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DHBS 365 > Immune System Gone Wrong: Part 2 > Flashcards

Immune System Gone Wrong: Part 2 Flashcards

1
Q

Type II hypersensitivity

A

Cytotoxic hypersensitivity

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2
Q

What are the three pathways of Type II hypersensitivity?

A
  • Activation of the complement system
  • Antibody dependent cellular cytotoxicity
  • Antibody-mediated cellular dysfunction
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3
Q

What antibodies mediates the activation of the complement system?

A

IgG or IgM

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4
Q

How is the complement system activated?

A

IgG or IgM antibodies bind to the antigen

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5
Q

What is Membrane Attack Complex?

A

Pokes holds and allows water influx into the red blood cell, causes lysis

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6
Q

What is hemolytic transfusion reactions and what do they involve?

A
  • Type II hypersensitivity reaction
  • Involves activation of complement system
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7
Q

When might hemolytic transfusion reactions occur?

A

Incompatible RBCs or incompatible plasma are transfused

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8
Q

What does hemolytic transfusion reactions lead to?

A

Intravascular hemolysis via MAC complex

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9
Q

What antibodies mediate antibody-dependent cellular cytotoxicity?

A

IgG or IgM

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10
Q

What do IgG or IgM antibodies bind during antibody-dependent cellular cytotoxicity?

A

Bind target cells and cytotoxic T cells or NK cells

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11
Q

During antibody-dependent cellular cytotoxicity, what do cytotoxic T cells and NK cells release? What does it cause?

A
  • Performs and granzymes
  • Apoptosis
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12
Q

Which of the three pathways of Type II hypersensitivity is non-cytotoxic?

A

Antibody-mediated cellular dysfunction

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13
Q

What two diseases are examples of antibody-mediated cellular dysfunction?

A
  • Grave’s Disease
  • Myasthenia Gravis
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14
Q

What happens during antibody-mediated cellular dysfunction?

A

Antibody binds to receptors and alters it’s activity

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15
Q

What antibodies are involved in Type III hypersensitivity?

A

IgG and IgM

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16
Q

What type of hypersensitivity is specifically in the vessel walls and/or tissues?

A

Type III

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17
Q

How does Type III hypersensitivity work?

A

When IgG or IgM bound antigens are in tissues, complement and neutrophils are activated

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18
Q

In Type III hypersensitivity, what do complements and neutrophils cause?

A

Inflammation, increased tissue permeability, tissue damage

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19
Q

Is Type III hypersensitivity local or systemic?

A

Can be both

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20
Q

Is local or systemic Type III hypersensitivity rare in humans?

A

Localized Type III

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21
Q

What is localized Type III hypersensitivity?

A

Damage is limited to area where immune complexes are first deposited

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22
Q

What is systemic Type III hypersensitivity?

A

Multiple sites in the body are damaged

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23
Q

What is serum sickness?

A

Immune system reacts to medicines that contain proteins to treat immune conditions, attacks it

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24
Q

What type of medication is specifically related to serum sickness?

A

Antivenoms

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25
Q

What hypersensitivity is serum sickness related to?

A

Type III

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26
Q

What is Type IV hypersensitivity mediated by?

A
  • Helper T cells
  • Cytotoxic T cells
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27
Q

When does Type IV hypersensitivity responses occur?

A

1-3 days after exposure

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28
Q

What do the helper T cells do during Type IV hypersensitivity?

A

Release cytokines that recruit macrophages and neutrophils, damage host tissue

29
Q

What do the cytotoxic T cells do during Type IV hypersensitivity?

A

Damage host tissues with granzymes

30
Q

What are two examples of Type IV hypersensitivity?

A
  • Contact hypersensitivity
  • TB test
31
Q

A poison ivy reaction is what type of hypersensitivity?

A

Type IV

32
Q

What is the sensitization stage of contact hypersensitivity (Type IV) of poison ivy?

A

Cytotoxic T cells are sensitived

33
Q

What is the effector stage of contact hypersensitivity (Type IV) of poison ivy?

A

Cytotoxic mechanisms of effector T cells cause host cellular destruction

34
Q

What is injected into a patient during a TB test?

A

Purified tuberculin protein

35
Q

Is a TB test immediate or delayed?

