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Med Student Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

Anaemia

Definition (2)

A

Low haemoglobin concentration, due to either a low red cell mass or increased plasma volume (eg. in pregnancy)
<135g/l for men, <115g/l for women

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2
Q

Anaemia

Signs + symptoms (7)

A 
Fatigue 
Faintness 
Dyspnoea
Palpitations 
Headache 
Pallor
In severe anaemia, there may be signs of hyperdynamic circulation, eg. tachycardia, flow murmurs (ejection systolic-loudest over apex)
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3
Q

Anaemia

Types (4)

A 
Low MCV (microcytic): iron deficiency, thalassaemia 
Normal MCV (normocytic): acute blood loss, anaemia of chronic disease, bone marrow failure, pregnancy, hypothyroidism 
High MCV (macrocytic): B12 deficiency, folate deficiency, alcohol, myelodysplastic, hypothyroid 
Haemolytic: normo/macrocytic, suspect if reticulocytosis and increased bilirubin, mild jaundice but no bilirubin in urine as it causes pre hepatic jaundice
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4
Q

Iron Deficiency Anaemia

Aetiology (3)

A

Blood loss (menorrhagia, GI bleeding)
Malabsorption (coeliac)
Hookworm most common cause in the Tropics

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5
Q

Iron Deficiency Anaemia

Signs + symptoms (3)

A

Koilonychia (spoon shaped nails)
Atrophic glossitis
Angular cheiolosis (ulceration at side of mouth)

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6
Q

Iron Deficiency Anaemia

Investigations (3)

A

Microcytic, hypochromic anaemia
Reduced ferritin
Reduced serum iron with increased total iron inding capacity

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7
Q

Iron Deficiency Anaemia

Treatment (4)

A

Treat cause
Oral iron, eg. ferrous sulfate (SE: nausea, abdo discomfort, constipation, black stool)
Continue treatment until Hb is normal and for at least 3 months to restore stores
IV iron almost never needed unless oral route is impossible or ineffective, eg. chronic renal failure with erythropoietin therapy

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8
Q

Anaemia of Chronic Disease

Aetiology (5)

A 
Chronic infection 
Vasculitis 
Rheumatoid 
Malignancy 
Renal failure
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9
Q

Anaemia of Chronic Disease

Pathology (3)

A

Poor use of iron in erythropoiesis
Cytokine-induced shortening of RBC survival
Reduced production of and response to erythropoietin

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10
Q

Anaemia of Chronic Disease

Investigations (3)

A

Mild normocytic anaemia
Normal/increased ferritin
Do blood film, B12, folate, TSH and tests for haemolysis

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11
Q

Anaemia of Chronic Disease

Treatment (2)

A

More vigorous treatment of underlying disease

Erythropoietin is effective in raising the haemoglobin level (SE: flu like symptoms, hypertension)

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12
Q

Macrocytic Anaemia

Aetiology (3)

A

Megaloblastic: B12 deficiency, folate deficiency, cytotoxic drugs
Non-megaloblastic: alcohol (most common cause of macrocytosis but not often anaemia), reticulocytosis (eg. haemolysis), liver disease, hypothyroidism, pregnancy
Other haematological disease: myelodysplasia, myeloma, myeloproliferative disorders

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13
Q

Macrocytic Anaemia

Investigations (5)

A

Blood film: hypersegmented polymorphs in B12 and folate deficiency
LFT
TFT
Serum B12 and serum folate
Bone marrow biopsy: megaloblastic, normoblastic marrow (eg. in liver disease, hypothyroidism), abnormal erythropoiesis (eg. leukaemia), increased erythropoiesis (eg. haemolysis)

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14
Q 
Macrocytic Anaemia
Folate deficiency (3)
A

Found in green vegetables, nuts and yeast
Causes: poor diet, increased demand (pregnancy, haemlysis, malignancy), malabsorption (coeliac disease), drugs (alcohol, anti-epileptics, methotrexate)
Treatment: folic acid for 4 months, never without B12 unless they have normal levels

