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FINALS > Haematology > Flashcards

Haematology Flashcards

1
Q

IRON DEFICIENCY ANAEMIA

What is the physiology of iron?

A
  • Bone marrow requires iron to produce Hb which is mainly absorbed in the duodenum + proximal jejunum enhanced by vitamin C + inhibited by tannin (tea)
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2
Q

IRON DEFICIENCY ANAEMIA

What are some causes of iron deficiency anaemia?

A
  • Increased loss = menorrhagia, GI bleeding (?colorectal cancer), hookworm
  • Inadequate intake/increased needs = poor diet, puberty growth, pregnancy
  • Malabsorption = IBD, coeliac disease
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3
Q

IRON DEFICIENCY ANAEMIA

What is the clinical presentation of iron deficiency anaemia?

A
  • Symptoms = fatigue, SOB, headaches, dizziness, palpitations
  • Generic signs = (conjunctival) pallor, tachycardia + tachypnoea
  • Pica = consumption of non-food materials
  • Koilonychia, angular stomatitis, atrophic glossitis + brittle hair/nails
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4
Q

IRON DEFICIENCY ANAEMIA

What investigations would you do in iron deficiency anaemia?

A
  • FBC = low Hb, low MCV + normal reticulocytes
  • Blood film = hypochromic microcytic RBCs, target cells + pencil poikilocytes
  • Iron studies
  • ?2ww suspected colorectal cancer for colonoscopy if ≥60
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5
Q

IRON DEFICIENCY ANAEMIA

What would iron studies show in iron deficiency anaemia?

A
  • Low = ferritin, iron + transferrin saturation (proportion of transferrin bound to iron)
  • High = total iron binding capacity (total space on transferrin for iron to bind)
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6
Q

IRON DEFICIENCY ANAEMIA
What is the management of iron deficiency anaemia?
Side effects of the treatment?

A
  • Diet = red meat, oily fish, green veg (broccoli, spinach), dried fruit (raisins)
  • PO iron supplementation (ferrous sulfate/fumarate)
  • Note SE: constipation, black coloured stools, nausea + abdo pain
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7
Q

THALASSAEMIA
What is thalassaemia?
What is the epidemiology?

A
  • Autosomal recessive disorders caused by ≥1 gene defect, resulting in a reduced rate of production of ≥1 alpha/beta globin chains making RBCs more fragile
  • Common in Mediterranean, Middle East + East Africa
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8
Q

THALASSAEMIA

How is alpha thalassaemia classified?

A
  • 1–2 alpha globin alleles affected = hypochromic + microcytic but Hb often ok
  • 3 = hypochromic microcytic anaemia with splenomegaly (Hb H disease)
  • 4 = death in utero due to foetal hydrops
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9
Q

THALASSAEMIA

How is beta thalassaemia classified?

A
  • Minor = 1 abnormal and 1 normal gene
  • Intermedia = 2 defective or 1 defective + 1 deletion
  • Major = homozygous for deletion genes
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10
Q

THALASSAEMIA
What is the clinical presentation of beta thalassaemia…

i) minor?
ii) intermedia?

A

i) Mild microcytic anaemia which only needs monitoring

ii) Jaundice + hepatosplenomegaly, monitoring ± blood transfusions

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11
Q

THALASSAEMIA

What is the clinical presentation of beta thalassaemia major?

A
  • Presents in first year with failure to thrive, hepatosplenomegaly, jaundice, microcytic anaemia
  • Extramedullary haemopoiesis = hepatosplenomegaly, bone marrow expansion (maxillary overgrowth + frontal bossing)
  • HbA2 + HbF raised but HbA absent
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12
Q

THALASSAEMIA
What investigations would you do in thalassaemia?
How do you differentiate from iron deficiency anaemia?
What investigation is diagnostic?

A
  • FBC = low Hb + MCV
  • Film = hypochromic + microcytic RBCs
  • Serum ferritin NORMAL
  • Hb electrophoresis = diagnostic
  • DNA testing via CVS
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13
Q

THALASSAEMIA
What is the management of thalassaemia?
What is a complication of this and how is it managed?

A
  • Blood transfusions (regular in beta thalassaemia major)
  • Require iron chelation with desferrioxamine to avoid overload + organ failure (cardiomyopathy, cirrhosis, DM, arthritis)
  • Splenectomy ± curative bone marrow transplant
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14
Q

B12 DEFICIENCY ANAEMIA

What is the physiology of vitamin B12?

A
  • Absorption occurs in the terminal ileum + is intrinsic factor (secreted by gastric parietal cells) dependent for transport across the intestinal mucosa
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15
Q

B12 DEFICIENCY ANAEMIA

What are some causes of B12 deficiency anaemia?

A
  • Malabsorption = Crohn’s, coeliac, ileal resection
  • Dietary (vegans) as B12 high in fish, meat, dairy
  • Autoimmune (pernicious) = atrophic gastritis leads to destruction of parietal cells > intrinsic factor deficient
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16
Q

B12 DEFICIENCY ANAEMIA

What is the clinical presentation of B12 deficiency anaemia?

A
  • Anaemia Sx = fatigue, SOB, headaches, dizziness, palpitations
  • B12 deficiency = dorsal column affected (proprioception, loss of vibration, peripheral neuropathy paraesthesia, neuropsych mood disturbance), glossitis (beefy-red sore tongue)
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17
Q

B12 DEFICIENCY ANAEMIA

What investigations would you do in B12 deficiency anaemia?

A
  • FBC = low Hb, high MCV (macrocytic, megaloblastic)
  • Haematinics = low B12
  • Blood film = hypersegmented neutrophil nuclei
  • Intrinsic factor Ab specific for pernicious, may have gastric parietal cell Ab
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18
Q

B12 DEFICIENCY ANAEMIA

What are some differentials of macrocytic anaemia which are normoblastic?

A
  • Alcohol
  • Liver disease
  • Hypothyroidism
  • Myelodysplasia
  • Reticulocytosis
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19
Q

B12 DEFICIENCY ANAEMIA
What should you check before managing B12 deficiency anaemia?
What is the management of B12 deficiency anaemia?

