Brainscape's Knowledge GenomeTM

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


See full index

Found. of Path. Processes - Block 1 > 7 - Hypersensitivity > Flashcards

7 - Hypersensitivity Flashcards

1
Q

What is hypersensitivity?

A

Harmful immunologic reaction developing in response to an otherwise harmless specific trigger

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

What is an Arthus reaction? What type of hypersensitivity reaction is this?

A

Skin rxn when sensitized people re-exposed to specific antigen

Causes hemorrhage/edema in 4-10 hrs, necrosis of the skin

Common after vaccination in pattients recently vaccinated (with high IgG titers already)

Type III hypersensitivity rxn

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

What is serum sickness?

A

Human immunization with serum of immunized horess triggered illness a week later:

  • joint pain
  • swelling
  • fever
  • malaise
  • rash
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

The word allergic and ____ are used interchangably.

A

Atopy.

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

What are the types of hypersensitivities as defiend by the Cell and Coombs framework? How is each mediated?

A

Type 1: immediate Allergy, IgE mediated

Type 2: direct antiBody mediated cytolytic

Type 3: immune Complex mediated

Type 4: Delayed type, T cell mediated

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

What are the two mechanisms of hypersensitivity shared by all four types of reactions?

A

1. Sensitization stage - development of immune response, symptoms silent, requires adaptive immnuity (antigen-specific T and B cell response)

2. Effector stage - secondary immune response, symptoms evident

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

What cells mediate the initial phase of anaphylaxis during a Type 1 hypersensitivity reaction?

A

Mast cells: tissue resident, (formed in BM)

Basophils: circulating and tissue residents

Both work as innate immune cells that wait for their trigger

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

What happens in a type I hypersensitivity reasion when an antigen triggers mast cells/basophils?

A

IgE cross-linking occurs causing rapid degranulation!

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

What occurs in the sensitization phase of a type 1 hypersensitivity reaction?

A
  1. BCR on naive B cell bind the venom protein
  2. Venom protein preocessed by APC and presented to CD4+ cell
  3. The naive CD4+ T helper cell matures into a Th2 oriented antigen specific cell and produces cytokines that support Bcell class switchign to IgE
  4. B cell and plasma cell make IgE
  5. Circulating IgE bind slong term onto FcgammaRI on mast cells and basopihls

*Remember this is clinically silent*

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

What occurs during the effector phase of a type 1 hypersensitivity reaction (after the second bee-sting)?

A
  1. Venom protein crosslinks anti-bee IgE already boudn to FCepsilonRI on mast cells/basophils
  2. Crosslinking triggers rapid release of preformed mediators
  3. Symptoms of anaphylaxis occur immediately
  4. Hours later, delayed phase symptoms develop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are FCepsilonRI receptors? Where are they found?

A

High affinity IgE receptors constituitively expressed on mast cells and basophils.

Allergen comes in and cross-links receptors, causing phosphorylation, signal transduction, and intracellular signaling.

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

What results from the intracellular signaling cascade initiated by the FCepsilonRI receptor in a type 1 hypersensitivity reaction?

A
  1. Degranulation: release of preformed mediators
  2. Leukotrienes made: takes a little longer
  3. Cytokines: longest because it requires transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What preformed mediators are released in a type 1 hypersensitivity reaction? How long does this take and what is the result?

A

Histamine, neutral proteases such as tryptase, proteoglycans such as heparin

  • cause vascular dilation, smooth muscle contraction, and tissue damage.

Takes seconds to minutes.

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

What is released in the minutes-hours during a type I hypersensitivity reaction? What is the result?

A

Platelet-activiting factors (PAF), prostaglandins (PGD2), and leukotrienes

  • causes vascular dilation and smooth muscle contraction

**basophils don’t make tryptase or PGD2

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

What is released in hours-days during a type I hypersensitivity reaction? What is the result of this?

A

Cytokines - takes awhile becasue it relies on transcription.

Causes inflammation through leukocyte recruitment.

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

What is anaphylaxis and what are signs and symptoms?

A

Systemic Type I hypersensitivity syndrome

  • swelling of conjunctive
  • light headedness
  • confusion
  • headache
  • fast or slow HR
  • low BP
  • hives, flushing, itchiness
  • abdominal cramping
  • vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What physiologic changes occur during anyphylaxis (type I hypersensitivity rxn)?

