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Haematology Flashcards

1
Q

What is the clinical presentation of iron deficiency anaemia?

A

Anaemia:

  • Fatigue
  • Low energy
  • Pallor
  • Dyspnoea on exertion.

Deficiency of iron:

  • Pica (appetite for non-food items).
  • Hair loss
  • Restless leg syndrome
  • Nail abnormality (spooning, flattening, thinning).
  • Angular stomatitis.
  • Glossitis.
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2
Q

What is the histological presentation of iron deficiency anaemia?

A
  • Microcytic, hypochromic.
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3
Q

What are the risk factors for iron deficiency anaemia?

A
  • Pregnant.
  • Vegan/vegetarian.
  • Menorrhagia.
  • Coeliac.
  • Excessive NSAID use (causes peptic ulcers).
  • CKD (low erythropoietin).
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4
Q

What are the diagnostic tests for iron deficiency anaemia?

A
  • FBC: Low RBCs, low MCV, low MCH (mean corpuscular haemoglobin).
  • Blood smear: Microcytic, hypochromic.
  • Low reticulocytes.
  • Low serum iron and low serum ferratin.
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5
Q

What is the treatment for iron deficiency anaemia?

A
  • 1st line: Ferrous sulfate (orally).
  • 2nd line: IV iron (used if ferrous sulfate is intolerated or the individual has IBD.)
  • RBC transfusion. Used if the individual begins to present with symptoms of CV compromise (chest pain, dyspnoea on rest).
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6
Q

What is pernicious anaemia?

A
  • Autoimmune disorder.
  • Destruction of the parietal cells of the stomach (that secrete IF) and production of intrinsic factor antibodies.
  • Causes malabsorption of B12, as If is required for the cotransportation process used for B12 absorption.
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7
Q

What are the symptoms of pernicious anaemia?

A

Anaemia:

  • Fatigue
  • Lack of energy
  • Pallor
  • Dyspnoea on exertion.

B12 deficiency:
- Neurological problems (peripheral neuropathy and dementia).

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8
Q

What is the histological presentation of pernicious anaemia?

A
  • Macrocytic, megaloblastic (presence of large, immature RBCs).
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9
Q

What are the risk factors for pernicious anaemia?

A
  • Old age (reduced stomach acid secretion).
  • FH.
  • Autoimmune endocrine disorders (e.g. Hashimoto’s thyroiditis).
  • Coeliac disease.
  • IBD (crohns, UC).
  • Partial/complete stomach resection.
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10
Q

What are the investigations used to confirm diagnosis of pernicious anaemia?

A

FBC - MCV increased, MCHC normal.

Blood film - Shows macrocytic, megaloblastic RBCs.

Intrinsic factor antibody test - Presence of these antibodies proves pernicious anaemia.

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11
Q

What is the treatment for pernicious anaemia?

A
  • Give hydroxocobalamin, a B12 analogue (1st line)
  • If there are neuro symptoms, refer to neurology/haematology.
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12
Q

What are the risk factors for folate-deficiency anaemia?

A
  • Pregnancy/lactation.
  • Old age.
  • Chronic alcohol abuse.
  • Low folate diet.
  • FH.
  • Coeliac disease.

Use of certain drugs:
- Trimethoprim.
- DMARDS (sulfasalazine, methotrexate).
- Anticonvulsants.
(therefore these drugs are contraindicated in pregnancy).

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13
Q

What is the histology of folate-deficiency anaemia?

A
  • Macrocytic, megaloblastic anaemia.
  • Hypersegmented neutrophils

NOTE: same as pernicious anaemia.

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14
Q

What is the clinical presentation of haemolytic anaemia?

A

Anaemia:

  • Fatigue
  • Lack of energy
  • Pallor
  • Dyspnoea on exertion

Folate deficiency:

  • Angular stomatitis.
  • Glossitis
  • Painful swallowing.
  • NO NEURO SYMPTOMS
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15
Q

What are the investigations used to diagnose folate-deficiency anaemia?

A
  • FBC. Raised MCV and MCHC.
  • Blood film. Macrocytic, megaloblastic cells with hypersegmented neutrophils.
  • Serum folate: 1st line screening tool.
  • RBC folate: Gold standard. More sensitive than serum folate, but more expensive/complex.
  • Serum B12. Should be done to exclude pernicious anaemia, which can be masked by folate supplementation.
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16
Q

What is the treatment for folate-deficiency anaemia?

A
  • Folic acid oral (1st line).
  • Consider RBC transfusion if severely anaemic.
  • Women planning/currently pregnant should be taking folic acid to reduce risk of neural tube defects.
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17
Q

What is haemolytic anaemia?

A

A number of conditions that occur due to increased destruction of RBCs.

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18
Q

What are the symptoms of haemolytic anaemia?

A

Anaemia:

  • Fatigue
  • Lack of energy
  • Pallor
  • Dyspnoea on exertion.

Haemolysis:
- Jaundice (due to bilirubin released from erythrocyte breakdown).

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19
Q

What type of anaemia is haemolytic anaemia?

A
  • Normocytic usually.
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20
Q

What are the differentials for haemolytic anaemia?

A
  • Blood loss.
  • Transfusion reaction.
  • Underproduction anaemia. Caused by reduced production of RBCs rather than increased breakdown. Will therefore have a low reticulocyte count (would be high in haemolytic anaemia).
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21
Q

What are the risk factors for haemolytic anaemia?

A
  • FH.
  • Autoimmune disorders (especially SLE).
  • CLL
  • Cephalosporins.
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22
Q

What are the investigations used to diagnose haemolytic anaemia?

A

FBC - Reduced Hb, increased MCH due to high amount of reticulocytes.

Blood film - High reticulocyte count, lots of abnormal RBC’s.

Coomb’s test - If positive indicates an autoimmune cause of haemolytic anaemia.

Consider ANA if SLE suspected.

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23
Q

What is the treatment for haemolytic anaemia?

A
  • If symptomatic, use RBC transfusion.
  • Give folic acid, as increased rates of reticulocytosis will deplete folic acid stores more quickly.
  • If coomb’s test +ve, give prednisolone (reduces production of autoantibodies that drive RBC breakdown in autoimmune haemolytic anaemia).
  • If caused by a drug (commonly cephalosporins) give prednisolone and discontinue the drug.
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24
Q

What is sickle cell anaemia?

A
  • Hereditary deformation of RBC’s as a result of faulty Hb molecule formation.
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25
What is the clinical presentation of sickle cell anaemia?
- Vaso-occlusion. Early childhood acute pain in the hands and feet due to small vessel occlusion. - In adults, pain in the long bones, ribs, spine and pelvis too. - OFTEN SYMPTOMS OF ANAEMIA DO NOT APPEAR AS HbS HAS A LOW OXYGEN AFFINITY. - If they do appear, anaemic symptoms are: - Tiredness - Fatigue - Dyspnoea - Palpitations - Headache - Faintness
26
What is the pathophysiology of sickle-cell anaemia?
- Changes in sequence of haemoglobin subunit causes faulty structure. - Distorts erythrocyte shape, making them sickle shaped. - Sickle cell RBC's block vessels easily, and are easily destroyed.
27
What is the investigation used for sickle cell anaemia?
- Usually identified in neonatal screening. - Otherwise, identified by presence of sickle cells on blood film.
28
What is the treatment for sickle cell anaemia?
- Anaphylactic penicillin until 5 years old (children). Because they are at substantially increased risk of invasive pneumococcal infection. - Hydroxycarbamide. Manages the pain. - Potentially blood transfusion. - Bone marrow stem cell transfusion if disease severe - still a very new treatment.
29
What is the alternative name for folic acid?
B9
30
What is the clinical presentation of a DVT?
- Often will have progressed to PE before clinical presentation. Classical features include: - Limb pain and tenderness. - Calf swelling. - Raised skin temperature. - Pitting oedema. - May resemble cellulitis.
31
What is the pathophysiology of DVT?
- Thrombus formation in the deep vein. - May then embolise and flow up into the pulmonary circulation, before becoming stuck and causing a PE.
32
What are the thrombotic risk factors?
- Obesity - Family history - Male - Smoking - Age - Cancer
33
What are the investigations used in a suspected DVT?
If Well's score \<2: - D-dimer testing. If negative, DVT ruled out. - If positive, arrange a venous ultrasound. If Well's score ≥2: - Venous ultrasound straight away, before D-dimer.
34
What is the treatment for a DVT?
Until DVT confirmed/ruled out: - apixaban (1st line) - If not tolerated, offer LMWH (2nd line). When confirmed: - Continue apixaban - Encourage mobilisation as soon as possible. - Compression stockings.
35
What are the 4 different types of leukaemia? And what are they?
- Acute lymphoblastic leukaemia (ALL). ACUTE malignant transformation of a clone of LYMPHOID PROGENITOR CELLS. - Chronic lymphoblastic leukaemia (CLL). CHRONIC malignant transformation of a clone of MATURE LYMPHOID CELLS. - Acute myeloid leukaemia (AML). ACUTE malignant transformation of a clone of MYELOID PROGENITOR CELLS. - Chronic myeloid leukaemia (CML). CHRONIC malignant transformation of a clone of MYELOID CELLS.
36
What is the typical presentation of ALL?
- Fatigue - Dizziness - Palpitations - Bone pain - Hepatosplenomegaly Bone marrow failure causes: - Anaemia (due to overpopulation of bone marrow with lymphoblastic cells). - Bleeding - Infection - ALL also has a propensity to include the CNS.
37
What is the pathophysiology of ALL?
- Uncontrolled proliferation of precursor B and T cells. - Leukaemic cells accumulate in the bone marrow, peripheral blood and other tissues. - Overproduction of leukaemic cells leads to reduced RBCs, platelets and neutrophils.
38
What are the risk factors for ALL?
- Genetic (Down's syndrome 20x risk). - Environmental. Benzene compounds, drugs (alkylating agents) and radiation exposure.
39
What is the most common cancer in children?
- Acute lymphoblastic leukaemia (ALL).
40
What are the investigations used to assess ALL?
- FBC. Anaemia, leukocytosis, thrombocytopenia may be found. - Peripheral blood smear. Presence of leukaemic lymphoblasts indicates ALL. - Bone marrow aspiration. Look for presence of leukaemic lymphoblasts.
41
What is the treatment for ALL?
Chemotherapy: - Prednisolone (corticosteroid) AND cyclophosphamide (immunosuppressant) AND vincristine (alkaloid chemo drug) AND doxorubicin (anthracycline antibiotic). - Potentially use methotrexate (antimetabolite immunosuppressant) depending on type of AML.
42
What is the prognosis for children with ALL?
- Only 1/5 die from it. Prognosis very good.
43
What is the clinical presentation of chronic lymphoblastic leukaemia (CLL)?
- Early on, it will often be asymptomatic with lymphocytosis (increased white cell count). Later on, will become symptomatic: - Anaemia - Bleeding and infection due to bone marrow failure. - Rubbery lymph nodes.
44
What is the histological presentation of CLL?
Smudge cells.
45
What is the pathophysiology of CLL?
- Uncontrolled proliferation of mature T/B cells. - Autoimmune haemolysis may occur, causing anaemia.
46
What is the aetiology of CLL?
- Mutation (11q or 17p deletion).
47
What is the epidemiology of CLL?
- Most common leukaemia in western world. - Usually affects older people.
48
What are the diagnostic tests for CLL?
FBC: Anaemia, raised white cell count. Blood film: smudge cells.
49
What is the treatment for CLL?
If asymptomatic, watch and wait. When symptomatic: - Chemotherapy. CLL is incurable.
50
What are the symptoms of AML?
- Fatigue - Dizziness - Palpitations - Hepatosplenomegaly Bone marrow failure causes: - Anaemia - Bleeding - Infection
51
What is the histological presentation of AML?
- Auer rod cells.
52
What is the pathophysiology of AML?
- Accumulation of leukaemic myeloid blast cells in the bone marrow, peripheral blood and other tissues. - There is also a reduction in erythrocytes, platelets and neutrophils.
53
What is the aetiology of AML?
- Can transform from myelodysplasia. - Can be genetic.
54
What is the epidemiology of AML?
- Most common in older adults.
55
What are the investigations used to diagnose AML?
Peripheral blood film: - Anaemia - Thrombocytopenia - Auer rods Bone marrow aspirate: - Leukaemic blast cells
56
What is the treatment for AML?
- Chemotherapy - For severe/relapsing AML, consider stem cell transplant.
57
What is the clinical presentation of CML?
- Insidious onset - Fever - Weight loss - Sweating - Anaemia - HUGE SPLENOMEGALY - Untreated, will last 3-4 years before disease progresses to AML.
58
What is the pathophysiology of CML?
- CML lasts around 3-4 years, before blast formation begins. - Blast formation causes AML, leading to rapid death if untreated.
59
What is the aetiology of CML?
- Genetic. Philadelphia chromosome translocation in 95% of cases.
60
What is the epidemiology of CML?
Most common in the elderly.
61
What are the investigations used to diagnose CML?
FBC: Anaemia, raised white cells. Cytogenetics: Philadelphia chromosome.
62
What is the treatment for CML?
If in chronic stage, 1st line is imatinib (tyrosine kinase inhibitor). When blast phase/acute phase reached, chemotherapy is 1st line.
63
What is lymphoma?
Malignant tumour of the lymphatic system.
64
What are the two types of lymphoma? What differentiates the two?
Hodgkin's lymphoma. Reed-Sternberg cells present. Non-Hodgkins lymphoma. No Reed-Sternberg cells present.
65
What are the symptoms of lymphoma?
- Painless, rubbery lymph node enlargement. - Hepatosplenomegaly. - Puritus - Fatigue - Alcohol induced pain in the affected nodes. Typical cancer symptoms: - Weight loss - Fever - Night sweats
66
What is the aetiology of non-Hodgkin's lymphoma?
- Usually unknown. - Could be H. Pylori in mucous associated lymphoid tissue lymphoma. - Could be EBV in Burkitt's lymphoma.
67
What is the aetiology of Hodgkin's lymphoma?
- Often unknown. - Could be previous EBV infection.
68
What is the epidemiology of both Hodgkin's and non-Hodgkin's lymphoma?
- Hodgkin's more common in young adults. - Non-Hodgkins is more common in older people (rare before 40).
69
What are the diagnostic tests used for lymphoma?
- Lymph node biopsy. Will show Reed-Sternberg cells (Hodgkin's lymphoma) or not (non-Hodgkin's lymphoma). - CT scan is used for staging the cancer. - FBC. Check for anaemia.
70
What is the treatment for Hodgkin's lymphoma?
- Radio + chemo (often doxorubicin). As disease progresses, treatment will be made more aggressive.
71
What is the treatment for non-Hodgkins lymphoma?
- Chemotherapy + radiotherapy.
72
Which form of lymphoma has a worse prognosis?
- Hodgkin's lymphoma has a worse prognosis than non-Hodgkin's lymphoma.
73
How is myeloma different to leukaemia?
- In myeloma, cancerous cells generally remain in the bone marrow. - In leukaemia, cancerous cells will circulate in the blood.
74
What is malaria?
- Infection by plasmodium transmitted by mosquitos.
75
What is the clinical presentation of malaria?
If infected with plasmodium falciparum, presentation occurs usually in the first month. Other types of malaria can incubate much longer than this. No specific symptoms, but symptoms can include: - Fever - Chills - Rigors (shivering + rise in temperature). - Cough - Myalgia - Splenohepatomegaly If severe: - Impaired consciousness - SOB - Bleeding - Fits - Hypovolaemia
76
What is the pathophysiology of malaria?
- Mosquito bite. - Sporozoites in the mosquito saliva travel to the liver, where they mature. - Eventually, the sporozoites rupture and are released back into the blood. - Invade RBC's and undergo asexual reproduction to create more sporozoites, which more mosquitos can pick up... - And the cycle continues.
77
What is the pathophysiology of malaria?
- Infection by plasmodium (usually plasmodium falciparum).
78
What is the epidemiology of malaria?
- Poor, pregnant, old and young all at more risk. - Consider if recently travelled abroad.
79
What is the investigation used to diagnose malaria?
- Giemsa stained thick and thin blood smears. - Will detect the malaria parasites inside the RBCs.
80
What is the treatment for malaria?
If infection is with plasmodium falciparum: - Quinine sulfate + doxycycline (as will usually be resistant to chloroquine). - Chloroquine phopshate if not resistant. If malaria infection is caused by another pathogen: - Chloroquine is first line.
81
What is thalassaemia?
- Anaemia due to defective subunit of the haemoglobin complex.
82
What are the two types of thalassaemia?
- Alpha and beta. - Determined by the subunit that has been affected.
83
What is the clinical presentation of thalassaemia?
Variable. - Alpha tends to present in utero, whereas beta in infancy. - Heterozygotes can be asymptomatic, whereas homozygotes may have severe symptoms such as failure to thrive and bone deformities.
84
What type of anaemia is thalassaemia?
Microcytic.
85
What is the pathophysiology of thalassaemia?
- Defective versions of either alpha or beta subunits of haemoglobin. - The globin chains within the erythrocytes precipitate and cause cell damage/death.
86
What is the aetiology of thalassaemia?
- Genetic. Homozygotes have severe anaemia, heterozygotes can vary.
87
What is the diagnostic testing used for thalassaemia?
- Firstly identify microcytic anaemia (blood film). - Either genetic testing or haemoglobin electrophoresis.
88
What is the treatment for thalassaemia?
- If iron too high: desferrioxamine - Blood transfusions if required. IF THALASSAEMIA SEVERE, USE BONE MARROW TRANSPLANT!
89
What are the potential complications of thalassaemia?
- Iron overload - Endocrine dysfunction.

Phase 2a diseases (18 decks)

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