A
  • Folate > do not give folic acid as can cause subacute combined degeneration of the cord = distal sensory loss, ataxia + mixed U/LMN signs
  • Initially IM hydroxocobalamin then maintenance with PO cyanocobalamin if diet-related or IM hydroxocobalamin every 2–3m
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20
Q

FOLATE DEFICIENCY ANAEMIA

What is the pathophysiology of folate deficiency anaemia?

A
  • Develops over 4m of deficiency due to bodily reserves

- Folate is absorbed in the proximal jejunum

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21
Q

FOLATE DEFICIENCY ANAEMIA

What are some causes of folate deficiency anaemia?

A
  • Increased demand = pregnancy, malignancy, haemolysis
  • Decreased intake = poor diet (green vegetables)
  • Decreased absorption = coeliac, Crohn’s, jejunal resection
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22
Q

FOLATE DEFICIENCY ANAEMIA

What is the clinical presentation of folate deficiency anaemia?

A
  • Anaemia = fatigue, SOB, headaches, dizziness, palpitations

- NO neuropathy

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23
Q

FOLATE DEFICIENCY ANAEMIA
What investigations would you do in folate deficiency anaemia?
What’s the management?

A
  • FBC = low Hb, high MCV, macrocytic megaloblastic
  • Haematinics = low folate
  • PO folic acid 5mg OD
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24
Q

HEREDITARY SPHEROCYTOSIS

What is the pathophysiology of hereditary spherocytosis?

A
  • Autosomal dominant mutation of structural RBC membrane proteins leading to removal of abnormal membrane as it passes by spleen resulting in reduced SA:V + becoming spheroidal leading to extravascular haemolysis + destroyed by spleen
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25
Q

HEREDITARY SPHEROCYTOSIS

What is the epidemiology and clinical presentation of hereditary spherocytosis?

A
  • Most common inherited haemolytic anaemia in Northern Europeans
  • Anaemia, jaundice, splenomegaly + gallstones (due to increased bilirubin excretion)
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26
Q

HEREDITARY SPHEROCYTOSIS

What are the investigations for hereditary spherocytosis?

A
  • FBC = raised MCHC, raised reticulocytes
  • Film = spherocytes (no central pallor) + schistocytes (haemolysis)
  • EMA binding test = diagnostic
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27
Q

HEREDITARY SPHEROCYTOSIS
What complication can occur in hereditary spherocytosis and why?
How does it present?
What is the management?

A
  • Aplastic crisis due to parvovirus B19 infection
  • Increased anaemia, extravascular haemolysis + jaundice without normal bone marrow (reticulocyte) response to create new RBCs
  • Supportive, ?transfusion
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28
Q

HEREDITARY SPHEROCYTOSIS

What is the management of hereditary spherocytosis?

A
  • PO folate replacement

- Splenectomy before 5y is curative > Hib, Men A + C, annual influenza, PCV 5 yearly, PO pen V for at least 2y

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29
Q

G6PD DEFICIENCY

What is G6PD deficiency?

A
  • X-linked recessive haemolytic anaemia so predominantly affects males, more common in Mediterranean, Middle Eastern + African background
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30
Q

G6PD DEFICIENCY

What is the clinical presentation of G6PD deficiency?

A
  • Neonatal jaundice often within 3d

- Anaemia, intermittent jaundice, splenomegaly + gallstones

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31
Q

G6PD DEFICIENCY
What investigations would you do in G6PD deficiency?
What is diagnostic?
What considerations would you take?

A
  • Blood film = Heinz bodies + bite & blister cells
  • Diagnostic = G6PD enzyme assay
  • 3m after acute episode of haemolysis as RBCs with most severely reduced G6PD activity will have haemolysed so false negative results
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32
Q

G6PD DEFICIENCY
What is a complication of G6PD deficiency?
What can trigger it?
How does it present?

A
  • Acute (intravascular) haemolysis
  • Infection, fava bean, henna + drugs (antimalarials primaquine, sulfa-drugs, ciprofloxacin)
  • Fever, malaise, dark urine (Hb + urobilinogen)
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33
Q

G6PD DEFICIENCY

What is the management of G6PD deficiency?

A
  • Avoid precipitants

- ?Transfusion if needed

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34
Q

SICKLE CELL DISEASE

What is the pathophysiology of sickle cell disease?

A
  • Autosomal recessive condition leads to amino acid substitution of glutamine > valine causing abnormal HbS variant
  • This polymerises when deoxygenated into sickle shape making them more fragile (haemolysis) + prone to getting trapped in microvasculature (thrombosis) leading to ischaemia/infarction
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35
Q

SICKLE CELL DISEASE
What are the different phenotypes in sickle cell disease?
What is the epidemiology and why is this significant?

A
  • Heterozygous = trait, homozygous = disease
  • More common in African descent in areas traditionally affected by malaria as having sickle-cell trait reduces severity of falciparum malaria making them more likely to survive + pass the gene on
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36
Q

SICKLE CELL DISEASE

What is the general clinical presentation of sickle cell disease?

A
  • HbF unaffected so usually manifests when HbF decreases around 6m
  • All have moderate anaemia with detectable jaundice from chronic haemolysis
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37
Q

SICKLE CELL DISEASE

What are the various acute presentations of sickle cell disease?

A
  • Vaso-occlusive painful crises
  • Sequestration crises
  • Aplastic crises
  • Acute chest syndrome
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38
Q

SICKLE CELL DISEASE
What is the clinical presentation of…

i) sequestration crises?
ii) aplastic crises?

A

i) Pooling of blood in spleen leads to severe anaemia + shock, if >2x = splenectomy
ii) Parvovirus B19 = acute sudden anaemia

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39
Q

SICKLE CELL DISEASE
What can cause vaso-occlusive painful crises?
How do they present?

