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haematology Flashcards

1
Q

Iron deficiency anaemia definition

A

• A common microcytic anaemia caused by low insufficient iron in the body to support red blood cell production

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2
Q

how common is iron deficiency anaemia

A
  • very common

- More common in pre-menopausal women due to heavy menstruation.

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3
Q

biological causes/risk factors for iron deficiency anaemia

A

• EXCESSIVE BLOOD LOSS:

  • Gut (upper or lower GI)
  • Menorrhagia
  • Trauma
  • Epistaxis
  • Following blood donation
  • Malignancy

• INCREASED DEMAND:

  • Pregnancy
  • Rapid growth in children

• REDUCED INTAKE:

  • Diet
  • Malabsorption – drugs, coeliac disease, H. pylori, low vitamin C
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4
Q

symptoms / history of iron deficiency anaemia

A
  • Dependent on how quickly the anaemia develops  people wiyth chronic, slow blood loss may be able to tolerate very low levels of haemoglobin with few symptoms
  • COMMON SYMPTOMS: fatigue, dyspnoea and palpitations
  • LESS COMMON SYMPTOMS: headache, tinnitus, taste disturbance, pruritus, pica (abnormal dietary cravings e.g. ice or clay), glossitis, dysphagia, impairment of body temperature regulation (in pregnant women)
  • SERIOUS SYMPTOMS: angina, marked ankle oedema, dyspnoea at rest are unlikely haemoglobin concentrations of more than 70g/L unless there is additional heart or lung pathology
  • Symptoms of iron deficiency may occur without anaemia  fatigue, hair loss, lack of concentration and irritability
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5
Q

signs of iron deficiency anaemia

A
  • May be no signs, even in severe anaemia
  • Pallor – mild anaemia
  • LESS COMMONLY: atrophic glossitis, angular cheilosis (or stomitis), nail changes
  • Nail changes – longitudinal marking and/or koilonychia (spoon shaped nails with longitudinal ridges)
  • Angular cheilitis – ulcerations at corners of mouth
  • Atrophic glossitis
  • Tachycardia
  • Systolic flow murmur/Cardiac failure plus epithelial cell changes induced by ↓ iron i.e. cardiac enlargement
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6
Q

DDx of iron deficiency anaemia

A

• Other causes of microcytic anaemia e.g. thalassaemia, chronic disease anaemia, sideroblastic anaemia

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7
Q

Investigations of iron deficiency anaemia

A 
•	1st LINE:
-	BLOOD TEST:
o	FBC
	Low MHC  hypochronic
	Low MCV  microcytic 
	Poikilocytosis (variation in shape)
	Anisocytosis (variation in size)
o	SERUM FERRITIN
	Should be measured to confirm iron deficiency 
	Reflects amount of stored iron
	However, ferritin levels can be raised during inflammation or infection even if iron stores are low
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8
Q

management of iron deficiency anaemia

A

• 1st LINE:
- Oral iron supplement
- Adjunct: ascorbic acid – enhances iron absorption
• 2nd LINE:
- Parenteral iron replacement
• If symptomatic at rest with dyspnea, chest pain or presyncope + red cell transfusion
• If Hb <7  blood transfusion

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9
Q

Macrocytic Anaemia – B12 Deficiency definition

A
  • Vit B12 OR Folate deficiency

* Presence of erythroblasts with delayed nuclear maturation due to defective DNA synthesis in the bone marrow

