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General Pathology -- Roecker > Gen Path Exam 2 Section 4: Disease of the Immune System > Flashcards

Gen Path Exam 2 Section 4: Disease of the Immune System Flashcards

1
Q

Immune System

A

specialized network of cells, proteins, tissues, and organs that serve to protect body from infectious pathogens and maintain health

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2
Q

Immunodeficiency

A

an insufficient level of immune activity

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3
Q

Hypersensitivity Reactions

A

excessive immune activity

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4
Q

Immunity

A

body’s ability to resist disease, esp. via resistance of infection

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5
Q

Leukocytes

A

= WBCs

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6
Q

Antigen (Ag)

A

a foreign substance that induces immune response, esp. production of anti-bodies

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7
Q

Antibody (Ab)

A

a blood protein produced in response to antigen exposure; also referred to as immunoglobulins (Ig)
Types: IgE, IgG, IgM, IgA

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8
Q

IgE

A

ass. with allergic reactions, mast cell degranulation/histamine release

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9
Q

IgG

A

most abundant, protects vs bacterial and viral infections

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10
Q

IgM

A

first antibody formed in response to new infection or antigen exposure

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11
Q

IgA

A

common in areas open to external env. (orifices)

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12
Q

Hypersensitivity Reactions

A

an injurious immune response; chronic and debilitating

AKA - hypersensitivities or immune-mediated reactions

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13
Q

Immune Reaction may cause tissue damage when:

A
  1. immune rxn inadequately controlled
  2. immune rxn is directed toward a harmless antigen
  3. immune rxn is directed against host’s tissues
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14
Q

Three categories of Hypersensitivity reactions

A
  1. Autoimmunity
  2. Persistent Rxn to Microbial Infections
  3. Allergic reactions
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15
Q

Autoimmunity (hypersensitivity)

A

immune reactions to self-antigens; inds. have lost of “self-tolerance”

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16
Q

Reactions to Microbes (hypersensitivity)

A

commonly involve excessive antibody production, following infection; may involve formation of immune complexes; may involve excessive T-cell-mediated rxns –> commonly produce severe inflammation and chronic inflammation
- Immune complex

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17
Q

Immune Complex

A

an antigen-antibody complex–> forms following binding of antibody to an antigen
- frequently deposited in walls of blood vessels and trigger immune rxn–> resulting in destructive vasculitis

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18
Q

Allergies (hypersensitivity)

A

allergic rxns; immune system reacting to harmless env. antigen; range from mild discomfort to life-threatening anaphylactic shock
~20% of US adults have at least one allergy

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19
Q

Types of Hypersensitivity Reactions

A

A - (Type I) degradation of mast cells, IgE
C - (Type II) antibodies (IgG, IgM) promote opsonization
I - (Type III) antigen + antibody = immune complex
D - (Type IV) T-cell mediated

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20
Q

Type I Hypersensitivity

A

allergic rxns; involve formation of IgE antibodies in response to harmless env. antigens; mast cell degranulation releases histamine –> initiates an acute inflam. rxn

  • “immediate” rxn ~5-30mins
  • can be localized or systemic
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21
Q

First exposure to antigen in Type I Hypersentivitity

A

produce excessive IgE and they bind to circulating mast cells–> mast cells now “sensitized” –> and a repeat exposure will result in sudden mast cell degranulation and release histamine

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22
Q

Features of Type I Hypersensitivity

A
  • endothelial contraction and increase vessel permeability leading to edema and erythema
  • accumulation of inflam. cells at site produces itching/irritation
  • “hives” (urticaria)
  • Bronchoconstriction
  • increase mucous secretion
  • GI tract inflammation (if ingest food allergic to)
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23
Q

Localized Type I Hypersentivitity

A

localized to region of body (skin or sinus); tend to occur where come into contact with antigen

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24
Q

Generalized Type I Hypersentivity

A

to entire body; commonly occur when ingested or injected allergen and travel circulatory system; more likely to produce anaphylaxis–> may be lethal

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2 Phases of Type I Hypersensitivity
1. Early-Immediate Phase | 2. Late Phase Reaction
26
1. Early- Immediate Phase (of Type I Hypersensitivity)
occurs withing minutes of allergic exposure; but quickly subsides; release of histamine; produces edema, itchiness, etc.
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2. Late Phase Reaction (of Type I Hypersensitivity)
occurs ~2-8 hours after exposure to allergen; involves cytokine-mediated tissue injury; attracts neutrophils to site and capable of more sig. injury--> esp. to mucous membranes and epithelia cells
28
Examples of Type I Hypersensitivity
Hay Fever | Asthma
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Hay Fever
allergic rhinitis; inflammation of nasal sinuses following inhalation of allergic antigen
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Asthma
upper respiratory reaction,may be triggered by inhalation of allergic antigen; difficult breathing--> result of bronchoconstriction and excessive mucous production
31
Hygiene Hypothesis
decrease infections during childhood may not allow immune system to develop and appropriate immune rxn to common allergens
32
Wheal-and-Flare test
"scratch test"; introduces common allergens into skin to evaluate which stimulate Type I Hypersensitivity rxn at site of contact
33
Type II Hypersensitivity
classic "antibody-mediated rxns"; produce cell injury (cytotoxicity); involves tissues being "targeted for death" via oponization; excessive oponization of host's cells with IgG or IgM antibodies; normal tissue being targeted (Coomb's Test--direct or indirect)
34
How does Type II Hypersensitivity target cells and get rid of them?
targets cells for phagocytosis via oponization - neutrophils or macrophages phagocytosize cells If targeted cell is in circulation--> splenic macrophages remove them when cells pass through spleen
35
IgG Antibodies (ass. with Type II Hypersensitivity)
may also induce injury by activating the complement system OR by recruiting NK cells
36
IgM Anitbodies (ass. with Type II Hypersensitivity)
may stimulate the complement system to utilize a membrane attack complex (MAC) to injury cells that have been opsonized
37
Conditions that fall under Type II Hypersensitivity
- Grave's Disease - Rheumatic Fever - Goodposture Syndrome - Pernicious Anemia - Myasthenia Gravis - Autoimmune Hemolytic Anemia - Blood Type Incompatibilities
38
Grave's Disease
hyperthyroidism; overproduction of thyroid hormones (T4 and T3) Features: - exophthalmoses (eyes bulge), pretibial myxedema (thick skin on shins), tachycardia, goiter, insomnia, weight loss, fatigue 7x greater chance in females at age 20-40 Antigen = TSH receptor
39
Type III Hypersensitivity
rxns ass. with formation of immune complexes (Ab+Ag); MC characteristic = acute vasculitis and fibrinoid necrosis of vessel wall Stimuli can be internal or external
40
Common Tissues Involved with Deposition for Type III Hypersensitivity
vessel wall --> vasculitis (possible fibrinoid necrosis) kidney --> glomerulonephritis joint surface --> arthritis
41
Immune complex (Type III Hypersensitivity)
composed of antigen fused to an antibody - antibodies ass. are IgG and IgM - form within circulatin blood and are deposited into tissues
42
Once Immune complexes are made and deposited in tissues, what happens?
an acute complement-mediated inflammatory reaction develops--> takes ~1-2 weeks to become apparent
43
Stimuli for Type III Hypersentivitiy
(widely varied, but) 1. external (exogenous) antigens ---> microbs or other foreign substances 2. internal (endogenous) antigens---> normal cells or tissues within body; self-antigens
44
Conditions of Type III Hypersensitivity
- systemic Lupus Erythematosus (SLE) - polyarteritis nodosa (PAN) - reactive arthritis - poststreptococcal glomerulonephritis - serum sickness - arthus reaction
45
Type IV Hypersensitivity
(*do NOT involve antibodies) ARE mediated by only T-cells --> specifically CD4+ T cells and CD8+ T cells - involved with many autoimmune conditions and common env. exposures
46
Tow Mechanisms that Type IV Hypersensitivity Occurs
1. CD4+ T cell Injury | 2. CD8+ T cell Injury
47
CD4+ T Cell Injury
involves cytokine production--> recruits injurious neutrophils and macrophages to inflammation site = "delayed" reaction b/c process takes ~24-48 hours - Granulomatous Inflammation - Contact Dermatitis (eczema)
