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PHRM 100 – APPP > APPP Quiz: Hematopoietic System and Body Defence Systems > Flashcards

APPP Quiz: Hematopoietic System and Body Defence Systems Flashcards

1
Q

What are the 3 major functions of blood?

A
  • transportation and distribution (O2, CO2, nutrients, hormones, wastes)
  • regulation and homeostasis (pH, body temperature, water content of cells)
  • protection and repair (blood loss, inflammation, wound healing)
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2
Q

What are the components of plasma? (6)

A
  • electrolytes
  • water
  • proteins (albumins, globulins, fibrinogen/blood coagulation components, complement proteins and cytokines)
  • wastes
  • nutrients/vitamins/hormones
  • gases (N2, O2, CO2)
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3
Q

What are the 3 different types of globulins and what are their functions?

A
  • alpha – transport of lipids/metals
  • beta – transport of hormones/vitamins
  • gamma – immunoglobulins/antibodies
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4
Q

Rank formed components by number, from most to least. (8)

A
  • erythrocytes
  • platelets
  • reticulocytes
  • neutrophils
  • lymphocytes
  • monocytes
  • eosinophils
  • basophils
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5
Q

Rank formed components by size, from largest to smallest. (8)

A
  • monocytes – largest WBCs
  • granulocytes (WBC) – all considered to have comparable sizes
  • lymphocytes – smallest WBCs
  • erythrocytes (RBC)
  • platelets
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6
Q

What are reticulocytes?

A

immature RBCs released by bone marrow

  • mature into final RBC after 1-2 days in peripheral circulation
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7
Q

Lifespan of Formed Components

A
  • erythrocytes: 100-120 days
  • platelets: 5-10 days
  • monocyte: months
  • lymphocyte: hours to years
  • neutrophil: 6 hours to few days
  • eosinophil: 5-10 days
  • basophil: few hours to few days
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8
Q

What is hematocrit?

A

% erythrocytes in whole blood

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9
Q

Describe the structure of hemoglobin.

A
  • 4 protein helixes: 2 alpha and 2 beta globin chains
  • heme molecule (porphyrin ring and Fe2+ core)
  • 4 sites for cooperative binding of O2
  • O2 binds to heme molecule in one monomer, which induces conformational change in the other three molecules, leading to increased O2 affinity
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10
Q

What are the 3 factors that affect O2 binding capacity?

A
  • hematocrit
  • other gases (CO2 and CO)
  • RBC diseases
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11
Q

What are the 4 factors that affect O2 binding affinity?

A
  • pH and temperature
  • 2,3-biphosphoglycerate
  • fetal hemoglobin (δ chain instead of β chain)
  • RBC diseases
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12
Q

How does erythropoeisis occur?

A

initiated by low O2 (reduced oxygen-carrying capacity of blood)

  • kidney senses drop in O2 and releases erythropoietin (hormone)
  • erythropoietin stimulates RBC production in bone marrow
  • increased O2 reduces erythropoietin production in kidney – NEGATIVE FEEDBACK
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13
Q

What is polycythemia?

A

overproduction of RBCs (high hematocrit)

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14
Q

What is secondary polycythemia?

A

caused by factors other than RBC production such as hypoxia, sleep apnea, certain tumours

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15
Q

What are alpha and beta thalassemias?

A

defects in production of the respective hemoglobins

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16
Q

What is sickle cell anemia?

A

HbS instead of HbA

  • sickle shape in hypoxic conditions
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17
Q

What are the 2 causes of anemia?

A
  • decrease production of RBC
  • increase turnover of RBC – abnormal hemoglobins
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18
Q

Granulocytes

A
  • polynucleated
  • activated through binding of ligands to cell surface receptors (toll-like, cytokines, immunoglobulins)
  • contain cytoplasmic granules of inflammatory cytokines that are released upon activation
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19
Q

Neutrophils

A
  • most abundant WBC
  • short lifespan (1-5 days)
  • mobile first responders – follow chemokine gradients
  • amplify response – secrete cytokines, recruit/activate other immune cells
  • kill invaders via phagocytosis (activation of PAMPs), degranulation (release soluble anti-microbials and lytic enzymes), neutrophil extracellular traps (NETs)
  • eliminated through apoptosis
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20
Q

Eosinophils

A
  • attack organisms that are too big for phagocytosis
  • role in asthma and allergies
  • counts increase with rheumatoid arthritis, Hodgkin’s disease, and Addison’s disease
  • release granule contents such as enzymes and cytokines to damage infectious organisms while creating localized tissue damages
  • release granule contents such as interleukins, leukotrienes, and PGE2 to amplify immune response
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21
Q

Basophils

A
  • histamine
  • serotonin
  • heparin
  • several proteases
  • degranulation induce by IgE or IgG – FceRI is receptor for IgE
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22
Q

Agranulocytes

A
  • no granules
  • single-lobe nucleus
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23
Q

Monocytes

A
  • migrate out of blood into tissue for local patrol
  • responsible for presenting foreign materials to immune systems
  • types include macrophages and dendritic cells
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24
Q

Lymphocytes – Natural Killer Cells

A
  • contain large granules
  • lack antigen-specific receptors
  • roles in tumour surveillance
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25
Q

Lymphocytes – T- and B-Lymphocytes

A
  • cellular mediators of adaptive/acquired immunity
  • activate and respond to innate immunity – cytotoxic, specificity (specific antigen receptor), generates memory
  • specialized and adaptable
  • eliminates pathogens and infected cells
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26
Q

When are neutrophil counts higher?

A
  • bacterial infection
  • fungal infection
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27
Q

When are lymphocyte counts higher?

A

viral infection

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28
Q

When are monocyte counts higher?

A

fungal/viral infection

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29
Q

When are eosinophil counts higher?

A
  • viral infection
  • parasite infection
  • allergic reaction
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30
Q

When are basophil counts higher?

A
  • allergic reaction
  • thyroid disease
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31
Q

What are the 2 functions of thrombocytes (platelets)?

A
  • hemostasis, coagulation, and wound healing
  • participation in innate and acquired immune functions – ie. serotonin storage and release
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32
Q

Platelet Morphology

A
  • originate in bone marrow as fragments of megakaryocytes
  • no nucleus
  • different types of cytoplasmic granules in which contents are released by surface receptor binding – dense (serotonin, ADP), alpha (clotting factors)
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33
Q

How does thrombopoiesis occur?

A

negative feedback pathway in bone marrow

  • hormonally regulated by thrombopoietin (TPO) produced by liver (main), kidney and bone marrow
  • TPO is bound to surface of platelets and destroyed, then free circulating TPO concentration increases with low platelet counts to induce production by megakaryocytes in bone marrow – NEGATIVE FEEDBACK
  • myeloid stem cell, megakaryoblast, megakaryocyte with platelet precursor extensions, platelets
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34
Q

Explain the process of the hematopoietic system renewal.

A
  • mature blood cells have short lifespan and constant renewal is necessary
  • hematopoiesis starts in bone marrow
  • hematopoiesis is regulated by vast network of cytokines and growth factors
  • synthetic versions of growth factors used as clinical therapies
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35
Q

What are the 5 properties of the immune system?

A
  • mobility – systemic protection against localized insults through rapid cell migration to infected area
  • replication – immune response is amplified through clonal expansion and signaling cascade
    -specificity – prevent recognition of non-cross-reacting antigens and identify self vs. non-self
  • memory – faster and stronger response to (similar) subsequent infection
  • diversity – combinatorial library of antigen receptors to recognize innumerable pathogens
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36
Q

What are the 4 areas of a lymph node?

A
  • cortex – unactivated mature T cells
  • germinal centre – activated B cell development (plasma cell development and antibody affinity maturation)
  • para-cortex – mix of unactivated and activated mature T cells
  • medulla – funnels to outgoing vessels to collect mature immune cells and antibodies for distribution to lymphatic/blood circulation
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37
Q

What are the cellular mediators of the innate response and what are their functions? (8)

A

blood:

  • neutrophils – ingest (phagocytotic) and destroy
  • eosinophils – release toxic molecules and destroy
  • monocytes – ingest, destroy and antigen presentation
  • natural killer cells – kills cancer or viral infected host cells
  • basophils – release first chemicals that start inflammation

peripheral tissues:

  • macrophage – ingest, destroy and antigen presentation
  • dendritic cells – ingest, recruit others and antigen presentation
  • mast cells – release first chemicals that start inflammation
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38
Q

How are pathogens detected in the innate response?

A

recognition of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors such as toll-like receptors (TLR)

  • recognize PAMPs essential to microorganism survival or pathogenecity
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39
Q

Tissue Monocyte Derivatives

Macrophages

A
  • located in every tissue
  • some circulate in blood and migrate with rapid response to insults in tissues
  • inactive lifespan: months to years
  • active lifespan: day to weeks
  • phagocytosis
  • antigen presentation (APC)
  • initiation of tissue repair
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40
Q

Monocyte Derivatives

Dendritic Cells

A
  • immature: in blood and tissues interfacing the outside (skin, nose, lungs, stomach)
  • mature: move to lump nodes and interact with T cells and B cells
  • phagocytes
  • antigen-presenting cells
  • activate adaptive immune response
  • regulate T cell activation
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41
Q

B cells vs. T cells

  • function
  • development
A
  • B: attack invaders outside cells, can act as antigen-presenting cells (only one type of antigen receptor) to activate helper T cells, can induce differentiation into plasma cells for antibody production, can induce differentiation into memory B cells
  • T: attack invaders inside cells (inaccessible to antibodies), no antigen-presenting properties
  • B: mature and negatively selected in bone marrow
  • T: mature in thymus (but produced in bone marrow)
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42
Q

Helper T cell

A

assist other immune cells with maturation/activation

  • CD4+ co-receptor (activates cytotoxic T cells and B cells)
  • binds to MHCII (antigen-presenting cell)
  • 70% of all T cells
43
Q

Cytotoxic T cell

A

virally infected cells and tumour cells

  • CD8+ co-receptor (induces release of cytotoxic molecules)
  • binds to MHCI (infected cells)
  • 25% of all T cells
44
Q

T Regulatory cell

A

suppress and regulate auto-reactive T cells

  • CD4 and CD25
45
Q

Memory T cell

A

proliferate when reintroduced to antigen

  • CD4+ or CD8+
46
Q

What are the 4 things that innate and acquired immunity overlap in?

A
  • co-activation of B cells through BCR and TLR
  • antigen-presentation by macrophage
  • complement proteins
  • cytokines (interferons, TNF, IL-1)
47
Q

What can occur if there is a reduction or dysfunction in the adaptive immune response?

A
  • over-activity of innate system
  • exaggerated cytokine response
  • compromised normal immune functions
  • coagulation dysfunctions and other organ system failures
48
Q

How does inflammation occur?

A

cross-talk and signaling through release of cytokines and inflammatory chemicals/hormones

49
Q

What are the 2 types of mediators of the inflammatory response?

A
  • pre-formed mediators
  • newly synthesized mediators
50
Q

Protein Mediators of the Immune Response

What are the 5 types of cytokines (protein signaling molecules) and their functions?

A
  • interferons (type 1 alpha and beta, type II gamma) – innate antiviral response
  • chemokines (MCP-I, IL-8, etc.) – chemotaxis proinflammatory
  • interleukins (IL-6, IL-10, etc.) – leukocyte development, responsible for cross-talk between RBCs
  • TNF-a – acute phase response, coagulation/stop inflammation and call for help
  • growth factors( VEGF, GM-CSF, TGF beta, etc.) – growth differentiation/proliferation of immune cells
51
Q

Chemical and Hormonal Mediators of Immune Response

A

signaling molecules activated or released by immune cells and injured cells

  • mediate inflammatory responses
  • amino acid derivatives: histamine, serotonin
  • lipid derivatives: prostaglandins, leukotrienes (both eicosanoids)
  • hormones and other neurotransmitters: bradykinin, substance P
52
Q

Amino Acid Mediators of Humoral Immune Response

Histamine

A
  • derived from amino acid histidine
  • produce, store, and release, mainly from mast cells
  • serves important roles in immune responses and inflammation process
  • binds to and activates GPCRs (H1 to H4 tissue-specific subtypes)
  • vasodilation, increase permeability
53
Q

Amino Acid Mediators of Humoral Immune Response

Serotonin

A
  • derived from amino acid tryptophan
  • produced by enterochromaffin cells and stored mainly in platelets
  • neurotransmitter serves multiple functions in homeostasis (GI, CNS, body defence)
  • binds to and activates GPCRs (5HT1 to 7 tissue- and function-specific subtypes)
  • vasodilation, increase permeability, pain, fever
54
Q

Lipid Mediators of Humoral Immune Response

Eicosanoids (Prostaglandins and Leukotrienes)

A
  • synthesized with arachidonic acids
  • made by oxidation of omega-6 fatty acids
  • 20 carbons, 4 double bonds
  • biosynthesis by cyclo-oxygenase (prostglandins) and lipo-oxygenase (leukotrienes)
55
Q

Lipid Mediators of Humoral Immune Response

Prostaglandins

A

vasodilation, pain, fever

56
Q

Lipid Mediators of Humoral Immune Response

Leukotrienes

A

increase permeability, leukocyte adhesion, and chemotaxis

57
Q

Lipid Mediators of Humoral Immune Response

Platelet Activating Factor

A

vasodilation, increase permeability, leukocyte adhesion, and chemotaxis

58
Q

What are the functions of eicosanoids?

