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Phase 2a > Haematology > Flashcards

Haematology Flashcards

1
Q

What is anaemia?

A

Reduced red cell mass +/- haemoglobin concentration

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2
Q

Three main causes of microcytic anaemia:

A

MCV <80

  1. Iron deficiency
  2. Chronic disease
  3. Thalassemia
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3
Q

Three main causes of normocytic anaemia:

A

MCV 80-100

  1. Acute blood loss
  2. Anaemia of chronic disease
  3. Combined haematinic deficiency
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4
Q

Three main causes of macrocytic anaemia?

A

MCV >100

  1. B12 deficiency
  2. Folate deficency
  3. Alcohol excess/liver disease
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5
Q

Specific symptoms of Fe deficiency?

A
  • Brittle nails and hair
  • Tongue inflammation
  • Angular stomatitis
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6
Q

What tests are carried out of Fe deficiency?

A
  • Ferritin
  • Reticulocyte count
  • Iron studies
  • FBC
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7
Q

What can cause Fe deficiency?

A
  • Cancer
  • Parasites (LCWW)
  • Menorrhagia
  • Pregnancy
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8
Q

Treatment for Fe deficiency?

A

Ferrous sulphate

Can cause black stools

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9
Q

General signs of anaemia?

A

Pale skin
Pale mucous membranes
Tachycardia

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10
Q

General symptoms of anaemia?

A 
Fatigue
Lethargy 
Dyspnoea 
Palpitations 
Headache
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11
Q

Causes of folate deficiency?

A

Poor folate diet
Malabsorption
Pregnancy
Antifolate drugs, methotraxate

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12
Q

Investigations of folate deficiency?

A

Blood film: macrocytyic anaemia

Erythrocyte folate level: indicated reduced blood stores

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13
Q

Treatment for folate deficiency?

A

Folic acid

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14
Q

How is vitamin B12 absorbed?

A

B12 is absorbed in the terminal ileum bound to intrinsic factor secreted by parietal cells

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15
Q

Causes of vitamin B12 deficiency?

A

Caused by the destruction of parietal cells or something effecting absorption in the terminal ileum

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16
Q

Investigations for B12 deficiency?

A

Blood film: macrocytic red blood cells

Autoantibody screen: check of IF antibiodyes

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17
Q

Treatment for B12 deficiency?

A

B12 tablets/injection

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18
Q

What is haemolytic anaemia?

A

RBCs usually removed by macrophages in red pulp of spleen after 120 days > haemolytic anaemia occurs when this happens before 120 days

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19
Q

Signs of haemolytic anaemia?

A 
Gallstones 
Jaundice 
Leg ulcers 
Splenomegaly 
Signs of underlying disease e.g. malar rash
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20
Q

Inherited causes of haemolytic anaemia?

A

Membranopathies
Enzymopathies
Haemoglobinopathies

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21
Q

Aquired causes of haemolytic anaemia?

A

Autoimmune
Infections
Secondary to systemic disease

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22
Q

Investigations of haemolytic anaemia?

A

FBC - reduced haemoglobin
Reticulocyte count - increased
Blood film - presence of SCHISTOCYTES

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23
Q

Treatments for haemolytic anaemia?

A

Folate and iron supplementation
Immunosurpressives
Splenectomy

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24
Q

Describe anaplastic anaemia?

A

(bone marrow failure) occurs when there is a reduction in the number of pluripotent stem cells causing a lack of haemopoiesis - reduced number of RBCs to replace old ones causes anaemia

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25
Q

What are the specific signs of anaplastic anaemia?

A

Increased susceptibility to infection
Increased bruising
Increased bleeding (especially from nose and gums)

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26
Q

What investigations would be carried out for anaplastic anaemia?

A

FBC - pancytopenia
Reticulocyte count - low
Bone marrow biopsy

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27
Q

What is the treatment for bone marrow failire (anaplastic anaemia)

A

Removal of causative agent
Blood/platelet transfusion
Bone marrow transplant
Immunosuppressive therapy

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28
Q

Describe sickle cell anaemia?

A

Autosomal recessive disease, point mutation of the B globin chain (valine to glutamine) resulting in a Hs variant

Carriers are protected against falciparum malaria

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29
Q

What causes the symptoms of sickle cell anaemia?

