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Medical Studies 1 > Week 11 Haematology > Flashcards

Week 11 Haematology Flashcards

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USMLE® Step 1 flashcards
1
Q

how are thrombocytes formed

A

-pluripotent HSC
-common myeloid progenitor
-megakaryoblast
-promegakaryocyte
-thrombocytes

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2
Q

how are erythrocytes formed

A

-pluripotent HSC
-common myeloid progenitor
-proerythroblast
-basophilic erythrocyte
-polychromatic erythroblast
-orthochromatic erythroblast (normoblast)
-polychromatic erythrocyte (reticulocyte)
-erythrocyte

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3
Q

how are basophils formed

A

-pluripotent HSC
-common myeloid progenitor
-myeloblast
-B.promyelocyte
-B.myelocyte
-B.metamyelocyte
-B.band
-basophil

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4
Q

how are neutrophils formed

A

-pluripotent HSC
-common myeloid progenitor
-myeloblast
-N.promyelocyte
-N.myelocyte
-N.metamyelocyte
-N.band
-neutrophils

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5
Q

how are Eosinophils formed

A

-pluripotent HSC
-common myeloid progenitor
-myeloblast
-E.promyelocyte
-E.myelocyte
-E.metamyelocyte
-E.band
-Eosinophil

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6
Q

how are mast cells formed

A

-pluripotent HSC
-common myeloid progenitor
-mast cell

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7
Q

how are macrophages and myeloid dendritic cells formed

A

-pluripotent HSC
-common myeloid progenitor
-myeloblast
-monoblast
-promonocyte
-monocyte
-macrophages and myeloid dendritic cells (3)

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8
Q

how are plasma cells formed

A

-pluripotent HSC
-common lymphoid progenitor
-lymphoblast
-prolymphocyte
-small lymphocyte (4)
-T and B lymphocyte
-Plasma cells

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9
Q

how are NKC formed

A

-pluripotent HSC
-common lymphoid progenitor
-lymphoblast
-prolymphocyte
-NKC

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10
Q

how are lymphoid dendritic cells formed

A

-pluripotent HSC
-common lymphoid progenitor
-lymphoid dendritic cells (3)

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11
Q

define leukopoiesis

A

the physiological process of white blood cell (leukocyte) formation and maturation within the bone marrow

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12
Q

what are HSC

A

undifferentiated cells capable of prosecuting all blood cell types

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13
Q

what are common progenitors

A

intermediate cells that give rise to both myeloid and lymphoid cell lineages

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14
Q

what are granulocyte/monoctes

A

differentiate into myeloid cells, leading to neutrophils, eosinophils,
basophils, and monocytes/macrophages.

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15
Q

what are megakaryocytes/platelets

A

megakaryocytes differentiate into platelets that are essential for clotting

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16
Q

what is lymphoid development

A

process that yields lymphocytes, including B and T cells within the lymphoid lineage

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17
Q

what is T lymphocyte differentiation

A

specific pathway leading to the development of T cells from lymphoid progenitors

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18
Q

morphology of neutrophils

A

polymorphonuclear with granules

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19
Q

function of neutrophils

A

phagocytosis of bacteria and fungi in innate immunity

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20
Q

location of neutrophils

A

circulate in blood, and migrate to site of infection

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21
Q

lifespan of neutrophils

A

relatively short lifespan (6-8 hours in circulation)

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22
Q

morphology of monocytes

A

kidney shaped nucleus, fine granules

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23
Q

function of monocytes

A

precursors of tissue macrophages and dendritic cells involved in immune response

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24
Q

location of monocytes

A

circulate in blood and migrate to tissues PRN

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25
Q

lifespan of monocytes

A

can circulate for a few days before entering tissue and living for weeks to months

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26
Q

morphology of macrophages

A

irregularly shaped nucleus and abundant cytoplasm

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27
Q

function of macrophages

A

phagocytosis of pathogens and debris, antigen presentation, and tissue repair

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28
Q

location of macrophages

A

found in various tissues such as the lung, liver and spleen

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29
Q

lifespan of macrophages

A

long lifespans, from months to years within tissues

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30
Q

morphology of eosinophils

A

bilobed nucleus and large granules

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31
Q

function of eosinophils

A

defence against parasitic infections and involvement in allergies

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32
Q

location of eosinophils

A

found in tissues and the bloodstream especially at sites of inflammation

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33
Q

lifespan of eosinophils

A

relatively short (8-12 hours)