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15
Q 
Macrocytic Anaemia
B12 deficiency (4)
A

Found in meat, fish and dairy
B12 binds to intrinsic factor in the stomach and then is absorbed in the terminal ileum
Causes: dietary (eg. vegan), malabsorption (lack of intrinsic factor = pernicious anaemia, often post gastrectomy or ileal restriction)
Can lead to subacute combined degeneration of the spinal cord with peripheral neuropathy

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16
Q 
Macrocytic Anaemia
Pernicious anaemia (4)
A

Caused by an autoimmune atrophic gastritis, leading to lack of intrinsic factor secretion
Associated with other autoimmune disease: thyroid disease, Addison’s disease, hypoparathyroidism, stomach cancer (so have low threshold for doing upper GI endoscopy)
Investigations: low Hb, high MCV, low serum B12, megaloblastic marrow, intrinsic factor antibodies
Treatment: treat cause, may need B12 injections

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17
Q

Haemolytic Anaemia

Pathology (3)

A

Haemolysis = premature breakdown of RBCs
Occurs in the circulation (intravascular) or in the reticuloendothelial system, ie. macrophages of liver, spleen and bone marrow (extravascular)
Haemolysis may be asymptomatic but if the bone marrow doesn’t compensate sufficiently, a haemolytic anaemia results

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18
Q

Haemolytic Anaemia

Signs + symptoms (5)

A 
Jaundice 
Dark urine 
Hepatosplenomegaly (when extravascular) 
Gallstones (pigmenteed, due to increased bilirubin from haemolysis) 
Leg ulcers (due to poor blood flow)
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19
Q

Haemolytic Anaemia

Investigations (7)

A 
FBC 
Reticulocytes 
Bilirubin 
LDH 
Urinary urobilinogen 
Blood film: macrocytes 
Direct antiglobulin (Coombs) test identifies red cells coated with antibody or complement, a +ve result indicates an immune cause of the haemolysis)
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20
Q

Haemolytic Anaemia

Causes (6)

A

Drug induced: causing formation of RBC autoantibodies binding to RBC membranes (eg. penicillin) or production of immune complexes (eg. quinine), Coombs +ve
Autoimmune: autoantibodies cause extravascular haemolysis, Coombs +ve
Hep B + C: Coombs -ve, autoimmune haemolytic anaemia
Enzyme defects: G6PD deficiency is chief one, most asymptomatic but can cause oxidative crisis –> rapid anaemia + jaundice
Membrane defects: Coombs -ve and need folate, eg. hereditary spherocytosis
Haemoglobinopathy: sickle, thalassaemia

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21
Q

Sickle Cell Anaemia

Definition (1)

A

Autosomal recessive disorder causing production of abnormal B-globin chains (mostly in those of African descent)

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22
Q

Sickle Cell Anaemia

Pathology (2)

A

An amino acid substitution in the gene coding for the B chain results in the production of HbS rather than HbA
HbS polymerises when deoxygenated causing RBCs to deform, producing sickle cells, which are fragile and haemolyse and also block small vessels

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23
Q

Sickle Cell Anaemia

Signs + symptoms (7)

A

Usually well tolerated unless in crisis (due to microvascular occlusion)
Often affects marrow, causing severe pain; triggered by cold, dehydration, infection, hypoxia
Occlusion may occur, causing mesenteric ischaemia, mimicking acute abdo
CNS infarction: stroke, seizures, cognitive defects
Dactylitis
Avascular necrosis
Leg ulcers

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24
Q

Sickle Cell Anaemia

Investigations (6)

A 
May have haemolysis 
Hb 60-90g/L 
Increased reticulocytes 
Increased bilirubin 
Blood film shows sickle cells 
Hb electrophoresis to confirm diagnosis
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25
Q

Sickle Cell Anaemia

Treatment of chronic disease (2)

A

Hydroxycarbamide if frequent crises

Splenic infarction leads to hyposplenism so give prophylactic antibiotics and immunisation

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26
Q

Sickle Cell Anaemia

Treatment of crises (4)

A

Analgesia
Crossmatch blood
Antibiotics if fever, unwell or chest signs
Give blood transfusion if Hb or reticulocytes fall sharply

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27
Q

Thalassaemia

Definition (2)

A

Genetic disease of unbalanced Hb synthesis, with under or no production of one globin chain
Unmatched globins precipitate damaging RBC membranes, causing their haemolysis while still in the marrow

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28
Q 
Thalassaemia 
alpha thalassaemia (6)
A

There are 4 alpha genes
Alpha thalassaemias are caused by gene deletions
If 4 genes are deleted, death in utero
If 3 genes are deleted, there may be moderate anaemia and features of haemolysis: hepatosplenomegaly, leg ulcers and jaundice
If 2 genes are deleted, there is asymptomatic carrier state with reduced MCV
If 1 gene deleted, clinical state is normal

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29
Q 
Thalassaemia 
beta thalassaemia (4)
A

Usually caused by point mutations in B-globin genes leading to reduced B chain production or absence
B thalassaemia minor: carrier state and usually asymptomatic or mild, well tolerated anaemia (often confused with iron deficiency)
B thalassaemia intermedia: moderate anaemia but not requiring trasnfusions
B thalassaemia major: abnormalities in both B-globin genes, presents in 1st year with severe anaemia and failure to thrive, extramedullary heamopoiesis in response to anaemia causing weird head shape + hepatosplenomegaly

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30
Q

Thalassaemia

Investigations (5)

A 
FBC 
MCV 
Blood film 
Iron 
Hb electrophoresis
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31
Q

Thalassaemia

Treatment (5)

A

Regular lifelong transfusions to suppress extramedullary haematopoiesis and allow normal growth
Iron-chelatores to prevent iron overload
Ascorbic acid to increase urinary excretion of iron
Splenectomy if hypersplenism persists
Marrow transplant may cure

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32
Q

Differential White Cell Count

Neutrophils (3)

A

Ingest and kill bacteria, fungi and damaged cells
Neutrophilia: bacterial infections, inflammation, myeloproliferative disorders, drugs (steroids), stress (trauma, haemorrhage), malignancy
Neutropenia: viruses, drugs (post chemo), severe sepsis, hypersplenism, bone marrow failure

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33
Q

Differential White Cell Count

Lymphocytes (4)

A

Divided into T and B
Important for cell-mediated immunity and antibody production
Lymphocytosis: acute viral infections, chronic infection (eg. TB, syphilis, hepatitis), leukaemia, lymphoma
Lymphopenia: steroid therapy, SLE, HIV, post chemo, radio

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34
Q

Differential White Cell Count

Eosinophils (2)

A

Mediate allergic reactions and defend against parasites

Eosinophilia: drug reactions eg. erythema multiforme, allergies, parasites, skin disease

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35
Q

Differential White Cell Count

Monocytes (2)

A

Precursors of tissue macrophages

Monocytosis: post chemo/radio, chronic infections, malignancy

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36
Q

Differential White Cell Count

Basophils (2)

A

Contain histamine, which is released on binding IgE
Basophilia: myeloproliferative disease, viral infections, IgE mediated hypersensitivity reactions (eg. urticaria), inflammatory disorders (eg. UC, RA)

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37
Q

Haemophilia

Definition (3)

A

Haemophilia A- factor VIII
Haemophilia B- factor IX deficiency
X-linked recessive

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38
Q

Haemophilia

Signs + symptoms (2)

A

Bleeds into joints leading to crippling arthropathy

Bleeds into muscles causing haematomas (increased pressure can lead to nerve palsies and compartment syndrome)

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39
Q

Haemophilia

Investigations (2)

A

Reduced factor VIII/IX assay

High APTT

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40
Q

Haemophilia

Treatment (4)

A

Avoid NSAIDs + IM injections
Minor bleeds: pressure and elevation, desmopressin works to increase factor VIII
Major bleeds eg. haemarthrosis: increases factor VIII levels to 50% of normal
Life threatening bleeds: need factor VIII levels of 100% eg. with recombinant factor VIII

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41
Q

von Willebrand’s Disease

Role of vWF (3)

A

Bring platelets into contact with exposed subendothelium
Make platelets bind to each other
Bind to factor VIII, protecting it from destruction in the circulation

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42
Q

von Willebrand’s Disease

Types (3)

A

Type I: most common, autosomal dominant, reduced levels of vWF, mild
Type II: autosomal dominant, abnormal vwF, bleeding tendency varies
Type III: least common, autosomal recessive, undetectable vWF so less factor VIII, severe

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43
Q

von Willebrand’s Disease

Signs + symptoms (4)

A

Bruising
Epistaxis
Menorrhagia
Increased bleeding post tooth extraction

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44
Q

von Willebrand’s Disease

Investigations (4)

A

Increased APTT
Increased bleeding time
Reduced factor VIIIC (clotting activity)
INR + platelets normal

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45
Q

von Willebrand’s Disease

Treatment (2)

A

Desmopressin for mild bleeding

vWF-containing factor VIII concentrate for surgery or major bleeds

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46
Q

Acute Lymphoblastic Leukaemia

Definition (2)

A

Malignancy of lymphoid cells, affecting T/B cells, arresting maturation and promoting uncontrolled proliferation of immature blast cells, with marrow failure and tissue infiltration
Commonest cancer in childhood

47
Q

Acute Lymphoblastic Leukaemia

Classification (3)

A

Morphological (microscopic appearance)
Immunological (surface markers- precursor/T/B cells)
Cytogenetic (chromosomal analysis, useful for prognosis- poor with Philadelphia chromosome, 9:22 translocation)

48
Q

Acute Lymphoblastic Leukaemia

Signs + symptoms (2)

A

Marrow failure: anaemia (low Hb), infection (low WCC), bleeding (low platelets)
Infiltration: hepatomegaly, splenomegaly, lymphadenopathy, CNS involvement (CN palsies, meningism)

49
Q

Acute Lymphoblastic Leukaemia

Investigations (4)

A

Blood film: characteristic blast cells
Bone marrow: characteristic blast cells
High WCC
CXR: CT for mediastinal or abdominal lymphadenopathy

50
Q

Acute Lymphoblastic Leukaemia

Treatment (7)

A

Platelet/blood transfusion
IV fluids
Allopurinol (prevents TLS)
Immediate antibiotics for infection
Start neutropenic regimen: prophylactic antivirals, antifungals, antibiotics
Chemo
Matched related allogeneic marrow transplant once in 1st remission (no evidence of leukaemia in blood)

51
Q

Acute Lymphoblastic Leukaemia

Prognosis (2)

A

Cure rates 70-90% for kids

40% cure rate in adults

52
Q

Acute Myeloid Leukaemia

Definition (2)

A

Neoplastic proliferation of blast cells that is derived from marrow myeloid elements
Commonest acute leukaemia of adults, progresses rapidly (death in 2 months if untreated)

53
Q

Acute Myeloid Leukaemia

Aetiology (3)

A

Age
Long term complication of chemo
Myelodysplastic syndromes

54
Q

Acute Myeloid Leukaemia

Signs + symptoms (2)

A

Marrow failure: anaemia, infection, bleeding

Infiltration: hepatomegaly, splenomegaly, gum hypertrophy, skin involvement

55
Q

Acute Myeloid Leukaemia

Investigations (5)

A 
WCC high/normal/low 
Blood film: blast cells may be few 
Bone marrow biopsy: multiple blasts 
Immunophenotyping 
Cytogenetic analysis effects treatment recommendations and guides prognosis
56
Q