A
  • Triggers = cold, infection, dehydration
  • Affects bones of limbs + spine, can lead to avascular necrosis
  • Hand-foot syndrome = dactylitis
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40
Q

SICKLE CELL DISEASE
What is the clinical presentation of acute chest syndrome?
What are some potential causes?

A
  • Pleuritic chest pain, fever, SOB, CXR = pulmonary infiltrates
  • Infective or non-infective (pulmonary vaso-occlusion, fat emboli)
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41
Q

SICKLE CELL DISEASE
What are the investigations for sickle cell disease?
What is the definitive diagnostic investigation?

A
  • Prenatal Dx with CVS and detected on neonatal heel prick test at 5d
  • FBC = normocytic anaemia, high reticulocytes
  • Blood film = sickled RBCs, Howell-Jolly bodies + schistocytes
  • Definitive = Hb electrophoresis showing high HbSS + absent HbA
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42
Q

SICKLE CELL DISEASE

What are some long-term complications of sickle cell disease?

A
  • Short stature + delayed puberty
  • Hyposplenism due to sequestration + infarction so increased infection risk
  • Stroke
  • Chronic renal failure
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43
Q

SICKLE CELL DISEASE

What is the management of acute crises in sickle cell disease?

A
  • PO/IV analgesia titrate to effect, IV fluids, oxygen, ?NIV
  • Infection = Abx
  • Blood transfusion if severe anaemia
  • Exchange transfusion if severe (e.g., neuro complications)
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44
Q

SICKLE CELL DISEASE

What is the chronic management of sickle cell disease?

A
  • PO hydroxyurea to increase HbF levels as prophylaxis for painful crises
  • PCV vaccine every 5y, may have prophylactic pen V
  • Bone marrow transplantation curative + offered if failed response
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45
Q

HAEMOLYTIC ANAEMIA

What is the pathophysiology of haemolytic anaemias?

A
  • Extravascular = RBC destruction within reticuloendothelial system (spleen + liver) > sickle cell, hereditary spherocytosis
  • Intravascular = RBC destruction within blood stream so release of contents into circulation > G6PD, AIHA, paroxysmal nocturnal haemoglobinuria
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46
Q

HAEMOLYTIC ANAEMIA

How are the causes of haemolytic anaemias split?

A

Inherited –
- Hereditary spherocytosis, G6PD, sickle cell disease
Acquired –
- Immune coombs +ve = autoimmune or alloimmune (transfusion reactions)
- Non-immune = paroxysmal nocturnal haemoglobinuria, microangiopathic haemolysis

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47
Q

HAEMOLYTIC ANAEMIA
What is the typical biochemical picture seen in haemolysis?
How does this differ between intravascular and extravascular?

A
  • Both = increased unconjugated bilirubin, LDH + reticulocytes
  • Intravascular = haemoglobinuria + decreased haptoglobin which binds to free Hb in blood (not seen in extravascular)
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48
Q

HAEMOLYTIC ANAEMIA

What are the 2 types of autoimmune haemolytic anaemia?

A
  • Warm = IgG mediated extravascular haemolysis where spleen tags cells for splenic phagocytosis occurring at body temp
  • Cold = IgM mediated where IgM fixes complement causing direct intravascular haemolysis (cold agglutinins) occurring in cold <4 degrees
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49
Q

HAEMOLYTIC ANAEMIA

What are the causes of warm and cold autoimmune haemolytic anaemia?

A
  • Warm = idiopathic, lymphoproliferative neoplasms (CLL, lymphoma), SLE
  • Cold = idiopathic, mycoplasma, EBV
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50
Q

HAEMOLYTIC ANAEMIA

What is the clinical presentation of warm and cold autoimmune haemolytic anaemia?

A
  • Warm = jaundice, splenomegaly

- Cold = acrocyanosis, Raynaud’s

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51
Q

HAEMOLYTIC ANAEMIA

What is the management of warm and cold autoimmune haemolytic anaemia?

A
  • Warm = steroids, rituximab or splenectomy

- Cold = keep warm (?blood warmers)

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52
Q

HAEMOLYTIC ANAEMIA
What are the features of paroxysmal nocturnal haemoglobinuria?
What is the management?

A
  • Early adulthood nocturnal episodes of intravascular haemolysis > anaemia, dark urine (haemoglobinuria) in morning
  • Flow cytometry diagnostic, eculizumab
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53
Q 
HAEMOLYTIC ANAEMIA
What is microangiopathic haemolytic anaemia?
What causes it?
How does it present?
What's the management?
A
  • Mechanical destruction of RBCs
  • TTP, HUS + DIC
  • Fever, renal failure, abdo pain, schistocytes on blood film
  • Plasma exchange to remove vWF multimers
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54
Q

ALL
What is acute lymphoblastic leukaemia (ALL)?
What is the epidemiology?
What are some risk factors?

A
  • Abnormal proliferation of lymphoid progenitor cells (usually B-lymphocytes)
  • Accounts for 80% of leukaemia in children + peaks at 2–5y
  • Trisomy 21 + immunocompromised
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55
Q

ALL
What is the general clinical presentation of ALL?
What causes the various clinical presentations of ALL?

A
  • Fever, weight loss, night sweats, lymphadenopathy

- Infiltration with leukaemic blast cells > bone marrow (pancytopaenia), reticuloendothelial, other organs

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56
Q

ALL
How does ALL present in terms of…

i) bone marrow infiltration?
ii) reticuloendothelial infiltration?
iii) other organ infiltration?

A

i) Anaemia (pallor, lethargy, SOB), neutropaenia (infection) + thrombocytopaenia (bruising, petechiae, epistaxis)
ii) Hepatosplenomegaly
iii) CNS (CN palsies), bone pain, testicular swelling

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57
Q

ALL
What investigations would you do in ALL?
What is diagnostic?

A
  • FBC + blood film = pancytopaenia, blast cells
  • CXR if ?mediastinal mass, LP if ?CNS involvement
  • Bone marrow examination via ASPIRATION = diagnostic
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58
Q

ALL

What are some complications of ALL?

