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MCIM 224 > 17 Immunology III: Disorders of the Immune System (allergies, autoimmunity, etc.) > Flashcards

17 Immunology III: Disorders of the Immune System (allergies, autoimmunity, etc.) Flashcards

1
Q

Three categories of immune sys defects?

A
  1. Hypersensitivity
  2. Immunodeficiency
  3. Autoimmunity
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2
Q

Define hypersensitivity

A

Overactive, harmful response to foreign antigens

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3
Q

Define immunodeficiency

A

Failure to mount an adequate immune response to foreign antigen

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4
Q

Define Autoimmunity

A

A harmful response to “self” antigens

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5
Q

What is the 2-stage process that causes hypersensitivity rxns?

A

i) First exposure to the Ag “sensitizes” the person to the Ag
ii) Second exposure to same Ag results in a strong immune reaction

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6
Q

Another name for the sensitizing antigen in hypersensitivity rxns?

A

“Allergen”

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7
Q

What is an allergen?

A

A normally harmless foreign antigen (eg. foods, pollen, nuts, etc.)
that can trigger an overly aggressive immune response

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8
Q

Two categories of hypersensitivity rxns? What do ea. involve?

A
  1. Immediate hypersensitivity (involves antigen, antibody, and various cells)
  2. Delayed hypersensitivity (involves antigen and T-cells only [no antibody])
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9
Q

What’re other names for “immediate hypersensitivity”?

A
  1. Type I hypersensitivity
  2. Anaphylactic rxns
  3. Alleries
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10
Q

What specific antibodies and cells does immediate hypersensitivity involve?

A

IgE antibodies and various “granulated” cells

eg. Basophils, Eosinophils, but mainly mast cells

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11
Q

What do mast cells carry inside them?

A

Numerous granules containing inflammatory chemicals (histamine, proteases, heparin, etc.)

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12
Q

Where’re mast cells found?

A

Tissues close to body surfaces (skin, airways, GI tract, etc.)

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13
Q

Mast cells strongly bind ____ to its cell surface during Type I hypersensitivity

A

IgE

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14
Q

In immediate hypersensitivity, what events does an allergen trigger during the 1st contact?

A

B-cells > IgE produced > IgE binds to surface of mast cells and “sensitizes” them

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15
Q

In immediate hypersensitivity, what events does an allergen trigger during the 2nd contact w/ identical allergen?

A

Allergen binds to IgE on sensitized mast cell > Mast cell “degranulates” and releases various inflammatory chemicals

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16
Q

Two types of anaphylaxes? Where do ea. occur?

A
  1. Localized (atopic) anaphylaxis
    >occurs only at site where allergen enters body
  2. Generalized (systemic) anaphylaxis
    >occurs throughout the body
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17
Q

What occurs during an anaphylactic shock? What type of anaphylaxis is this associated w/?

A
  1. Airways constrict
  2. Leakage of fluids from capillaries > tissue swelling and serious drop in blood pressure due to lg histamine release

Anaphylactic shock is associated w/ generalized (systemic) anaphylaxis.

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18
Q

How are atopic and/or mild systemic rxns treated? (3)

A
  1. anti-histamines
  2. steroids and bronchodilators > reduce inflammation and open airways
  3. Mast cell stabilizers (e.g. Cromolyn) > prevents degranulation
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19
Q

How is an anaphylactic shock treated?

A

Epinephrine > relaxes smooth muscles and reduces vascular permeability

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20
Q

What does desensitization immunotherapy involve?

A

Expose pt to increasing amts of allergen over time

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21
Q

How are allergy testing conducted?

A

Suspected allergen is administered underneath skin > examine for inflammation after 20-30 mins

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22
Q

Why isn’t everyone hypersensitive to one or more allergens?

A
  1. genetics
  2. failure to regulate IgE production
  3. “Hygiene hypothesis” > lack of early childhood exposure to dirt and microbes leads to a weaker, less trained immune sys
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23
Q

How many adults think they’re allergic to a food? What’s the actual statistic?

A

25% think they’re allergic

3-4% have an actual immune sys hypersensitivity

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24
Q

Delayed hypersensitivity synonym?

