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2420 Pathology > Module 5 Immunocellular Alterations > Flashcards

Module 5 Immunocellular Alterations Flashcards

1
Q

Innate Immunity

A
  • Physical protective barrier of skin & mucosal surfaces
  • Automated response to physical/infectious injury
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2
Q

Processes

A
  • Phagocytosis
  • Inflammation
  • Complement activation
  • Coagulation
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3
Q

Stratum Corneum

A
  • Physical impermeable barrier
  • Works with granular & spinous cell layer
  • Corneocytes embedded in lipid matrix
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4
Q

Sebaceous Gland

A
  • Secrete sebum
  • Coats skin in antimicrobial lipid
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5
Q

Physical Barrier

A
  • Acidic pH
  • Antimicrobial lipids & peptides
  • Disrupt bacterial membranes
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6
Q

Mucosal Surface Barrier

A
  • Bacteria trapped in mucus
  • Mucus contains antimicrobial peptides & secretory IgA
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7
Q

Goblet Cells

A
  • Attract bacteria
  • Intestinal
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8
Q

Skin Infection Barrier

A
  • Keratin
  • Mucous
  • Tight junctions between epithelial cells
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9
Q

Microbe Death via Antibiotics

A
  • Defensins
  • Dermcidin
  • Acidic pH
  • Sebum
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10
Q

Epithelial Functions

A
  • Portals of entry of microbes
  • Provide physical barriers
  • Produce antimicrobial substances
  • Harbor lymphocytes
  • Kill microbes & infected cells
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11
Q

Granulocytes

A
  • Multi-lobed nucleus
  • Spotted surface (protein, peptides)
  • Cytoplasm packed with granules
  • Granules loaded with antimicrobial enzymes
  • All contribute to innate immunity
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12
Q

Polymorphonuclear Cell (PMN) /Neutrophils

A
  • Recognized by multi-lobed nucleus
  • 60% of bone marrow
  • Develop within bone marrow
  • 10hr lifespan
  • 10^11 enter & leave circulation daily
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13
Q

Neutrophil Granules Function

A
  • Kills bacteria by iron restriction
  • Destruction of cell wall & membrane
  • Oxidation
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14
Q

Phagocytosis

A
  • Optimised by antibody
  • Compliment protein binds to bacteria receptor
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15
Q

NADPH Oxidase System

A
  1. Electrons pumped into vacuole
  2. Convert oxygen into super oxygen animes
  3. Interact with protons to form hydrogen peroxide
  4. MPO reacts with hydrogen peroxide & halide (Cl, Br, I)
  5. Form toxic oxidizing agents (HOCl, OH,)
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16
Q

Chronic Granulomatous Disease

A
  • Genetic defect X-linked & autosomal recessive
  • Failure to produce cytochrome b558
  • Unable to generate superoxide (NADPH Oxidase)
  • Can’t kill bacteria, form granulomatous lump
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17
Q

Basophils

A
  • Fight parasitic & allergic reactions
  • Produce heparin (anticoagulant)
  • Produce histamine (vasodilator)
  • Initiate chronic allergy & anaphylaxis
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18
Q

Eosinophils

A
  • Fight parasitic infection
  • Pathology of asthma
  • Produce reactive oxygen species
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19
Q

Macrophage Lifespan

A
  • Emerge from bone marrow as stem cell
  • Circulate as monocytes
  • Migrate into tissue (differentiation) take up properties
  • Activated macrophage
  • Inject microbe
  • Life span several months
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20
Q

Macrophage Function

A
  • Efflux of iron & manganese (nutrition)
  • Influx of copper & zinc (support oxidate killing)
  • Produce nitric oxide synthase
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21
Q

Pattern Recognition Receptors

A
  • Recruitment of adapter proteins
  • Recruitment & activation of protein kinases
  • Activation of transcription factors
  • Gene transcription
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22
Q

TLR 1, 2, 6

A
  • Peptidoglycan
  • Lipoproteins
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23
Q

TLR 4

A
  • Bacterial LPS
  • Fungal mannans
  • Viral envelope proteins
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24
Q

TLR 5

A
  • Bacterial flagellin
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25
Q