A
  • CNS development
  • Growth impact
  • Infertility
  • Cardiac + renal toxicity
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59
Q

ALL
What is the management of ALL?
What are good prognostic factors in ALL?

A
  • Supportive = IV fluids, transfusions, allopurinol to protect kidneys from tumour lysis syndrome
  • Chemo = remission, consolidation & CNS protection + maintenance
  • Ages 2–10, female, WCC <20, no CNS disease, Caucasian
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60
Q

AML

What is acute myeloid leukaemia (AML)?

A
  • Neoplastic proliferations of myeloid precursor cells

- Commonest acute leukaemia in adults, over 75y affected

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61
Q

AML

What are some causes of AML?

A
  • Myelodysplastic + myeloproliferative syndromes

- Radiation + chemotherapy

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62
Q

AML

What is the clinical presentation of AML?

A
  • Bone marrow failure (pancytopaenia) = anaemia, neutropaenia + thrombocytopaenia
  • Infiltration = lymphadenopathy, hepatosplenomegaly + gum hypertrophy
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63
Q

AML
What are the investigations for AML?
What is diagnostic?

A
  • FBC = pancytopaenia, may present in DIC
  • Blood film = blast cells + auer rods
  • Bone marrow examination via ASPIRATION diagnostic
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64
Q

AML

What is the management of AML?

A
  • Supportive = IV fluids, transfusions, allopurinol

- Chemotherapy or bone marrow transplant but generally poor prognosis

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65
Q

CLL
What is CLL?
What is the epidemiology?

A
  • Monoclonal proliferation of functionally incompetent malignant B cells
  • Most common in those >60y
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66
Q

CLL

What is the clinical presentation of CLL?

A
  • Often none but incidental lymphocytosis on FBC

- Anaemia, hepatosplenomegaly + B symptoms (weight loss, fever, night sweats)

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67
Q

CLL

What are the investigations for CLL?

A
  • FBC = anaemia + lymphocytosis
  • Blood film = smudge/smear cells
  • Immunophenotyping (flow cytometry) diagnostic
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68
Q

CLL

What are the complications of CLL?

A
  • Richter transformation to high grade lymphoma = CLL > large B cell lymphoma
  • Hypogammaglobulinaemia
  • Warm autoimmune haemolytic anaemia
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69
Q

CLL

What is the management of CLL?

A
  • Chemotherapy
70
Q

CML
What is chronic myeloid leukaemia (CML)?
What are the phases?
What is the epidemiology?

A
  • Uncontrolled clonal proliferation of myeloid cells
  • 3 phases = chronic (5y asymptomatic), accelerated + blast phase
  • Ages >65
71
Q

CML

What is the clinical presentation of CML?

A
  • Anaemia + thrombocytopaenia
  • Systemic = fever, weight loss + night sweats
  • Massive splenomegaly which can cause abdominal pain
72
Q

CML

What are the investigations in CML?

A
  • FBC = anaemia, thrombocytopaenia + leukocytosis of neutrophils, monocytes, basophils + eosinophils
  • Philadelphia chromosome t(9:22) in almost all leading to BCR-ABL gene coding for fusion protein with excess tyrosine kinase activity
  • Bone marrow aspiration + biopsy = diagnostic
73
Q

CML

What is the management of CML?

A
  • Imatinib = tyrosine kinase inhibitor
74
Q

LYMPHOMA
What is Hodgkin’s lymphoma?
What is the epidemiology?
What are some risk factors?

A
  • Proliferation of lymphocytes
  • Bimodal age distribution with peaks around 20 + 75 years
  • HIV, EBV, autoimmune conditions like RA, sarcoidosis
75
Q

LYMPHOMA

What is the clinical presentation of Hodgkin’s lymphoma?

A
  • Non-tender, rubbery lymphadenopathy at neck with alcohol-induced pain
  • Pruritus
  • Compression Sx = SOB, abdominal pain
  • B symptoms (night sweats, fever, weight loss) imply poorer prognosis
76
Q

LYMPHOMA
What are some investigations for lymphoma?
What is diagnostic?
What is the characteristic finding of Hodgkin’s lymphoma?

A
  • Bloods = normocytic anaemia, LDH raised
  • CT CAP/PET for staging
  • Lymph node biopsy = diagnostic for Reed-Sternberg cells (mirror-image nuclei, often multinucleate malignant lymphocytes)
77
Q

LYMPHOMA
What staging system is used in both lymphomas?
How is it categorised?

A

Ann Arbor –

  • I = confined to single LN region
  • II = ≥2 nodal areas on same side of diaphragm
  • III = nodal areas on both sides of diaphragm
  • IV = spread beyond LN
  • A = no systemic Sx, B = systemic B symptoms
78
Q

LYMPHOMA

What is the management of Hodgkin’s lymphoma?

A
  • Chemotherapy ± radiotherapy
79
Q

LYMPHOMA
What is non-Hodgkin’s lymphoma?
Give some key types

A
  • All lymphomas without Reed-Sternberg cells
  • Diffuse large B cell lymphoma most common = rapidly growing mass in >65y + hepatitis C
  • Burkitt = associated with EBV, malaria + HIV
  • Mucosa-associated lymphoid tissue (MALT) = associated with H. pylori
80
Q

LYMPHOMA

What is the clinical presentation of non-Hodgkin lymphoma?

A
  • Non-tender, firm lymphadenopathy often symmetrical at multiple sites
  • B symptoms (poor prognostic marker)
81
Q

LYMPHOMA
What are the investigations for non-Hodgkin’s lymphoma?
What is the management of non-Hodgkin’s lymphoma?

A
  • Bloods = normocytic anaemia, elevated LDH
  • LN biopsy diagnostic + Ann Arbor staging with CT CAP/PET
  • Chemotherapy
82
Q

TUMOUR LYSIS SYNDROME
What is tumour lysis syndrome?
What is it related to?

A
  • Breakdown of tumour cells + subsequent release of chemicals from the cell
  • Treatment of high-grade lymphomas + leukaemias
83
Q

TUMOUR LYSIS SYNDROME

What is the clinical presentation of tumour lysis syndrome?