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34
Q

define chemotaxis

A

biological process in which cels, such as immune cells, move in response to chemical signals or gradients

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35
Q

define phagocytosis

A

process by which certain cells, notably phagocytes like neutrophils, macrophages and Dc, engulf and internalise solid particles, such as bacteria, debris or foreign material

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36
Q

morphology of T cells

A

T cells have a round or irregularly shaped nucleus and minimal cytoplasm
-several types Tc (CD8+), Th (CD4+), Treg, T memory

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37
Q

function of T cells

A

-cell mediated immunity
-recognise and attack infected or abnormal host cells such as virally infected cells or cancer cells

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38
Q

location of T cells

A

-T cells are found in the blood and lymphatic system, but are also in lymphoid organs (spleen, thus, LN)
-they move to the site of infection

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39
Q

lifespan of T cells

A

varies, some circulate for weeks and months while memory T cells can circulate for many years

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40
Q

morphology of B cells

A

B cells have a round nucleus and a larger amount of cytoplasm compared to T cells

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41
Q

function of B cells

A

-B cells are responsible for humeral immunity
-produce immunoglobulins (anitbodies) that can neutralise pathogens, mark them for detrsution or enhance phagocytosis
-B cells also play a role in presenting antigens to T cells

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42
Q

location of B cells

A

-found in lymphoid organs, lymph nodes, the spleen and in the bloodstream, they can also be found in peripheral tissues

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43
Q

lifespan of B cells

A

variable lifespans; some differentiate into short lived plasma cells while others form long living b memory cells

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44
Q

define leukocytosis

A

An abnormal increase in the number of white blood cells (leukocytes) in the blood,
often indicative of an immune response to infection or other underlying medical conditions
*WBC > 11,000/microL

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45
Q

define leukopenia

A

A decrease in the total white blood cell count in the blood, potentially increasing the
risk of infections and impairing the immune system’s function.

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46
Q

define neutropenia

A

condition characterized by a deficiency of neutrophils (a type of white blood cell), which can make individuals more susceptible to bacterial infections.

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47
Q

define monocytopenia

A

A reduction in the number of monocytes (a type of white blood cell) in the blood, potentially affecting the body’s ability to fight certain infections and inflammatory conditions.

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48
Q

define lymphopaenia

A

A lower-than-normal count of lymphocytes (a type of white blood cell), which can weaken the immune response and increase vulnerability to infections.

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49
Q

function of chemokine

A

subset of cytokines that specifically attract immune cells to sites of infection or inflammation

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50
Q

function of cytokines

A

small signalling proteins produced by immune cells to regulate inflammation, cell communication and immune responses

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51
Q

function of mast cells

A

tissue resident immune cells that release inflammatory mediators like histamine in response to allergens or pathogens, playing a central role in allergic reactions

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52
Q

function of NK cells

A

cytotoxic lymphocytes that recognise and destroy infected cells without prior sensitisation, contributing to early defence against infections and tumour surveillance

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53
Q

functions of neutrophil

A

-phagocytosis: ingest and release into phagosome
-degranulation: release granules into extracellular environment
-netosis: expulsion of nuclear material in the form of neutrophil extracellular traps (NET)

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54
Q

functions of macrophages

A

-phagocytosis: ingest harmful wastes, pathogens and microbes
-inflammation: secrete pro inflammatory cytokines and antimicrobial mediators

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55
Q

function of dendritic cells

A

-antigen capturing : detect PAMP’s
-antigen presentation: process antigens into smaller peptides for antigen presentation

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56
Q

list the steps in pathogen recognition

A

-pathogen exposure
-antigen identification
-PRR binding
-phagocytosis
-antigen presentation
-T cell recognition
-B cell recognition

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57
Q

describe ‘pathogen exposure’ in pathogen recognition

A

immune system encounters a pathogen, such as bacterium, virus or fungus through inhalation, digestion other physical contact