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10
Q

who does Macrocytic Anaemia – B12 Deficiency

A
  • Peak age of diagnosis is 60 years.
  • F:M 1.6:1
  • Accounds for 80% of megaloblastic anaemia
  • Prevalence of Vit B12 deficiency was abound 5% in people 65-74 years of age, and more than 10% in people 75 years of age or older
  • Dietary Vit B12 deficienct is unusual in younger people, except those eating strict long-term vegan diets
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11
Q

biological causes/ risk factors of Macrocytic Anaemia – B12 Deficiency

A 
•	Macrocytosis is caused by a problem in the synthesis of red blood cells as opposed to microcytosis which is due deficiency of haemoglobin production.
•	Megaloblast = a cell in which nuclear maturation is delayed compared with the cytoplasm.
•	Causes of macrocytosis:
-	MEGALOBLASTIC:
o	VITAMIN B12 DEFICIENCY
	Pernicious Anaemia (80%) - autoimmune disorder causing atrophic gastritis of parietal cells in gastric mucosa  intrinsic factor not released and vit B12 not absorbed - IF transports vit B12 to specific receptors in illeum for absorption but remains in the lumen itself. 1% vit B12 absorbed if no IF
	Post gastrectomy/ilieal resection
	Bacterial overgrowth or parasitic infestation
	HIV infection
	Dietary deficiency – rare even in vegans
o	FOLATE DEFICIENCY
	Dietary deficiency
	Malabsorption
	Increased demand in pregnancy, haemolysis, leukaemia
	Drug-induced deficiency
-	NON-MEGALOBLASTIC:
o	Alcohol abuse
o	Liver disease
o	Reticulocytosis
o	Severe hypothyroidism
o	Pregnancy
-	OTHER:
o	Myelodysplasia
o	Myeloma
o	Myeloproliferative disorders
o	Aplastic anaemia
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12
Q

how does Macrocytic Anaemia – B12 Deficiency present

A
  • ANAEMIA – fatigue, lethargy, dyspnoea, faitness, palpitations, headache, tinnitus, anorexia, angina (if the person has pre-existing coronary heart disease)
  • B12 DEFICIENCY – person reports unexplained neurologival symptoms  paraesthesia, numbness, cognitive changes, visual disturbances
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13
Q

signs of Macrocytic Anaemia – B12 Deficiency

A
  • ANAEMIA - pallor, if severe (HB<80g/L) signs of hyperdynamic circulation may be present (tachycardia, flow murmurs) – sometimes progressing to HF
  • B12 DEFICIENCY – lemon tinge skin (gradual onset, due to pallor and haemolysis-induced jaundice), glossitis, oropharyngeal ulceration, neuropsychiatric: irritability, depression, psychosis and dementia, neurological: impaired response to vibration, touch, pain and position, visual disturbance and abnormal gait – should come back and mention sub-acute degeneration of the cord
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14
Q

investigations of Macrocytic Anaemia – B12 Deficiency

A

• 1st LINE:

  • FBC - if Hb is low and the MCV is high  check serum vit B12 and serum folate concentrations, if Hb is low and the MCV is normal  check ferritin, B12 and folate levels
  • Reticulocyte Count – low Hb, hypersigmented nuclei, reticulocytes (indicate rapid turnover or erythrocytes)
  • Serum Vit B12
  • Peripheral Blood Smear
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15
Q

treatment of Macrocytic Anaemia – B12 Deficiency

A

• SEVERE SYMPTOMS:
- 1ST LINE: parenteral cyanocobalamin or hydroxocobalamin + referally to neurologist/haematrologist
- Adjunct: blood transfusion +/- diuretic, oral folic acid
• MILD TO MODERATE:
- 1ST LINE: oral or parenteral cyanocobalamin or parenteral hydroocobalamin
• ASYMPTOMATIC/BORDERLINE DEFICIENCY:
- VEGAN/>65/GI ILLNESS: Dietary supplementation + multivitamins
- AFTER BARIATRIC SURGERY: oral, parenteral or intranasal cyanocobalamin or parenteral hydroxocobalamin

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16
Q

DDx of Macrocytic Anaemia – B12 Deficiency

A

• Vit B12 and Folate deficiencies are not the only causes of macrocytosis
• Other causes includes:
- Alcohol  may cause macrocytosis with neither anaemia nor a change in liver function
- Drugs (hydroxycarbamide and azathioprine)
- Severe thyroid deficiency – modest increase in mean cell volume may be seen
- Pregnancy and the neonatal period
- Haematological causes
o Myelodysplasia – progressive bone marrow failure, with variable changes seen in the quantity and quality of RBCs and platelets
o Aplastic anaemia – pancytopenia is noted
o Pure red cell aplasia
o Plasma protein changes (myeloma)
• IF THE CAUSE OF MACROCYTIC ANAEMIA IS UNCERTAIN  BLOOD FILM ANALYSIS MAY HELP

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17
Q

Macrocytic Anaemia – Folate Deficiency definition

A
  • Vit B12 OR Folate deficiency

* Presence of erythroblasts with delayed nuclear maturation due to defective DNA synthesis in the bone marrow

18
Q

who does Macrocytic Anaemia – Folate Deficiency affect

A
  • Peak age of diagnosis is 60 years.
  • F:M 1.6:1
  • Accounds for 80% of megaloblastic anaemia
  • Prevalence of Vit B12 deficiency was abound 5% in people 65-74 years of age, and more than 10% in people 75 years of age or older
  • Dietary Vit B12 deficienct is unusual in younger people, except those eating strict long-term vegan diets
19
Q

causes of Macrocytic Anaemia – Folate Deficiency

A

• FOLATE DEFICIENCY: absorbed in the upper part of the small intestine, only have about 4 months’ store, can occur because of:

  • DIETARY DEFICIENCY – alcoholism
  • MALANSORPTION – coeliac disease, tropical sprue, congenital specific malabsoprtio, jejunal resection or IBD
  • EXCESSIVE REQUIREMENTS – pregnancy, prematurity and infancy, malignancy, blood disorders, inflammation, metabolic disorders (homocystinuria)
  • EXCESSIVE URINARY EXCRETION – CHF, acute liver damage, or chroic dialysis
  • SOME DRUGS
20
Q

risk factors of Macrocytic Anaemia – Folate Deficiency

A

• Linked to causes

21
Q

how does Macrocytic Anaemia – Folate Deficiency present

A
  • ANAEMIA – fatigue, lethargy, dyspnoea, faitness, palpitations, headache, tinnitus, anorexia, angina (if the person has pre-existing coronary heart disease)
  • FOLATE DEFICIENCY – mild symptoms of peripheral neuropathy or psychiatric disturbance e.g. depression
22
Q

signs of Macrocytic Anaemia – Folate Deficiency

A

• ANAEMIA - pallor, if severe (HB<80g/L) signs of hyperdynamic circulation may be present (tachycardia, flow murmurs) – sometimes progressing to HF
FOLATE DEFICIENCY – mild symptoms of peripheral neuropathy or psychiatric disturbance e.g. depression

23
Q

investigations of Macrocytic Anaemia – Folate Deficiency

A

• 1st LINE:

  • FBC - if Hb is low and the MCV is high  check serum vit B12 and serum folate concentrations, if Hb is low and the MCV is normal  check ferritin, B12 and folate levels
  • Reticulocyte Count – low Hb, hypersigmented nuclei, reticulocytes (indicate rapid turnover or erythrocytes)
  • Peripheral Blood Smear
24
Q

DDx Macrocytic Anaemia – Folate Deficiency

A

• Vit B12 and Folate deficiencies are not the only causes of macrocytosis
• Other causes includes:
- Alcohol  may cause macrocytosis with neither anaemia nor a change in liver function
- Drugs (hydroxycarbamide and azathioprine)
- Severe thyroid deficiency – modest increase in mean cell volume may be seen
- Pregnancy and the neonatal period
- Haematological causes
o Myelodysplasia – progressive bone marrow failure, with variable changes seen in the quantity and quality of RBCs and platelets
o Aplastic anaemia – pancytopenia is noted
o Pure red cell aplasia
o Plasma protein changes (myeloma)
• IF THE CAUSE OF MACROCYTIC ANAEMIA IS UNCERTAIN  BLOOD FILM ANALYSIS MAY HELP