A
  • Often 2 days post chemo with dysuria/oliguria, abdo pain + weakness
84
Q

TUMOUR LYSIS SYNDROME
What investigations would you do for tumour lysis syndrome?
What laboratory findings would you expect?

A
  • U&Es + serum uric acid
  • AKI
  • High K+, phosphate, uric acid (25% increase)
  • Low calcium (25% decrease)
85
Q

TUMOUR LYSIS SYNDROME

How do you diagnose tumour lysis syndrome?

A
  • Laboratory confirmation

- PLUS 1 of increased serum creatinine (1.5x upper limit of normal), cardiac arrhythmias/sudden death, seizure

86
Q

TUMOUR LYSIS SYNDROME

What is the management of tumour lysis syndrome?

A
  • High risk = IV allopurinol OR rasburicase immediately prior to + during first days of chemo for prophylaxis
  • Low risk = PO allopurinol during chemo cycles to prevent
87
Q

TUMOUR LYSIS SYNDROME

What is the mechanism of action of rasburicase?

A
  • Recombinant urate oxidase an enzyme that metabolises uric acid to more water soluble allantoin so excreted more easily via kidneys
88
Q

MYELOMA
What is the pathophysiology of myeloma?
What are the risk factors?

A
  • B cell malignancy causing clonal proliferation of plasma cells > increased monoclonal Igs (paraprotein), mostly IgG = hypogammaglobulinaemia
  • Older age, male, Black African ethnicity
89
Q

MYELOMA

What condition may be seen before developing myeloma?

A
  • Monoclonal gammopathy of undetermined significance (MGUS) = excess of a single type of antibody (components) without other features of myeloma
90
Q

MYELOMA

What is the clinical presentation of myeloma?

A

OLD CRAB –

  • Old age (peak incidence 60–70)
  • Calcium high
  • Renal failure (light chain deposition within renal tubules)
  • Anaemia (classically pancytopaenia)
  • Bone lesions = pathological #, pain
91
Q

MYELOMA
What are some investigations of myeloma?
What is diagnostic

A
  • Bloods = FBC (normocytic anaemia), U&Es, Ca2+ & ESR high, normal ALP + phosphate
  • Blood film = rouleaux formation (RBCs stacked)
  • Monoclonal proteins in serum/urine electrophoresis = Bence Jones protein
  • Imaging for bone lesions (whole body MRI/CT or skeletal XR survey)
  • Bone marrow biopsy = diagnostic
92
Q

MYELOMA

What are some complications of myeloma?

A
  • Renal failure
  • Hypercalcaemia
  • Peripheral neuropathy
  • Spinal cord compression
93
Q

MYELOMA

What is the management of myeloma?

A
  • Bone pain = bisphosphonates or radiotherapy for localised pain
  • Influenza + PCV vaccination for infection prevention
  • Chemo
  • Stem cell transplant
94
Q

NEUTROPENIC SEPSIS
What is neutropenic sepsis?
Why does it commonly occur?

A
  • Neutrophils <0.5x10^9/L in a patient on anticancer treatment with 1 of: temp >38 or other signs/symptoms of clinical sepsis
  • Complication of cancer therapy often chemo, often occurring 7–14d after
95
Q

NEUTROPENIC SEPSIS

What are the investigations for neutropenic sepsis?

A
  • Blood gas
  • Blood cultures
  • FBC, CRP, U&E, LFT, clotting
  • Urine MC&S
  • CXR
96
Q

NEUTROPENIC SEPSIS

What is the management of neutropenic sepsis?

A
  • SEPSIS 6 = BUFALO
  • Piperacillin + tazobactam (Tazocin) within 1h (do NOT wait for FBC)
  • If febrile + unwell after 48h meropenem ± vancomycin
97
Q

NEUTROPENIC SEPSIS

What is the prophylaxis of neutropenic sepsis?

A
  • If anticipated to have neutrophils of <0.5 due to their treatment then offer fluoroquinolone
98
Q

HAEMOPHILIA
What is haemophilia?
What are the 2 types?

A
  • X-linked recessive deficiency of one of the clotting factors (more common in males)
  • Haemophilia A (more common) = factor VIII, haemophilia B = factor IX
99
Q

HAEMOPHILIA

What is the clinical presentation of haemophilia?

A
  • Large bleeds into joints (haemoarthrosis) or muscles (haematoma)
  • Prolonged bleeding after surgery/trauma
  • Neonates = intracranial haemorrhage + cord bleeding
100
Q

HAEMOPHILIA

What are the investigations for haemophilia?

A
  • PT (F2/5/7/10, extrinsic) = normal
  • APTT (intrinsic) = greatly elevated
  • Diagnosis with factor VIII/IX assay
  • Prenatal Dx with CVS DNA testing
101
Q

HAEMOPHILIA

What is the management of haemophilia?

A
  • Avoid NSAIDs + IM injections
  • Minor bleeds = desmopressin which stimulates vWF release
  • Major bleeds = IV infusion of recombinant FVIII/FIX concentrate, TXA
102
Q

HAEMOPHILIA

What prophylactic treatment can you give in haemophilia but what is a potential risk of this?

A
  • Recombinant factor VIII/IX concentrate to reduce risk of arthropathy
  • Risk of antibodies forming against the factor + making treatment ineffective
103
Q

VON WILLEBRAND DISEASE

What is the role of von Willebrand factor?

A
  • Facilitates platelet adhesion to damaged endothelium

- Acts as carrier protein for FVIII:C, protecting it from inactivation + clearance

104
Q

VON WILLEBRAND DISEASE
What is the pathophysiology of von Willebrand disease (vWD)?
What causes it?

A
  • Defective platelet plug formation + deficient FVIII:C > bleeding
  • Most common inherited bleeding disorder, mostly autosomal dominant
105
Q

VON WILLEBRAND DISEASE
What is the clinical presentation of vWD?
How does this differ to haemophilia?