Acute Myeloid Leukaemia

Treatment (5)

A

Blood/platelet transfusions
IV fluids
Allopurinol (prevents TLS)
V. intensive chemo for marrow suppression
Bone marrow transplant (+ ciclosporin +/- methotrexate to reduce graft vs host disease- new marrow attacking patient’s body)

57
Q

Acute Myeloid Leukaemia

Complications (2)

A

Infection is major problem

Chemo causes increased urate levels (from TLS)

58
Q

Chronic Myeloid Leukaemia

Definition (2)

A

Uncontrolled clonal proliferation of myeloid cells

Myeloproliferative disorder

59
Q

Chronic Myeloid Leukaemia

Aetiology (2)

A

40-60

Philadelphia chromosome present in >80% (those without it have a worse prognosis)

60
Q

Chronic Myeloid Leukaemia

Signs + symptoms (12)

A 
Mostly chronic and insidious
Weight loss 
Fatigue 
Fever 
Sweats 
Features of gout (purine breakdown) 
Bleeding (platelet dysfunction) 
Splenomegaly (>75%), often massive 
Hepatomegaly
Anaemia 
Bruising 
Abdo discomfort (organomegaly)
61
Q

Chronic Myeloid Leukaemia

Investigations (5)

A

Really high WCC (especially myeloid cells- neutrophils, myelocytes, basophils, eosinophils)
Low/normal Hb
High urate
High B12
Ph chromosome found on cytogenetic analysis or bone marrow

62
Q

Chronic Myeloid Leukaemia

Phases (4)

A

Median survival 5-6 years
Chronic phase: lasting months/years, no symptoms
Accelerated phase: increased symptoms, increased splenomegaly
Blast transformation phase: acute leukaemia +/- death

63
Q

Chronic Myeloid Leukaemia

Treatment (2)

A

Tyrosine kinase inhibitor

Stem cell transplant (offers only cure but significant morbidity + mortality, may be 1st line for young patients)

64
Q

Chronic Lymphocytic Leukaemia

Definition (2)

A

Accumulation of mature B cells that have escaped programmed cell death
Commonest leukaemia

65
Q

Chronic Lymphocytic Leukaemia

Signs + symptoms (6)

A 
Often asymptomatic and found on a routine FBC 
Anaemia
Prone to infections 
Enlarged, rubbery non-tender nodes 
Splenomegaly
Hepatomegaly
66
Q

Chronic Lymphocytic Leukaemia

Investigations (2)

A

Increased lymphocytes

Later, marrow infiltration: low Hb, low neutrophils, low platelets

67
Q

Chronic Lymphocytic Leukaemia

Complications (3)

A

Autoimmune haemolysis
Increased rate of infection due to hypogammaglobulinaemia (low IgG)- often the cause of death
Marrow failure

68
Q

Chronic Lymphocytic Leukaemia

Treatment (4)

A

Consider drugs if symptomatic, immunoglobulin genes are unmutated
Rituximab
Radiotherapy for lymphadenopathy and splenomegaly
Supportive: transfusions, IV human immunoglobulin if recurrent infection

69
Q

Chronic Lymphocytic Leukaemia

Prognosis (3)

A

1/3 never progress
1/3 progress slowly
1/3 progress actively

70
Q

Hodgkin’s Lymphoma

Definition (2)

A

Lymphomas are disorders caused by malignant proliferations of lymphocytes (accumulate in lymph nodes causing lymphadenopathy)
In Hodgkin’s, characteristic cells are found (with mirror-image nuclei) called Reed-Sternberg cells

71
Q 
Hodgkin's Lymphoma
Risk factors (7)
A 
2 peaks: young adults and elderly 
Male 
Affected sibling 
EBV 
SLE 
Post-transplant
Obesity
72
Q

Hodgkin’s Lymphoma

Signs + symptoms (5)

