Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

IMM Exam 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Hypersensitivity

A

defect in regulation or targeting of the usually beneficial immune response

i.e. overreaction of normal immune response triggered by self/microbial/environmental antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Triggers of hypersensitivity

A

3 types of antigens

  1. “self” antigens -autoimmunity
  2. microbial antigens - excessive inflammation
  3. Environmental antigens - allergy/atopy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 4 types of hypersensitivity?

A

Type I - Immediate hypersensitivity

Type II - Antibody-mediated

Type III - Immune complex-mediated

Type IV - T cell-mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Names for Type 1 Hypersensitivity

A

Immediate, IgE-mediated, allergy/atopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Timing of Type 1 Hypersensitivity

A

within minutes (very rapid)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Mechanism of Type 1 Hypersensitivity

A

cross-linking of IgE triggering mediator release in mast cells

Involve antigen-specific IgE on effector cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Various mediators in Type 1 Hypersensitivity

A

vasoactive mediators (e.g. histamine)

lipid mediators

cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Most common type of hypersensitivity

A

Type 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Allergy =

A

histamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Examples of allergic diseases (Type 1 Hypersensitivity)

A
  • Allergic rhinitis (“hay fever”)
  • Atopic asthma
  • Anaphylaxis (food allergy, stinging insect allergy, drug allergy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Potential causes of increase in Type 1 Hypsersensitivity prevalence within the past 50 years

A
  • hygiene hypothesis

- environmental factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Similarities between Type II and III hypersensitivity

A

both mediated by antibodies (involve IgG and IgM)

frequently involve auto-antibodies (failure in developing or loss of self-tolerance)

less commonly involve foreign antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type II Hypersensitivity

A
  • Injury related to antibody directly binding to target

- Antigens are specific cells or extracellular matrix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Differences between Type II and III Hypersensitivity

A

Type II: Local, tissue/cell specific (i.e. “targeted”)

Type III: Systemic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Type III Hypersensitivity

A
  • Injury related to immune complex deposition

- Antigens are present in circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Names for Type II Hypersensitivity

A

antibody-mediated, cytotoxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Timing for Type II Hypersensitivity

A

couple days up to a week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mechanism of Type II Hypersensitivity

A

3 mechanisms:

  • complement/Fc receptor inflammation
  • opsonization/phagocytosis
  • receptor activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

1st mechanism of Type II Hypersensitivity

A

“Complement- and Fc receptor-mediated inflammation”

Antibody binds antigens and attract neutrophils and/or complement which lead to inflammation and injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Goodpasture syndrome

A

Anti-glomelular basement membrane disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are antibodies directed against in Goodpasture syndrome?

A

Abs against basement membrane in kidney and lung

Activate complement and Fc receptors (of neutrophils), leading to inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Symptoms of Goodpasture syndrome

A

Blood in urine, Blood in lung, kidney failure and fatigue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

2nd Mechanism of Type II hypersensitivity

A

Opsonization and phagocytosis

Ab coat the outside of cells and then phagocytes come and eat them up

24
Q

ITP (Idiopathic thrombocytopenic purpura)

A

Autoantibodies against platelets –> opsonization

25
Q

Symptoms of ITP

A
  • Recurrent nose bleeds
  • Easy bruising
  • Petechiae
26
Q

AIHA (Autoimmune hemolytic anemia)

A

Autoantibodies against RBC membrane proteins

Pts. have symptoms of anemia

On blood smear, less RBCs; not donut shaped - vary in size; no central pallor

27
Q

3rd mechanism of Type II Hypersensitivity

A

Abnormal physiologic responses without cell/tissue injury - Abs turn things on or off

  • Antibody stimulates receptor without hormone (e.g. Grave’s disease: Ab against TSH receptor leads to hyper-stimulation of thyroid and production of thyroid hormones)
  • Antibody inhibits binding of NT to receptor (e.g.: Myasthenia Gravis: Ab bind ACh receptors, preventing ACh from signaling from nerve to muscle)
28
Q

Why are Grave’s disease and Myasthenia Gravis examples of Type II Hypersensitivity?

