Skin > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

(52 cards)

Study These Flashcards
1
Q

Type I hypersensitivity immune reactant

A

IgE

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

Hypersensitivity

A

An excessive immune response against foreign, often innocuous, antigens - which may result in tissue damage or death

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

Sensitization

A

The initial exposure to an antigen that primes the immune system to elicit a reaction to a subsequent exposure to that antigen

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

Allergen

A

Antigen that elicits immediate hypersensitivity

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

Allergy

A

A reaction caused by an allergen

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

Atopy

A

Familial predisposition (genetic) reaction to allergen

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

Cells involved in type I hypersensitivity

A

Mast cells, basophils, and eosinophils

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

Histamine

A

An amine derivative of histidine that is involved in vasodilation and increase capillary permeability

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

Where is histamine released from?

A

Exosomes; means immediate result (no transcription/translation)

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

What do mast cells and basophils release to mediate type I hypersensitivity reaction?

A
  • Histamines
  • Lipid mediators: Leukotrines and prostaglandins
  • Cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Leukotrienes function

A

Smooth muscle contraction, increase capillary permeability, and mucus secretion

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

Prostaglandins function

A

Vasodilation and increase capillary permeability, PMN recruitment

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

Cytokines involved in type I hypersensitivity with mast cells/basophils and their functions

A

TNF-alpha: proinflammatory cytokine

IL-4, IL-5, IL-13: Th2 response

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

Sensitization response

A
  1. ) Prior to the hypersensitivity reaction, the individuals must have been exposed to the allergen
  2. ) Prototypical immune response for adaptive immunology takes place
  3. ) Production of plasma cells that secrete allergen-recognizing IgE
  4. ) IgE associates with the Fc receptor (FcεRI) on mast cells and primes, or sensitizes it for quick activation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

2 phases of immediate reaction

A

Effector or elicitation phase and late-phase reaction

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

Effector/elicitation phase in immediate reaction

A
  1. ) Exposure to the antigen again is immediately recognized by the IgE-bound antibody on mast cells (crosslinking of the FcεRI receptors activate mast cells)
  2. ) Activation of mast cells result in degranulation and release of mediators (the vasoactive amines and lipid mediators result in the immediate reaction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Late-phase reaction in immediate reaction

A
  • Cytokines result in this a few hours after exposure
  • Few hours post exposure
  • Accumulation of PMNs, eosinophils, basophils, T helper cells, and their mediators
  • May occur without prominent immediate reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Immediate reaction in immediate hypersensitivity

A
  • Seconds to minute exposure
  • Histamine and lipid mediators increase vascular permeability
  • Wheal-and-flare response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Wheal

A

Redness and local swelling due to initial vessel dilation

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

Flare

A

Subsequent dilation promotes red rim

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

Chronic allergic inflammation

Study These Flashcards
A

repeated exposure that results in persistent inflammation – may alter tissue (asthma, eczema, hay fever)

22
Q

Immediate hypersensitivity anaphylaxis

Study These Flashcards
A

Systemic activation of mast cells (such as from a bee sting) can lead to severe anaphylaxis

23
Q

Anaphylaxis leads to…

Study These Flashcards
A

Widespread vascular permeability and fluid leaving blood, may cause BP to drop

24
Q

Clinical features of anaphylaxis

Study These Flashcards
A

Resp: nasal obstruction, increased mucus, dyspnea, wheezing
CV: hypotension, shock
Skin: urticaria, angioedema, pruritus, erythema
GI: pain, nausea, diarrhea
Hematological: thrombocytopenia, DIC