A

Often presents with enlarged, painless, non-tender superficial lymph node, typically cervical (size may increase and decrease in size spontaneously)
Constitutional upset: fever, weight loss, night sweats, pruritus and lethargy
Mediastinal lymph node involvement can cause features due to mass effect, eg. bronchial/sVT obstruction
Anaemia
Spleno-or hepatomegaly

73
Q

Hodgkin’s Lymphoma

Investigations (5)

A

Tissue diagnosis: lymph node excision biopsy
FBC
Blood film
High ESR or low Hb indicates a worse prognosis
LDH is raised as it is released during cell turnover

74
Q

Hodgkin’s Lymphoma

Staging (5)

A

I- confined to single lymph node region
II- involvement of 2+ nodal areas on same side of diaphragm
III- involvement of nodes on both sides of diaphragm
IV- spread beyond lymph nodes, eg. liver/bone marrow
Each stage is either A (no systemic symptoms) or B (presence of B symptoms- weight loss, >10% in 6 month, unexplained fever >38, night sweats)

75
Q

Hodgkin’s Lymphoma

Treatment (2)

A

Radiotherapy +/- short courses of chemo for stages IA+IIA

Longer courses of chemo for more advanced disease

76
Q

Hodgkin’s Lymphoma

Prognosis (2)

A

> 95% in IA

<40% with IVB

77
Q

Non-Hodgkin’s Lymphoma

Definition (2)

A

All lymphomas without Reed-Sternberg cells

Most are derived from B cells

78
Q

Non-Hodgkin’s Lymphoma

Signs + symptoms (3)

A

Superficial lymphadenopathy (75% at presentation)
Possible sites: skin, oropharynx, stomach, small bowel, bone, CNS, lung
Pancytopenia from marrow involvement: anaemia, infection, bleeding

79
Q

Non-Hodgkin’s Lymphoma

Investigations (2)

A

Blood: FBC, U&E, LFT, high LDH (worse prognosis, reflecting high cell turnover)
Marrow and node biopsy for classification

80
Q

Non-Hodgkin’s Lymphoma

Treatment (3)

A

May need no treatment if no symptoms
Radiotherapy may be curative in localised disease
Rituximab

81
Q

Non-Hodgkin’s Lymphoma

Prognosis (2)

A

Very variable

30% for high grade + >50% for low grade (5 year survival)

82
Q

Bleeding

Physiological processes of stopping bleeding (3)

A

Vasoconstriction
Gap-plugging by platelets
Coagulation cascade

83
Q 
Bleeding
Vascular defects (3)
A

Lead to prolonged bleeding from cuts, bleeding into skin (bruising, purpura) and bleeding from mucus membranes (epistaxis, menorrhagia)
Congenital: Ehlers-Danlos
Acquired: seile purpura, steroids, Henoch-Schonlein purpura

84
Q 
Bleeding
Platelet disorders  (4)
A

Leads to prolonged bleeding from cuts, bleeding into skin and bleeding from mucous membranes
Decreased marrow production: marrow infiltration (leukaemia, ,yeloma), marrow suppression (cytotoxic drugs, radiotherapy)
Excess destruction: immune thrombocytopenic purpura (acute in children following infection or chronic in women), TTP or HUS
Poorly functioning platelets: myeloproliferative diseae, NSAIDs

85
Q 
Bleeding
Coagulation disorders (3)
A

Cause delayed bleeding into joints and muscle
Congenital: haemophilia, von Willebrand’s
Acquired: anticoagulatns, liver disease, DIC

86
Q

Bleeding

Investigations (5)

A

FBC, film + coagulation tests
Prothrombin time: thromboplastin is added to test the extrinsic system (coagulation), tests for abnormalities in factor I, II, V, VII, X, prolonged by warfarin, vit K deficiency, liver disease (shown as INR)
Activated partial thromboplastin time (APTT): kaolin added to test intrinsic system (coagulation) tests for abnormalities in factor I, II, V, VIII, IX, X, XI, XII, prolonged by heparin, haemophilia, DIC, liver disease
Thrombin time: prolonged by heparin, DIC
D-dimers: fibrin degradation product, occurs in DIC or in presence of venous thromboembolism

