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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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25
Q

2 Phases of Type I Hypersensitivity

A
  1. Early-Immediate Phase

2. Late Phase Reaction

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26
Q
  1. Early- Immediate Phase (of Type I Hypersensitivity)
A

occurs withing minutes of allergic exposure; but quickly subsides; release of histamine; produces edema, itchiness, etc.

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27
Q
  1. Late Phase Reaction (of Type I Hypersensitivity)
A

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
Q

Examples of Type I Hypersensitivity

A

Hay Fever

Asthma

29
Q

Hay Fever

A

allergic rhinitis; inflammation of nasal sinuses following inhalation of allergic antigen

30
Q

Asthma

A

upper respiratory reaction,may be triggered by inhalation of allergic antigen; difficult breathing–> result of bronchoconstriction and excessive mucous production

31
Q

Hygiene Hypothesis

A

decrease infections during childhood may not allow immune system to develop and appropriate immune rxn to common allergens

32
Q

Wheal-and-Flare test

A

“scratch test”; introduces common allergens into skin to evaluate which stimulate Type I Hypersensitivity rxn at site of contact

33
Q

Type II Hypersensitivity

A

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
Q

How does Type II Hypersensitivity target cells and get rid of them?

A

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
Q

IgG Antibodies (ass. with Type II Hypersensitivity)

A

may also induce injury by activating the complement system OR by recruiting NK cells

36
Q

IgM Anitbodies (ass. with Type II Hypersensitivity)

A

may stimulate the complement system to utilize a membrane attack complex (MAC) to injury cells that have been opsonized

37
Q

Conditions that fall under Type II Hypersensitivity

A
  • Grave’s Disease
  • Rheumatic Fever
  • Goodposture Syndrome
  • Pernicious Anemia
  • Myasthenia Gravis
  • Autoimmune Hemolytic Anemia
  • Blood Type Incompatibilities
38
Q

Grave’s Disease

A

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
Q

Type III Hypersensitivity

A

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
Q

Common Tissues Involved with Deposition for Type III Hypersensitivity

A

vessel wall –> vasculitis (possible fibrinoid necrosis)
kidney –> glomerulonephritis
joint surface –> arthritis

41
Q

Immune complex (Type III Hypersensitivity)

A

composed of antigen fused to an antibody

  • antibodies ass. are IgG and IgM
  • form within circulatin blood and are deposited into tissues
42
Q

Once Immune complexes are made and deposited in tissues, what happens?

A

an acute complement-mediated inflammatory reaction develops–> takes ~1-2 weeks to become apparent

43
Q

Stimuli for Type III Hypersentivitiy

A

(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
Q

Conditions of Type III Hypersensitivity

A
  • systemic Lupus Erythematosus (SLE)
  • polyarteritis nodosa (PAN)
  • reactive arthritis
  • poststreptococcal glomerulonephritis
  • serum sickness
  • arthus reaction
45
Q

Type IV Hypersensitivity

A

(*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
Q

Tow Mechanisms that Type IV Hypersensitivity Occurs

A
  1. CD4+ T cell Injury

2. CD8+ T cell Injury

47
Q

CD4+ T Cell Injury

A

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
Q

Granulomatous Inflammation

A

(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
Q

Contact Dermatitis (eczema)

A

(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
Q

CD8+ T Cell Injury

A

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
Q

Conditions of Type IV Hypersentivitity

A
  • Rheumatoid Arthritis
  • Multiple sclerosis
  • Type I Diabetes Mellitus
  • Crohn’s disease
  • psoriasis
  • contact sensitivity (eczema)
  • Transplant rejection
  • poison ivy
52
Q

Urushiol oil

A

= an oil in poison ivy and poison oak; initiates Type IV Hypersensitivity rxn; a “poison ivy” rxn

53
Q

Autoimmunity

A

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
Q

Localized Autoimmunity

A

to specific tissue type
Examples: Type I Diabetes mellitus, MS, Crohn’s disease, ulcerative colitis, Grave’s disease, myasthenia gravis, goodpasture syndrome

55
Q

Systemic Autoimmunity

A

spread throughout body; many involve attack against vasculature, CT–like joint surfaces
Examples: SLE (lupus), rheumatoid arthritis, systemic sclerosis, Sjogren syndrome, polyarteritis nodosa

56
Q

Immunologic Tolerance

A

= when there is a lack of immune rxn to one’s own tissues; a state of normally or optimal health and homeostasis

57
Q

2 Main Mechanisms Body uses to kill immune cells that lack self-tolerance

A
  1. Central Tolerance

2. Peripheral Tolerance

58
Q

Central Tolerance

A

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
Q

Peripheral Tolerance

A

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
Q

Genetic Risk Factors for Autoimmunity

A

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
Q

Human Leukocyte Antigens (HLAs)

A

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
Q

Ankylosing Spondylitis

A

ass. with HLA; advanced stages may result in ankylosis of sacroiliac joints
ankylosis = fusion

63
Q

Gender and Autoimmunity

A

Females = much more likely to develop autoimmune conditions; thought various genetic and or hormonal influences are responsible (but not well understood)

64
Q

Environmental Risk Factors for Autoimmunity

A

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
Q

Examples of Environmental Triggers

A

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
Q

Cross-Reactivity

A

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
Q

What is an example of Cross-Reactivity

A

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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