25
How does epinephrine counteract the disease state during anaphylaxis?
Vascular smooth muscle contraction, increased cardiac output, and inhibit mast cell degranulation
26
Hygiene hypothesis
- Allergy is on the rise in developed countries - Treg cells and IL-10 production capacity are low - skew towards Th2 response - IgE, IL-4, IL-5, IL-13
27
Function of chemokines in type I hypersensitivity
Recruit PMNs, monocytes, and macrophages
28
Late-phase reaction in immediate hypersensitivity
- Few hours post exposure - Accumulation of PMNs, eosinophils, basophils, T helper cells, and their mediators - May occur without prominent immediate reaction
29
Immediate hypersensitivity clinical responses
- Food/drug allergies (hives, anaphylaxis, flushing, angioedema) - Atopic dermatitis (eczema) - Atopic urticaria (hives) - Atopic rhinoconjunctivitis (allergic rhinitis, hay fever) - Asthma
30
Genetics of atopy (reaction to allergen)
MHCII, TCR-alpha, IL-4, FcεRI, and Th1/2 balance
31
IL-10 function
- Elevated in helminth infested individuals | - Blocks mast cell degranulation
32
Type I hypersensitivity diagnostics
- Application (skin prick or intradermal injection) of allergen in skin to visualize wheal and flare - Blood test to detect specific IgE (results take days)
33
Type I desensitization
To gradually decrease IgE-dominant response towards IgG or Treg response (IL-10)
34
Type II hypersensitivity
- Antibody mediated disease caused by anti-tissue antibody - Main antibody – IgG, IgM - Antibody targets tissues or extracellular matrix - 2 - 24 hours
35
Effector mechanisms of type II hypersensitivity
1. ) Opsonization and phagocytosis 2. ) Complement and Fc receptor-mediated inflammation 3. ) Abnormal physiologic response w/o injury
36
HDNB
Rh- mothers may carry an Rh+ fetus; fetal erythrocytes enter mother's circulation during childbirth and anti-Rh antibodies produced in the mother; subsequent pregnancies in which the fetus is Rh+ may result in fetal erythrocyte destruction due to IgG crossing placenta (RhIG administration w/i 72 hours after first Rh+ birth)
37
Type II hypersensitivity reactions
``` Blood transfusions Autoimmune hemolytic anemias Autoimmune thrombocytopenic purpura Goodpasture syndrome Pemphigus vulgaris Penicillin sensitivity (non allergic) Acute rheumatic fever ```
38
Grave's
receptor of thyroid gland targeted by TSI (triggers production of TSH); symptoms: irregular heartbeat, bulging eyes, anxiety, heat sensitivity, weight loss, goiter
39
Myasthenia gravis
- Autoantibody targets acetylcholine receptors - Blocks acetylcholine binding, resulting in defective neuromuscular transmission - Symptoms: muscle weakness, localized paralysis, strabismus (eye misalignment), ptosis (drooping eyelids), difficulty swallowing
40
Type III hypersensitivity
- Antibody mediated disease caused by immune complexes - Main antibody – IgG, IgM - Antibody targets soluble antigen - Hours, days, weeks
41
Effector mechanisms of type III hypersensitivity
- Immune complex formation (normally cleared by classical complement and phagocytes) - Certain immune complexes may get deposited on tissue - Phagocytes (PMNs) recognize antibody via Fc receptors and complement via CRs (receptors activate cells to secrete inflammatory mediators>>tissue inflammation and injury)
42
Most common sites of immune complex deposition
``` Small arteries (vasculitis) Renal glomeruli (nephritis) Joint synovium (arthritis) ```
43
Serum sickness
- Individuals w/ no prior exposure - Antitoxin administration from horse serum - Controls toxin but mounts response against horse antibodies - Symptoms: fever, weakness, rash, edema (7-21 days later)
44
Arthus reaction
- Localized form of type III hypersensitivity that causes vasculitis - Subcutaneous antigen is delivered to a previously immunized individual to that antigen - Antibody-antigen complexes form in the area of injection - Symptoms: inflammation, pain, and necrosis in severe cases
45
Type III hypersensitivity reactions
Systemic lupus erythematosus Polyarteritis nodosa Granulomatosis with polyangiitis (Wegener’s disease) Farmer’s lung
46
Type IV hypersensitivity
-Type IV hypersensitivity is also delayed type hypersensitivity (DTH) -Cell-mediated reaction Th1 Th2 CTL (CD8+) -2 days to weeks post exposure
47
Effector mechanisms of type IV
-Antigen processed by APC, -Th1 activated (IFN-gamma, macrophage activation and inflammatory mediators released)>>tissue damage -Th2 cells are activated IL-5 – Eosinophil activation and inflammatory mediators released>>tissue damage -Th17 cell are activated IL-17 – PMN recruitment and activation>>tissue damage -CTL activation – direct cytotoxicity of recognized MHCI-antigen
48
Basis of tuberculin/PPD/Mantoux test
- Individuals who have had Mycobacterium tuberculosis infection have produced memory CD4+ T cells to mycobacterial antigens - Exposure to PPD (tuberculin purified protein derivative) will activate these memory CD4+ T cells, release proinflammatory cytokines, and recruit macrophage, resulting in an indurated skin lesion 48-72 hours later
49
Allergic contact dermatitis
- skin inflammation including pruritic papules and vesicles on an erythematous base - Upon first contact with an allergen, sensitization may take 10 - 14 days (Langerhans cells (DCs)) - Subsequent contact = hours to days (T cell mediated) - most common chemicals that cause ACD are: - Nickel Preservatives, dyes, and fragrances - Chemicals in rubber gloves - Many are haptens
50
Poison Ivy
- ACD reaction - component of plant penetrates skin and associated with proteins in keratinocytes - Primary exposure: memory T cells - Secondary exposure: Th1, macrophage, and CTL cells target skin
51
Chronic DTH reactions
- Cell types involved derived from macrophages - Epithelioid cells - Multinucleated giant cells - Tissue damage due to size and location of granuloma - Granulomas often form in diseases with persistent antigen - Tuberculosis - Leprosy - Leishmaniasis
52
Type IV hypersensitivity reactions
``` Hashimoto thyroiditis Rheumatoid arthritis Type I Diabetes Celiac disease Crohn disease Multiple Sclerosis ```
Skin
flashcards
Decks in class (9)
# Cards
Brainscape helps you reach your goals faster, through stronger study habits.
© 2026 Bold Learning Solutions. Terms and Conditions