A

Delayed, takes a few days to get the memory cells to come to the site

36
Q

A negative TB test means…

A

There is no swelling and no prior exposure

37
Q

What is the sensitization stage for Type I hypersensitivity?

A

Mast cells and basophils become sensitized to the allergen, produces IgE

38
Q

What is the sensitization stage for Type II hypersensitivity?

A
  • Production of antibodies to recognize substances
  • IgG and IgM
39
Q

What is the sensitization stage for Type III hypersensitivity?

A
  • Presence of antibodies against the offending antigen in the serum of affected individuals
  • IgG or IgM
40
Q

What is the sensitization stage for Type IV hypersensitivity?

A

T cells are sensitized and memory T cells are produced 7-10 days later

41
Q

Autoimmune diseases have what kind of T cell response?

A

TH1

42
Q

What is an autoimmune disease the result of?

A

When mechanisms meant to preserve tolerance of self breakdown and cause disease

43
Q

What are the three conditions for autoimmunity to occur?

A
  • MHC molecules determine susceptibility to autoimmune diseae
  • Lymphocyte receptors recognize a particular self antigen
  • Environmental factors (bacterial or viral infection)
44
Q

What is molecular mimicry?

A
  • Structural similarity between foreign and self molecules
  • Can induce autoimmunity
45
Q

There must be what in the same tissues that express the self-antigen?

A

An inflammatory reaction

46
Q

What are the two groups of autoimmune diseases?

A
  • Organ specific
  • Systemic disease
47
Q

Is Type I diabetes organ-specific or systemic?

A

Organ specific

48
Q

What does Type I diabetes target?

A

Insulin producing beta cells of the pancreas

49
Q

What are the noticeable symptoms of plaque psoriasis?

A

Thickening and scaling of skin’s surface

50
Q

What causes plaque psoriasis?

A

CD8 T cells that produce high levels of IL-17

51
Q

How does molecular mimicry play a role in plaque psoriasis?

A

MHC molecules recognize both a particular keratin protein and a protein made by streptococcal bacteria

52
Q

What is rheumatoid arthritis?

A

Chronic inflammation of the joints

53
Q

What antibodies are abundant in the joints in rheumatoid arthritis?

A

IgM antibodies that can bind tot he Fc regions of IgG

54
Q

What happens in rheumatoid arthritis when IgM and IgG bind together in the joints?

A

Forms antibody complex, activates macrophages that have entered the joints, increases inflammation

55
Q

What is celiac disease?

A

Intestinal immune system mounts strong inflammatory response which damages the villi of the intestinal epithelium

56
Q

What do villi do?

A

Absorption of nutrients in intestine

57
Q

Is celiac disease caused by molecular mimicry?

A

No

58
Q

What type of inflammatory response is activated in celiac disease?

A

TH1

59
Q

What are the symptoms of lupus erythematosus?

A
  • Red rash on forehead and cheeks
  • Inflammation of lungs, arthritis, kidney damage, hair loss, paralysis, convulsions
60
Q

What is lupus erythematosus caused by?

A

Breakdown in B and T cell tolerance and causes diverse collection of IgG antibodies that recognize self antigens

61
Q

Is there a specific microbial infection associated with lupus erythematosus?

A

No

62
Q

Type I autoimmune diseases?

A
  • Anaphylaxis
  • Bronchial asthma
  • Allergic rhinitis
  • Food allergies
63
Q

Type II autoimmune diseases?

A
  • Rheumatic fever
  • Myasthenia gravis
  • Grave’s disease
  • Acute hemolytic transfusion reactions
64
Q

Type III autoimmune diseases?

A
  • Serum sickness
  • SLE
  • Rheumatoid arthritis
65
Q

Type IV autoimmune diseases?

A
  • Plaque psoriasis
  • Poison ivy contact dermatitis
  • TB test
  • Type I diabetes
66
Q

Can rheumatoid arthritis be in the TMJ?

A

Yes

67
Q

What is Sjogren’s syndrome?

A

Erythematous oral mucus, enlarged salivary glands, difficulty swallowing, altered taste

68
Q

What is a fissured tongue?

A

Atrophy of papillae

DHBS 365 (10 decks)

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