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Pathology > Immunity and Diseases of Immune Origin > Flashcards

Immunity and Diseases of Immune Origin Flashcards

1
Q

The Body’s Defenses – Three Lines of Defense

A

Barriers
Inflammatory Response
Immune Response

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2
Q
  1. Barriers –
A

skin, mucous membranes, secretions

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3
Q
  1. Inflammatory Response –
A

cells (leukocytes),
molecules (mediators)

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4
Q
  1. Immune Response –
A

Antibodies (humoral),
Cytotoxic T cells (cellular)

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5
Q

Antigen (Ag) -

A

A substance that can induce an
immune response when introduced into an
animal.

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6
Q

Antibody (Ab) -

A

A protein that is produced in
response an antigen. The antibody binds the
antigen that stimulated its production. All
antibodies are immunoglobulins.

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7
Q

Immunoglobulin (Ig) -

A

A glycoprotein composed
of heavy and light chains that functions as an
antibody.

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8
Q

Schematic Structure of a Typical Immunoglobulin (Antibody) Molecule
(5)

A

• Heavy chains (2)
• Light chains (2)
• Variable regions form
antigen-binding site (Fab)
• Constant end (Fc) receptor
for attachment of phagocytic
cells)
• Complement binding

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9
Q

• IgM -

A

first immunoglobulin to
appear in an immune response

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10
Q

• IgG -

A

principal immunoglobulin of
the secondary immune response.
Only immunoglobulin capable of
crossing the placental barrier

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11
Q

• IgA -

A

principal immunoglobulin in
external secretions of mucosal
surfaces, tears, saliva, and
colostrum

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12
Q

• IgE -

A

plays an important role in
immediate hypersensitivity
reactions and parasitic infections

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13
Q

• IgD -

A

thought to activate the B-
lymphocyte

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14
Q

Primary and Secondary Lymphoid Organs
• All lymphocytes arise in the

A

bone marrow

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15
Q

Primary lymphoid organs
(2)

A

– Bone marrow
– Thymus

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16
Q

• Secondary lymphoid organs
(4)

A

– Lymph nodes
– Tonsils
– Spleen
– Mucosal-associated lymphoid tissue (MALT)

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17
Q

There are two
types of
lymphocytes,

A

B
cells and T cells
• They look alike in
their H&E
phenotype, but
they are
completely
different

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18
Q

B lymphocytes

A

become
plasma cells and secrete
antibodies when
challenged by antigen
• Antibodies are essential
for humoral immunity

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19
Q

X-linked Agammaglobulinemia (Bruton Agammaglobulinemia) XLA

A

• X-linked genetic disease – more common in males
• X-linked agammaglobulinemia (XLA)
• A primary immunodeficiency disease
• B lymphocytes unable to mature to plasma cells
• Can’t make antibody and are deficient in opsonization
• Recurrent bacterial infections

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20
Q

X-linked Agammaglobulinemia (Bruton Agammaglobulinemia) XLA
tx

A

Treatment: intravenous infusions of immunoglobulin every 3-
4 weeks for life (passive immunity)

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21
Q

Natural Killer Cell – NK Cell
(3)

A

• A component of the innate immune system
• A type of cytotoxic lymphocyte
• Do not have markers for B or T cells

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22
Q

T Lymphocytes
(3)

A

• CD4+ (T Helper Cell) - quarterback
• CD8+( Cytotoxic T Cell) - effector
• Cell-mediated defense against intracellular pathogens
– Viruses, fungi and one important bacterial disease (tuberculosis)

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23
Q

Function of the Thymus
(3)

A

• T cells become educated
• Learn self from non-self
• Self-reacting T cells are
deleted

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24
Q

B lymphocytes leave the — and populate lymph nodes

A

bone
marrow

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25
Q

T lymphocytes leave the
and populate lymph nodes

A

thymus

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26
Q

Immune System
(7)

A

• Self / non-self recognition
• General / specific
• Natural / adaptive
• Innate / acquired
• Humoral / cell-mediated
• Active / passive
• Primary / secondary

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27
Q

Extracellular pathogens
(2)

A

– Most bacteria
– Humoral immunity

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28
Q

Intracellular pathogens
(2)

A

– Viruses, fungi, some bacteria
– Cellular immunity

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29
Q

Innate immunity (born with)
(4)

A

– Physical and chemical barriers
(epithelia and antimicrobial
substances)
– All phagocytic cells (neutrophils,
macrophages, NK cells)
– Complement proteins
– Cytokines (TNF, IL-1, interferon)

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30
Q

Adaptive immunity (not born with,
requires exposure)
(3)

A

– Antibodies
– Lymphocytes
– Cytokines (IL-2, IL-12)

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31
Q

Antibody-Dependent Immunity: First Exposure (no antibody available)

A

• Innate immunity – phagocytosis and killing by macrophages and neutrophils with the help of
complement proteins
– C3b – opsonization
– C3a – histamine release from mast cells enhancing inflammation
– C5a - histamine release and chemotaxis of neutrophils
– C5b, 6, 7, 8, 9 – membrane attack complex (MAC)
• Formation of antibodies
– Too late for first exposure
– Memory B cells formed

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32
Q

Antibody-Dependent Immunity: Second Exposure (antibody available)
• Memory B cells quickly make specific antibody
(4)

A

– Neutralize toxins
– Bind pathogens
– Serve as opsonins
– Activate complement cascade via classic pathway

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33
Q

Humoral immunity is the
first line of defense against
— pathogens

A

extracellular
Antibody-dependent immunity

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34
Q

Cellular immunity is the
first line of defense against
— pathogens

A

intracellular
Antibody-independent immunity

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35
Q

Major Histocompatibility Complex (MHC) Molecules
(3)

A

• MHC molecules were originally discovered on leukocytes and called
Human Leukocyte Antigens (HLA)
• All cells of the body have MHC molecules
• MHC molecules are recognition molecules that allow the immune system
to distinguish self from non-self

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36
Q

• MHC Class 1 molecules are located

A

on the surface of most cells

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37
Q

• MHC Class 2 molecules are found on

A

Antigen-Presenting Cells (APCs)

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38
Q

– APCs:
(3)

A

dendritic cells, macrophages, Langerhans cells

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39
Q

If the invading organism is a virus, fungus or Mycobacterium, the first
line of defense is

A

cellular immunity, not humoral immunity

organism
APC
CD4
CD8

Phagocytosis by antigen presenting cell
Coupling of antigen to MHC-II molecule and presentation to CD-4 T lymphocyte
Secretion of cytokines to generate CD8 cytotoxic T lymphocyte
Elimination of cells that harbor the pathogen

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40
Q

CD4+ T Helper Lymphocyte
(2)

A
  • The recognition arm of cellular
    immunity – the bloodhounds
  • Role is to look at all the MHC-2
    molecules in the body (on APCs) to
    determine if they’re clean or dirty
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41
Q

CD4 Helper T- Lymphocytes are — Restricted

A

MHC-2

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42
Q

CD4+ T Helper cell
secretes

A

IL-2

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43
Q

IL-2

A

• IL-2 signals naïve
lymphocytes to
differentiate into CD8+
cytotoxic lymphocytes

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44
Q

CD8 Killer T-Lymphocytes
(3)

A

• The effector arm of cellular immunity –
the Marines
• Role is to scout the body for dirty
MHC-1 molecules on somatic cells and
kill them
• AKA: Cytolytic T-cells, Killer T cells,
Cytotoxic lymphocytes, CTLs

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45
Q

CD8 Killer T-Lymphocytes are — Restricted

A

MHC-1

46
Q

exposing virus to humoral
immune system

A

hepatocyte (perforins),

47
Q

MMUNE INJURY
DISEASE:
TYPE I
HYPERSENSITIVITY

A

Immediate hypersensitivity
Recipe
• Antigen
• IgE antibodies
• Mast cells

48
Q

TYPE I REACTION: IMMEDIATE HYPERSENSITIVITY –
CLINICAL RESPONSE PATTERNS
(5)

A

• “Hay fever”
• Asthma
• Hives
• Angioedema
• Anaphylactic shock

49
Q

TYPE I REACTION: IMMEDIATE HYPERSENSITIVITY –
ANAPHYLAXIS
(3)

A

• Anaphylaxis (Greek) – ana (excessive) + phylaxis (protection)
• Systemic anaphylaxis
• Local anaphylaxis

50
Q

IMMUNE INJURY DISEASE:
TYPE II HYPERSENSITIVITY

A

• Antibody mediated
hypersensitivity

51
Q

• Antibody mediated
hypersensitivity
• Cells – (2)
• Cell surface receptors –
(1)
• Extracellular matrix
material – (1)

A

• Cells – erythrocytes,
platelets
• Cell surface receptors –
acetylcholine receptor
• Extracellular matrix
material – laminin,
desmoglein

52
Q

Outcome of Antibody-Dependent Cytotoxic Reactions Against Cells
(2)

A

• Lysis – complement mediated (MAC)
• Phagocytosis - opsonization

53
Q

Blood Transfusion Reaction - ABO Blood Incompatibility (2)

A

• ABO mismatch leads to
intravascular hemolysis
• Antibody-coated
erythrocytes destroyed
by both complement-
mediated lysis and by
phagocytosis in spleen

54
Q

Myasthenia Gravis (1)

A

Antibody blocks
acetylcholine receptor

55
Q

Grave’s disease (2)

A
  • Antibody-mediated
    stimulation of cell function
  • Antibody stimulates TSH
    receptor
56
Q

IMMUNE INJURY DISEASE:
TYPE III HYPERSENSITIVITY

A

• Immune Complex Disease

57
Q

Target Antigens in Type III Disease
• Exogenous antigen –
• Endogenous antigen –

A

post-streptococcal glomerulonephritis
lupus erythematosus

58
Q

Post-Streptococcal Glomerulonephritis
(7)

A

• Pharyngitis caused by certain strains of
Streptococci (“Strep throat”) – exogenous antigen
• Immune complexes formed in antigen excess
(small)
• Failure of the immune system to quickly clear
complexes from the circulation
• Immune complexes filter out in renal glomeruli
• Complexes fix complement and generate pro-
inflammatory molecules
• Glomerulonephritis – proteinuria, hematuria,
hypertension, fever, lower back pain
• No infection – only sterile inflammation

59
Q

Lupus Erythematosus
(8)

A

• A multisustem autoimmune disease
most common in adult women in
child-bearing years
• Type III Hypersensitivity -
Immune Complex Disease
• Immune complexes are deposited
throughout the body, especially
kidney and blood vessels
• Renal failure due to immune-
mediated glomerulonephritis
• The patient’s own tissues are the
antigen
• Autoantibodies - anti-nuclear
antibodies (ANA)
• Involves many tissues and organs
• Butterfly rash

60
Q

Type III Reaction – Immune Complex Disease
(2)

A

• Glomerulonephritis
• Vasculitis

61
Q

Organs Involved in SLE
(7)

A

• Skin
• Joints
• Kidney
• Heart – Libman-Sachs
endocarditis
• Serosal Surfaces
(pericardidits, pleuritis)
• Central nervous system
• Arthritis, arthralgia,
heart and lung
involvement, anemia,
bone marrow depression,
vasculitis, skin rashes

62
Q

Examples of Type IV Reactions – Cell-Mediated Hypersensitivity (3)

A

• Tuberculin reaction
• Contact mucositis (nickel, cinnamon)
• Contact dermatitis (nickel, poison
ivy)

63
Q

Mantoux Tuberculin Skin Test – PPD Test (4)

A

• Type IV delayed hypersensitivity reaction to
protein from M. tuberculosis
• Intracutaneous tuberculin injection
• T-cells sensitized by prior infection
recruited to area
• Produces an area of induration

64
Q

Poison Ivy Contact Dermatitis (2)

A

• CD8 cytotoxic lymphocytes
• Type IV immune injury

65
Q

Development of Autoimmunity
• Loss of
• Arises from a combination of
(2)

A

self-tolerance

– Susceptibility genes
– Environmental triggers (infections and tissue damage)

