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Medical Studies 1 > Haem Week 11 > Flashcards

Haem Week 11 Flashcards

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USMLE® Step 1 flashcards
1
Q

Describe the development and differentiation of HSCs into neutrophils

A

HSC

Then, common myeloid progenitor

Then, myeloblast

Then, N.promyelocyte

Then, N.myelocyte

Then, N.metamyelocyte

Then, N.band

Then, neutrophil

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2
Q

Describe the development and differentiation of HSCs into monocyte/macrophages

A

HSC

Then, common myeloid progenitor

Then, myeloblast

Then, monoblast

Then, promonocyte

Then, monocyte

Then, macrophage

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3
Q

Describe the development and differentiation of HSCs into basophils

A

HSC

Then, common myeloid progenitor

Then, myeloblast

Then, B.promyelocyte

Then, B.myelocyte

Then, B.metamyelocyte

Then, B.band

Then, basophil

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4
Q

Describe the development and differentiation of HSCs into eosinophils

A

HSC

Then, common myeloid progenitor

Then, myeloblast

Then, E.promyelocyte

Then, E.myelocyte

Then, E.metamyelocyte

Then, E.band

Then, eosinophil

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5
Q

Describe the development and differentiation of HSCs into platelets

A

HSC

Then, common myeloid progenitor

Then, megakaryoblast

Then, promegakaryocyte

Then, megakaryocyte

Then, thrombocytes (platelets)

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6
Q

Describe the development and differentiation of HSCs into erythrocytes

A

HSC

Then, common myeloid progenitor

Then, proerythroblast

Then, basophilic erythroblast

Then, polychromatic erythroblast

Then, orthochromatic erythroblast (normoblast)

Then, polychromatic erythrocyte (reticulocyte)

Then, erythrocyte

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7
Q

Describe the development and differentiation of HSCs into B lymphocytes

A

HSC

Then, common lymphoid progenitor

Then, lymphoblast

Then, prolymphocyte

Then, small lymphocyte

Then, B lymphocyte

Then, plasma cell

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8
Q

Describe the development and differentiation of HSCs into T lymphocytes

A

HSC

Then, common lymphoid progenitor

Then, lymphoblast

Then, prolymphocyte

Then, small lymphocyte

Then, T lymphocyte

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9
Q

Describe the development and differentiation of HSCs into NKCs

A

HSC

Then, common lymphoid progenitor

Then, lymphoblast

Then, prolymphocyte

Then, NKC

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10
Q

Define leukopoiesis

A

The physiological process of WBC formation and maturation within the bone marrow

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11
Q

Outline the morphology of neutrophils

A

Polymorphonuclear w granules

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12
Q

Outline the function of neutrophils

A

Migrate to sites of infection through chemotaxis, engage in phagocytosis to engulf and ingest foreign materials like bacteria, and kill pathogens by releasing antimicrobial substances

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13
Q

Outline the location of neutrophils

A

Circulate in the blood and migrate to sites of infection

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14
Q

Outline the lifespan of neutrophils

A

Relatively short of around 6-8 hrs in circulation

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15
Q

Outline the morphology of monocytes

A

Kidney-shaped nucleus

Fine granules

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16
Q

Outline the function of monocytes

A

Precursors of tissue macrophages and dendritic cells, involved in immune responses

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17
Q

Outline the location of monocytes

A

Circulate in the blood and migrate to tissues when needed

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18
Q

Outline the lifespan of monocytes

A

Can circulate for a few days before entering tissues, where they can live for weeks to months

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19
Q

Outline the morphology of macrophages

A

Irregularly shaped nucleus and abundant cytoplasm

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20
Q

Outline the function of macrophages

A

Respond to chemotactic signals to migrate to areas of infection, conduct phagocytosis to engulf foreign materials, and play a central role in antigen presentation, inflammation regulation and tissue repair in addition to destroying pathogens