TLR 3, 7, 8, 9

A
  • Microbial & viral nucleic acids
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26
Q

Innate Immunity Specificity

A
  • Structures shared by classes of microbes/damaged cells
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27
Q

Innate Immunity Receptors

A
  • Tool-like
  • N-formyl peptide
  • Mannose
  • Scavenger
  • Identical on each cell
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28
Q

Adaptive Immunity Specificity

A
  • Structural detail of microbial molecules
  • May recognize nonmicrobial antigens
  • Distinct antibody molecules
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29
Q

Adaptive Immunity Receptors

A
  • Encoded by genes
  • Produced by recombination of gene segments
  • Greater diversity
  • Clonal distribution
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30
Q

Cytokine Production

A
  • Complement
  • Microbe engagement of toll receptors
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31
Q

Cytokine Function

A
  • Modify functionality of immune cells & vascular endothelium
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32
Q

TLR Engagement

A
  • Immune cells produce cytokines & chemokines
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33
Q

Tumour Necrosis Factor (TNF)

A
  • Macrophages & t cells
  • Endothelial & neutrophils activation
  • Hypothalamus fever
  • Upregulate expression of adhesion proteins
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34
Q

Interleukin -1 (IL-1)

A
  • Macrophages & endothelial cells
  • Endothelial activation (inflammation/coagulation)
  • Hypothalamus fever
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35
Q

Chemokines (IL8)

A
  • Macrophages, dendric cells
  • Activated endothelial cells
  • Attract neutrophils
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36
Q

Chemokines Function (IL8)

A
  • Upregulate oxidative capacity
  • Change in shape
  • Promote adhesion to endothelium
  • Promotes granulation (protein to surface)
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37
Q

Interleukin -12 (IL12)

A
  • Dendritic cells & macrophages
  • Act on t & NK cells
  • IFN production
  • Activate macrophage killing capacity
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38
Q

Interleukin-10 (IL-10)

A
  • Macrophages, endothelial cells, T cells
  • Inhibit IL-12 production
  • Anti-inflammatory
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39
Q

Cytokines Process

A
  1. Phagocytosis, macrophage/dendritic cell produces IL-12, IL-1, TNF
  2. IL12 instructs NK-cells to produce IFN-y
  3. Macrophages produces more inflammatory mediators
  4. TNF & IL-1 pro-inflammatory mediators acting on other immune cells
  5. Promotes adhesion & extravasation of neutrophils
40
Q

Complement Cascade Activation

A
  • Alternative pathway (C3)
  • Classical pathway
  • Lectin pathway
41
Q

Membrane Attack Complex (MAC)

A
  • Cascade pathway
  • 9 protein complex on bacteria surface
  • Bacteria opsonized for phagocytosis by deposition of C3b
  • C3a & C5a (proinflammatory) chemo attractants
  • Poke hole in bacteria
42
Q

Alternative Complement Pathway

A
  • Deposition of C3b on bacterial surface
  • No specific antibody required
43
Q

Classical Pathway

A
  • Antibody binds to antigen on bacteria
  • C1 engages antibody
  • Initiate complement activation
  • Production of C3a&b
44
Q

Lymphocyte Functionality

A
  • Recognize pathogens
  • Antigen specific receptors
  • Like antibodies on cell surface
45
Q

B cells

A
  • Produce antibodies
  • Develop within bone marrow
46
Q

Antibodies of B cells

A
  • Circulate in blood
  • Bind to specific bacteria/viruses to neutralize
  • Assist other immune cells in killing
47
Q

Clonal Expansion of B cells

A
  • Aided by T-helper
  • Produce cytokines
  • Promote b-cell development
48
Q

T cells

A
  • Develop in thymus
  • Regulatory & immune effector functions
49
Q

Th1

A
  • Facilitate macrophage & cytotoxic t-cell responses
  • Produce cytokines IFN-y & IL-2
50
Q

Th2

A
  • Stimulate antibody production by B-cells
  • Produce cytokines IL-4, IL-6, IL-10
51
Q