87
Q

Bleeding

Treatment (2)

A

If bleeding continues in presence of clotting disorder or massive transfusion, may need FFP + platelets
In ITP, steroids +/- IV immunoglobulin may be used

88
Q

Blood Transfusion

Packed red cells (3)

A

Used in transfusion for chronic anaemia
Used for acute haemorrhage
Usually over 2h but in an emergency stat

89
Q

Blood Transfusion

Platelets (3)

A

Highest risk of bacterial infection as stored at room temp.
Used for bleeding in thrombocytopenia
Used pre-op in thrombocytopenia to prevent bleeding

90
Q

Blood Transfusion

Fresh frozen plasma (4)

A

Contains clotting factors, albumin and immunoglobulin
Risk severe allergic reactions
Prophylaxis in major surgery, where risk of significant bleeding
Plasma replacement in massive transfusion

91
Q

Blood Transfusion

Acute haemolytic transfusion reaction (4)

A

Caused by ABO incompatibility
Red cells react with patients anti-A or anti-B antibodies causing rapid intravascular haemolysis of transfused cells and release of inflammatory cytokines leading to shock, AKI, DIC
Agitation, pyrexia, hypotension, abdo/chest pain, AKI, DIC
Stop transfusion, check identity and name on unit and inspect pack, inform haematologist, send samples to lab

92
Q

Blood Transfusion

Anaphylaxis (2)

A

More likely with platelets/FFP

Bronchospasm, cyanosis, hypotension, angioedem

93
Q

Blood Transfusion

Transfusion associated lung injury (TRALI) (3)

A

Happens when donor blood antibodies react with patient neutrophils/monocytes/pulmonary endothelium causing leakage of plasma into alveolar spaces + ARDS
SOB, pyrexia, hypotension, cough
Stop transfusion, give O2, manage as ARDS, donor removed from panel

94
Q

Blood Transfusion

Transfusion Associated Circulatory Overload (TACO) (4)

A

Circulatory overload from red cell or high dose FFP transfusions
Within 6h of transfusion
SOB, hypoxia, tachycardia, elevated JVP, basal crackles, HTN
Stop transfusion, give O2, give furosemide

95
Q 
Bone Marrow Failure 
Marrow physiology (3)
A

Responsible for haemopoiesis
Normally takes place in central skeleton (vertebrae, sternum, ribs, skull) and proximal long bones
In some anaemias (eg. thalassaemia), increased demand induces haematopoiesis beyond the marrow, eg. in liver, spleen, causing organomegaly

96
Q

Bone Marrow Failure

Pancytopenia (3)

A

Reduction in all the major cell lines

Due to reduced marrow production: aplastic anaemia, infiltration (eg. acute leukaemia, myelodysplasia, myeloma)

97
Q 
Bone Marrow Failure 
Aplastic anaemia (4)
A

Rare stem cell disorder leading to pancytopenia and hypoplastic marrow (it stops making cells)
Presents with features of anaemia (low Hb), infection (low WCC) or bleeding (reduced platelets)
Most cases are autoimmune
Do allogeneic marrow transplant

98
Q

Myeloproliferative Disorders

Pathology (6)

A

Proliferation of a clone of haematopoietic myeloid stem cells in the marrow
Classification by cell type which is proliferating
RBC –> polycythaemia rubra vera
WBC –> chronic myeloid leukaemia
Platelets –> essential thrombocythaemia
Fibroblasts –> myelofibrosis

99
Q

Myeloproliferative Disorders

Polycythaemia rubra vera (4)

A

Cause: JAK2 mutation
Pathology: myeloproliferative disorder of red cells casing hyperviscosity and thrombosis
Signs + symptoms: hyperviscosity- headache, visual disturbance, dizziness, thrombosis, gout (high urate from RBC turnover)
Treatment: venesection in young or hydroxycarbamide if >60

100
Q 
Myeloproliferative Disorders
Essential thrombocytopenia (2)
A

Pathology: myeloproliferative disorder of megakaryocytes causing increased platelets leading to bleeding, thrombosis and microvascular occlusion
Treatment: aspirin or hydroxycarbamide

101
Q

Myeloproliferative Disorders

Myelofibrosis (4)

A

Epidemiology: elderly
Pathology: myeloproliferative disorder with hyperplasia of megakaryocytes which produce platelet-derived growth factor, leading to intense marrow fibrosis and myeloid metaplasia (haemopoiesis in spleen and liver) –> massive hepatosplenomegaly
Signs + symptoms: night sweats, fever, weight loss, organomegaly, bone marrow failure (low Hb, infections, bleeding)
Median survival 4-5 years

102
Q

Myeloma

Aetiology (1)

A

Neoplastic disorder of plasma cells result in the excessive production of a single immunoglobulin (paraprotein)

103
Q

Myeloma

Pathology (5)

A

Plasma cells cause osteolytic bone lesions + bone marrow failure
Paraproteins deposited in kidney causing cast nephropathy and AKI
Hyperviscosity leads to microvascular congestion and bleeding
Hypogammaglobinaemia leads to imunoparesis (infections)
Hypercalcaemia occurs due to increased osteoclastic bone resorption caused by local cytokines released by myeloma cells

104
Q

Myeloma

Signs + symptoms (4)

A 
Calcium increased (due to increased osteoclast activation by signalling myeloma cells) 
Renal failure (amyloidosis, hyperviscosity, light chain deposition, monoclonal immunoglobulins cause glomerular changes) 
Anaemia (or neutropenia/thrombocytopenia from marrow infiltration by plasma cells) 
Bony lesions (causing back ache, pathological fractures and vertebral collapse)
105
Q

Myeloma

Investigations (8)

A

FBC: normocytic normochromic anaemia
Blood film: rouleaux formation
ESR: persistently elevated
Increased urea and creatinine
Increased calcium
Bone marrow biopsy: plasma cells increased
Screening test: serum and urine electrophoresis (monoclonal protein band)
X-rays: lytic lesions (‘punched out’ appearance)

106
Q

Myeloma

Treatment (8)

A

Analgesia for bone pain
Bisphosphonates
Transfusion + erythropoietin for anaemia
Renal failure: fluid intake increase, may need dialysis
Treat infections
Chemotherapy
Autologous stem cell transplant
Allogeneic transplant can be curative in younger people but carries high risk of mortality

107
Q

Myeloma

Prognosis (1)

A

Median survival 3 years

108
Q 
Amyloidosis 
Aetiology (2)
A

Primary (AL amyloid): myeloma, lymphoma

Secondary (AA amyloid): reflects chronic inflammation in RA, UC, Crohn’s

109
Q 
Amyloidosis 
Prognosis (1)
A

Median survival 1-2 years

110
Q

Thrombophilia

Definition (1)

A

An inherited or acquired coagulopathy predisposing to thrombosis

111
Q

Thrombophilia

Inherited (2)

A

Factor V Leiden: main cause, mutation in factor V Leiden stops it being broken down by APC (activated protein C)
Prothrombin gene mutation: high prothrombin levels due to down-regulation of fibrinolysis

112
Q

Thrombophilia

Acquired (2)

A

COCP

Antiphospholipid syndrome

113
Q

Thrombophilia

Investigations (2)

A

FBC + film

Clotting profile: PT, thrombin time, APTT, fibrinogen

114
Q

Thrombophilia

Treatment (2)

A

Standard VTE treatment

Recurrence: consider lifelong warfarin

Med Student Finals (23 decks)

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