarism, hypothyroidism or hypoadrenalism)
  • renal failure
  • pregnancy
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15
Q

How is normocytic anaemia diagnosed?

A
  • normal B12 and folate
  • raised reticulocytes
  • low haemoglobin
  • blood count and film
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16
Q

How is normocytic anaemia managed?

A
  • treat underlying cause
  • improve diet with vitamins
  • erythropoietin injections
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17
Q

What is the aetiology of macrocytic anaemia?

Megaloblastic and non-megaloblastic

A

Megaloblastic:
- vitamin B12 deficiency, folate deficiency

Non-megaloblastic:
- alcohol, liver disease, hypothyroidism, haemolysis, bone marrow failure, bone marrow infiltration, antimetabolite therapy, myeloma

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18
Q

What are the risk factors of of folate deficiency anaemia?

A
  • low dietary folate intake
  • age > 6y
  • alcoholism
  • pregnant or lactating
  • prematurity
  • intestinal malabsorptive disordes
  • use of methotrexate
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19
Q

What is the clinical presentation of folate deficiency anaemia?

A
  • prolonged diarrhoea
  • loss of appetite and weight
  • fatigue
  • shortness of breath
  • dizziness
  • pallor
  • tachycardia
  • heart murmur
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20
Q

What are the differential diagnoses of folate deficiency anaemia?

A
  • vitamin B12 deficiency
  • thiamine-responsive megaloblastic anaemia
  • alcoholic liver disease
  • hypothyroidism
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21
Q

How is folate deficiency anaemia diagnosed?

A
  • peripheral blood smear
  • FBC
  • reticulocyte count
  • serum folate
  • RBC folate
  • serum vitamin B12
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22
Q

How is folate deficiency anaemia managed?

A
  • oral folic acid and multivitamin supplementation
  • folonic acid
  • treat underlying disorder
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23
Q

What is the aetiology of sickle cell anaemia?

type and location of genetic defect

A

Autosomal-recessive single gene defect in the beta chain of haemoglobin

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24
Q

What is the pathophysiology of sickle cell anaemia?

A
  • RBCs become rigid and distorted in crescent shape
  • defamed cells cause vast-occlusion in the small vessels or adhere to vascular endothelium resulting in intimacy hyperplasia in larger vessels, slowing blood flow
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25
Q

What is the risk factor for sickle cell anaemia?

A
  • family history (genetic)
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26
Q

What is the clinical presentation of sickle cell anaemia?

A
  • persistent pain in skeleton, chest and/or abdomen
  • dactylitis (inflammation of the digits)
  • high temperature
  • pneumonia-like syndrome
  • bone pain
  • visual floaters
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27
Q

What are the differential diagnoses of sickle cell anaemia?

A
  • gout
  • septic arthritis
  • connective tissue diseases
  • avascular necrosis
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28
Q

How is sickle cell anaemia diagnosed?

A
  • DNA-based assays
  • haemoglobin isoelectric focusing
  • cellulose acetate electrophoresis
  • haemoglobin solubility testing
  • peripheral blood smear
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29
Q

How is sickle cell anaemia managed?

A
  • only curative treatment is bone marrow transplantation
30
Q

What is the aetiology of pernicious anaemia?

A

B12 deficiency

31
Q

What are the risk factors of pernicious anaemia?

A
  • elderly
  • female
  • fair-haired and blue-eyed
  • blood group A
  • thyroid and Addison’s disease
32
Q

What is the clinical presentation of pernicious anaemia?

general and neurological features

A
  • insidious onset with progressively increasing symptoms of anaemia
  • may have a lemon-yellow skin colour (from pallour and mild jaundice)
  • red sore tongue and ulceration of corners of the mouth

Neurological features:

  • only occur if B12 is very low
  • burning or prickling pain/ tingling in fingers and toes
  • early loss of vibration sense and proprioception
  • progressive weakness and ataxia
  • paraplegia
  • dementia, psychiatric problems, hallucinations, delusions
33
Q

What are the differential diagnoses of pernicious anaemia?

A
  • folate deficiency
  • any disease in the terminal ileum or bacterial overgrowth in the small bowel
  • gastrectomy
34
Q

How is pernicious anaemia diagnosed?

A
  • blood count and film (large RBCs that may be oval-shaped on a peripheral film)
  • raised bilirubin
  • low B12
  • low Hb
  • low reticulocytes
35
Q

How is pernicious anaemia managed?