Th17

A
  • Promote inflammation
  • Produce cytokines IL-17
52
Q

Treg

A
  • Suppress inflammation
  • Produce cytokines TGF-b & IL-10
53
Q

CD8 T-cells

A
  • Receptor recognizes viral antigen present in infected cell
  • T-cell receptor & CD8 engage MHC
  • T-cell releases perforin & granzyme
54
Q

Perforin & Granzyme

A
  • Proteins that damage membrane & nucleus of target cell
55
Q

Major Histocompatibility Complex 1 (MHC)

A
  • Expressed by all nucleated cells
  • Self-antigen
  • Any infected cell can also present an antigen to CD8 T-cells
  • Presents antigens from virus infected cells
56
Q

MHC 2

A
  • Only present on professional antigen presenting cells (CD4 helper T-cells)
  • Present antigens from extracellular pathogens
57
Q

Professional Antigen Presenting Cells

A
  • B-cells
  • Macrophage
  • Dendritic cells
  • Langerhan cells
  • Activated T-cells
58
Q

Immune Disorders Linked to Variant MHC

A
  • Psoriasis
  • Ankylosing spondylitis
  • Type 1 diabetes
  • Multiple sclerosis
  • Rheumatoid & reactive arthritis
59
Q

Natural Killer (NK) Cells

A
  • Recognize activating ligands expressed on nucleated cells
  • If inhibitory receptor not engaged NK degranulates
  • Release perforin & granzyme to kill target cells
60
Q

Type 1 Hypersensitivity

A
  • IgE-mediated allergic reaction
  • Immediate (occurs within minutes)
  • 2 phases (sensitization & re-exposure)
61
Q

Sensitization Phase (Type 1)

A
  • Allergens detected by dendritic cells
  • CD4+ T cells develop into Th2 cells
  • Cytokines mediate production of IgE antibodies
  • IgE binds to surface receptors
  • Tissue mast cells & blood basophils are sensitized
62
Q

Re-Exposure Phase (Type 1)

A
  • Allergen binds to IgE on surface receptors
  • 2 IgE receptors are cross-linked by allergen
  • Signal transduction through y chains of receptor
  • Influx of calcium
  • Degranulation & release of mediators
63
Q

Systemic Anaphylaxis

A
  • IV or oral absorption
  • Edema (laryngeal)
  • Increased vascular permeability
  • Circulatory collapse
  • Death
64
Q

Acute Urticaria

A
  • Skin entry
  • Local increase in blood flow & vascular permeability
  • Edema
65
Q

Seasonal Rhinoconjunctivitis

A
  • Eye/nasal mucosa contact
  • Edema of eye/nasal mucosa
  • Sneezing
66
Q

Asthma

A
  • Contact with mucosa lining of airway
  • Bronchial constriction
  • Increased mucous production
  • Airway inflammation
67
Q

Food Allergy

A
  • Oral entry
  • Vomit/diarrhea
  • Itching/hives
  • Anaphylaxis
68
Q

Type 2 Hypersensitivity

A
  • IgG & IgM mediated
  • Antibodies directed against antigen (slef/non-self)
  • Cells of particular tissues only
  • 3 mechanisms
69
Q

Antibody Mechanisms of Type 2

A
  • Activate normal cell function (hyperactive)
  • Activate complement cascade causing target cell destruction
  • ADCC exhibited by NK/phagocytic cells
70
Q

Graves Disease

A
  • Antibodies bind to TSH receptor
  • Activation of receptor
  • Cells produce hormone
  • No natural shut off mechanism
  • Overproduction of thyroid hormone
71
Q

Rheumatic Fever

A
  • Following throat infection by bacterium streptococcus pyogenes
  • Production on antibodies against tissues
  • IgG-mediated cytotoxic hypersensitivity
72
Q

Rheumatic Fever Process

A
  1. Bacterium infects susceptible host
  2. T-cells & antibodies against M protein of streptococcus
  3. T cells & antibodies may attack look-alike proteins of body
  4. Bacterial infection clears
  5. Development of rheumatic heart disease
73
Q

Type 3 Hypersensitivity

A
  • IgG bind to free antigens forming immune complexes
  • Complexes circulate in free state
74
Q