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21
Q

Outline the location of macrophages

A

Found in various tissues such as lungs, liver and spleen

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22
Q

Outline the lifespan of macrophages

A

Long lifespan, from months to years within tissues

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23
Q

Outline the morphology of eosinophils

A

Bilobed nucleus

Large granules

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24
Q

Outline the function of eosinophils

A

Defence against parasitic infections and involvement in allergies

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25
Q

Outline the location of eosinophils

A

Found in tissues and the bloodstream, especially at sites of inflammation

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26
Q

Outline the lifespan of eosinophils

A

Relatively short of around 8-12 hours

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27
Q

Outline the morphology of basophils

A

Bilobed nucleus

Large granules

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28
Q

Outline the function of basophils

A

Release histamine, heparin, and other mediators involved in allergic responses

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29
Q

Outline the location of basophils

A

Circulate in blood but are rare compared to other WBC

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30
Q

Outline the lifespan of basophils

A

Short lifespan, usually few hours to few days

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31
Q

What is chemotaxis

A

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

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32
Q

Outline the morphology of T lymphocytes

A

Round or irregularly shaped nucleus and minimal cytoplasm

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33
Q

Outline the function of T lymphocytes

A

Cell mediated immunity

Central role in recognising and attacking infected or abnormal host cells

Each type (cytotoxic, helper, regulatory) has distinct function

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34
Q

Outline the location of T lymphocytes

A

Blood and lymphatic system, but also present in lymphoid organs such as thymus, lymph nodes and spleen

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35
Q

Outline the lifespan of T lymphocytes

A

Varies, some circulate for weeks or months while memory T cells can persist for many years

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36
Q

Outline the morphology of B lymphocytes

A

Round nucleus and larger amount of cytoplasm compared to T cells

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37
Q

Outline the function of B lymphocytes

A

Humoral immunity

Produce antibodies that can neutralise pathogens, mark them for destruction, or enhance phagocytosis, and has a role in antigen presentation to T cells

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38
Q

Outline the location of B lymphocytes

A

Found in lymphoid organs, lymph nodes, the spleen, and in bloodstream

Can also be found in peripheral tissues

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39
Q

Outline the lifespan of B lymphocytes

A

Variable lifespans; some differentiate into short lived plasma cells that produce antibodies, while other form memory B cells that can persist for years

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40
Q

Define leukocytosis

A

Abnormal increase in number of WBC in blood, often indicative of immune response to infection or other underlying medical conditions

WBC >11,000/microL

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41
Q

Define leukopaenia

A

Decrease in the total WBC count in the blood, potentially increasing the risk of infections and impairing the immune system’s function

42
Q

Define neutropaenia

A

Condition characterised by a deficiency of neutrophils which can make individuals more susceptible to bacterial infections

43
Q

Define monocytopaenia

A

Reduction in the number of monocytes in the blood, potentially affecting the body’s ability to fight certain infections and inflammatory conditions

44
Q

Define lymphopaenia

A

Lower than normal count of lymphocytes, which can weaken the immune response and increase vulnerability to infections

45
Q

What is netosis

A

When a neutrophil expels nuclear material in the form of neutrophil extracellular traps (NETs)

46
Q

Outline the process of pathogen recognition

A
  1. Pathogens exposure - immune system encounters pathogen
  2. Antigen ID - immune cells equipped w PRRs recognise conserved molecular patterns found on pathogens
  3. PRR binding - PRRs on immune cells bind to PAMPs on pathogen surface > activates immune cell which triggers series of intracellular signalling events to initiate immune response
  4. Phagocytosis - engulf pathogen
  5. Antigen presentation - dendritic cells present fragments of pathogen’s antigen on surface using MHC markers
  6. T cell recognition - Th cells (CD4+) recognise antigen-MHC complexes on dendritic cells, so they then release cytokines that orchestrate immune response / T cytotoxic cells (CD8+) also recognise antigens presented by infected host cells
  7. B cell recognition - B cells recognise antigens directly which activates them so that they can differentiate into plasma cells that can produce specific and complementary antibodies
47
Q

Describe the role of the complement system in initiating an inflammatory response

A

Contributes to host defence by enhancing body’s ability to fight infections and remove damaged cells

Activation of complement system leads to cascade of events, including opsonisation of pathogens, inflammation, and formation of membrane attack complexes to directly lyse and destroy target cells