A

Autoantibodies are involved, and the Abs bind particular cells and disease is tissue specific

29
Q

Clinical examples of Type II Hypersensitivity

A
  • Acute rheumatic fever - Abs against myocardial Ags ( cross-reactive anti-strep Abs)
  • Pemphigus vulgaris - Abs against desmosomes
  • Pernicious anemia - Abs against intrinsic factor
30
Q

Names for Type III Hypersensitivity

A

Immune-complex mediated

31
Q

Timing for Type III Hypersensitivity

A

several days up to a couple weeks

32
Q

Mechanism of Type III Hypersensitivity

A
  1. Abs bind Ags forming complexes
  2. Complexes not efficiently cleared
  3. Deposit in vessels or tissue
  4. Trigger complement/Fc receptor inflammation

(e.g.: vasculitis)

33
Q

Type III Hypersensitivity and diphtheria treatment from horse serum

A
  • Horse injected w diphtheria toxin –> induce Abs
  • Anti-diphtheria horse serum injected into humans to treat diphtheria
  • Some patients receiving the anti-diphtheria horse serum developed (1) fever, (2) hives and (3) joint pain
    note: symptoms occured with anti-diphtheria horse serum AND with horse serum alone

repeated exposure to horse serum led to quicker and quicker rxns because already had developed antibodies

34
Q

Type III Hypersensitivity and SLE (systemic lupus erythematosus)

A

Multiple nuclear autoantibodies: dsDNA, ribo-nucleopreotins, histones

35
Q

SLE also has examples of Type II Hypersensitivity with the blood issues

A

but joint pain, nephritis and vasculitis are classic of Type III

36
Q

Clinical examples of Type III Hypersensitivity

A

Poststreptococcal glomerulonephritis - group A strep Ag

Polyarteritis nodosa - Hep B surface Ag

37
Q

Slowest Hypersensitivity type

A

Type IV

38
Q

Names for Type IV Hypersensitivity

A

delayed type, cell-mediated

39
Q

Timing for Type IV Hypersensitivity

A

1-3 days

40
Q

Mechanism of Type IV Hypersensitivity

A

2 mechanisms: (both T cell mediated)

  • CD4 T-cell cytokine-mediated inflammation
  • CD8 T-cell direct cytotoxic killing
41
Q

Type IV Hypersensitivity and antibodies

A

T-cell mediated rather than antibodies - not transferrable by serum

42
Q

1st mechanism of Type IV Hypersensitivity (Cytokine-mediated inflammation)

A

CD4 indirectly causes injury by releasing inflammatory cytokines (e.g. IFNgamma)

43
Q

What is FoxP3

A

TF associated with regulatory T cells

44
Q

Suppressive cytokines secreted by Tregs

A

IL-10 and TGFbeta

45
Q

Cytokine associated with allergy

A

IL-4

46
Q

TB test is example of what type of hypersensitivity

A

Delayed-type hypersensitivity (DTH)

Type IV Hypersensitivity since CD4+ T cells are involved

47
Q

Clinical examples of Type IV Hypersensitivity (cytokine-mediated inflammation)

A

MS

Type 1 diabetes

IBD

Rheumatoid arthritis

48
Q

2nd mechanism of Type IV Hypersensitivity

A

T cell-mediated killing of host cells; direct tissue injury by CD8+ cytotoxic T cells

49
Q

Examples of CTL mediated Type IV Hypersensitivity

A

poison ivy (contact dermatitis)

50
Q

Poison ivy (contact dermatitis)

A

Urushiol - colorless oil

  • low molecular weight, lipid soluble so crosses cell membrane
  • modifies intracellular ksin proteins; presented on MHC Class I –> cells appear FOREIGN
  • CTLs trigger cell destruction by apoptosis

delayed, develops over 12-48 hours

51
Q

Poison ivy (contact dermatitis) onset

A

delayed, develops over 12-48 hours

note: this is Type IV Hypersensitivity (not Type I so not immediate)

52
Q

Treatment options for Types I-IV Hypersensitivity

A
  • Antihistamines, epinephrine
  • Plasmapheresis, immune biologics (target specific cytokine)
  • IVIG (high doses lead to immune suppression)
  • Corticosteroids (reduce inflammatory cytokines produced)
53
Q

Diseases involving Type II Hypersensitivity

A

Goodpasture, AIHA, ITP, Graves, Myasthenia gravis

54
Q

Diseases involving Type I Hypersensitivity

A

Allergic diseases and anaphylaxis

55
Q

Diseases involving Type III Hypersensitivity

A

Lupus, serum sickness, post-strep glomerulonephritis, polyarteritis nodosa

56
Q

Diseases involving Type IV Hypersensitivity

A

TB, contact dermatitis

IMM Exam 2 (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions