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Pathology > immunity > Flashcards

immunity Flashcards

1
Q

bodys lines of defense, which are specific?

A
  1. Barriers – skin, mucous membranes, secretions
  2. Inflammatory Response – cells (leukocytes),
    molecules (mediators)
  3. Immune Response – only one that is specific
    Antibodies (humoral),
    Cytotoxic T cells (cellular)
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2
Q

Antigen (Ag) -

A

Antigen (Ag) - A substance that can induce an
immune response when introduced into an
animal.

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3
Q

Antibody (Ab)

A

Antibody (Ab) - 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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4
Q

Immunoglobulin (Ig) -

A

Immunoglobulin (Ig) - A glycoprotein composed
of heavy and light chains that functions as an
antibody.

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5
Q

Schematic Structure of a Typical Immunoglobulin (Antibody) Molecule

A
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6
Q

• IgM -

A

• IgM - first immunoglobulin to
appear in an immune response

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7
Q

IgG -

A

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

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8
Q

IgA -

A

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

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9
Q

IgE -

A

IgE - plays an important role in
immediate hypersensitivity
reactions and parasitic infections

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10
Q

IgD

A

gD - thought to activate the B-
lymphocyte

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11
Q
A

lymphocyte

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12
Q

Primary and Secondary Lymphoid Organs

A

• All lymphocytes arise in the bone marrow
• Primary lymphoid organs
– Bone marrow
– Thymus
• Secondary lymphoid organs
– Lymph nodes
– Tonsils
– Spleen
– Mucosal-associated lymphoid tissue (MALT)

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13
Q

Subsets of
Lymphocytes

A

B and T

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14
Q

distinguishing b and t cells

A

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

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15
Q

B lymphocytes become? role?

A

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

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16
Q

Agammaglobulinemia (Bruton Agammaglobulinemia)
inheritence?
more common in?
type of dx?
result?
deficeint in what immune function?
susceptiable to?
tx?

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
  • Treatment: intravenous infusions of immunoglobulin every 3-4 weeks for life (passive immunity)
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17
Q

QB of IS?

A

Tcells (CD4)

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18
Q

types of t cells

A

T Lymphocytes
• CD4+ (T Helper Cell) - quarterback
• CD8+( Cytotoxic T Cell) - effector

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19
Q

role of t cells

A

• Cell-mediated defense against intracellular pathogens
– Viruses, fungi and one important bacterial disease (tuberculosis)

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20
Q

Natural Killer Cell

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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21
Q

Function of the Thymus

A

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

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22
Q

Lymph Nodes and lymphocytes

A

• B lymphocytes leave the bone
marrow and populate lymph nodes
• T lymphocytes leave the thymus and populate lymph nodes

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23
Q

IS balance

A

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

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24
Q

classifications of pathogens, examples and immunity responsible for defense

A

• Extracellular pathogens
– Most bacteria
– Humoral immunity
• Intracellular pathogens
– Viruses, fungi, some bacteria
– Cellular immunity

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25
Q

innate immunity
components?

A

(born with)
– 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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26
Q

Adaptive immunity
components?

A

(not born with, requires exposure)
– Antibodies
– Lymphocytes
– Cytokines (IL-2, IL-12)

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27
Q

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

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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28
Q

Antibody-Dependent Immunity: Second Exposure (antibody available)

A

• Memory B cells quickly make specific antibody
– Neutralize toxins
– Bind pathogens
– Serve as opsonins
– Activate complement cascade via classic pathway

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29
Q

arms of adaptive immunity, depend on?

A

humoral and cellular, both Ab dependent

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30
Q

• Humoral immunity is the
first line of defense against?

A

extracellular pathogens

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31
Q

• Cellular immunity is the
first line of defense against?

A

intracellular pathogens

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32
Q

MHC

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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33
Q

• MHC Class 1

A

• MHC Class 1 molecules are located on the surface of most cells

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34
Q

• MHC Class 2

A

• MHC Class 2 molecules are found on Antigen-Presenting Cells (APCs)
– APCs: dendritic cells, macrophages, Langerhans cells

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35
Q

activation path of CD8 cells thru CD4 cells

A

• If the invading organism is a virus, fungus or Mycobacterium, the first line of defense is cellular immunity, not humoral immunity

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36
Q

CD4+ T Helper Lymphocyte
Role?

A

• The recognition arm of cellular
immunity – the bloodhounds
• Role is to look at all the MHC-2molecules in the body (on APCs) to determine if they’re clean or dirty
CD4 Helper T- Lymphocytes are MHC-2 Restricted

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37
Q

CD4 releases what cytokine with activation, results in?

A

CD4+ T Helper cell
secretes IL-2
• IL-2 signals naïve
lymphocytes to
differentiate into CD8+
cytotoxic lymphocytes

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38
Q

CD8 Killer T-Lymphocytes
role? names?

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
• CD8 Killer T-Lymphocytes are MHC-1 Restricted

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39
Q

how CD8 cells kill

A

• CD8 Killer T-Lymphocytes kills
hepatocyte (perforins),
exposing virus to humoral
immune system

OR perforin+granuzymes/ FAS

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40
Q

Immune Injury Disease
Hypersensitivity Reactions
types?

A

Types I, II, III, IV

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41
Q

type 1 hypersensitivity
recipe?

A

Immediate hypersensitivity
Recipe
• Antigen
• IgE antibodies
• Mast cells

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42
Q

clinical responses seen in type 1 hypersensitivity

A

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

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43
Q

most common clinical manifestation of type 1 hyper

A

hay fever

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44
Q

hives of types 1 hyper

A

can form but also be more profound with bronchoconstriction

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45
Q

anaphylaxis of type 1 hyper
local?

A

mass release of immune chemicals that can lead to shock
can be localized or systemic

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46
Q

localized type 1 hyper rxn

A

angioedema (lips)

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47
Q

systemic type 1 hyper rxn

A

can be due to exaggerated response such as bee stings

48
Q

type 2 hyper sensitivity
can target what?

A

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

49
Q

examples of type 2 hypersensitivity

A
50
Q

Outcome of Antibody-Dependent Cytotoxic Reactions Against Cells

A

type 2 rxn
• Lysis – complement mediated (MAC)
• Phagocytosis - opsonization

51
Q

Blood Transfusion Reaction - ABO Blood Incompatibility
what kind of hypersensitivity is this?
what happens?

A

type 2 rxn
* ABO mismatch leads to
intravascular hemolysis
* Antibody-coated
erythrocytes destroyed
by both complement-
mediated lysis and by
phagocytosis in spleen

52
Q

Autoimmune Thrombocytopenic Purpura
presentation?

A

type 2
Ab produced in spleen against plattlet Ag (GPIb)= macrophage destruction of plattlet in spleen

53
Q

type 2 hyper against cell receptors

A

myasthenia gravis
graves dx

54
Q

Myasthenia Gravis

A

Myasthenia Gravis
• Antibody blocks
acetylcholine receptor

55
Q

graves dx

A

• Antibody-mediated
stimulation of cell function
• Antibody stimulates TSH
receptor
hyperthyroidism

56
Q

type 2 rxns against ECM
examples

A

laminin and desmoglein
mucus membrane pemphigoid
pemphigus vaulgaris

57
Q

type 3 rxns due to?

A

immune complexes

58
Q

type 3 rxn mechanism

A
59
Q

PMN role in type 3 rxn

A

act as pahgo but have regurrgitatiojn of lysozomal enzymes leading to fibrinoid necrosis of endothelial wall

60
Q

Target Antigens in Type III Disease
example dx?

A

• Exogenous antigen – post-streptococcal glomerulonephritis
• Endogenous antigen – lupus erythematosus

61
Q

Post-Streptococcal Glomerulonephritis
results from?
signs?
does infection occur?

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
62
Q

Lupus Erythematosus
what kind of hypersensitivity?
involves what systems? especially which ones?
renal failure possible?
demographic?
renal?
what is the Ag?
lab finding?
common superficial manifestation?

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
63
Q

type 3 diseases of vessels

A

vasculitis and glomerulonephritis

64
Q

organs involved in
SLE

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
65
Q

type 4 hypersensitivity due to?

A

cell mediated hypersensitivty

66
Q

examples of type 4 hypersensitivity

A

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

67
Q

contact dermititis

A

usually seen on the skin with exposure to allergenic agent

68
Q

allergic contact stomatitis mechanism

A

Ag bind langerhans cells
present Ag to LN in conn tissue for T cell sensitization
secondary expsoure to the Ag results in activation of sensitzed T cells causing cytokine release and hypersensititvty

69
Q

PPD test

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

70
Q

how could contact mucositis occur in the mouth

A

buccal mucosa, to cinnamon chewing gum or nickel

71
Q

type of hyper? cell involved?

poison ivy contact dermatitis

A
  • CD8 cytotoxic lymphocytes
  • Type IV immune injury
72
Q

development of autoimmunity, arises from?

A

• Loss of self-tolerance
• Arises from a combination of
– Susceptibility genes
– Environmental triggers (infections and tissue damage)

73
Q

Mechanisms of Immunological Tolerance

A

central and peripheral

74
Q
  • Central tolerance
A

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

75
Q

• Peripheral tolerance

A

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

76
Q

Rheumatoid Arthritis
what tissues are effected?
genetic/environment?
TNF role?

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, plays a role in tissue damage by preventing osteoblast maturation

77
Q

RA histology

A

Hyperplastic synovium with dense chronic inflammatory infiltrate = pannus
• Pannus errodes articular cartillage, leading to joint destruction and ankylosis

78
Q

RA due to

A

• Rheumatoid factor is an antibody against an antibody
• IgM autoantibody to the Fc portion of IgG

79
Q

Skin Involvement in RA

A

Rheumatoid Nodules= presssure points/ granulomas

80
Q

key cytokine of RA pathogenesis

A

TNF

81
Q

RA pathogenesis/ flow chart

A

CD4 activated w unknown Ag and stimulate autoab production
CD4 will also activate macrophages and other cells of the joint synovium to cause pannus formation

82
Q

systemic sclerosis
type of dx?
demographic?
characterized by?
what systems can be affected?
can be associated with?

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 other autoimmune diseases

83
Q

spectrum of systemic sclerosis
tissue involvement?

A
84
Q

what accumulates in systemic sclerosis/what happens?
what does this cause?

A
  • Slow continuous replacement of loose fibrovascular connective tissue with dense collagen
  • Fibrosis causes loss of mobility and altered function of organs - skin, esophagus, salivary glands, kidneys, lungs, heart, muscle
85
Q

systemic sclerosis oral findings

A

• Microstomia
• Xerostomia
• Generalized widening of PDL space
• Mandibular resorption: Condyle, Corinoid Process and Angle

86
Q

systemic Sclerosis
face?
blood vessels?
hands?

A

• Mask-like face
• Telangiectasia-pinpoint areas
• Raynaud phenomenon

87
Q

Raynaud Phenomenon

A

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

88
Q

Hands and Fingers of systemic scleroderma

A

Fibrosis, stiffness, deformity
• Ischemia= atrophy and ulceration

89
Q

CREST syndrome

A

limited form of scleroderma

Calcinosis
– Calcium deposits in the skin

• Raynaud Phenomenon
– Spasm of vessels
– Response to cold or stress

• Esophageal dysfunction
– Decrease in motility
– Acid reflux

• Sclerodactly
– Thickening and tightening of the skin
– Fingers and hands

• Telangiectasia
– Dilation of capillaries
– Red lesions on skin

90
Q

Sjogren Syndrome
type of dx?
can be associated with?
presents as what histo?
signs?
demogrpahics?
increased risk of? classified as?

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
    classified as an Autoimmune Exocrineopathy
91
Q

lab findings of SS

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 (non-specific)

• Anti-nuclear antibodies (ANA), non-specific
• Anti-salivary duct antibodies, non-specific

92
Q

sicca complex of SS

A

• Xerostomia
• Xerophthalmia -keratoconjunctivitis sicca

93
Q

oral patholgy associated with xerostomia

A

caries

94
Q

Improper Immune reaction against external “antigens”: result in

A

ALLERGY or HYPERSENSITIVITY

95
Q

Immune reaction against
your own tissues: results in?

A

AUTOIMMUNITY

96
Q

Too little immunity: results in?

A

Immune deficiency

97
Q

Spectrum of Immunodeficiency Diseases

A
98
Q

Primary and Secondary Immune Deficiencies

A
99
Q

Defects in humoral immunity examples

A

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

100
Q

Defects in cellular immunity examples

A

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

101
Q

Bruton Agammaglobulinemia
what is wrong?
result?
recurrent infection?
demographics? why is one sex protected?

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
commnality?
mortality?
recurring infections where?

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
due to?
susceptiable to?
inheritance?

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)
primary or secondary?
group of dx?
symptom?
susceptiable to?
tx ?

A
  • Common primary immunodeficiency
  • A heterogenous group of 20–30 immunodeficiencies
  • Symptoms: all exhibit hypogammaglobulinemia (decreased Ig) due to different causes
  • Recurring bacterial infections
  • Treatment: intravenous infusion of immunoglobulins
105
Q

DiGeorge Syndrome

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
what is wrong?
mutation? result?

A

• 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)

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 mechanism
what fails?
what can occur as a result?

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 can arise

109
Q

Possible Oral Lesions in AIDS

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

candidasis in AIDS

A

can appear in a variety of forms; pseudomembraneous, erthymatous

111
Q

karposi sarcoma with AIDS

A

appear as lesions on the face or gingiva; red in appearence

112
Q

HSV oral presentation in AIDS

A

similarly ulcerative but can vary due to the immune compromised state

113
Q

in immunocompromised pts the clinical appearance of a lesion depends on

A

• Effect of the immune system
• Effect of the agent

114
Q

AIDS – Oral Hairy Leukoplakis

A

can occur on lateral aspect of the tongue and have similar appearence to EBV
bilateral lesion

115
Q

AIDS – Human Papilloma Virus

A

can form papillomas on lip

116
Q

AIDS – Necrotizing Ulcerative Periodontitis

A

gingiva can undergo necrosis

Pathology (20 decks)

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