48
Q

Describe the classical activation pathway of complement system

A

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

49
Q

Describe the alternative activation pathway for complement system

A

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

50
Q

Describe the lectin activation pathway for complement system

A

Mannose binding lectin (MBL) attaches to the mannose sugar residues on bacterial surfaces

51
Q

What are 3 key mechanisms of action of the complement system and provide a brief description of each

A

Opsonisation - process by which complement proteins coat pathogens, making them more susceptible to phagocytosis

Inflammation - increased blood flow and increased recruitment of immune cells and release of inflammatory mediators

Punching holes - complement components create pores in membranes of target cells leading to their lysis

52
Q

What is HLA

A

Genes that code for MHC proteins in humans

53
Q

What are two classes of HLA/MHC, give 3 examples, and a brief description of their function

A

HLA/MHC class 1: HLA-A, HLA-B, HLA-C —> present on almost all nucleated cells and present endogenous peptides to CD8+ cytotoxic cells

HLA/MHC class 2: HLA-DP, HLA-DQ, HLA-DR —> primarily found on APCs where they present exogenous peptides to CD4+ helper T cells

54
Q

What does idiotype mean

A

Refers to the unique set of characteristics that define an antibody, including the specific shape and structure of its variable domains

It is determined by the combination of CDRs within an antibody, and it plays a crucial role in the antibody’s ability to bind to a specific antigen

55
Q

Describe how antigen-antibody complexes are formed

A

Epitopes (specific regions on antigens recognised by antibodies) bind to CDRs on antibodies. These interactions are highly specific, like a lock and key mechanism ensuring that each antibody binds only to its corresponding antigen

56
Q

Distinguish between innate and adaptive immune response with regards to time course, specificity and discrimination between self and non self

A

Innate immunity has a rapid defence whereas adaptive is slower acting

Innate immunity is non specific whereas adaptive is tailored to a pathogen

Innate immunity has tolerance to self antigens whereas adaptive immunity can distinguish between self and non self

57
Q

What is AML

A

Acute myeloblastic leukaemia

Fast growing cancer of the blood and bone marrow characterised by the rapid proliferation of immature myeloid WBC

58
Q

what is ALL

A

Acute lymphoblastic leukaemia

Rapidly progressing cancer of the blood and bone marrow, primarily affecting lymphoid WBC and often seen in children

59
Q

What is CML

A

Chronic myelogenous leukaemia

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

60
Q

What is CLL

A

Chronic lymphocytic leukaemia

A slowly progressing leukaemia primarily affecting lymphocytes, characterised by the accumulation of abnormal WBC in the blood and bone marrow

61
Q

What is MM

A

Multiple myeloma

Cancer of plasma cells in the bone marrow, leading to overproduction of abnormal monoclonal antibodies and weakened bone structure

62
Q

Define leukaemia

A

Malignancy characterised by an excess of clonal WBC

63
Q

Define lymphoma

A

A heterogenous group of malignancies that arise from the clonal proliferation of various cell subsets of lymphocytes at different stages of maturation

64
Q

Define indolent lymphoid malignancy

A

Malignancies that refer to cancers that have a slow and relatively non-aggressive growth pattern

65
Q

Define aggressive lymphoid malignancy

A

Malignancies that are characterised by a faster growth rate and a more invasive nature

66
Q

Define acute lymphoid malignancies

A

Lymphoid malignancies that progress rapidly and involve immature or underdeveloped cells

67
Q

Define chronic lymphoid malignancies

A

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

68
Q

What are two types of acute leukaemias

A

ALL

AML

69
Q

Describe the pathogenesis of acute leukaemias

A

Leukaemia cells (arising from early HSCs) lose their ability to differentiate, resulting in an early block, however they retain their ability to replicate

Then, these myeloblasts or lymphoblasts proliferate uncontrollably, occupying space in the bone marrow

Then, these cells replace most of the bone marrow cells, crowding sites of normal haematopoiesis

Then, they enter peripheral blood

Then, they metastasise throughout the body, forming a malignant leukaemia

70
Q

What are 8 clinical features of acute leukaemias

A

Fatigue - due to decrease healthy RBC leading to decreased O2 transport

Infection - due to fewer functional WBC

Bleeding - due to decrease platelets

Hepatosplenomegaly - due to infiltration of leukemic cells in these organs

Lymphadenopathy - swelling of lymph nodes in response to abnormal proliferation of leukaemia cells

Headache - due to increased ICP due to accumulation of leukemic cells and reduced blood flow

Arthralgia - joint pain due to leukemic cells infiltration leading to inflammation

Skin rashes - T cell infiltration to peripheral skin

71
Q

Outline the pathogenesis of chronic leukaemias

A

Same as acute but it is a monoclonal disorder of LATE HSCs rather than early, meaning the cells are more mature but non-functional

72
Q

What are 4 clinical features of chronic leukaemia

A

Fatigue - due to reduced healthy RBC and O2 transport

Hepatosplenomegaly - infiltration of leukemic cells in these organs

Lymphadenopathy - swelling of lymph nodes due to abnormal proliferation of leukaemia cells

Arthralgia - joint pain due to leukemic cell infiltration leading to inflammation and discomfort

73
Q

What are 6 common complications of haematologic malignancies

A

Organomegaly - due to uncontrolled growth and accumulation of cancerous cells within an organ

Bleeding/bruising - malignant tumours invade blood vessels, impairing their integrity or when cancer disrupts normal clotting processes

Infection - underproduction of immune cells > weakened immune system

Anaemia - abnormal cancerous cells crowd out healthy blood-forming cells in bone marrow

Renal failure - abnormal proteins produced by cancer cells > clog and damage filtering units of kidneys

Bone pain - infiltration of abnormal cells into bone marrow and subsequent disruption of normal bone structure

74
Q

What are 6 risk factors for haematological malignancies

A

Chemicals/radiation - damages DNA increasing risk of mutations

Genetic abnormalities - ppl w trisomy 21 have an increased risk of haematological cancers due to genetic factors and abnormal immune function

Smoking - carcinogens which increases the risk of developing haematological cancers

Viruses - can lead to genetic changes which increases risk of developing haematological cancers

Past medical history - history of certain conditions like myelodysplastic syndrome can increase risk of progression to more aggressive cancers

Family history - indicate genetic predisposition

75
Q

Describe peripheral blood films

A

Lab 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 ells

Enables observation of size, shape, colour, arrangement and inclusions of blood cells

76
Q

Describe how erythrocytes are seen in peripheral blood films

A

Darker cells with central pallor

77
Q

Describe how neutrophils are seen on peripheral blood films

A

Larger, segmented purple nuclei

78
Q

Describe how platelets can be seen on peripheral blood films

A

Represented as small dots

79
Q

Outline the role of bone marrow biopsies in the investigation of suspected haematological malignancy

A

Diagnosis - crucial for confirming or ruling out haematological malignancies such as leukemia, lymphoma and myeloma

Classification - classify specific subtype and stage of malignancy

Staging - determine extent and progression of malignancy and spread

Monitoring - response to Rx, assess disease remission, and detect relapse

Rx guidance - determine most appropriate Rx strategies, including chemotherapy, targeted therapy, or bone marrow transplantation

80
Q

Describe flow cytometry

A

Enables the analysis of cell surface markers and intracellular proteins on individual cells in a blood or bone marrow sample

Detect and quantify abnormal cell populations such as leukemic blasts, lymphoma cells, and myeloma cells

Helps differentiate b/w diff types of haem malignancies

Allows assessment of Rx response

Provides immunophenotypic info which is crucial for tailoring Rx

81
Q

CD34 marker viewed on flow cytometry indicates what

A

Immaturity of cell

82
Q

CD19 marker viewed on flow cytometry indicates what

A

Lymphoid lineage

83
Q

CD117 marker viewed on flow cytometry indicates what

A

Myeloid lineage

84
Q

What are 5 investigative methods that can be used to differentiate between different haem malignancies

A

Cytogenics

Flow cytometry

Next gen sequencing

Gene profiling

PCR

85
Q

What is the Binet staging system

A

Used for staging CLL

Categorises Pt into one of 3 clinical stages based on extent of lymphocyte involvement and presence of anaemia or thrombocytopaenia

Helps in determine the prognosis and guiding Rx decisions w early typically requiring less aggressive Rx compared to late stages