A

Leaky/dilated blood vessels: angioedema, low BP, shock

Cardiac effects: myocardial depression, tachy/bradycardia

Smooth muscle spasm: bronchospasm, GI/GU tract spasm, coronary spasm

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

What is the most important preformed mediator involved in a type I hypersensitivity reaction? What are its receptors and the associated symptom when it binds?

A

Histamine! Short lived in the serum (gone in minutes)

Receptors:

  • H1R: itching, incerased vasc. perm (edema), smooth muscle contraction
  • H2R: gastric acid secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What releases tryptase during a type I hypersensitivity reaction? What are the different types and when are they released? How long does it last in serum?

A

Tryptase released from mast cells NOT basophils

Immature: constit. released (a and b protryptase)

Mature: only released when degranulation (b tryptase)

Lasts up to 4 hours in serum.

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

What is the best clinical indicator of mast cell activation? What is the purpose of this?

A

Tryptase; leads to remodeling of connective tissue matrix

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

Other than tryptase, what are other preformed mediator enzymes released during a type I hypersensitivity rxn? What is their function?

A

Proteases such as chymases, cathepsin G, and carboxypeptidases.

Degrade toxins and lead to connective tissue remodeling.

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

Which cytokines are rapidly synthesised during a type I reaction? What is the function of each?

A

IL-1 and IL-3: associated with Th2 and promote Bcell class switching

IL-3, IL-5, and GM-CSF: promote survival and activate eosinophils

TNF-alpha: activates endothelium and leads to adhesion molecule expression.

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

What chemokines are rapidly synthesized during a type I reaction? What is the function of each?

A

MIP-1a (CCL3): chemotactic for monocytes, macrophages, neutrophils, T cells, and eosinophils

RANTES (CCL5) and Eotaxin (CCL11): chemotactic for T cells and eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What lipid mediators are rapidly synthesized during a type I reaction? What is the function of each?

A

Cysteinyl leukotrienes (LTC4, D4, E4): leads to eosinophil migration, smooth muscle contraction, vascular permeability, and mucus secretion

Platelet activiating factor (PAF): attracts/activates eosinophils, activates PMNs adm platements, and increases lipid mediator production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Most atopic (allergic) diseases have _______-induced recruitment and associated pathology. This cell type has crystalloid granules that contain __________.

A

Eosinophil

Major basic protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the function of major basic protein?

A

MAst cell activation, helminthotoxic, and core protein.

27
Q

What major mediators do eosinophils have?

A
  1. Major basic protein
  2. Eosinophilic cationic protein (same as MBP)
  3. Lysophospholipase
  4. Eosinophil derived neurotoxin (EDN)
  5. Platelet activating factor (PAF): bronchoconstriction
  6. LTC4 (leukotrience C4): bronchoconstriction, mucus secretion
28
Q

What is the importance of IL-5 in a type I hypersensitivity reaction? Why is it important clinically?

A

Produced by Th2 CD4+ cells; In vivo causes hypereosinophilic syndrome and incases fluids frmo allergic late phase reactions.

Important clinically to make anti-IL5 antibodies.

29
Q

What effect do corticosteroids have on eosinophils?

A

Binds glucocorticoid receptor which goes to nucleus to inhibit AP-1 and NFkB

Inhibits production of IL-5 via decreased release from marrow and rapid apoptosis.

**steroids seem to make eosinophils disappear!

30
Q

What are three examples of type I hypersensitivity reactions?

A
  1. Allergic rhinitis
  2. Drug*, food, venom, and allergies
  3. Asthma* (reversible airway obstruction)

*not all cases are due to or triggered by teyp I hypersensitivity or allergen

31
Q

What are two disorders of mast cells?

A
  1. Urticaria/angioedema (hives/swelling)
    * contact (dog licking) or chronic (autoimmune, direct activation)
  2. Mastocytosis (increased MC burden)
    * spontaneous anaphylaxos, osteoporosis, chronic diarrhea
32
Q

How do you clinically confirm sensitization for type I hypersensitivity?