A

Chronic haemolysis produced stable Hb so patients often dont have symptoms, if Hb suddenly falls then there are symptoms! Possible causes

  • Splenic sequestration/infarction
  • Bone marrow aplasia
  • Further haemolysis
  • Gallstones, leg ulcers, AVN femoral head
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30
Q

What happens to sickle cells under stress?

A

Under stress e.g. cold, infection, dehydration, hypoxia the RBCs deoxygenate and the Hs polymerises causing the cells to become rigid and sickled

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31
Q

What are the complications of sickle cells anaemia?

A

Acute: painful crisis, sickle chest crisis, mesenteric ischaemia

Chronic: renal impairment, pulmonary HTN, joint damage

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32
Q

Investigations for sickle cell anaemia?

A

Screen neonates: BLOOD/HEEL TEST
FBC: reticulocyte count
Blood film: SICKLED erythrocytes
Hb ELECTROPHORESIS for diagnosis: HbSS present and HbA absent

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33
Q

Management of sickle cell anaemia?

A

Supportive: aggressive analgesia, treat underlying cause (e.g. antibiotics) fluids, folic acid, transfuse with falling Hb

Disease modifying: hydroxycarbamide, transfusion, stem cell transplant

If hyposplenic: prophylactic antibiotics, pneumococcal and meningococcal vaccinations

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34
Q

Describe thalassemia?

A

Autosomal recessive - decreased production of one or more globin chains in the red cell precursors/mature cells

Precipitation of the globin chains red cell precursors causes ineffective erythropoiesis

Precipitation of the globin chain in mature red cells causes haemolysis

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35
Q

What are the types of thalassemia?

A

a. Alpha thalassemia (decreased a chain synthesis)

b. B thalassemia (decreased b chain synthesis)

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36
Q

Describe alpha thalassemia?

A

Varies from mild to severe

4 deletions - no a chain synthesis (incompatible with life)
3 deletions - severe haemolytic anaemia
2 deletions - asymptomatic with possible mild anaemia
1 deletion - blood picture normal

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37
Q

Describe beta thalassemia?

A

B thal minor - mild/absence anaemia, low MCV, Fe stores normal Hetrozg

B thal intermediate - doesnt require transfusions, moderate anaemia, splenomegaly and bone abnormalities

B thal major = severe anaemia, failure to thrive, chronic infection, Homozg

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38
Q

Investigations for thalassemia?

A

FBC and film - hypochromic and microcytic anaemia

Irregular and pale RBCs

Diagnosis by Hb electrophoresis - shows HbF + low HbA

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39
Q

Treatment for thalassemia?

A 
Blood transfusions (2-4 per week) 
\+ Risk of iron overload so give iron chelation &amp; ascorbic acid

Long term folic acid
Bone health, endocrine supplements and psych support

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40
Q

Describe membranopathy?

A

Autosomal dominant conditions, causes a deficiency in a protein that is used to make red cell membrane = deformed cells that get trapped in the spleen

Spherocytosis - vertical
Elliptocytosis - horizontal

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41
Q

Symptoms of membranopathy?

A

Neonatal jaundice and haemolytic anaemia exacerbated during infection (splenomegaly)

Excess bilirubin

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42
Q

What investigations would you carry out for membranopathy?

A

FBC and reticulocyte count

Blood film: osmotic fragility tests (RBC = fragility in hypotonic solutions)

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43
Q

Treatment for membranopathy?

A

Folic acid and splenectomy

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44
Q

Describe glucose 6 phoshphate deficiency?

A

X linked - can effect women

Mainly effects males in mediterranean, Africa and middle/far east

May get oxidative crisis
+ preciptated by drugs or illness
+ in attacks: rapid haemolysis - jaundice - anaemia

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45
Q

Diagnosis for glucose 6 phosphate deficiency?

A

Blood film: bite and blister cells

Diagnosis: enzyme essay

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46
Q

Management of glucose 6 phosphate deficency?

A

Avoid precipitants e.g. HENNA

Transfuse if severe

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47
Q

What kinds of patients might be over anticoagulated?

A

Vit K antagonists - WARFARIN

NOACs e.g.apixaban (do not need regular review, cannot be reversed

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48
Q

Why might patients be over anticoagulated?