A
  • Mucosal bleeding (epistaxis, menorrhagia, bleeding gums) + bruising
  • Spontaneous large soft tissue bleeding is uncommon
106
Q

VON WILLEBRAND DISEASE

What are the investigations for vWD?

A
  • Prolonged bleeding time as primary haemostasis affected

- PT normal, APTT elevated

107
Q

VON WILLEBRAND DISEASE

What is the management of vWD?

A
  • Avoid NSAIDs + IM injections
  • Desmopressin causes release of vWF + FVIII antigen
  • TXA for mild bleeding
  • Severe vWD may require plasma derived FVIII concentrate or vWF infusion
108
Q

MYELODYSPLASIA

What is the pathophysiology of myelodysplastic syndromes?

A
  • Hypercellular bone marrow with abnormal maturation of all three cell lineages
  • Decreased peripheral blood cells as cells can’t get out > bone marrow failure
109
Q

MYELODYSPLASIA
What causes myelodysplastic syndromes?
How do they present and what’s a key complication?

A
  • Secondary to radio or chemotherapy
  • Bone marrow failure (pancytopaenia) Sx
  • May progress to AML
110
Q

MYELODYSPLASIA

What investigations would you do in myelodysplastic syndromes?

A
  • FBC = pancytopaenia, decreased reticulocytes
  • Blood film = ring sideroblasts
  • Bone marrow aspiration + biopsy diagnostic = hypercellular bone marrow
111
Q

MYELODYSPLASIA

What is the management of myelodysplastic syndromes?

A
  • Supportive = transfusions, EPO + G-CSF

- Stem cell transplant

112
Q

MYELOPROLIFERATIVE
What are the 3 myeloproliferative disorders to know?
What are their similarities?

A
  • Polycythaemia vera, essential thrombocytosis + myelofibrosis
  • All linked to JAK2 mutation which can be targeted by JAK2 inhibitors ruxolitinib
  • All have potential to progress + transform to AML
113
Q

MYELOPROLIFERATIVE
What is polycythaemia vera?
What are some causes?

A
  • Proliferation of erythroid cell line = RBCs

- Primary or secondary to hypoxia, increased EPO

114
Q

MYELOPROLIFERATIVE

What is the clinical presentation of polycythaemia vera?

A
  • Hyperviscosity = thrombotic complications (DVT, PE, TIA)
  • Plethoric complexion
  • Splenomegaly + pruritus (esp. after hot bath)
115
Q

MYELOPROLIFERATIVE

What investigations would you do in polycythaemia vera?

A
  • Bloods = raised Hb, haematocrit + ALP
  • 95% JAK2 +ve
  • Bone marrow = hypercellular
116
Q

MYELOPROLIFERATIVE

What is the management of polycythaemia vera?

A
  • First-line = venesection to aim for haematocrit <0.45
  • Aspirin 75mg OD to reduce risk of thrombotic events
  • Hydroxyurea as chemo
117
Q

MYELOPROLIFERATIVE
What is essential thrombocytosis?
How does it present?

A
  • Proliferation of the megakaryocyte cell line > platelets
  • Both thrombosis + bleeding
  • Platelet count >600
118
Q

MYELOPROLIFERATIVE

What is the management of essential thrombocytosis?

A
  • Aspirin 75mg OD to reduce risk of thrombotic events

- Hydroxyurea to reduce platelet count

119
Q

MYELOPROLIFERATIVE

What is myelofibrosis?

A
  • Megakaryocyte hyperplasia producing increased platelet derived growth factor = intense bone marrow fibrosis
120
Q

MYELOPROLIFERATIVE

What is the clinical presentation of myelofibrosis?

A
  • Most commonly elderly presenting with anaemia (fatigue)
  • Systemic = fever, weight loss + night sweats
  • Massive splenomegaly
121
Q

MYELOPROLIFERATIVE

What are the investigations in myelofibrosis?

A
  • Bloods = anaemia, high urate + LDH due to increased cell turnover
  • Blood film = teardrop poikilocytes
  • Bone marrow aspirate difficult resulting in ‘dry tap’ so biopsy needed
122
Q

MYELOPROLIFERATIVE

What is the management of myelofibrosis?

A
  • Stem cell transplantation
  • Hydroxyurea + folic acid
  • ?Splenectomy
123
Q

DIC
What is disseminated intravascular coagulation (DIC)?
What causes it?

A
  • Dysregulated coagulation + fibrinolysis leading to widespread clotting with resultant bleeding
  • Sepsis, trauma, malignancy, obstetrics (HELLP syndrome)
124
Q

DIC

What is the clinical presentation of DIC?

A
  • Bleeding from unrelated sites (epistaxis, cannula, haematuria)
  • Petechiae/purpura, confusion + shock
125
Q

DIC

What are the classic investigation findings in DIC?

A

FBC + clotting crucial –
- Raised = PT, APTT, bleeding time, fibrinogen degradation products
- Decreased = platelets, fibrinogen
Schistocytes may be seen due to microangiopathic haemolytic anaemia

126
Q

DIC

What is the management of DIC?

A
  • Treat underlying

- Supportive = FFP + platelets

127
Q

ITP

What is the pathophysiology of immune thrombocytopaenic purpura (ITP)?

A
  • Type 2 hypersensitivity reaction with platelet destruction by anti-platelet IgGs
128
Q

ITP

What is the clinical presentation of ITP in paeds/adults and in general?

A
  • Paeds = acute 1-2w post-viral infection or vaccine
  • Adults = more chronic condition, commoner in older females
  • Petechiae/purpuric rash, bruising, bleeding (less common)
129
Q

ITP

What investigations would you do for ITP?

A
  • FBC = isolated thrombocytopaenia
  • Blood film
  • Bone marrow examination only required if atypical features
130
Q

ITP

What is the management of ITP in paeds/adults + in both?

A
  • Paeds = first-line often no treatment
  • Adults = first-line PO pred
  • IVIg or platelet transfusions may be required based on platelet count or bleeding
131
Q

TTP

What is the pathophysiology of thrombotic thrombocytopaenic purpura (TTP)?