A
  • B12 injections if due to malabsorption

- oral B12 if due to dietary deficiency

36
Q

What is the aetiology of a DVT?

general, genetic, acquired

A
  • surgery, immobility, leg fracture, oral contraceptive pill, long haul flights, malignancy

Genetic:
- Factor V Leiden, antithrombin deficiency, protein C or S deficiency

Acquired:
- anti-phospholipid syndrome, lupus anticoagulant

37
Q

What is the pathophysiology of a DVT?

A

Blood clots develop in the deep vein system of the leg just above and behind a venous vein

38
Q

What are the risk factors of a DVT?

A
  • increasing age
  • pregnancy
  • synthetic oestrogen
  • hospitalisation within the past 2 months
  • major surgery within 3 months
  • recent long haul flights
  • active cancer
  • lower extremity trauma
39
Q

What is the clinical presentation of a DVT?

A
  • may be asymptomatic
  • calf swelling
  • localised pain along deep venous system, often with swelling, redness and engorged superficial vein
  • affected calf is often warmer and there may be ankle oedema
  • asymmetric anaemia
  • complete occlusion can cause cyanotic discolouration of the limb and severe oedema
  • pulmonary embolism can also occur (more frequent from an iliofemoral thrombosis)
40
Q

How is a DVT diagnosed?

A
  • Wells’ score
  • plasma D-dimer level
  • proximal Duplex US
  • whole-leg US
41
Q

How is a DVT managed?

A
  • low molecular weight heparin (e.g., sc enoxaparin)
  • oral warfarin
  • direct acting Oral Anti-Coagulants (DOAC)
  • compression stockings
  • inferior vena cava filters to reduce risk of pulmonary emboli

Prevention:

  • early mobilisation post-op
  • compression stockings
  • thromboprophylaxis for low and high risk
42
Q

What is the aetiology of leukaemia?

A

Presence of rapidly proliferating immature blast blood cells in the bone marrow that are non-functional

43
Q

What is the pathophysiology of leukaemia?

A

Bone marrow is not able to make as many normal functioning cells resulting in fewer functioning blood cells in the blood

44
Q

What is the aetiology of acute lymphoblastic leukaemia?

A
  • increased proliferation of immature lymphoblast cells (B cells in children, T cells in adults)
  • combination of genetic susceptibility and environmental trigger
45
Q

What is the clinical presentation of acute lymphoblastic leukaemia?

A

Marrow failure

  • low Hb → breathlessness, fatigue, angina, clarification, pallor
  • low WCC → infections, fever, mouth ulcers
  • low platelets → bleeding and bruising
  • bone pain from bone marrow infiltration
  • headache and cranial nerve palsies from CNS infiltration
  • hepatosplenomegaly from liver/ spleen infiltration
46
Q

How is acute lymphoblastic leukaemia diagnosed?

A
  • FBC and blood film → high WCC, blast cells on film and in the bone marrow
  • CXR and CT scan to look for mediastinal and abdominal lymphadenopathy
  • lumbar puncture to look for CNS involvement
47
Q

How is acute lymphoblastic leukaemia managed?

A
  • blood and platelet transfusions
  • allopurinol
  • prophylactic antivirals, antibacterial and antifungals
  • IV fluids through a Hickman line
  • chemotherapy
  • marrow transplantation
48
Q

What is the aetiology of acute myeloid leukaemia?

A

Neoplastic proliferation of blast cells derived from marrow myeloid elements

49
Q

What is the clinical presentation of acute myeloid leukaemia?

A

Marrow failure

  • low Hb → breathlessness, fatigue, angina, clarification, pallor
  • low WCC → infections, fever, mouth ulcers
  • low platelets → bleeding and bruising
  • hepatomegaly and splenomegaly
  • gum hypertrophy
  • disseminated intravascular coagulation
50
Q

What is the differential diagnoses of acute myeloid leukaemia?

A

Acute lymphoblastic leukaemia

51
Q

How is acute myeloid leukaemia diagnosed?

A
  • WCC often raised, but can be normal or low
  • may be blast cells in the peripheral blood so diagnosis depends on bone marrow biopsy
  • differentiation from acute lymphoblastic leukaemia is based on microscopy, immunophenotyping and molecular methods
52
Q

How is acute myeloid leukaemia managed?

A
  • blood and platelet transfusions
  • allopurinol
  • prophylactic antivirals, antibacterial and antifungals
  • IV fluids through a Hickman line
  • chemotherapy
  • marrow transplantation
53
Q

What is the aetiology of chronic lymphoblastic leukaemia?