A
  • essential control of inflammation and immunity
  • synthesized upon activation signals
  • specific inhibition of major biosynthesis enzymes is a major mechanism to control inflammation
  • role in systemic inflammatory response and cellular defense functions
59
Q

Eicosanoid

Prostacyclin and Prostaglandin D/E

A

vasodilation

60
Q

Eicosanoid

Thromboxane A2 and Leukotrienes C/D/E

A

vasoconstriction

61
Q

Eicosanoid

Leukotrienes C/D/E and Prostaglandin D

A

vascular permeability

62
Q

Eicosanoid

Leukotriene B and HETE

A

chemotaxis and leukocyte adhesion

63
Q

Eicosanoid

Leukotrienes C/D/E

A

bronchoconstriction

64
Q

Explain how the immune system distinguishes self from non-self.

A

major histocompatibility complex (MHC) – I and II

  • cell surface molecules
  • present as peptide epitope on surface of cell
  • normal functions include playing essential roles in immune system engagement
  • known as the human leukocyte antigen (HLA)
  • unique to each of us – highly polymorphic
65
Q

MHC I

A
  • present on all nucleated cells and platelets
  • display infectious epitopes – from hijacked cells’ synthesis of infectious agent (non-self), and recognized by cytotoxic T cells (CD8+ receptor)
  • special breaks to ensure a regulated immune activation (CTLA4 and PD1 receptors)
66
Q

MHC II

A
  • present on antigen-presenting immune cells (macrophages, dendritic cells, and B cells)
  • display degraded/digested pathogen epitopes that are recognized by helper T cells (CD4+ receptor)
  • special breaks to ensure a regulated immune activation (CTLA4 and PD1 receptors)
67
Q

Genetic Recombination of T cell Receptors (TCR)

A
  • receptor has alpha and beta chain subunits
  • each subunit is generated through recombination of 1 segment each from the V and J loci (alpha), and D and J loci (beta)
  • generates immunological diversity, as each mature T cell will have a different combination of subunits that recognize different antigens
68
Q

Positive and Negative Selection of T cells in Thymus

A
  • occurs during development/maturation
  • positive selection of affinity for MHC I or MHC II (antigen presentation cell surface molecules) with either CD4 or CD8 receptors
  • negative selection of cells that recognize self-antigens cannot be autoreactive
  • 2% survival
69
Q

Diversity of B cell Receptors (BCR)

A
  • each mature B cell is covered with a single type of BCR
  • BCRs are predecessors of antibody that recognized one antigen
  • two identical binding sites on each fork of the Y
  • BCR can bind antigen directly in absence of co-receptors
  • B cells with BCR that recognizes self-antigens are destroyed (central and peripheral tolerance)
70
Q

Explain how B cells are activated via the T-cell dependent pathway.

A
  1. antigen binds to BCR
  2. internalization and MHC II presentation to helper T cells
  3. helper T cell releases cytokines
  4. activated B cell differentiates into plasma cells for antibody production and memory B cells
71
Q

What are immunoglobulins?

A

family of globular proteins (Ig)

  • bind with specificity and affinity to antigen
  • produced and secreted by activated B- lymphocytes following earlier encounter with the infectious materials
72
Q

Describe the structure of immunoglobulins.

A
  • Y-shaped molecule made of 4 protein chains – 2 identical light, 2 identical heavy
  • constant region
  • variable region
72
Q

What is the constant region of immunoglobulins?

A

stem of monomer and lower part of Y

  • Fc region: recognized by Fc receptor on leukocytes/complement factors
73
Q

What is the variable region of immunoglobulins?

A

gives specificity and affinity to singular antigen

  • two identical regions on Y arms (mirror images)
  • Fab-binding sites – antigen-binding region
  • identical on same antibody, but highly variable across antibodies
74
Q

What is second recombination?

A

switching the Fc region and the class switching mechanism

  • constant (Fc) region of BCR can go through a second recombination after the activation of a mature B-cell (CLASS SWITCHING)
  • generates antibodies with the same antigen recognition region (Fab), but different constant region (Fc)
  • creates functional diversity by increasing the numbers of effector processes Ab-binding can engage
75
Q

What are the 5 immunoglobulin classes and what is classification based on?

A

based on which heavy chain is present

  • IgA – alpha
  • IgD – delta
  • IgE - e
  • IgG - gamma
  • IgM – mu
76
Q

What is the function of IgM?

A
  • main antibody of primary responses
  • best at fixing complement
  • the monomer form of IgM serves as the B cell receptor
77
Q

What is the function of IgG?

A
  • main blood antibody of secondary responses
  • neutralizes toxins
  • opsonization
  • Fc binds to phagocytes
78
Q

What is the function of IgA?