A
  • Deficiency of ADAMTS13 protease which usually inactivates vWF to reduce platelet adhesion to vessel walls + clot formation so vWF overactivity + sticky multimers > clots in small vessels which haemolyses RBCs = microangiopathic haemolytic anaemia
132
Q

TTP

What are some causes of TTP?

A
  • Post-infection (urinary, GI), pregnancy + SLE

- Congenital absence of ADAMTS13 or autoimmune disease with Ab against it

133
Q

TTP

What is the clinical presentation of TTP?

A
  • Fever
  • Fluctuating neuro signs from microemboli
  • Renal failure
  • Abdominal pain
    (Overlap with HUS)
134
Q

TTP

What is the investigations and management of TTP?

A
  • Bloods = raised LDH, film = schistocytes from haemolysis

- Plasma exchange, steroids + rituximab (monoclonal Ab against CD20 B cells)

135
Q

THROMBOPHILIA

What are some causes of thrombophilia?

A

Inherited
- Factor V leiden = activated protein C resistance #1 cause
- Protein C & S deficiency = usually inactivates factors V + VIII respectively
- Antithrombin III deficiency = usually inactivates factors IIa, IXa, Xa + XIa
Acquired
- Antiphospholipid syndrome
- COCP

136
Q

THROMBOPHILIA
What are some investigations you would do in thrombophilias?
What is the management?

A
  • FBC, clotting + fibrinogen levels
  • Assays = protein C & S, antithrombin
  • Factor V Leiden mutation analysis
  • Anticoagulated so INR 2-3 or 3-4 if recurrence on warfarin
137
Q

TRANSFUSIONS
What are the RBC transfusion thresholds?
What are the Hb targets post-transfusion?
How much does 1 unit raise Hb and how quickly do you transfuse it?

A
  • 70g/L or 80g/L if ACS
  • 70–90g/L or 80–100g/L if ACS
  • 10g/L + if non-urgent transfuse over 90-120m
138
Q

TRANSFUSIONS

What are the platelet transfusion thresholds in active bleeding?

A
  • Clinically significant (haematemesis, melaena, prolonged epistaxis) + platelets <30
  • Severe bleeding/critical site (CNS) + platelets <100
139
Q

TRANSFUSIONS
What are the platelet transfusion thresholds for…

i) pre-invasive procedure prophylaxis?
ii) no active bleeding or planned invasive procedure?

A

i) >100 if surgery at critical site, 50–75 if high bleeding risk or >50 for most
ii) 10

140
Q

TRANSFUSIONS
What is an important risk of platelet transfusions?
How quickly do you transfuse it?
When would you not perform a platelet transfusion?

A
  • Highest risk of bacterial contamination
  • 1 unit/30m
  • Chronic bone marrow failure, autoimmune thrombocytopaenia, HIT or TTP
141
Q

TRANSFUSIONS
What is present in FFP and the indications?
What is present in cryoprecipitate and the indications?
How quickly do you transfuse them both?

A
  • All clotting factors > major bleeding, DIC, liver disease, TTP
  • Factors 8, vWF + fibrinogen > major bleeding, DIC
  • 1 unit/30m
142
Q

TRANSFUSIONS

What are the 6 main acute and 2 late transfusion reactions that can occur?

A

Acute –
- Minor allergic reaction
- Anaphylaxis
- Acute haemolytic transfusion reaction
- Febrile non-haemolytic transfusion reaction
- Transfusion-related acute lung injury (TRALI)
- Transfusion-associated circulatory overload (TACO)
Late –
- Delayed haemolytic transfusion reaction
- Transfusion-associated graft versus host disease

143
Q

TRANSFUSIONS

What are the features and management of minor allergic reactions?

A
  • Pruritus, urticaria

- Temporarily stop, antihistamine + monitor

144
Q

TRANSFUSIONS

What are the risk factors, features and management of anaphylaxis?

A
  • Increased risk in patients with IgA deficiency with anti-IgA Ab
  • Hypotension, SOB, wheeze, angioedema
  • Stop transfusion, usual Mx (ABC, IM adrenaline)
145
Q

TRANSFUSIONS

What are the causes, features and management of acute haemolytic transfusion reaction?

A
  • ABO-incompatibility due to RBC destruction by IgM Ab
  • Fever, hypotension minutes after, later DIC
  • Stop transfusion, fluid resus, send blood for direct Coombs
146
Q

TRANSFUSIONS

What are the features and management of febrile non-haemolytic transfusion reactions?

A
  • Fever, rigors but otherwise well

- Slow transfusion, antipyretic (paracetamol), monitor

147
Q

TRANSFUSIONS

What are the features and management of TRALI?

A
  • Hypoxia, fever, HYPOtension, CXR = pulmonary infiltrates

- Stop transfusion, oxygen + supportive care

148
Q

TRANSFUSIONS

What are the features and management of TACO?

A
  • Pulmonary oedema, raised JVP, HYPERtension

- Slow transfusion, ?furosemide

149
Q

TRANSFUSIONS
What are the features of…

i) delayed haemolytic transfusion reaction?
ii) transfusion-associated graft versus host disease?

A

i) Jaundice, anaemia + fever often 5d post-transfusion
ii) Donor blood lymphocytes attack the recipient’s body (irradiated blood products are depleted of T-lymphocytes to avoid this)

150
Q

ANTICOAGULATION
What is the mechanism of action of warfarin?
What monitoring is required?

A
  • Vitamin K antagonist so decreases vitamin K dependent factors 2, 7, 9 + 10 (1972)
  • INR (patient’s PT ÷ normal PT)
151
Q

ANTICOAGULATION
What are some indications for warfarin?
What are the target INRs?

A
  • First line (+ aspirin) for mechanical heart valves (mitral usually higher INR than aortic)
  • 2nd line after DOACs for VTE + AF
  • Usually 2.5 but 3.5 if recurrent VTE
152
Q

ANTICOAGULATION
What are some side effects of warfarin?
What can lower INR?
What can increase INR?