A

Bad patient compliance
Artificial valves
New/interacting drugs

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49
Q

Symptoms of over antigcoagulated?

A 
Bruising 
Bleeding 
Melena 
Epistaxis 
Hamatemesis 
Haemoptysis
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50
Q

Assessments for bleeding?

A 
APTT = intrinsic pathway 
PTT = extrinsic pathway
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51
Q

Describe disseminated intravascular crisis?

A

Rare but life threatening disease

Generation of FIBRIN WITHIN the blood vessels also consumption of platelets/coagulation factors causing secondary activation of fibrinolysis

ie. there will be an initial thrombosis followed by bleeding tendency

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52
Q

Causes of disseminated intravascular crisis?

A 
Malignancy 
Septicaemia 
Obstetric causes 
Trauma 
Infections 
Haemolytic transfusion reactions 
Liver disease
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53
Q

Treatment of disseminated intravascular disease?

A

Treat underlying cause: maintain blood volume and perfusion

May need transfusions

Activated protein C

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54
Q

Causes of thrombocytopenia? (both types)

A
  • Reduced platelet production in the bone marrow
  • Excessive peripheral destruction of platelets
  • Problem of an enlarged spleen

ITP more common than TTP

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55
Q

Physiology of thrombotic thrombocytopenic purpura?

A

Extensive microvascular clots form in small vessels in the body resulting in a low platlet count and organ damage

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56
Q

Clinical features of thrombocytopenia? (both types)

A

Easy bruising
Purpura
Epistaxis/mennorragia

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57
Q

Investigation of thrombocytopenia?

A

Reduced platelets so normal/increased megakaryocytes

ITP = may have detection of platelet autoantibodies

58
Q

Treatment for thrombocytic thrombocytopenic purpura?

A

Plasma exchange and immunosupression

59
Q

Physiology of immune thrombocytopenic purpura?

A

Often triggered by VIRAL INFECTION OR MALIGNANCY

Due to autoimmune destruction of platelets, the antibodies coat the platelets which are then removed by binding to Fc receptors on macrophages

Is autoimmune so may be associated with other autoimmune diseases

60
Q

Treatment for immune TP?

A

Corticosteriods
Splenectomy
IV Ig
Anti D

61
Q

What are the two types of haemophilia?

A

Haemophilia A - factor 8 deficiency: treatment is IV factor 8

Haemophilia B - factor 9 deficiency: treatment is IV factor 9

62
Q

Describe haemophilia?

A

X linked recessive disorders, females rarely severely affected

Haemophilia A is more common

Symptoms are anything associated with excess bleeding

Normal PTT (extrinsic) but prolonged APTT (intrinsic)

63
Q

What is polycythaemia?

A

Defined as an increase in haemoglobin, PCV and RBCS

64
Q

What are the primary causes of polycythaemia?

A

Increases sensitivity of the bone marrow to EPO

Polycythaemia rubra vera - genetic mutation in the JAK2 gene

Primary familial and congenital polycythaemia - mutation in the EPOR gene

65
Q

What are the secondary causes of polycythaemia?

A

The are more RBCs due to more circulating EPO

Due to: chronic hypoxia, poor oxygen delivery (e.g. high altitude), abnormal RBC structurea and tumours which release high levels of RPO

66
Q

Symptoms of polycythaemia?

A

May present with no symptoms

May have: easy bleeding /brusing, fatigue, dizziness, headaches etc

67
Q

Investigations for polycythaemia?

A

FBC
Bone marrow biopsy
Genetic testing for JAK2 gene

68
Q

Treatment for polycythaemia?

A

Polycythaemia rubra vera - bloodletting, aspirin

Secondary - treat the cause

69
Q

What is acute lymphoblastic leukemia?

A

Neoplasm within the bone marrow, systemically unwell - B symtoms

Generalised cytopenia - infection and bleeding

Progenitors cant mature - too many blasts

70
Q

Risk factors for acute lymphoblastic leukemia?

A

Epi: 2-5 years

Chromosomal abnormalities
Downs sydrome
Radiation

71
Q

Presentation of acute lymphoblastic leukaemia?

A

Bone marrow failure

Neutropenia - infections

Anaemia - fatigue, pallor

Thrombocytopenia - brusing

72
Q

Infiltration of Acute lymphoblastic leukaemia?