A
  1. Prick/scratch test: first line that balances sensitivity/specificity
  2. Intradermal testing: 1000x more sensitive, never used on foods
  3. Serum IgE ELISA: tests serum for specific IgE
33
Q

How do you clinically manage type I hypersensitivity?

A
  1. Avoid known allergies
  2. Suppression of mediators: nasal steroid, oral antihist, nasal mast cell inhibitors
  3. Immunotherapy (allergy shots): SubQ of sublingual
34
Q

What is the prevelance of asthma and what are sommon symptoms?

A

Reversible airway obstruction that effects 5% of population

Symptoms: non-productive cough, wheezing, shortness of breath, and chest tightness.

35
Q

What are basic (first choice) treatments for asthma? What doesn’t work?

A
  • Trigger avoidance
  • Corticosteroids (Apoptose eosinophils)
  • Bronchodilators: short-acting B-agonists (albuterol)

Antihistamines ineffective

36
Q

What are some second-line treatments for asthma?

A
  • Anti-leukotrienes: Montelukast
  • Biologics: omalizumab
  • Immunotherapy: SCIT SubQ allergy shots
  • Long acting B-agonists (LABA) - only given with inhaled steroids too
37
Q

What are characteristics of a type II hypersensitivty reaction?

A

Antibody (IgG or IgM) binds cell or matrix bound antigen.

Bound Ab to antigen leads to:

  • future immunologic attack and/or
  • functional interference (inhibition or activation)
38
Q

What are the four types of type II hypersensitivity?

A
  1. Complement activation
  2. Antibody dependent cellular cytotoxicity (ADCC)
  3. Phagocytosis (opsonization)
  4. Antibody alteration of normal function (anti-receptor_
39
Q

Type II hypersensitivity reactions are usually _____ or ______. Name a few examples.

A

Infectious or autoimmune.

Exp: goodpasture syndrome, bullous pemphigold, pernicious anemia, vasculities, thrombotic phenomena, and acute rheumatic fever.

40
Q

What type of hypersenvitity reaction is drug-induced hemolytic anemia/thrombocytopenia? What occurs?

A

Type II

Medicien becomes antigenic when bound to RBCs or platelets and IgG may target the drug-cell antigen (hapten formation)

Antibody tagged RBCs/platelets are targets for destruction (ADCC) in the spleen.

41
Q

Fetal Rh incompatibilityl is an example of a type II hypersen. reaction. What occurs in this disease? How would you prevent this?

A
  1. Rh neg mother becomes sensitized againt Rh factor from fetus and developes IgG against fetal Rh antigen.
  2. Next pregnancy, mom anti-Rh IgG crose placenta and tags fetal RBC
  3. Fetal RBC destruction leads to hydrops/stillbirth from severe anemia

Treat mom with anti-Rh antibody to prevent disease

42
Q

What is a type III hypersensitivity reaction? What occurs?

A

Immune complex mediated reaction.

IgG targeted against a soluble foreign antigen forms a large polymeric immune complex

  • may be cleared by mononuclear-phagocyte system.
  • Certain cases can trigger self injury
43
Q

What is the “zone of equivalence” for type III hypersensitivity reactions?

A

Immune complex formation is promoted in a range where the ratio of antigen to antibody is closer to 1:1. This is the “perfect storm” scenario.

44
Q

In type III reactions, how do immune complexes trigger injury?

A
  1. Activate FcYR expressing phagocytic cells (proinflammatory)
  2. Activating complement at sites of deposition

IC deposit in preferential sites where they get stuck and cause inflammation

  • kidneys, vessels, joints, skin
  • sites of high antigen concentration
45
Q

What is serum sickness? What type of reaction is this?

A

Type III hypersensitivity rxn

Systemic reaction following large quant. of foreign protein usually from animals.

  • Flu like symptoms with rash, arthritic, and glomerulonephritis
  • Onset 7-10 days, with more rapid onset with subsequent exposure
46
Q

NAme some exogenous and endogenous sources of “foregin” antiben in type III hypersensitivity reactions?

A

Exogenous: infectious agents like streptocicci, hepB, or plasmodium; drugs or chemicals like foreign serum or heroin.

Endogenous: nuclear antigens, immunolglobulins, tumor antigens

47
Q

What type of immune response does SLE represent? Why would someone with systemic lupus erythematosus (SLE) develop disease in the lungs and kidneys?

