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Haemotology > week 3 part 1 > Flashcards

week 3 part 1 Flashcards

1
Q

Haemopoiesis

A

the production of blood cells and platelets, which occurs in the bone marrow.

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2
Q

Erythropoiesis

A

Produces red blood cells (erythrocytes),

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3
Q

Lymphopoiesis

A

Refers to the production of new lymphocytes, including B lymphocytes, T lymphocytes, and natural killer (NK) cells.

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4
Q

Neutrophils lifespan

A

7-8 hrs

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5
Q

Platelets lifespan

A

7-10 days

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6
Q

What do “blasts” mean at the end of cells - e.g. erythrobasts?

A

Nucleated precursor cell

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7
Q

Megakaryocytes

A

platelet precursor, polyploid

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8
Q

Reticulocytes

A

Immediate red cell precursor

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9
Q

Myelocytes

A

nucleated precursor between neutrophils and blasts

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10
Q

Where do these precursor cells come from?

A

Progenitors, and ultimately all haemopoietic cells come from haemopoietic stem cells (HSC)

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11
Q

What are the sites of haemopoiesis?

A

Embryonically, haemopoietic stem cells originate in the mesoderm

Circulating committed progenitors detectable as early as week 5

Yolk sac, the first site of erythroid activity, stops by week 10

Liver starts by week 6

Bone marrow by week 16

In adults, haemopoiesis is restricted to the marrow within axial skeleton, pelvis and proximal long bones

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12
Q

Venous sinuses

A

Arterioles drain into ‘sinuses’ – wide venous vessels, which open into larger central sinuses

In contrast to capillaries, ‘sinuses’ are larger and have a discontinuous basement membrane

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13
Q

Release of mature cells from marrow

A

Formed blood cells can pass through fenestrations in endothelial cells to enter circulation

Release of red cells is associated with sinusoidal dilatation and increased blood flow

Neutrophils actively migrate towards the sinusoid

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14
Q

Myeloid:erythroid ratio

A

Myeloid:erythroid ratio: relationship of neutrophils and precursors to proportion of nucleated red cell precursors (ranges from 1.5:1 to 3.3:1) – can change (eg reversal in haemolysis as a compensatory response)

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15
Q

How do we assess haemopoiesis?

non-lymphoid mature cells

A
  1. Routinely undertaken- blood count, cell indices (by non-specialists), morphology (blood film-specialist)
  2. Less common (specialist)-bone marrow
    examination
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16
Q

Immunophenotyping

A

Identify patterns of protein (antigen) expression unique to a cell lineage

Use antibodies (in combination) specific to different antigens

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17
Q

What regulates haemopoiesis?

A

Intrinsic properties of cells (e.g stem cells vs progenitor cells vs mature cells)

Signals from immediate surroundings and the periphery (microenvironmental factors)

Specific anatomical area (‘niche’) for optimal developmental signals

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18
Q

What happens in Malignant Haemopoiesis?

A

Malignant haemopoiesis is usually characterised by increased numbers of abnormal & dysfunctional cells & loss of normal activity

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19
Q

What causes haematological malignancies?

A

Genetic, epigenetic, environmental interaction

ACQUIRED somatic mutations in regulatory genes [driver mutations vs passenger mutations (‘noise’)]

Recurrent cytogenetic abnormalities (eg deletions, chromosomal translocations etc): NOT causal in most, but contributory

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20
Q

What are clones?

A

Clone: population of cells derived from a single parent cell

This parent cell has a genetic marker (driver mutation or chromosomal change) that is shared by the daughter cells

Clones can diversify but contain a similar genetic ‘backbone’

Normal haemopoiesis is polyclonal; malignant haemopoiesis is usually monoclonal

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21
Q

Driver’ mutations

A

Confer growth advantage on the cells and are selected during the evolution of the cancer
A term used to describe changes in the DNA sequence of genes that cause cells to become cancer cells and grow and spread in the body.

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22
Q

Passenger mutations

A

Do not confer growth advantage, but happened to be present in an ancestor of the cancer cell when it acquired one of its drivers

Passenger mutations are defined as those which do not alter fitness but occurred in a cell that coincidentally or subsequently acquired a driver mutation, and are therefore found in every cell with that driver mutation.

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23
Q

Types of haematological malignancies based on:

A
  1. Lineage: Myeloid, Lymphoid
  2. Developmental stage
  3. Blood involvement: leukaemia
  4. Lymph node involvement with lymphoid malignancy: lymphoma
  5. Myeloma: plasma cell malignancy in marrow
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24
Q

Features of clinical aggression

A

rapid progression of symptoms

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25
Q

Features of histological aggression

A

Large cells with high nuclear-cytoplasmic ratio, prominent nucleoli, rapid proliferation

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26
Q

Difference between histology and presentation of acute leukaemias/high-grade lymphomas and chronic leukaemias/low-grade lymphomas

A

acute leukaemias & high-grade lymphomas are histologically and usually clinically more aggressive than chronic leukaemias & low-grade lymphomas

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27
Q

Leukaemia

A

Leukaemia is the name for cancer of a particular line of the stem cells in the bone marrow. This causes unregulated production of certain types of blood cells. Types of leukaemia can be classified depending on how rapidly they progress (chronic is slow and acute is fast) and the cell line that is affected (myeloid or lymphoid).

28
Q

Leukaemia types

A
  • Acute lymphoblastic leukaemia (ALL) is the most common in children
  • Acute myeloid leukaemia (AML) is the next most common
  • Chronic myeloid leukaemia (CML) is rare
29
Q

Ages of onset of the leukaemias

A

ALL peaks aged 2 – 3 years

AML peaks aged under 2 years

30
Q

Leukemia pathophysiology

A

Leukaemia is a form of cancer of the cells in the bone marrow. A genetic mutation in one of the precursor cells in the bone marrow leads to excessive production of a single type of abnormal white blood cell.

The excessive production of a single type of cell can lead to suppression of the other cell lines, causing underproduction of other cell types. This results in a pancytopenia, which is a combination of low:
Red blood cells (anaemia),
White blood cells (leukopenia)
Platelets (thrombocytopenia)

31
Q

Blood features of leukaemia

A

The excessive production of a single type of cell can lead to suppression of the other cell lines, causing underproduction of other cell types. This results in a pancytopenia, which is a combination of low:
Red blood cells (anaemia),
White blood cells (leukopenia)
Platelets (thrombocytopenia)

32
Q

Risk factors for Leukemia

A

Down’s syndrome
Kleinfelter syndrome
Noonan syndrome
Fanconi’s anaemia

33
Q

Features of Leukemia

A 
Persistent fatigue
Unexplained fever
Failure to thrive
Weight loss
Night sweats
Pallor (anaemia)
Petechiae and abnormal bruising (thrombocytopenia)
Unexplained bleeding (thrombocytopenia)
Abdominal pain
Generalised lymphadenopathy
Unexplained or persistent bone or joint pain
Hepatosplenomegaly
34
Q

Diagnosis of Leukemia

A

Full blood count, which can show anaemia, leukopenia, thrombocytopenia and high numbers of the abnormal WBCs
Blood film, which can show blast cells
Bone marrow biopsy
Lymph node biopsy

Further tests may be required for staging:
Chest xray
CT scan
Lumbar puncture
Genetic analysis and immunophenotyping of the abnormal cells

35
Q

Management of Leukemia

A

Treatment of leukaemia will be coordinated by a paediatric oncology multi-disciplinary team. Leukaemia is primarily treated with chemotherapy.

Other therapies:
Radiotherapy
Bone marrow transplant
Surgery

36
Q

Complications of Chemotherapy

A 
Failure to treat the leukaemia
Stunted growth and development
Immunodeficiency and infections
Neurotoxicity
Infertility
Secondary malignancy
Cardiotoxicity
37
Q

Prognosis of Leukemia

A

The overall cure rate for ALL is around 80%, but prognosis depends on individual factors. The outcomes are less positive for AML.

38
Q

Infective causes of lymphadenopathy

A 
infectious mononucleosis
HIV, including seroconversion illness
eczema with secondary infection
rubella
toxoplasmosis
CMV
tuberculosis
roseola infantum
39
Q

Neoplastic causes of lymphadenopathy

A

leukaemia

lymphoma

40
Q

Lymphadenopathy

A

Lymphadenopathy refers to the enlargement of one or more lymph nodes, the bean-shaped glands found in the neck, armpits, chest, groin, and abdomen

41
Q

Symptoms of Lymphadenopathy

A

A ‘lump’: lymphadenopathy

General Symptoms (‘B symptoms’)
Fever or
night sweats or
weight loss – (10% over a 6-month period)

Itch without rash, alcohol-induced pain

Symptoms relevant to known/suspected systemic illness (INDAM)

42
Q

What do tender lymph nodes suggest?

A

Caused by bacteria/virus rather than neoplasia

43
Q

What do non-tender lymphadenopathy siggest?

A

Lymphoma and metastatic cancers

44
Q

What does a rubbery/soft lymphadenopathy suggest?

A

Lymphoma

45
Q

Lymphomas

A

Lymphomas are a group of cancers that affect the lymphocytes inside the lymphatic system. These cancerous cells proliferate within the lymph nodes and cause the lymph nodes to become abnormally large (lymphadenopathy).

46
Q

The two types of lymphomas

A

There are two main categories of lymphoma: Hodgkin’s lymphoma and non-Hodgkin’s lymphoma. Hodgkin’s lymphoma is a specific disease and non-Hodgkins lymphoma encompasses all the other lymphomas.

47
Q

Hodgkin’s lymphoma

A

Hodgkin’s lymphoma is a malignant proliferation of lymphocytes characterised by the presence of the Reed-Sternberg cell. It has a bimodal age distributions being most common in the third and seventh decades

48
Q

Risk factors for Hodgkin’s lymphoma

A

HIV
Epstein-Barr Virus
Autoimmune conditions such as rheumatoid arthritis and sarcoidosis
Family history

49
Q

Features of Hodgkin’s lymphoma

A

Lymphadenopathy is the key presenting symptom. The enlarged lymph node or nodes might be in the neck, axilla (armpit) or inguinal (groin) region. They are characteristically non-tender and feel “rubbery”.
B symptoms are the systemic symptoms of lymphoma: Fever, Weight loss, Night sweats

Other symptoms can include:
Fatigue
Itching
Cough
Shortness of breath
Abdominal pain
Recurrent infections
50
Q

Diagnosis/investigations in Hodgkin’s lymphoma

A

Lactate dehydrogenase (LDH) is a blood test that is often raised in Hodgkin’s lymphoma but is not specific and can be raised in other cancers and many non-cancerous diseases.

Lymph node biopsy is the key diagnostic test.

The Reed-Sternberg cell is the key finding from lymph node biopsy in patients with Hodgkin’s lymphoma.

CT, MRI and PET scans can be used for diagnosing and staging lymphoma and other tumours.

51
Q

The Reed-Sternberg cell

A

The Reed-Sternberg cell is the key finding from lymph node biopsy in patients with Hodgkin’s lymphoma. They are abnormally large B cells that have multiple nuclei that have nucleoli inside them. This can give them the appearance of the face of an owl with large eyes. The Reed-Sternberg cell is a popular feature in medical exams.

52
Q

The Ann Arbor staging system

A

The Ann Arbor staging system is used for both Hodgkins and non-Hodgkins lymphoma. The system puts importance on whether the affected nodes are above or below the diaphragm.

53
Q

The Ann Arbor staging system (what are the stages?)

A

Stage 1: Confined to one region of lymph nodes.
Stage 2: In more than one region but on the same side of the diaphragm (either above or below).
Stage 3: Affects lymph nodes both above and below the diaphragm.
Stage 4: Widespread involvement including non-lymphatic organs such as the lungs or liver.

54
Q

Management of Hodgkin’s lymphoma

A

The key treatments are chemotherapy and radiotherapy. The aim of treatment is to cure the condition. This is usually successful however there is a risk of relapse, other haematological cancers and side effects of medications.

Chemotherapy creates a risk of leukaemia and infertility.

Radiotherapy creates a risk of cancer, damage to tissues and hypothyroidism.

55
Q

A common type of Non-Hodgkin’s lymphoma

A

Diffuse large B cell lymphoma

56
Q

Different types of Non-Hodgkin’s lymphoma

A

A few notable ones are:

  1. Burkitt lymphoma is associated with Epstein-Barr virus, malaria and HIV.
  2. MALT lymphoma affects the mucosa-associated lymphoid tissue, usually around the stomach. It is associated with H. pylori infection.
  3. Diffuse large B cell lymphoma often presents as a rapidly growing painless mass in patients over 65 years.
57
Q

Risk factors for Non-Hodgkin’s lymphoma

A 
HIV
Epstein-Barr Virus
H. pylori (MALT lymphoma)
Hepatitis B or C infection
Exposure to pesticides and a specific chemical called trichloroethylene used in several industrial processes
Family history
58
Q

Management of Non-Hodgkin’s lymphomas

A 
Watchful waiting
Chemotherapy
Monoclonal antibodies such as rituximab
Radiotherapy
Stem cell transplantation
59
Q

Use of monoclonal antibodies in Non-Hodgkin’s lymphomas

A

Rituximab (CD20) in B cell NHL

Brentuximab (CD30) in T cell NHL

60
Q

Burkitt tumours

A

Fastest growing human tumour

Endemic type (EBV link) vs sporadic

HIV association

Disease sites

Chromosomal translocations involving c-myc

High cure rates in high income countries – beware of tumour lysis at the start

61
Q

Microscopy findings of Burkitt’s lymphoma

A

starry sky’ appearance: lymphocyte sheets interspersed with macrophages containing dead apoptotic tumour cells

62
Q

Nodular sclerosing Hodgkin’s lymphoma

A

Nodular sclerosing - Most common (around 70%), Good prognosis, More common in women. Associated with lacunar cells

63
Q

Mixed cellularity Hodgkin’s lymphoma

A

Around 20%
Good prognosis
Associated with a large number of Reed-Sternberg cells

64
Q

Lymphocyte predominant Hodgkin’s lymphoma:

A

Around 5%

Best prognosis

65
Q

Lymphocyte depleted Hodgkin’s lymphoma:

A

Rare

Worst prognosis

66
Q

Gastric MALT lymphoma

A

associated with H. pylori infection in 95% of cases
good prognosis
if low grade then 80% respond to H. pylori eradication
paraproteinaemia may be present

67
Q

Prognosis of non-Hodgkin’s lymphomas

A

Low-grade non-Hodgkin’s lymphoma has a better prognosis

High-grade non-Hodgkin’s lymphoma has a worse prognosis but a higher cure rate

Haemotology (9 decks)

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