A

secreted into mucus, tears, saliva, colostrum

79
Q

What is the function of IgE?

A
  • antibody of allergy and antiparasitic activity
  • Fc binds to mast cells and basophils
80
Q

What is the function of IgD?

A

B cell receptor

81
Q

What are the functional outcomes of antibody binding? (6)

A

recruit cytotoxic immune cells and complement proteins by providing recognition and destruction signals – protective mechanism of binding antibodies to antigens

  • agglutination
  • neutralization
  • opsonization
  • antibody-mediated cytotoxicity (ADCC)
  • inflammation
  • complement activation
82
Q

What is agglutination?

A

clumping of antigen-containing pathogens

  • enhances phagocytosis
  • reduces number of infectious units to be dealt with
83
Q

What is neutralization?

A

blocking active sites

  • blocks toxins from binding
  • blocks adhesion of pathogens to host cells
84
Q

What is opsonization?

A

coating pathogens with antibody for recognition/to enhance phagocytosis

85
Q

What is antibody-mediated cytotoxicity (ADCC)?

A

antibodies attached to target cell cause destruction by non-specific immune system cells

  • NKC, macrophages, neutrophils, and eosiniphils
  • antibodies assist in detection of virus- and bacteria-infected host cells
  • cytotoxic immune-cell-surface Fc receptor binds immunoglobulin motif (Ig) on antibody
  • binding causes degranulation leading to cell apoptosis
86
Q

What is inflammation?

A

amplification of the immune response and attract other immune effectors

  • disruption of cell by complement/reactive protein attracts phagocytic and other defensive immune system eclls
87
Q

What is complement activation?

A

opsonization and membrane attack complex

  • cell lysis
88
Q

Complement System

What are complement factors?

A

protein and glycoprotein components

  • around 30 small peptides (‘C’ designation– ie. C1)
  • synthesized primarily in liver
  • represent 5% of globulin content in blood
  • activated through cascade of proteolytic activities
89
Q

Complement System

What are the 3 activation pathways?

A
  • classical
  • alternative
  • lectin

(C3b is deposited on microbe)

90
Q

Complement System

What is the classical pathway?

A

antigen:antibody complexes for activation (adaptive/specific)

91
Q

Complement System

What is the alternative pathway?

A

non-specific (antibody-independent, C3 autolysis)

92
Q

Complement System

What is the lectin pathway?

A

binding of specific carbohydrates on pathogens, aided by C-reactive proteins

93
Q

Complement System

What are the 3 functional outcomes of complement system activation? What mediates all 3 processes?

A

C3b binding mediates all 3 processes

  • opsonization: coats infected cells for recognition by phagocytes
  • chemotaxis: directs immune cells to infection (inflammation)
  • infected-cell lysis: formation of membrane attack complex (MAC)
94
Q

Direct Cell Lysis from Complement Activation

What is the membrane-attack complex (MAC)?

A
  • result of classical, alternative, and lectin pathways
  • forms on membrane of bacteria – multiple complement factors come together, interact to insert into/through lipid bilayer
  • forms transmembrane channels – non-specific (free diffusion of molecules and water), cell death occurs if sufficient MAC complexes form
95
Q

Acquired Immune System

What is the primary response?

A

after 1st exposure to antigen

  • response 5-10 days
  • after contact with Ag
  • IgM secretion
  • low IgG production
  • lower antibody affinity
96
Q

Acquired Immune System

What is the secondary response?

A

after 2nd exposure to antigen

  • fast response (1-3 days after contact)
  • IgG secretion
  • heavy chain class switching
  • higher antibody affinity
97
Q

What is immune memory?

A
  • conferred by the acquired immune system through generation of memory T cells and B cells from the first encounter
  • second encounter with same pathogen will lead to a response with greater magnitude and with faster kinetics
  • basis of vaccination – first encounter is deliberately introduced through injected materials
  • immunocompromised individuals generate weaker or shorter-lived immune responses to infections and vaccination compared to those who are not
98
Q

Properties of the Immune System

Which branch of the immune system is ‘mobility’ attributed to?

A

innate

99
Q

Properties of the Immune System

Which branch of the immune system is ‘replication’ attributed to?

A

acquired = innate

100
Q

Properties of the Immune System

Which branch of the immune system is ‘specificity’ attributed to?

A

acquired&raquo_space; innate

101
Q

Properties of the Immune System

Which branch of the immune system is ‘memory’ attributed to?

A

acquired

102
Q

Properties of the Immune System

Which branch of the immune system is ‘diversity’ attributed to?

A

acquired

PHRM 100 – APPP (23 decks)

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