A
  • Haemorrhage, teratogenic (safe in breastfeeding)
  • P450 inducers = PC BRAS (Phenytoin, Carbamazepine, Barbiturates, Rifampicin, Alcohol chronic, sulfonylureas & vitamin K food (green leafy veg)
  • P450 inhibitors = AO DEVICES (allopurinol, omeprazole, disulfiram, erythromycin, valproate, isoniazid, ciprofloxacin, ethanol acute, sulfonamides
153
Q

ANTICOAGULATION
A patient on warfarin presents with an INR between 5.0–8.0 and…

i) no bleeding
ii) minor bleeding

what is the management?

A

i) Withhold 1–2 doses, reduce subsequent maintenance dose

ii) Stop warfarin (restart when INR <5.0), IV vitamin K 1–3mg (phytomenadione)

154
Q

ANTICOAGULATION
A patient on warfarin presents with an INR >8 and…

i) no bleeding
ii) minor bleeding

what is the management?

What about any INR and major bleeding?

A

i) Stop warfarin (restart when INR <5.0), PO vitamin K 1–5mg (IV prep PO), repeat after 24h if required
ii) Stop warfarin (restart when INR <5.0), IV vitamin K 1–3mg, repeat after 24h if required

  • IV vitamin K 5mg and prothrombin complex concentrate (Beriplex) or FFP
155
Q

ANTICOAGULATION
What is the mechanism of action of DOACs?
What is the reversal agent?
What would you use in renal impairment?

A
  • Apixaban, rivaroxaban = direct Xa inhibitors reverse with andexanet alfa
  • Dabigatran = direct thrombin (IIa) inhibitor reverse with idarucizumab
  • Apixaban
156
Q

ANTICOAGULATION
What is the mechanism of action of heparin?
How would you monitor it?
What are some side effects?

A
  • Activate antithrombin III
  • Unfractionated = APTT, LMWH = factor Xa
  • Bleeding, osteoporosis hyperkalaemia + HIT
157
Q

ANTICOAGULATION
What is heparin-induced thrombocytopaenia (HIT)?
How is it managed?

A
  • Low platelets BUT prothrombotic due to increased activation of platelets
  • Stop heparin, monitor platelets, reversal with protamine sulfate
158
Q

BONE MARROW FAILURE
What are some causes of bone marrow failure?
What anaemia pattern is seen?

A 
Pancytopaenia –
- Inherited = Fanconi's anaemia
- Acquired = aplastic anaemia, leukaemia
Single cell cytopaenia –
- Acquired = red cell aplasia
- Normochromic, normocytic
159
Q

BONE MARROW FAILURE
What is Fanconi anaemia?
How does it present?
What is the management?

A
  • AR condition with pancytopaenia leading to aplastic anaemia
  • Skin = café-au-lait spots, skeletal = absent thumbs, GU = horseshoe kidney
  • Bone marrow transplant as high mortality from failure or acute leukaemia
160
Q

BONE MARROW FAILURE
What is aplastic anaemia?
What causes it?

A
  • Hypocellularity of bone marrow + pancytopaenia

- Fanconi’s anaemia, parvovirus B19

161
Q

BONE MARROW FAILURE
What investigations would you do in aplastic anaemia?
What is the management?

A
  • FBC, blood film, bone marrow biopsy diagnostic (hypocellular marrow)
  • Supportive (transfusions), immunosuppression, stem cell transplant
162
Q

BONE MARROW FAILURE
What is red cell aplasia?
How does it present?
How is it managed?

A
  • Parvovirus B19 infection destroys erythroid precursor cells + erythropoiesis stops for 5–10d
  • Slapped cheek syndrome
  • PCR/serology, supportive or transfusion
163
Q

ANAEMIA OF CHRONIC DISEASE
What are some causes of anaemia of chronic disease?
What would investigations show?
What is the management?

A
  • Autoimmune/connective tissue disease (SLE), inflammation (RA, Crohn’s), cancer
  • Normocytic anaemia with reduced TIBC, high ferritin
  • Treat underlying + ?EPO
164
Q

MALARIA

What is malaria?

A
  • Disease caused by plasmodium protozoa which is transmitted by the female anopheles mosquito
165
Q

MALARIA

What is the pathophysiology of malaria?

A
  • Sporozoites in saliva > enter hepatocytes and mature > rupture to release merozoites into blood + enter RBCs > sporozoites a mosquito can pick up
166
Q

MALARIA

What are the causes of malaria?

A
  • Plasmodium falciparum = causes almost all severe malaria cases, #1 cause overall
  • Plasmodium vivax = #1 non-falciparum malaria, more benign
  • Plasmodium ovale
  • Plasmodium malariae
167
Q

MALARIA

What are some protective factors from malaria?

A
  • Sickle cell trait
  • G6PD deficiency
  • HLA-B53
168
Q

MALARIA

What is the clinical presentation of malaria?

A
  • Flu-like prodrome = headache, myalgia, malaise
  • Fever paroxysms (vivax/ovale is cyclical every 48h, malariae every 72h)
  • Anaemia + splenomegaly
  • Hx of foreign travel = Central America, Indian subcontinent, Africa
169
Q

MALARIA

How do you investigate malaria?

A
  • Thick + thin blood films with Giemsa stain

- FBC = anaemia, blood gas may show acidosis

170
Q

MALARIA

What are some complications with malaria?

A
  • Cerebral malaria = confusion, seizures
  • Hypoglycaemia
  • AKI
  • DIC
171
Q

MALARIA

What is the management of non-falciparum malaria?

A
  • Artemisinin-based combination therapy (ACT) or chloroquine (ACT if chloroquine-resistance or pregnancy)
  • Primaquine following acute treatment if vivax or ovale to prevent relapse
172
Q

MALARIA

What is the management of falciparum malaria?

A
  • Uncomplicated = ACT first line

- Severe = IV artesunate

FINALS (20 decks)

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