A

LYMPHADENOPATHY, HSM, orchidomegaly

CNS INVOLVEMENT

Bone pain

73
Q

Systemic features of ALL?

A

Fever, weight loss

74
Q

Epidemiology of acute myeloid leukaemia?

A

60-70 years

75
Q

Risk factors of AML?

A

Chromosomal abnormalities

Chemotherapy

Myelodysplastic/proliferative disorders

76
Q

Presentation of acute myeloid leukaemia?

A

Bone marrow failure

Neutropenia - Infection

Anaemia - fatigue pallor

Thrombocytopenia - brusing - DIC WITH ANPL

77
Q

Infiltration with AML?

A

GUM INFILTRATION

HSM

Bone pain

78
Q

Systemic features of AML?

A

Leukaemia

79
Q

What is acute promyeleocytic leukaemia?

A

Subtype of AML, translocation t15;t17

Good prognosis but associated with DIC, add all-trans retinoic acid to standard management

80
Q

Investigations for acute leukaemia? ALL and AML

A 
FBC: 
White cell count = increased 
Polymorphonuclear leukocytes = decreased 
RBCs = decreased 
Platelets = decreased

BONE MARROW ASPIRATION AND IMMUNOPHENOTYPING & CYTOGENETICS

Lumbar puncture is also indicated in ALL to check for CNS involvement

81
Q

What is the name given to the cell that is diagnostic of AML if seen on bone marrow aspiration?

A

Auer rods

82
Q

Management of acute leukaemia?

A

Chemotherapy (ATRA in APML)

Bone marrow transplant

Supportive:

+ Anaemia/thrombocytopenia: blood products
+ Infections: prophylactic abc
+ Allopurinol: tumour lysis syndrome

83
Q

Side effects of chemotherapy - immediate?

A 
\+ alopecia 
\+ neutropenia 
\+ anaemia/fatigue 
\+ thrombocytopenia - bruising/bleeding 
\+ N&amp;V/ mucosistis/loss of appetite
84
Q

Side effects of chemotherapy - late?

A 
\+ cardiotoxicity 
\+ nephrotoxicity 
\+ pulmonary fibrosis 
\+ infertility 
\+ increased risk of other malignancy 
\+ psychological
85
Q

Describe chronic lymphocytic leukaemia?

A

Proliferation of B lymphocytes

Arrested in G0/G1 - do not develop into B plasma cells

86
Q

Presentation of chronic lymphocytic leukaemia?

A

Epi: eldery 70+

ASYMPTOMATIC in 50%
Symmetrical painless lymphadenopathy
Bone marrow infiltration (anaemia/infection)
Systemic B symptoms

87
Q

Investigation of chronic lymphocytic leukaemia?

A

FBC - increased white cell count
Ig - HYPOGAMMAGLOBULINEMIA
Blood film - SMUDGE/SMEAR celd
Immunophenotyping - distinguish from NHL

88
Q

Management of CLL?

A

If symptomatic

Supportive - abx/blood products
RT - lymphadenopathy
Chemotherapy
Bone marrow transplant

89
Q

Presentation of chronic myeloid leukaemia?

A

Slow onset/incidental finding
Systemic symptoms
Abdominal discomfort/ SPLENOMEGALY

90
Q

Investigation of CML?

A

<5% blasts - chronic phase
>10% blasts - accelerated phase
>20% blasts - blast phase (AML)

91
Q

With bone marrow aspiration and cytogenetics what would you find in chronic myeloid leukemia?

A

PHILIDELPHIA CHROMOSOME

92
Q

Management of chronic myeloid leukaemia?

A

1st line = TYROSINE KINASE INIHIBITORS e.g. imatinib

Stem cell transplant if TK resistant or blast crisis

93
Q

What is tumour lysis sydrome

A

Chemotherapy given >

Cancer cell broken down >

Released contents - hyperkalaemia and nucleic acids >

Produce crystals that get deposited in the kidneys >

Damage and loss of function

Prevention: allopurinol
Treatment: IV fluid and correct electrolytes

94
Q

Describe the presentation of non Hodgkins lymphoma?

A

Epi - elderly

Lymphadenopathy
+ painless
+ symmetrical
+ discontinuous spread

Extranodal
+ skin/cns/lymphomas
+ BM: pancytopenia
+ spenomegaly

B symtoms

95
Q

Describe the presentation of Hodgkins lymphoma?