48
Granulomatous Inflammation
(Type IV Hypersensitivity ass.) ass. with chronic inflammation rxn ass. with CD4+ T cells mediated rxns granuloma = walled off collection of macrophages); "epitheloid cells" or "giant cells"
49
Contact Dermatitis (eczema)
(Type IV Hypersensitivity ass.) common skin pathology develops from CD4+ T cell mediated rxn Eczema = a group of skin conditions that manifest with similar features following exposure to env. antigen
50
CD8+ T Cell Injury
involves specialized CD8+ T cells that directly bind to and kill cells that express a triggering antigen - responsible to injury to pancrease in Type I Diabetes mellitus and in tissue/organ rejection following transplantation
51
Conditions of Type IV Hypersentivitity
- Rheumatoid Arthritis - Multiple sclerosis - Type I Diabetes Mellitus - Crohn's disease - psoriasis - contact sensitivity (eczema) - Transplant rejection - poison ivy
52
Urushiol oil
= an oil in poison ivy and poison oak; initiates Type IV Hypersensitivity rxn; a "poison ivy" rxn
53
Autoimmunity
someone has an immune rxn against own tissues; rxn against own tissue antigens (self-antigens) - involve a "loss of self-tolerance" - can be localized or systemic
54
Localized Autoimmunity
to specific tissue type Examples: Type I Diabetes mellitus, MS, Crohn's disease, ulcerative colitis, Grave's disease, myasthenia gravis, goodpasture syndrome
55
Systemic Autoimmunity
spread throughout body; many involve attack against vasculature, CT--like joint surfaces Examples: SLE (lupus), rheumatoid arthritis, systemic sclerosis, Sjogren syndrome, polyarteritis nodosa
56
Immunologic Tolerance
= when there is a lack of immune rxn to one's own tissues; a state of normally or optimal health and homeostasis
57
2 Main Mechanisms Body uses to kill immune cells that lack self-tolerance
1. Central Tolerance | 2. Peripheral Tolerance
58
Central Tolerance
recognition and deletion of auto-reactive immune cells in area where they mature - T Cells mature in thymus gland - B Cells mature in bone marrow (is not perfect and some get released into peripheral circulation)
59
Peripheral Tolerance
mechanisms that deactivate and kill auto-reactive immune cells in peripheral circulation - occurs via stimulation of mitochondrial and death receptor pathways - regulatory T-cells suppress auto-reactive immune cells via poorly understood mechanisms
60
Genetic Risk Factors for Autoimmunity
Multigenic = something is caused by or effected by more than one gene (most autoimmune conditions are complex and involve multiple genes) - high risk Human Leukocyte antigens (HLAs)
61
Human Leukocyte Antigens (HLAs)
cellular surface molecules involved with antigen presentation; help regulate immune system and some place ind. and increased risk of developing a specific autoimmune condition Ex: HLA-B27 places some at increased risk 100-200-fold for developing ankylosing spondylitis
62
Ankylosing Spondylitis
ass. with HLA; advanced stages may result in ankylosis of sacroiliac joints ankylosis = fusion
63
Gender and Autoimmunity
Females = much more likely to develop autoimmune conditions; thought various genetic and or hormonal influences are responsible (but not well understood)
64
Environmental Risk Factors for Autoimmunity
many env. exposures combined with individuals underlying genetic risk--> may push ind. past a threshold--> and result in initiation of specific autoimmune condition - cross-reactivity
65
Examples of Environmental Triggers
infections, ultraviolet (UV) light exposure, mechanical trauma, or injury from smoking ~thought: these harmful env. triggers cause injury--> initiates a positive-feedback loop in inds. with lack of self-tolerance--> lead to injury, inflam., injury, and more = explains chronicity and reoccurring characteristics of autoimmune conditions
66
Cross-Reactivity
occurs when immune system develops antibodies to antigen (typically infectious origin) and the newly-formed antibodies react with host's normal tissues *example of Type II Hypersensitivity
67
What is an example of Cross-Reactivity
occurs in rheumatic valve disease - a case of untreated "strep throat" results in formation of strep antibodies--> these antibodies inadvertently become cross-reactive with host's normal cardiac valves--> may cause valvular injury known as rheumatic heart disease

General Pathology -- Roecker (7 decks)

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