86
Q

Outline stage A (low risk) CLL according to the Binet staging system

A

Patients have fewer than 3 enlarged lymph node groups and no anaemia or thrombocytopenia

Prognosis of >15 yrs

87
Q

Outline stage B (intermediate risk) CLL according to the Binet staging system

A

Patients have 3 or more enlarged lymph node groups and no anaemia or thrombocytopenia

Prognosis 7-8 years

88
Q

Outline stage C (high risk) CLL according to the Binet staging system

A

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

Prognosis of 5-6 years

89
Q

What are the 3 phases of Rx for haematological malignancies

A

Induction - primary goal is to rapidly reduce number of cancer cells using intensive therapy e.g chemo

Consolidation - following success phase, aims to eliminate any remaining cancer cells often involving additional chemo or stem cell transplantation

Maintenance - lower dose, long term therapy administer to prevent re-emergence of malignancy

90
Q

Describe allogenic stem cell transplant

A

Curative option for some haematological malignancies, involving the infusion of healthy stem cells from a donor to replace the patients diseased bone marrow, enabling new blood and immune system to develop

91
Q

Outline the use of monoclonal antibodies for Rx of haematologic

A

Targeted therapies that can be designed to recognise and bind to specific antigens present on surface of cancer cells

Used as standalone Rx or combined w chemo

Can exert therapeutic effects through various mechanisms including immune system activation, interference w cell signalling pathways and direct cytotoxicity against cancer cells

E.g rituximab for B cell lymphomas and alemtuzumab for CLL

92
Q

Describe the pathophysiology of CML

A

Reciprocal translocation between chromosomes 9 and 22 leads to the BCR-ABL fusion gene

This encodes for a constitutively active tyrosine kinase

This activation stimulates intracellular signalling pathways that promote cell growth, survival and division

This results in uncontrolled proliferation of myeloid cells, especially granulocytes, in the bone marrow and peripheral blood

The accumulation of these abnormal myeloid cells can lead to symptoms of CML such as fatigue, enlarged spleen, and increased WBC counts

93
Q

Explain how tyrosine kinase inhibitors work

A

TKIs such as imatinib and dasatinib work by binding to active site of 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

94
Q

What are myeloproliferative neoplasms

A

MPNs are a group of rare blood disorders characterised by the overproduction of mature blood cells in the bone marrow

Caused by genetic mutations in HSCs leading to uncontrolled growth of blood cells

95
Q

What are the 4 main types of MPNs

A

Essential thrombocythemia (ET)

Polycythemia Vera (PV)

Primary Myelofibrosis (PMF)

Chronic myeloid leukemia (CML)

96
Q

Describe polycythemia Vera

A

Rare blood disorder where the bone marrow produces too many RBC, WBC and platelets leading to an increased risk of blood clots and other complications

Has raised haemtocrit, may have Splenomegaly, may have high platelets, may have high leukocytes

97
Q

Describe essential thrombocythemia

A

Overproduction of platelets, potentially resulting in abnormal blood clotting or bleeding

Has normal haematocrit, may have Splenomegaly, may have high leukocytes

98
Q

Describe primary myelofibrosis

A

MPN where bone marrow develops fibrous tissue, impairing its ability to produce normal blood cells and leading to anaemia and an enlarged spleen

99
Q

Provide an outline of aplastic anaemia

A

Rare and serious blood disorder characterised by a significant reduction in the number of blood cells, including RBC and platelets in the bone marrow

Occurs when bone marrow fails to produce adequate amount of blood cells

Can be acquired or congenital, but it can also be idiopathic

100
Q

Describe the diagnosis of aplastic anaemia

A

CBC to assess low blood cell counts

Bone marrow biopsy or aspiration to confirm reduction in haematopoietic cells

101
Q

Outline Rx for aplastic anaemia

A

Blood transfusions

Medications to stimulate blood cell production

Immunosuppressive therapy

Bone marrow transplantation

102
Q

What are 7 signs/symptoms of aplastic anaemia

A

Fatigue

Pallor

Petechiae

Infection

Dyspnea

Bleeding

Headache

Medical Studies 1 (16 decks)

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