A

Type IV hypersensitivity

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25
Q

What does a delayed (Type IV) hypersensitivity rxn involve?

A

allergen and T-cells ONLY

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26
Q

Why do delayed hypersensitivity rxns take longer (>24h)?

A

T-cell response takes a while to become fully active

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27
Q

What occurs during the 1st exposure to allergen during a delayed hypersensitivity rxn?

A

Exposure to allergen causes Th cell activation and production of memory Th cells

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28
Q

What occurs during the 2nd exposure to allergen during a delayed hypersensitivity rxn?

A

Memory Th cells respond and release cytokines > attracts macrophages and cytotoxic T-cells to site of allergen > tissue damage, inflammation, etc.

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29
Q

What is type of test is used to test for sensitization to Mycobacterium tuberculosis?

A

Tuberculin skin test (Mantoux test)

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30
Q

How is a tuberculin skin test done?

A
  1. Inject non-infectious extract of M. tuberculosis under the skin
  2. Look for inflammation at the site of injection after 48-72 h
31
Q

What can a positive TB skin test indicate? (3)

A 
1. Previous disease, followed by full recovery
or 
2. Vaccination against TB
or 
3. A current active infection with TB
32
Q

T or F: The tuberculin skin test can tell you whether you’re suffering from an active tuberculosis infection or not.

A

F

33
Q

What do immunodeficiency disorders entail?

A

Failure to mount an effective immune response to foreign antigens due to a defect in the innate or the adaptive immune system

34
Q

What happens to our immune systems as we get older?

A

Body’s ability to produce new T and B-cells

gradually declines with age

35
Q

How long does it take for kids’ immune systems to develop fully?

A

12-18 months

36
Q

What type of antibody are kids protected by, and which they receive from their mothers?

A

IgG (it can cross the placenta)

37
Q

What’re two possible causes of abnormal immunodeficiencies?

A
  1. Congenital

2. Acquired

38
Q

Synonym for congenital immunodeficiency?

A

“Primary immunodeficiency”

39
Q

What causes primary immunodeficiency?

A

Mutation (spontaneous or inherited) in any one of many genes responsible for regulating immune response or encoding critical components

40
Q

Five types of congenital (“Primary”) immunodeficiency?

A
  1. B-cell deficiencies (most common)
  2. T-cell deficiencies
  3. Combined B and T-cell deficiencies
  4. Defects in phagocytic cell number or fn
  5. complement deficiencies
41
Q

Examples of specific primary immunodeficiency conditions? (3)

A
  1. Agammaglobulinemia (B-cell deficiency)
  2. DiGeorge Syndrome (T-cell deficiency due to abnormalities in thymus)
  3. Severe combined immunodeficiency (SCID)
42
Q

What’re inds esp. susceptible to in agammaglobulinemia?

A

Infection w/ normally harmless microbes

43
Q

What’re inds esp. susceptible to in DiGeorge Syndrome?

A

Intracellular microbes (e.g. viruses)

44
Q

This type of primary immunodeficiency disorder requires isolation from all microbes to prevent infections.

A

Severe Combined Immunodeficiency (SCID)

45
Q

Define acquired immunodeficiency.

A

Suppression of the immune response due to EXTERNAL agents (usually microbial or chemical)

46
Q

T or F: Acquired immunodeficiencies are permanent.

A

F

Not necessarily

47
Q

Name a popular microbial infection that induces acquired immunodeficiency.

A

HIV infection

48
Q

How does HIV cause an acquired immunodeficiency?

A
  1. They attach to receptor molecule (CD4) of Helper T-cells
  2. Replicates in, and kills, Th cells
  3. Number of Th cells decrease over time > immunodeficiency
49
Q

Name a type of drug used for temp. suppression of an over-active immune response. How does it suppress the immune sys?

A

Corticosteroid > inhibits synthesis of inflammatory chemicals and phagocytes/lymphocytes

50
Q

When are drugs used to suppress the immune sys?

A

After transplantation

51
Q

T or F: Other things, such as stress, malnutrition, and alcoholism, can cause temporary immunodeficiency, leading to increased susceptibility to microbial infections

A

T

52
Q

Define autoimmunity.

A

Immune rxn against your OWN cells due to an inability to distinguish self from non-self

53
Q

What types of cells are involved in autoimmunity? What occurs to cause autoimmune rxns?

A

B-cells and T-cells

They recognize antigens on NORMAL host cells > antibodies form complexes w/ self antigens > inflammation, tissue damage, etc.

54
Q

What causes autoimmunity? (possible hypotheses) (2)

A
  1. High similarity between a foreign Ag and a cellular Ag?
  2. Mutation which causes a structural change in one of the body’s proteins so that it looks “foreign” to the immune system?
55
Q

Genetic and environmental probabilities that contribute to autoimmune diseases?

A

Genetic: 30%

Envir: 70%

56
Q

Are men or women more likely to develop autoimmune disease?

A

Women

57
Q

Examples of specific autoimmune conditions? (4)

A
  1. Type I (juvenile) diabetes
  2. Acute Rheumatic fever
  3. Rheumatoid Arthritis
  4. Celiac disease
58
Q

What occurs during Type I (juvenile) diabetes?

A

Cytotoxic T-cells destroy insulin-producing pancreatic cells

→ Lack of insulin = increased blood & urine glucose

59
Q

What occurs during Acute Rheumatic fever?

A

Antibodies produced vs. Streptococcus pyogenes cell wall proteins recognize similar antigens on heart valves (“cross-reaction”)
→ Inflammation & damage to heart & valves

60
Q

What occurs during Rheumatoid arthritis?

A

T-cells activated by UNKNOWN self-antigen > Immunoglobulins attach to these unknown self-antigens > Ig+antigen complexes deposit into joints > damage to joint cartilage

61
Q

Define celiac disease

A

Autoimmune condition triggered by GLUTEN

62
Q

Symptoms of celiac disease?

A

Abdominal pain, chronic diarrhea, anorexia, failure to thrive (kids),
+/- many non-specific symptoms (anemia, fatigue, etc.)

63
Q

Ultimately, what causes the symptoms associated w/ celiac disease?

A

loss of gut absorptive capacity because of autoimmune damage to intestinal tract epithelial villi

64
Q

What is a hypothesis as to how gluten causes celiac disease (an autoimmune disease)?

A
  1. Gut = more permeable to gluten > gluten enters underlying gut tissues
  2. Gluten gets acted on by tissue transglutaminase (tTG)
  3. tTG produces a. deamidated gluten and b. complexes of gluten bound to tTG (both of these activate T-cells and stimulate B-cells)
  4. Anti-gluten antibodies, anti-tTG antibodies, and activation of Th cells result
65
Q

What’s the autoantigen in celiac disease?

A

tissue transglutaminase (tTG)

66
Q

Where’re T-cells directed towards in celiac disease? Why?

A

All directed to site where gluten & tTG are present (ie. gut epithelium)

67
Q

How is “Helminthic Therapy” used to treat some immune disorders?

A
  1. Consume live parasitic worms
  2. Worms attach to gut wall and start infection
  3. Th cells increase in activity
  4. Cytokines are stimulated > suppress some parts of the immune sys
  5. Composition of intestinal “normal” flora is changed
  6. Inflammation and other symptoms associated w/ autoimmunity is DECREASED
68
Q

Places where helminth infestations are more common are associated w/…

A

reduced autoimmune disorders

69
Q

Name a condition where both over- and under-immune reactions occur. What does it entail.

A

Sepsis

Life-threatening organ failure / tissue damage caused by an un-regulated immune response to a microbial infection (or other things – major trauma,
circulatory shock, etc.)

70
Q

Stages of sepsis?

A
  1. Sepsis (systemic inflammation due to infection)
  2. Severe sepsis (sepsis + organ failure)
  3. Septic shock (severe sepsis + refractory hypotension)
71
Q

How does the immune sys react to sepsis?

A
  1. Hyper-inflammation, followed by…

2. immunosuppression

72
Q

Two main causes of death during sepsis?

A
  1. Overwhelming inflammation

2. Recurrent infections due to persistent immunosuppression

73
Q

T or F: Anyone who has an infection is at risk of developing sepsis.

A

T

MCIM 224 (25 decks)

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