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58
Q

describe ‘antigen identification’ in pathogen recognition

A

immune cells (macrophages, Dc, neutrophils) are equipped with receptors called pattern recognition receptors (PRR) that recognise conserved molecular patterns found on pathogens

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59
Q

describe ‘PRR binding’ in pathogen recognition

A

when PRR’s on immune cells bind to PAMP’s on the pathogens surface, this binding activates the immune cell, activation triggers a series of intracellular signalling events, leading to the initiation of the immune response

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60
Q

describe ‘phagocytosis’ in pathogen recognition

A

phagocytes engulf the pathogen through phagocytosis, internalising pathogens in a vesicle called a phagosome

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61
Q

describe ‘antigen presentation’ in pathogen recognition

A

dendritic cells capture pathogens and digest them, they then present fragments of the pathogen’s antigens on their cells surfaces using MHC molecules

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62
Q

describe ‘T cell recognition’ in pathogen recognition

A

-Th cells (CD4+) recognise antigen-MHC complexes on Dc
-this activates Th cells, which release cytokines that orchestrate immune response
-Tc cells (CD8+) can also recognise antigens presented by infected host cells and directly kill them

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63
Q

describe ‘B cell recognition’ in pathogen recognition

A

-B cells recognise antigens directly, without need for antigen presentation
-once activated they produce s+c antibodies to pathogens antigens
-pathogen is neutralised or tagged for destruction by antibodies

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64
Q

what is the classical complement pathway

A

C1 recognises immune complexes formed by the binding of IgG or IgM to an antigen.

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65
Q

what is the alternative complement pathway

A

Non-specific activation by bacteria, fungi, and parasites via C3b deposition on the surface of microbes

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66
Q

what is the lectin complement pathway

A

Mannose Binding Lectin (MBL) attaches to the mannose sugar residues on bacterial surfaces

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67
Q

what are the actions of complements

A

opsonisation: complements coat pathogens, making them more susceptible to phagocytosis

inflammation: increased blood flow, immune cells, inflammatory mediates to combat infection + promote repair

punching holes: create pores in membranes of cells leading to lysis and destruction

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68
Q

Describe the process of T cell recognition and activation

A

-immune cells recognise specific antigens on pathogens
-MHC proteins display antigens for T cell recognition
-HLA genes code for MHC proteins in humans
-antigen presenting cells process and display antigens using MHC molecules
-TCR’s interact with MHC molecules to recognise antigens
-TCR’s become activated when their receptors bind to MHC-antigen complexes

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69
Q

list the immunoglobulins

A

IgM
IgD
IgG
IgE
IgA

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70
Q

what is the IgM antibody

A

the first antibody produced during an initial immune response, characterised by pentameric structure and potent agglutination properties

71
Q

what is the IgD antibody

A

primarily found on the surface of B cells, serving as a receptor to initiate B cell activation and maturation

72
Q

what is the IgG antibody

A

the most abundant antibody class in the blood, providing long-term protection against infections and facilitating immune memory

73
Q

what is the IgE antibody

A

involved in allergic and hypersensitivity reactions, particularly by triggering mast cells degranulation in response to allergies

74
Q

what is the IgA antibody

A

predominantly found in the mucosal secretions and plays a crucial role protecting mucosal surfaces from pathogens

75
Q

epitopes are also known as

A

also known as Antigenic Determinants

76
Q

what is the idiotype

A

variable region of an immunoglobulin (determines its characteristics and its ability to bind to a specific antigen)

77
Q

what is complementary determining region

A

Regions within the variable region that actually comes into contact with the epitope on the antigen

78
Q

Features of antigen-antibody complex

A

-antibodies have specific regions known as CDR’s, which are the antibody’s variable domain
-CDR’s are responsible for binding to antigens
-works like the lock and key process

79
Q

distinguish between innate and adaptive immunity

A

*I= non specific vs A= specific and tailored
*I=rapid defence vs A=slower defence
*I=tolerance to self antigen (mainly works against non self) vs A=distinguish between self and non self
*I=pattern recognition only vs A=specific recognition of all possible antigens
I=no memory vs A=memory

80
Q

MHC vs HLA

A

MHC and HLA are both protein complexes that respond to antigens
-MHCI and HLA I are for Tc (CD8+)
-MHCII and HLA II are for Th (CD4+) and B cells

-MHC is for all organisms whereas HLA (human leukocyte agent) is only for humans

81
Q

what is the epitope/antigenic determinant

A

a specific part of an antigen that is recognized and bound by an antibody or immune cell receptor

82
Q

what are the five key leukaemia

A

-Acute myeloblastic leukaemia (AML)
-Acute lymphoblastic leukaemia (ALL)
-Chronic myelogenous leukaemia (CML)
-Chronic lymphocytic leukaemia (CLL)
-Multiple myeloma (MM)

83
Q

what is acute myeloblastic leukaemia (AML)

A

fast growing cancer of blood and bone marrow characterised by rapid proliferation of immature myeloid white blood cells

84
Q

what is acute lymphoblastic leukaemia

A

rapidly progressing cancer of the blood and bone marrow, primarily affecting lymphoid white blood cells and often seen in children

85
Q

what is chronic myelogenuous leukaemia (CML)

A

slow growing form of leukaemia that originates in myeloid white blood cells, characterised by the presence of Philadelphia chromosome and a chronic phase that can transform into an acute phase

86
Q

what is chronic lymphocytic leukaemia (CLL)

A

slowly progressing leukaemia primarily affecting lymphocytes, characterised by accumulation of abnormal white blood cells in blood and bone marrow

87
Q

what is multiple myeloma (MM)

A

cancer of plasma cells in the bone marrow, leading to the overproduction of MAb and weakened bone marrow structure

88
Q

define leukaemia

A

malignancy characterised by an excess of clonal white blood cells

89
Q

define lymphoma

A

heterogenous group of malignancies that arise from the clonal proliferation of various cell subsets of lymphocytes at different stages of maturation
-generally arise from lymph nodes

90
Q

what are indolent lymphoid malignancies

A

malignancies that have a slow and relatively non aggressive growth pattern

91
Q

what are aggressive lymphoid malignancies

A

malignancies that are characterised by faster growth rate and more invasive nature

92
Q

what are acute lymphoid malignancies

A

lymphoid malignancies that progress rapidly and involve immature or undeveloped cells

93
Q

what are chronic lymphoid malignancies

A

lymphoid malignancies that progress more slowly and involve mature but abnormal cells

94
Q

pathophysiology of acute leukaemia

A

HSC–> common myeloid –> myeloblast with reduced differentiability–> Accumulation of immature myeloid cells (myeloblasts) that cannot mature

HSC–> common lymphoid–> lymphoblast with increased proliferative ability–> Excessive accumulation of immature lymphoid cells (lymphoblasts) that overpopulate

95
Q

list the clinical features of acute leukaemia

A

fatigue
infection
bleeding
hepatosplenomegaly
lymphadenopathy
headache
arthalgia
skin rashes

96
Q

describe fatigue in acute leukaemia

A

due to decrease in healthy erythrocytes (bone marrow overcrowded), less oxygen transported and lesser energy levels

97
Q

describe infection in acute leukaemias

A

due to fewer functional WBC’s (bone marrow overcrowded) , body is less able to fight off infection

98
Q

describe bleeding in acute leukaemia

A

due to increase in platelets (bone marrow overcrowded), results in impaired blood clotting and increased risk of bleeding

99
Q

describe lymphadenopathy in acute leukaemia

A

Swelling of lymph nodes is a result of the body’s response to the abnormal proliferation of leukemia cells that collect in lymph nodes (Note, only painful in infection)

100
Q

describe hepatosplenomegaly in acute leukaemia

A

enlargement of the liver and spleen occurs due to the infiltration of leukaemic cells in these organs.

101
Q

describe headache in acute leukaemia

A

experienced due to increased intracranial pressure due to accumulation of leukaemia cells and reduced blood flow

102
Q

describe arthralgia in acute leukaemia

A

joint pain is a manifestation of leukaemic cell infiltration into the joints, leading to inflammation and discomfort

103
Q

define skin rashes in acute leukaemia

A

T cell infiltration to the peripheral skin leads to the rashes and erythema

104
Q

pathophysiology of chronic leukaemia

A

Hematopoietic Stem Cell (HSC) → Common Myeloid Progenitor → Myeloblast → Mature Myeloid Cells with abnormal proliferation and accumulation, especially mature cells like neutrophils, eosinophils, or basophils. These cells are more differentiated compared to acute leukemia but proliferate excessively and don’t function properly.

Hematopoietic Stem Cell (HSC) → Common Lymphoid Progenitor → Lymphoblast → Mature Lymphocytes (mostly B-cells) with excessive proliferation and accumulation. These lymphocytes are partially differentiated but still function abnormally and accumulate over time.

105
Q

list the clinical features of chronic leukaemia

A

fatigue
hepatosplenomegaly
lymphadenopathy
arthralgia

106
Q

describe fatigue in chronic leukaemia

A

due to a decrease in healthy red blood cells, leading to reduced oxygen transport and energy levels

107
Q

describe hepatosplenomegaly in chronic leukaemia

A

enlargement of the liver and spleen occurs due to the infiltration of leukaemia cells in these organs

108
Q

describe lymphadenopathy in chronic leukaemia

A

swelling of lymph nodes is a result of the body’s response to the abnormal proliferation of leukaemia cells (only painful in infection)

109
Q

describe arthralgia in chronic leukaemia

A

joint pain is a manifestation of leukaemia cell infiltration into the joints, leading to inflammation and discomfort

110
Q

list the common complications of haemtological malignancies

A

organomegaly
bleeding/bruising
infection
anaemia
renal failure
bone pain

111
Q

describe organomegaly as a complication of haematological malignancies

A

typically occurs because of the uncontrolled growth and accumulation of cancerous cells within an organ, leading to its enlargement and disruption of normal tissue structure and function

112
Q

describe bleeding/bruising as a complication of haematological malignancies

A

occurs when malignant tumours invade blood vessels, impairing their integrity, when cancer disrupts the normal clotting process by affecting platelet production or function

113
Q

describe infection as a complication of haematological malignancies

A

underproduction of immune cells results in a weakened immune system and increased exposure to pathogens such as viruses

114
Q

describe anaemia as a complication of haematological malignancies

A

Occurs when the abnormal cancerous cells crowd out healthy blood-forming cells in the bone marrow, leading to reduced production of red blood cells

115
Q

describe renal failure as a complication of haematological malignancies

A

can occur due to the abnormal proteins (eg MAb) produced by cancerous cells, which can clog and damage the filtering units of the kidneys, impairing their function

116
Q

describe bone pain as a complication of haematological malignancies

A

bone pain in haematological malignancies can result from the infiltration of abnormal cells into the bone marrow and the subsequent disruption of the normal bone structure and function

117
Q

describe the incidence and prevalence of leukaemia

A

-leukaemia comprises 3.2% of new cancer diagnoses (between 2014 and 2018)
-rate of new cases of leukaemia was 14.3 per 10000 men and women over the same time
-Acute LL is more common in paediatric population

118
Q

list the risk factors for haematological malignancies

A

-chemicals/radiation
-genetic abnormality
-smoking
-viruses
-past medical history
-family history

119
Q

how are chemicals/radiation a risk factor for haematological malignancies

A

exposure to certain chemicals or ionising radiation can damage DNA, increasing the risk of mutations that can lead to haematological cancers

120
Q

how are genetic abnormality a risk factor for haematological malignancies

A

people with trisomy 21 (downs syndrome) have an increased risk of haematological cancers due to genetic factors and abnormal immune function

121
Q

how is smoking a risk factor for haematological malignancies

A

smoking introduces carcinogens into the body, increasing the risk of developing haematological cancers, particularly leukaemia and lymphoma

122
Q

how are viruses a risk factor for haematological malignancies

A

viruses like Epstein-bar virus can lead to genetic changes in infected cells, increasing the risk of developing haematological cancers Hodgkins lymphoma

123
Q

how is PMHx a risk factor for haematological malignancies

A

history of certain conditions such as myelodysplastic syndrome (MDS), can increase the risk of progression to more aggressive haematological cancer

124
Q

how is FHx a risk factor for haematological malignancies

A

FHx of haematological cancers can indicate a genetic predisposition, potentially increasing. an individual’s risk of developing these cancers

125
Q

basophil morphology

A

bi/tri loped nucleus

126
Q

lymphocyte morphology

A

deep staining, eccentric

127
Q

erythrocyte morphology on stain

A

darker cells with central pallor (neutrophil are larger with purple nuclei)

128
Q

platelet morphology on stain

A

small dots

129
Q

what are peripheral blood film

A

laboratory test in which a drop of
blood is spread thinly on a glass slide and then stained to allow for the microscopic examination of blood cells

130
Q

functions of bone marrow biopsy

A

diagnosis
classification
staging
monitoring
treatment guidance

131
Q

what is flow cytometry

A

-dx tool in haem malignancies
-enables analysis of cell surface markers and intracellular proteins on individual cells in blood or bone marrow samples

132
Q

CD34 marker =

A

indicates immaturity

133
Q

CD19 marker =

A

Indicative of lymphoid
lineage

134
Q

CD117 marker=

A

Indicative of myeloid
lineage

135
Q

what is the Binet staging system

A

a widely used method for staging chronic lymphocytic leukemia (CLL).

136
Q

stage 1 of Binet staging system for CLL

A

Patients have fewer than three enlarged lymph node groups and no anaemia or thrombocytopenia

137
Q

stage 2 of Binet staging system for CLL

A

Patients have three or more enlarged lymph node groups and no anaemia or thrombocytopenia

138
Q

stage 3 of Binet staging system for CLL

A

Patients have anaemia and/or thrombocytopenia, regardless of number of enlarged lymph node groups

139
Q

Outline use of PCR in haematological malignancies

A

Identifies specific gene rearrangements, translocations, or mutations (allows to check for genes present in CML, AML and minimal residual disease)

140
Q

Outline use of next generation sequencing in haematological malignancies

A

Allows for comprehensive sequencing of multiple genes simultaneously/mutations of multiple genes

141
Q

Outline the use of gene profiling in haematological malignancies

A

Examines expression patterns of genes across a cell population used in lymphomas and leukaemia

142
Q

Outline use of cytogenics for haematological malignancies

A

Purpose: Detects chromosomal abnormalities in malignant cells eg philadelphia in CML

143
Q

List the phases of leukaemia treatment

A

induction
consolidation
maintenance
allogenic stem cell transplant

144
Q

induction phase of leukaemia treatment

A

the primary goal is to rapidly reduce the number of cancer cells in the body using intensive therapy, such as chemotherapy, to induce remission.

145
Q

consolidation phase of leukaemia treatment

A

Following successful induction, the consolidation phase aims to eliminate any remaining cancer cells and further reduce the risk of relapse, often involving additional chemotherapy or stem cell transplantation

146
Q

maintenance phase of leukaemia treatment

A

Lower-dose, long-term therapy is administered to prevent the re-emergence of the malignancy, maintaining the patient’s remission, and improving their long-term
outcomes.

147
Q

allogenic stem cell transplant in leukaemia treatment

A

A curative option for some haematological malignancies, involving the infusion of
healthy stem cells from a donor (typically a family member) to replace the patient’s diseased bone marrow, enabling new blood and immune system development

148
Q

Outline the use of MAb in treatment of haematological malignancies

A

-MAb can be designed to recognise and bind to specific antigens on surface of cancer cells
-can be used alone or combined with chemo etc
-they work via immune system activation/interference with cell signalling pathways/direct cytoxicity
-examples: rituximab for B cell lymphomas and alemtuzumab for CLL

149
Q

Describe the pathophysiology of CML

A

-reciprocal translocation (chromosome9/chromosome22) forms BCR-ABL fusion gene
-BCR-ABL fusion gene codes for active tyrosine kinase
-tyrosine kinase initiates uncontrolled cell signalling and proliferation, particularly of granulocytes in the bone marrow and peripheral blood
-abnormal accumulation of myeloid cells in the marrow and blood –> fatigue, splenomegaly and leukocytosis

150
Q

What are TKI’s

A

-TKIs, such as imatinib, dasatinib, and nilotinib, work by binding to the active site of the BCR-ABL protein,
inhibiting its kinase activity.
* By blocking the BCR-ABL kinase, these drugs effectively suppress the aberrant signalling pathways that drive
uncontrolled cell proliferation in CML.
* Tyrosine kinase inhibitors end in the suffix ‘-inib’.

151
Q

list the common myeloproliferative neoplasms

A

-polycythaemia vera (PV)
-myelofibrosis (MF)
-essential thrombocythaemia (ET)
-CML

152
Q

what is polycythaemia vera

A

A rare blood disorder where the bone marrow produces too many red blood cells, white blood cells, and platelets, leading to an increased risk of blood clots and other complications.

153
Q

what is essential thrombocythaemia

A

A myeloproliferative neoplasm characterized by the overproduction of platelets, potentially resulting in abnormal blood clotting or bleeding.

154
Q

what is myelofibrosis

A

A myeloproliferative neoplasm in which the bone marrow develops fibrous tissue, impairing its ability to produce normal blood cells and leading to anaemia and an enlarged spleen.

155
Q

outline dx of aplastic anaemia

A

-involves a complete blood count (CBC) to assess low blood cell counts,
as well as a bone marrow biopsy or aspiration to confirm the reduction in hematopoietic (blood-forming) cells
in the bone marrow.

156
Q

what is aplastic anaemia

A

rare and serious blood disorder characterized by a significant reduction in the number of blood cells, including red blood cells, white blood cells, and platelets, in the bone marrow

157
Q

treatment for aplastic anaemia

A

-blood transfusions, immunosuppressive therapy, bone marrow transplants

158
Q

list the clinical signs of aplastic anaemia

A

fatigue
pallor
petechiae
infection
dyspnoea
bleeding
dyspnoea
headache

159
Q

describe fatigue in aplastic anaemia

A

Persistent tiredness and weakness due to low red blood cell count, leading to reduced oxygen delivery to tissues.

160
Q

describe pallor in aplastic anaemia

A

A pale complexion or paleness of the skin and mucous membranes, resulting from decreased red blood cell production.

161
Q

describe petechiae in aplastic anemia

A

increased susceptibility to bruising and petechiae (small red or purple dots) due to low
platelet counts, causing impaired blood clotting

162
Q

describe infection in aplastic anaemia

A

Weakened immune system because of low white blood cell count, making the body
more susceptible to infections.

163
Q

describe dyspnoea in aplastic anaemia

A

Breathlessness and rapid heart rate, especially during physical activity, due to
reduced oxygen-carrying capacity of the blood.

164
Q

describe bleeding in aplastic anaemia

A

Excessive bleeding from minor cuts, scrapes, or dental procedures due to inadequate
platelet function

165
Q

describe headache in aplastic anaemia

A

Occasional or persistent headaches, which can be a result of anaemia-induced
reduced oxygen supply to the brain

166
Q

what are cold sores and their relevance

A

neuropathic pain, herpes virus resides in the nerves of the mouth or genitals, sores occur when individual is immunosuppressant

167
Q

how to assess splenomegaly on palpation (criteria)

A

-if able to balot then its the kidney
-if able to feel over it then not spleen
-if able to feel one notch its the spleen

168
Q

glandular fever/mononucleosis can increase risk of

A

Hodgkins lymphoma

169
Q

propose of urine protein electrophoresis/bence jones tests

A

check for MAb/proteins in the urine due to multiple myeloma

170
Q

smudge cells are characteristic of

A

chronić lymphocytic leukaemia

171
Q

what is PET scan checking for in malignancy

A

checking for active/functional myeloma lesions in bones and other tissues (in Mutliple myeloma)

172
Q

watch and wait vs active surveillance in haem malignancies

A

watch and wait- waiting until patient comes back or is worried
active surveillance- constant surveillance due to possible for acute disease progression

173
Q

list some broad treatment options for haematological malignancies

A

-chemotherapy (broader)
-immunotherapy (more specific)
-radiation therapy (at bone marrow)
-bone marrow transplant
-full bloods
-vaccines (non live)
-MAb
-long lasting opioids (oxycontin)
-screen for other cancers (bowel, prostate, cervical)

174
Q

list some lifestyle advice for haematological malignancies

A

-avoid sick contacts (risk for febrile neutropenia)
-diet
-exercise
-avoid smoking an alcohol
-medicine compliance
-mental health support

Medical Studies 1 (15 decks)

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