A

Epi - bimodal 20s and 60s

Lymphadenopathy
+ painless but pain with alcohol
+ asymmetrical
+ continuous spread

Other
+ itch
+ pel ebstein fever
+ splenomegaly

B symptoms

96
Q

What would be seen in a lymph node biopsy of hodgkins lymphoma?

A

Reed Sternberg cells in histology

97
Q

What investigations would be carried out for a lymphoma?

A 
FBC 
U&amp;E 
LFT 
Ca
Blood film 
LN biopsy

Staging using CT and ann arbor classificaition

98
Q

Describe the ann arbor classification?

A
  1. Singular lymph node region
  2. > 2 nodal areas on the same side of diaphragm
  3. Nodes on both sides of diaphragm
  4. Disseminated e.g. liver, BM
99
Q

Management of non Hodgkins lymphoma?

A

Low grade - follicular: watch and wait

High grade - large diffuse b cell: chemo, BMT

100
Q

Management of Hodgkins lymphoma?

A

Chemo +/- radiotherapy

Bone marrow transplant for relapse

101
Q

Describe multiple myeloma?

A

Neoplastic proliferation of bone marrow plasma cells, IgG is most common

Characterised by monoclonal protein in the serum or urine and CRAB - calcium, renal, anaemia, bone

102
Q

Aetiology of multiple myeloma?

A

Clone of B plasma cells in the body

Monoclonal antibodies, repeat infections as no other Ig

Bence jones protein deposition in the urine

Cancer symptoms - confusion, repeat infection, pathological fractures e.g. slipped in garden and fractured L1 and L2, bone pain, renal impairment

103
Q

Common presenting features of multiple myeloma?

A

Tiredness and malaise
Bone/back pain +/- fractures
Recurrent infection
Laboratory - anaemia/abnormal FBC, renal failure, hypercalcaemia, raised globulins, raised ESR, serum urine/urine paraprotein

104
Q

Diagnosis of multiple myeloma?

A

Monoclonal band on protein electrophoresis

BM aspiration shows excess plasma cells

Xray = pepperpot skull, lyses in long bones, pelvis and spine

105
Q

Treatment of multiple myeloma?

A

Radiotherapy - spot welding

Chemotherapy

BMT in some

106
Q

Management of multiple myeloma?

A

C - Ca - hydration/bisphosphates

R - renal - hydration/dialysis

A - anaemia - transfusion +/- EPO

B - bone - analgesia + bisphosphates

107
Q

Complications of multiple myeloma?

A

Hypercalaemia
AKI
Cord compression
Amyloid

108
Q

Describe malarial infection?

A

+ protazoa infection transmitted by plasmodia falciparum
+ transmitted by female anopheles mosquito
+ stages are:
1. exo-erythrocytic
2. endo-erythrocytic
3. hypnozoite

109
Q

What are the symptoms of a malarial infection?

A

FEVER + EXOTIC TRAVEL = MALARIA

Chills, sweats, jaundice, hepatosplenomegaly, anaemia, fatigue, black urine

110
Q

Pathogenesis of malaria?

A

Parasite matures in RBC - knobs in RNC surface - infected cells bind to eachother and receptors on endothelial walls

Sequestration in small vessels becoming trapped

Microcirculation obstruction = tissue hypoxia

Cerebral malaria, ARDS, hypoglycaemia, renal failure shock

111
Q

Investigation of malaria?

A

+ Thick and thin film ( thick - if you havent) (thin - what type)
+ RDT rapid diagnostic test: detects plasmodium antigens in the blood
+ RULE OUT MENIGITIS
+ PREGNANCY TEST

112
Q

Management of malaria?

A

Quinine and doxycycline

113
Q

Risk factors for deep vein thrombosis?

A

+ Age, obesity, varicose
+ Surgery, immobility, leg fracture, post op
+ OC pil, HRT, pregnancy - high oestrogen state
+ Long haul flights/ travel (rare)
+ Inherited thrombophilia - genetic predisposition

114
Q

DVT diagnosis?

A

Symptoms and signs - non specfic, clincial diagnosis unreliable

Symptoms - pain, swelling, (usually in calves)

Signs: tenderness, warmth, discolouration, pitting oedema

115
Q

Investigation of DVT?