A
  • accumulation of mature B cells that have escaped apoptosis and undergone cell-cycle arrest
  • may be triggered by pneumonia
54
Q

What is the clinical presentation of chronic lymphoblastic leukaemia?

A
  • often asymptomatic and found on routine FBC
  • may be anaemic or infection prone
  • if severe, then weight loss, sweats and anorexia
  • hepatosplenomegaly
  • enlarged, rubbery, non-tender nodes
55
Q

How is chronic lymphoblastic leukaemia diagnosed?

A
  • FBC - normal/ low Hb, raised WCC (very high lymphocytes)

- blood film - smudge cells may be seen in vitro

56
Q

How is chronic lymphoblastic leukaemia managed?

A
  • blood transfusions
  • human IV immunoglobulins
  • chemo/radiotherapy
  • try a stem cell transplant
57
Q

What is the aetiology of lymphoma?

A
  • primary immunodeficiency: ataxia telangiectasia, Wiscott-Aldrich syndrome
  • secondary immunodeficiency: HIV, transplant recipients
  • infection: EBV, H.pylori
  • autoimmune disorders e.g SLE
58
Q

What are the risk factors of Hodgkin’s lymphoma?

A
  • affected sibling
  • EBV
  • SLE
  • obesity
  • post-transplantation
59
Q

What is the clinical presentation of Hodgkin’s lymphoma?

A
  • painless cervical lymphadenopathy (commonly described as rubbery)
  • may present with generalised disease (weight loss, fever, night sweats)

Emergency presentation:

  • infection
  • superior vena cava obstruction with increased venous jugular pressure
  • dyspnoea
  • blackouts
  • facial oedema
60
Q

How is Hodgkin’s lymphoma diagnosed?

A
  • CT/ MRI for chest, abdomen and pelvis for staging
  • lymph node for excision or bone marrow biopsy
  • bloods: high ESR or low Hb indicated worse prognosis
  • PET scan
  • cytogenetics
  • immunophenotyping
61
Q

How is Hodgkin’s lymphoma managed?

A

Combination therapy (ABVD):

  • adriamycin
  • bleomycin
  • vinblastine
  • dacarbazine
62
Q

What is the risk factor of non-Hodgkin’s lymphoma

A

Family history

63
Q

What is the clinical presentation of non-Hodgkin’s lymphoma?

A
  • nodal disease
  • extra nodal disease
  • systemic B symptoms: fever, night sweats, weight loss
  • pancytopenia: anaemia, infection and bleeding
64
Q

How is non-Hodgkin’s lymphoma diagnosed?

A
  • marrow and node biopsy
  • CT/MRI of chest, abdomen and pelvis for staging
  • lymph node excision or bone marrow biopsy
  • cytogenetics
  • immunophenotyping
  • cytogenetics
65
Q

How is non-Hodgkin’s lymphoma managed?

A

R-CHOP regimen:

  • rituximab
  • cyclophosphamide
  • hydroxydaunorubicin
  • oncovin
  • prednisolone
66
Q

What is the aetiology of malaria?

A

Protozoa from Plasmodium transmitted to humans through a bite from one of the 40 species of female Anopheles mosquitos

67
Q

What is the pathophysiology of malaria?

A

Mosquito infects malaria sporozoites during a blood meal which enter hepatocytes

68
Q

What are the risk factors of malaria?

A
  • travel to endemic area
  • inadequate or absent chemoprophylaxis
  • low host immunity
  • pregnancy
  • age <5y
  • immunocompromised
  • older age
69
Q

What is the clinical presentation of malaria?

A
  • headache
  • weakness
  • myalgia
  • arthralgia
  • anorexia
  • diarrhoea
  • seizures
70
Q

What are the differential diagnoses of malaria?

A
  • dengue fever
  • Zika virus infection
  • yellow fever
  • pneumonia
  • influenza
71
Q

How is malaria diagnosed?

A
  • Giemsa-stained thick and thin blood films
  • rapid diagnostic tests
    FBC
  • clotting profile
  • serum electrolytes, urea and creatinine
  • serum LFTs
  • serum blood glucose
72
Q

How is malaria managed?

A
  • depends on the infecting species
  • no treatment until diagnosis is confirmed
  • antimalarial drugs e.g. hydroxychloroquine
  • multiple agents are used to avoid selective resistance

2a high tier (10 decks)

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