25
Q

treatment of Macrocytic Anaemia – Folate Deficiency

A

• AT RISK:
- 1ST LINE: oral folic acid and multivitamin supplementation
• ACUTE:
- ACQUIRED 1st LINE: oral folic acid replacement + tx of underlying disorder
- CONGENITAL 1ST LINE: parenteral folic acid replacement + methionine

26
Q

Non-Hodgkins Lymphoma definition

A
  • Neoplastic transformations of normal B or T cells which reside predominantly in lymphoid tissues
  • They are commoner than the leukaemia’s and are increasing in incidence for reasons that are unclear
  • The disease is classified based on histological appearance into Hodgkin and non-Hodgkin lymphomas
  • NON-HODGKIN’S: heterogenous group of malignancies of the lymphoid system which stems from the function of the lymphoid arm of the immune system, which employs various types of lymphocytes that defend the organism from external (infectious) and internal (neoplastic) threats
27
Q

who does Non-Hodgkins Lymphoma affect

A

• Increasing in incidence by about 4% per year from the 70s

28
Q

causes of Non-Hodgkins Lymphoma

A

• B-CELL LYMPHOMA:
- Malignant phenotype in NHL is due to a multi-step accumulation of genetic aberrations that confer a growth advantage and expansion of a monoclonal population of malignant lymphocytes
- Normal B cells originate and mature in the bone marrow (central lymphoid tissue compartment), they leave bone marrow to undergo subsequent differentiation in secondary lymphoid tissues such as the lymph nodes and speen and go on to perform their function in these tissues (peripheral lymphoid tissue compartment)
- B-cell lymphomas may arise during the different stages of B-cell maturation as a result of abnormal genetic mutations and represent the malignant counterparts of these normal maturing B-cells  e.g. abnormal mutations can happen at at the stage of early precurosrs and lead to corresponding subtypes of acute lymphoblastic leukaemia, similarly immature B-cells, mature antigen-naïve B cells and mature anitgen-activated B cells may transform to various types of NHL such as Burkitt’s lymphoma, diffuse large B-cell lymphoma and mantle cell lymphoma
- Most transformation from follicular to large cell lymphoma are of the germinal centr B-cell like phenotype
• T-CELL LYMPHOMA:
- Pluripotent haematopoietic stem cell CD34 gives rise to a lymphocyte (both b and T)-committed stem cell from which early T-cells originate, T-cells migrate to the thymus where they develop into mature cells, process starts from thymic lymphoid cells developing into T-cell receptor (TCR) alpha, forming the mature TCR complex and then developing into CD4+/CD8+ cells, interaction between TCR and peptide/MHC leads to commitment to be either CD4+ or CD8+ cells, subsequently T cells undergo a positive selection (to recognise host MHC, self-MHC restriction) and negative selection (to not bind MHC too strongly, which would lead to autoreactive clone, self-MHC tolerance) and are ready to leave the thymus, those that do not pass double selection die in the thymus through apoptosis
- Abnormal mutations can happen at different stages of t-cell development and can lead to different malignant phenotypes

29
Q

risk factors for Non-Hodgkins Lymphoma

A
  • Over 50
  • Male
  • Immunocompromised
  • EBV
  • H.pylori
  • Coeliac, Herpes
  • HIV
  • Hep c
  • Sjogren’s syndrome
30
Q

how does Non-Hodgkins Lymphoma present / signs

A
  • Night sweats – usually drenching
  • Weight loss – weight loss should be more than 10%
  • Fatigue/malaise – from anaemia
  • Fever – over 38 degrees
  • Lymphadenopathy – peripheral, often in the posterior triangle of the neck, painless swellings
  • Spenomegaly – can be massive in marginal one lymphoma, may cause splenic infarction
  • Pain when consuming alcohol
31
Q

investigations of Non-Hodgkins Lymphoma

A

• 1st LINE:

  • FBC: thrombocytopenia, pancytopenia, lymphocytosis
  • BLOOD SMEAR: nucleated RBCs, left shift
  • LYMPH NODE BIOPSY: preferably excisional or core biopsy to provide info on lymph node architecture, positive
  • SKIN BIOPSY: may have cutaneous T-cell, positive
  • BONE MARROW BIOPSY: gives definitive diagnosis, positive
  • BASIC METABOLIC PANEL: assess kidney, electrolyte and glucose function, may be normal or deranged
  • LFTs: elevated if liver involved in lymphoma
  • LDH: elevated
32
Q

treatment of Non-Hodgkins Lymphoma

A

• 1st LINE: dependent on subtype

- R-CHOP 21 WITH OR WITHOUT RADIOTHERAPY: rituximab, cyclophosphamide

33
Q

DDx of Non-Hodgkins Lymphoma

A
  • Hodgkin’s lymphoma
  • Acute lymphocytic leukaemia
  • Infectious mononucleosis
  • Hep C
  • TB
  • HIV
34
Q

Hodgkin’s Lymphoma definition

A
  • Neoplastic transformations of normal B or T cells which reside predominantly in lymphoid tissues
  • They are commoner than the leukaemia’s and are increasing in incidence for reasons that are unclear
  • The disease is classified based on histological appearance into Hodgkin and non-Hodgkin lymphomas
  • HODGKIN’S LYMPHOMA: uncommon haematological malignancy arising from mature b cells, characterised by the presence of Hodgkin’s cells and Reed-Sternberg cells
35
Q

who does Hodgkin’s Lymphoma affect

A

• Very uncommon

36
Q

causes of Hodgkin’s Lymphoma

A
  • Unclear
  • EBC is thought to play a role
  • HL is a B-cell malignancy and immunoglobulin expression is typically absent despite gene re-arrangements and somatic hyper-mutation
  • Surface immunoglobulin (B-cell receptors) is required for B-cell maturation and survival
  • In EBV-positive disease, it is though that viral proteins allow infected, abnormal B cells to evade apoptosis and/or replicate in an uncontrolled manner by mimicking constituively active cellular receptors that are essential for B-cell growth, survival and evasion of apoptosis
37
Q

risk factors of Hodgkin’s Lymphoma

A
  • Hx of EBV
  • Fx of Hogdkin’s lymphoma
  • Young adults from higher SES
38
Q

how does Hodgkin’s Lymphoma present / signs

A
  • Presence of risk factors
  • Lymphadenopathy – typically painless and most commonly invpving the cervical and/or supraclavicular nodula chain, most common presenting symptom of HL, often in the posterior triangle of the neck, painless swellings
39
Q

investigations of Hodgkin’s Lymphoma

A

• 1ST LINE:

  • FBC: low Hb and platelets, WBC count may be high or low
  • METABOLIC PANEL: performed to evaluate baseline liver and renal function prior to commencement of treatment, normal in most pts
  • ESR: elevated
  • CXR: mediastinal mass, large mediastinal adenopathy
  • PET-CT SCAN: involved sites appear FDG-avid (bright) with PET imaging
  • GALLIUM SCAN: involved sites appear bright on gallium scans
  • CONTRAST CT NECK, CHEST AND ABDOMEN/PELVIS: may show enlarged lymph nodes and other sites of disease
  • EXCISIONAL LYMPH NODE BIOPSY: hogdkin’s cells within an appropriate background cellular mileu
40
Q

treatment of Hodgkin’s Lymphoma

A

• 1st LINE:

- ABVD: doxorubicin, bleomycin, vinblastine and decarbazine +/- radiotherapu

41
Q

DDx of Hodgkin’s Lymphoma

A
  • NHL
  • Lymphadenopathy from other malignancies
  • Infectious mononucleosis
  • Reactive lymph nodes

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