A

D-dimer: normal excludes diagnosis - positive DOES NOT CONFIRM
Ultrasound compression test in proximal veins
Venogram calf, recurrence uncertain

116
Q

Treatment for DVT?

A

LMW heparin s/c od for minimum of 5 days > short acting injectable

Oral warfarin, INR 2-3 for 6 months > long acting but takes a while to get up a therapeutic range

DOAC > dont have to give an injectable component so can be treated as an outpatient

Compression stockings

Treat/seek underlying cause
Spontaneous DVT more likely to recur 10% per year

117
Q

Prevention of DVT?

A

Mechanical - hydration early mobilisation, compression stocking, foot pumps

Chemical - LMW heparin

118
Q

Describe thromboprophylaxis?

A

Low risk <40 yrs, surgery <30 min, early mobilisation and hydration

High risk: hip, knee and pelvis malignancy, prolonged immobility

119
Q

Describe pulmonary embolisms?

A

+ Massive = haemodynamically significant
+ Hypotension, cyanosis, severe dyspnoea , right heart strain/failure
+ Near death experience/medical emergency
+ Rare
+ Consider embolectomy/thrombolysis

120
Q

Symptoms of PE?

A

Breathlessness

Pleuritic chest pain

121
Q

Signs of PE?

A

Tachycardia
Tachypnoea
Pleural rub
No signs of alternative diagnosis

122
Q

Prevention of PE?

A

+ Same as DVT
+ Early mobilisation and hydration
+ Mechanical
+ Chemical: LMW heparin s/c OD

123
Q

PE initial investigations?

A

CXR usually normal
ECG sinus tachy - (QI, SI, TIII)
Blood gases - type 1 resp failure, decreased O2 and CO2
Mainly done to exclude alternative causes

124
Q

PE further investigations?

A

D dimer: normal excludes diagnosis > if abnormal then CTPA imaging

V/Q scan

CTPA spiral with contrast - visualise major segmental thrombi

125
Q

Treatment for PE?

A

+ As for DVT
+ Ensure normal Hb, platelets, renal function, baseline clottning
+ LWM hepatic and weight adjusted warfarin for 6 months (2-3 INR)
+ DOAC outpatient only with minor PE
+ If cannot anticoagulate then consider IVC filter

126
Q

What is neutropenic sepsis?

A

Temperature >38 degrees and absolute neutrophil count = 1x10^9

127
Q

Treatment for acute sickle cell crisis?

A

Pain relief and IV fluid

128
Q

Treatment for chest crisis?

A

IV fluid and abx

129
Q

Treatment for spinal cord compression?

A

Steroids and MRI

130
Q

Which of the following is NOT a complication of sickle cell anaemia?

A. Mesenteric ischaemia
B. Sequestration crisis
C. Acute chest sydrome
D. Acute lateral degloblanation

A

D. Acute lateral degloblanation

131
Q

Which of the following is not a cause of secondary polycythaemia?

A. Endogenous EPO
B. High altitude
C. JAK-2
D. COPD

A

C. JAK-2

132
Q

Patient has myeloma with side of the diaphragm and weight loss - which stage?

A

3b

133
Q

Which of the following is an innappropriate investigation for lymphoma?

PET
Histology
FBC
PR

A

PR

134
Q

Inappropriate test for malaria?

Pregnancy
RDT
Thick and thin film
Laprarotomy

A

Lapraotomy

135
Q

Which of the following is a sign of iron deficiency anaemia?

Fatigue
Pale mucous membranes
Dysponea
Palpitations

A

Pale mucous membranes

136
Q

Where in the GI tract is vitamin B12 absorbed?

A

Terminal ileum bound to intrinsic factor

137
Q

In which type of anaemia would you fine a raised reticulocyte count?

A

Haemolytic

138
Q

In histology which cells are seen in glucose 6 phosphate deficiency?

A

Bite and blister

139
Q

Histology in Hodgkins lymphoma will show which cell?

A

Reed sternberg

140
Q

Lady with DVT suddenly has chest pain, what is the most likely diagnosis?

A

Pulmonary embolism

141
Q

What does virchows triad contain?

A

Hypercoagulability
Hemodynamic changes
Endothelial injury/dysfunction

Phase 2a (13 decks)

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