Increased Vascular Permeability

A
  • Complexes deposit within tissues
  • Blood vessel walls (vasculitis)
  • Synovial joints (arthritis)
  • Glomerular basement membrane
75
Q

Deposition of Immune Complexes

A
  • Activation of complement system
  • Chemotaxis of neutrophils to sites of complex deposition
  • Local tissue damage & inflammation
76
Q

Vasculitis

A
  • Immune complexes in blood vessels
77
Q

Type 4 Hypersensitivity

A
  • Reaction occurs within 24-48hrs (delayed type)
  • Mediated by T-cells
  • Antibody independent
  • Sensitization & effector phase
78
Q

Sensitization Phase (Type 4)

A
  • Primary exposure CD4+ T cells develop into Th1 cells
  • Sensitizing agents (metals, chemicals, natural)
79
Q

Effector Phase

A
  • Re-exposure activates Th1 cells & cytotoxic T cells
  • Release pro-inflammatory cytokines & chemokine
  • Attract & activate macrophages & T-cells
  • Causing inflammation & tissue damage
80
Q

Poison Ivy

A
  • Biological agent inducing type 4
  • Delayed response (24-48)
  • Skin reaction
  • Red, itchy, blisters
81
Q

Nickle Exposure

A
  • Type 4 sensitizer
82
Q

Patch Test

A
  • Number of different compounds onto skin
  • 3-5 days (allow delayed response)
83
Q

Hypofunction Consequences

A
  • Disorders in defense
  • Disorders in surveillance
84
Q

Disorders in Defence

A
  • Increased susceptibility to infections
  • Infection type dependent on form of immunity affected
85
Q

Disorders of Surveillance

A
  • Increased frequency of malignant disease
  • Immunodeficiency syndromes & immunosuppressive meds increase cancer risk
86
Q

Clinical Features with Immunodeficiency

A
  • Chronic infection
  • Recurrent infection
  • Unusual infecting agents
  • Poor response to antibiotic treatment
87
Q

Primary Immunodeficiency Disorders

A
  • Pure B cell dysfunction
  • Cell-mediated immune deficiencies
  • Both T & B cell deficiency can occur in same patient
88
Q

Pure B cell Dysfunction

A
  • T cells unaffected
  • Detected at 5-6 months old
  • Protection by maternal IgG antibodies
  • Bruton’s syndrome
89
Q

Cell Mediated Immune Deficiencies

A
  • T-cell dysfunction
  • Presents early in neonatal period
  • DiGeorge syndrome
90
Q

Chronic Granulomatous Disease

A
  • Phagocytic dysfunction
  • Absence of lysosomal enzymes in monocytes & granulocytes
91
Q

Secondary Immunodeficiency Disease Causes

A
  • Infections
  • Immunosuppressive therapy
  • Malignancy (lymphoma especially)
  • Chronic illness
  • Malnutrition
  • Aging
92
Q

Infections

A
  • Rubella, measles, mycoplasma (temporary)
  • HIV, AIDS cell-mediated & humoral immunity
93
Q

Immunosuppressive Therapy

A
  • Cytotoxic drugs (cancer chemo)
  • Irradiation
  • Anti-lymphocyte serum globulin (ALG)
94
Q

Autoimmune Disease (Hyper)

A
  • Breakdown of normal processes to maintain self-antigen tolerance
  • Discrimination of antigens by reactive T-cells
  • Suppression of immune responses to self-antigen by T-cells
95
Q

Genetic Factors

A
  • Inheritance of susceptibility genes that disrupt different tolerance
  • Autoimmunity runs in families
  • Common to have 1+ autoimmune diseases
  • Particular HLA alleles are linked to autoimmune diseases
  • Genetic polymorphisms are linked to autoimmune diseases
96
Q

Environmental Factors

A
  • Infections & tissue injury expose self antigens
  • Activate antigen presenting cells & lymphocytes in tissues
  • Microbes including viruses & bacteria may trigger autoimmune
  • UV radiation & smoking cause tissue damage
97
Q

Clinical Presentation Factors

A
  • Target (antigen)
  • Immune reaction type (cell-mediated, humoral, both)
  • Changes secondary to destruction of target organ/immune reaction

2420 Pathology (13 decks)

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