66
Q

Central tolerance
– Developing T cells –
– Developing B cells –

A

deletion of self-reacting T cells in the thymus
receptor editing or deletion of self-reacting B cells in
the bone marrow

67
Q

Peripheral tolerance
(3)

A

– Anergy – functional inactivation
– Supression by regulatory T cells
– Deletion by activation-induced cell death

68
Q

Rheumatoid Arthritis (4)

A

• Chronic, systemic inflammatory
disease that may affect many
tissues and organs – joints, skin,
blood vessels, lungs, muscles
• Genetic susceptibility
• Environmental arthritogen
• Tumor necrosis factor (TNF) –
therapeutic target

69
Q

Hyperplastic synovium with dense chronic inflammatory infiltrate –

A

pannus

70
Q

Pannus errodes articular cartillage, leading to

A

joint destruction and
ankylosis

71
Q

Rheumatoid Factor
Rheumatoid factor is an antibody against an

A

antibody

72
Q

Rheumatoid Factor
IgM autoantibody to the

A

Fc portion of IgG

73
Q

Skin Involvement in RA - Rheumatoid Nodules (2)

A

• Pressure points
• Granulomas

74
Q

Systemic Sclerosis
(3)

A

• An autoimmune disease of adults, predominately females,characterized by excessive fibrosis
• May be limited to the skin or be widespread affecting various organ systems
• May be associated with otherautoimmune diseases

75
Q

Localized Form

A

• Skin involvement only
• No organ involvement

Morphea – mild localized disease

76
Q

Limited Form

A

C R E S T Syndrome

77
Q

Diffuse Form (2)

A

• Generalized involvement
• Skin and viscera

78
Q

• Slow continuous replacement
of

A

loose fibrovascular
connective tissue with dense
collagen

79
Q

• Fibrosis causes

A

loss of
mobility and altered function
of organs - skin, esophagus,
salivary glands, kidneys, lungs,
heart, muscle

80
Q

Scleroderma
(4)

A

• Acute myelogenous leukemia
• Bone marrow transplant
• Graft versus host disease
• Scleroderma

81
Q

Systemic Sclerosis – Oral Findings
(4)

A

• Microstomia
• Xerostomia
• Generalized widening of PDL
space
• Mandibular resorption

82
Q

Systemic Sclerosis
(3)

A

• Mask-like face
• Telangiectasia
• Raynaud phenomenon

83
Q

Raynaud Phenomenon
(3)

A

• Arterial spasm in
response to cold or
emotional stress
• Pallor, cyanosis and
then erythema
• Numbness, tingling or
pain on recovery.

84
Q

Hands and Fingers
(2)

A

• Fibrosis, stiffness, deformity
• Ischemia, atrophy and ulceration

85
Q

CREST Syndrome: A Limited Form of Scleroderma

A

• Calcinosis
• Raynaud Phenomenon
• Esophageal dysfunction
• Sclerodactly
• Telangiectasia

86
Q

• Calcinosis

A

– Calcium deposits in the skin

87
Q

• Raynaud Phenomenon
(2)

A

– Spasm of vessels
– Response to cold or stress

88
Q

• Esophageal dysfunction
(2)

A

– Decrease in motility
– Acid reflux

89
Q

• Sclerodactly
(2)

A

– Thickening and tightening of the skin
– Fingers and hands

90
Q

• Telangiectasia
(2)

A

– Dilation of capillaries
– Red lesions on skin

91
Q

Sjogren Syndrome
(5)

A

• Chronic, systemic autoimmune
disease that may be associated
with other autoimmune diseases
• Middle-aged females (9:1)
• Benign lymphoepithelial lesion
(BLEL) with variable salivary gland
enlargement
• Dry eyes and dry mouth (sicca
syndrome
• Increased risk of lymphoma

92
Q

Laboratory Findings in Sjogren Syndrome

A

• Autoantibodies to ribonucleoproteins
– Anti-SS-A (anti-Ro)
– Anti-SS-B (anti-La)
• Rheumatoid factor (RF) – IgM
autoantibody to the Fc portion of IgG
• Anti-nuclear antibodies (ANA)
• Anti-salivary duct antibodies

93
Q

Sicca Complex
(2)

A

• Xerostomia
• Xerophthalmia -
keratoconjunctivitis sicca

94
Q

immune reaction against
external “antigens”:

A

ALLERGY or HYPERSENSITIVITY

95
Q

Immune reaction against
your own tissues:

A

AUTOIMMUNITY

96
Q

Too little immunity:

A

Immune deficiency

97
Q

• IgA deficiency –

A

little morbidity

98
Q

• Severe combined immunodeficiency (SCID) –

A

mortality

99
Q

Defects in humoral immunity
(4)

A

• Bruton X-linked agammaglobulinemia
• IgA deficiency
• Hyper IgM syndrome
• Common variable immune deficiency (CVID)

100
Q

Defects in cellular immunity
(4)

A

• DiGeorge syndrome
• Bare lymphocyte syndrome
• Severe combined immunodeficiency (SCID)
• Acquired immumodeficiency syndrome (AIDS)

101
Q

Bruton X-Linked Agammaglobulinemia
(7)

A

• Failure of B cell maturation to plasma cells
• No plasma cells
• No antibodies
• No germinal centers in lymphoid tissue
• Recurrent bacterial infections
• X-linked inheritance – affects only males
• Lyonization protects females who are carriers

102
Q

IgA Deficiency
(5)

A

• Common immune deficiency (1:700)
• Defect in differentiation of IgA secreting plasma cells
• Low levels of circulating and secretory IgA
• Low morbidity
• Recurring infections of respiratory and gastrointestinal tracts

103
Q

Hyper IgM Syndrome
(5)

A

• Defect in class switching from IgM to IgG and IgA antibody production
• High levels of IgM
• No IgG or IgA
• Recurring bacterial infections
• X-linked inheritance

104
Q

Common Variable Immune Deficiency (CVID)
(5)

A

• Common primary immunodeficiency
• A heterogenous group of 20–30
immunodeficiencies
• Symptoms: all exhibit hypogammaglobulinemia
due to different causes
• Recurring bacterial infections
• Treatment: intravenous infusion of
immunoglobulins

105
Q

DiGeorge Syndrome
(5)

A

• Congenital absence of structures
derived from the 3rd and 4th branchial
pouches
• Thymic and parathyroid aplasia
• No cellular immunity - no T Cells
(neither CD4 nor CD8)
• Hypoparathyroidism
• Defects in humoral immunity

106
Q

Bare Lymphocyte Syndrome
(6)

A

• Antigen presenting cells don’t express MHC Class II molecules
• Mutations in the genes encoding transcription factors
• No MHC Class II molecules on APCs
• No antigen presentation to CD4 T cells
• No cellular immune response
• Misnomer – “bare APC syndrome” would be more accurate

107
Q

Severe Combine Immune Deficiency (SCID)
(4)

A

• A heterogenous group of diseases caused by defective development of both T and B cells
• No T cells
• No B cells
• No humoral and cellular immunity - lethal

108
Q

Human Immunodeficiency Virus - AIDS
(7)

A

• HIV gp 120 is a perfect fit for the
CD4 receptor on T cells
• HIV gp 41 promotes fusion
• HIV kills CD4 cells
• As CD4 cells are killed, cellular
immunity fails, followed by humoral
immunity
• Infections by intracellular pathogens
as cellular immunity fails
• Infections by extracellular pathogens
as humoral immunity fails
• Neoplasms

109
Q

Oral Lesions in AIDS
(9)

A

• Aphthous-like ulcers
• Candidiasis
• Kaposi sarcoma (HHV-8)
• Human papilloma virus lesions - papillomas
• Herpes simplex virus lesions
• Hairy leukoplakia (Epstein Barr virus)
• Accellerated periodontitis
• Necrotizing ulcerative gingivitis, periodontitis, stomatitis
• Neoplasms (squamous cell carcinoma, lymphoma)

110
Q

Lesions in Immunocompromised Patients
The clinical appearance of a lesion depends on:
(2)

A

• Effect of the immune system
• Effect of the agent

Pathology (23 decks)

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