A

SLE represents a type III immune response due to the antibody complex and complement activation (with some type IV components too).

These sites are favorable for immune complex deposition.

48
Q

What are the characteristics of a type IV hypersensitivity reaction?

A

Cell-mediated, delayed type involved T cells (CD4+ and/or CD8+)

Antigen binds to self-proteins to create haptenated self-protein (which then looks foreign to the immune system) and is processed by APCs and presented to T cells.

49
Q

When happens in a type IV reaction when a haptenated protein is presented to a T cell by an APC?

A

T cells proliferate and secrete mediators:

  • IFNg: induces expression of adhesion molecules and activates mø
  • TNFa and LT (lymphotoxin): causes local tissue destruction and induces expression of adhesion molecules
  • IL-3 and GM-CSF
  • Chemokines that recruit macrophages
50
Q

What is allergic contact dermatitis an example of? What occurs?

A

Type IV hypersensitivity

Haptens bind to self-proteins (haptenization) creting a foreign protein presented to APC and recognized by TCRs.

Triggers mø mediated inflammation

51
Q

What are some common sensitizers that cause allergic contact dermatitis (type IV hypersensitivity rxn)?

A

Poison ivy (rhus dematitis) caused by allergen pentadecacatechol (urushiol)

  • Formaldehyde
  • Methacrylates
  • Nickel, gold, cobalt
  • Fragrances
  • preservatives
  • Rubber accelerators
52
Q

How are sensitizers to allergic contact dermatitis confirmed? How are they treated?

A

Confirmed by patch testing

Treated with topical corticosteroids.

53
Q

What is an example of intradermal diagnostic testing for a type IV hypersensitivity? What is the speed of this?

A

Tubreculin (PPD) skin test: screening for sensitization to TB

Slow to test positive: 24-72 hours

54
Q

How does patch testing work for type IV hypersensitivities? How long does it take?

A

Adhesive patches with sensitizer applied to skin, interpreted after 2-3 days and 1 week.

Slow to test positive.

55
Q

Descibe the reactor, antigen, and effector mechanism of a type I hypersensitivity? What are examples?

A

Reactor: IgE

Antigen: soluble

Effector: mast cell activation

Examples: allergic rhinitis, asthma, anaphylaxis

56
Q

Descibe the reactor, antigen, and effector mechanism of a type II hypersensitivity? What are examples?

A

Reactor: IgG or IgM

Antigen: cell or matric associated

Effector mechanism: FcR+ cells (phagocytes and NK)

Examples: penicillin induced thrombocytopenia

57
Q

Descibe the reactor, antigen, and effector mechanism of a type III hypersensitivity? What are examples?

A

Reactor: IgG

Antigen: soluble, large quantities in a 1:1 ratio

Effector mechanism: macrophage activation

Examples: serum sickness, arthus reactoin

58
Q

Descibe the antigen and effector mechanism of a type IV hypersensitivity that uses Th1 cells as a reactor? What are examples?

A

Antigen: soluble

Effector mechanism: macrophage activation

Examples: contact dermatitis, tuberculin skin test

59
Q

Descibe the antigen and effector mechanism of a type IV hypersensitivity that uses CD8+ cells as a reactor? What are examples?

A

Antigen: cell associated

Effector mechanism: cytotoxicity

Examples: contact dermatitis

60
Q

What is the mechanism of allergic contact sensitivity (type IV)?

A
  1. Sensitizing agent penetrates skin and binds self-protein to be taken up by cells.
  2. Cells present self peptides hapenated with contact-sensitiving agent to Th1 cells which secrete IFN-Y
  3. Activated keratinocytes secrete cytokines (IL-1, TNFa) and chemokines (IL-8, IP-9, and MIG) which activate macrophages to secrete mediators of inflammation
61
Q

What is anergy? What are examples?

A

Ignorance or failure to clear harmful self/foreign antigens

Examples: cancer, HIV, TB

62
Q

What is autoimmunity and what are examples?

A

Reactivity to self antigens

Examples: lupus, rheumatoic arthritis, thyroiditis, MS

63
Q
A

Found. of Path. Processes - Block 1 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions