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immuno/micro exam 2 > hypersensitivity- stiner > Flashcards

hypersensitivity- stiner Flashcards

1
Q

what is hypersensitivity?

A

Exaggerated or aberrant immune response to an antigen resulting in inflammation and tissue damage

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2
Q

what are hypersensitivity diseases?

A

Disorders that are caused by aberrant immune responses.

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3
Q

another name for Type 1 hypersensitivity is:

A

allergy, atopy, or immediate hypersensitivity

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4
Q

when does a type 1 hypersensitivity occur?

A

Occurs within minutes after reexposure to antigen/allergen.

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5
Q

what are the characteristics of a type 1 reaction?

A

Rapid IgE and mast cell mediated vascular and smooth muscle reaction

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6
Q

give examples of type 1 reactions

A

hives, hay fever, food allergies, bronchial asthma, anaphylaxis.

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7
Q

what is the first step in a type 1 reaction

A

Initial exposure to antigen and production of IgE antibodies (Ab) = Sensitization.

1) TH2 cells secrete IL’s
2) TH2 cell CD40L binds to B cell CD40

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8
Q

what is the second step in a type 1 reaction?

A

Binding of IgE Ab to Fc receptors on mast cells

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9
Q

what are the immediate and late responses of a type 1 hypersensitivity reaction

A

A) Immediate Effects
—Dilation of blood vessels, increased vascular permeability, smooth muscle contraction (immediate reaction).
B) Late Response
—Inflammation (late phase reaction).

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10
Q

Mast cell degranulation

A

Immediate Response

  • Vasoactive amines (histamine and serotonin) and proteases
  • Synthesis and secretion of lipid mediators (prostaglandins and leukotrienes made from arachidonic acid)
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11
Q

what are the 2 lipid mediators in type 1 reactions?

A

Prostaglandins and Leukotrienes

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12
Q

prostoglandins cause what to occur?

A

vasoconstriction in the lungs or dilation in vascular smooth muscle

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13
Q

leukotrienes are made by what process? what do they induce?

A
  • Made via the lipoxygenase pathway
  • powerful inducer of bronchoconstriction, increased vascular permeability, increased secretion and accumulation of mucus, and inflammatory cell infiltration into airways
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14
Q

what are the most common asthma signs and symptoms

A

coughing, wheezing and shortness of breath

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15
Q

what are the most common asthma triggers?

A

Airborne allergens, such as pollen, animal dander, mold, cockroaches and dust mites

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16
Q

during dust mite induced asthma, what enzyme cleaves the occludins in tight junctions?

A

Der P 1

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17
Q

what are the 2 main treatments for asthma?

A

1) Inhaled corticosteroids- These medicines are the most effective long-term control medicine
2) Leukotriene modifiers- These medicines help block the chain reaction that increases inflammation in your airways

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18
Q

what Determines the Type of IgE-mediated Allergic Rxn that occur?

A

the dose and route of entry

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19
Q

type 1 hypersensitivity key points

A

1) All clinical and pathologic features of immediate hypersensitivity reactions are driven by mediators produced by mast cells.
2) The most severe form of immediate hypersensitivity is anaphylaxis.

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20
Q

what is anaphylaxis

A

1) Response driven by the systemic release of vasoactive amines and lipid mediators from mast cells
2) Causes life-threatening drop in BP accompanied by severe bronchoconstriction
3) Treated with epinephrine (vasoconstrictor and bronchodilator) and antihistamine

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21
Q

what is type 2 hypersensitivity?

A

A) antibodies produced by the immune response that bind to antigens on our own cell surfaces
—Primarily IgG and IgM isotypes
B) host Ab binds foreign Ag on cell surfaces
or binds self Ag
C) can activate complement resulting in membrane attack complex formation
—leads to destruction of cells, inflammation, or interfere with normal cellular function

22
Q

what is Hemolytic Disease of the Newborn (Erythroblastosis fetalis)

A

Maternal Ab’s target fetal RBC’s for destruction

23
Q

what is Hemolytic anemia?

A

Auto-antibodies are produced against self Ag’s on the surface of RBC’s. This triggers the rapid destruction of RBC’s leading to anemia

24
Q

Grave’s Disease

A

TSH receptor Ab’s stimulate TSH receptor to over produce thyroid hormone

25
Q

Myasthenia Gravis

A

Ach receptor Ab’s bind to and block the Ach receptor

26
Q

strategies to treat type 2 diseases

A 
Autoimmune hemolytic Anemia
-Prednisone or blood transfusion
HDNB
-Anti-Rh Ab
Graves Disease
-Radioactive iodine, anti-thyroid drugs, or thyroid removal
Myasthenia Gravis
-cholinesterase inhibitors and corticosteroids
27
Q

type 2 summary

A

Host Ab binds foreign Ag on cell surfaces or binds self Ag

IgG

28
Q

type 3 hypersensitivity

A

1) Ag-Ab complexes clump and deposit in blood vessels or tissues attracting an acute inflammatory reaction.
2) An immune complex is a complex consisting of an Ag bound to its specific Ab

29
Q

examples of type 3 hypersensitivity

A

Systemic lupus, Arthus reaction, serum sickness, lupus nephritis, and rhematoid arthritis.

30
Q

What can cause type 3 hypersensitivity?

A

Can be caused by exogenous or endogenous Ag

31
Q

what are immune complexes?

A

aggregations of antigens and IgG and IgM antibodies

32
Q

where are deposits usually found in type 3?

A

generally accumulate at sites where antigen is localized or at sites of turbulence (vessel branches) or high pressure (kidney)

33
Q

Immune complexes trigger inflammation via three mechanisms

A
  1. Mast cell activation
  2. Macrophages release TNF-alpha and IL-1 that induce the inflammatory cascade.
  3. Cells bearing Fc receptors for IgG (or IgM) and IgE may be crucial for antibody complex mediated hypersensitivity
34
Q 
Arthus reaction
(type 3)
A

1) Triggered in the skin by IgG
2) Immune complexes form
3) Complexes bind Fc receptors on mast cells and other leukocytes

(Can occur as a result of repeated subcutaneous injections of tetanus toxoid)

35
Q

symptoms of Arthus reaction

A

Swelling, induration, severe pain, edema, hemorrhage, and occasionally by necrosis (which can lead to gangrene in extreme cases).
Usually occur within a few hours after exposure

36
Q

Serum sickness is a classic example of what?

A

transient systemic immune complex-mediated syndrome. (type 3 reaction)

37
Q

what causes serum sickness?

A

Caused by an injection of a foreign protein or proteins which leads to an antibody response.

1) Antivenin (serum from horses immunized with snake venoms)
2) Antibiotics

3) Streptokinase (a bacterial enzyme

38
Q

therapeutic treatments for type 3 hypersensitivity

A

Arthus Reaction
-Avoidance or anti-inflammatory agents
Serum Sickness
-Drug avoidance, antihistamines, corticosteroids, etc
Lupus
-NSAID’s, corticosteroids, immunosuppressive agents, etc

39
Q

type 3 summary

A

Type III Hypersensitivity/Immune-Complex mediated: Ag-Ab complexes clump and aggregate in or near blood vessels attracting an acute inflammatory reaction.
Primarily IgG (possibly IgM or IgE)
Immune complex
Ex. Arthus Rxn, serum sickness, and SLE

40
Q

type 4 hypersensitivity

A

mediated by Ag specific T cells which induce macrophage infiltration in a sensitized individual

41
Q

is type 4 hypersensitivity antibody mediated?

A

NO

mediated by Ag specific T cells which induce macrophage infiltration in a sensitized individual

42
Q

Generally, what initiates type 4 reactions?

A

Small molecules that must become bound to a larger carrier molecule in order to illicit an immune or inflammatory response

Th cells secrete cytokines with activate macrophages

43
Q

Tuberculin Test (Mantoux PPD test) determines what? which type of sensitivity does it rely on?

A

determine previous exposure/infection with Mycobacterium tuberculosis

uses type 4 sensitivity
-The response is mediated by TH1 cells and infiltrating macrophages and other inflammatory mediators, causing visible swelling

44
Q

Contact Dermatitis

A
  • hapten complexed with skin proteins and become internalized by APC’s in the skin
  • CD4 or CD8 T cells
  • Inflammation occurs as a result of the inflammatory response initiated by T cells
45
Q

what are the 2 phases of contact hypersensitivity?

A

sensitization and elicitation

46
Q

when does Sensitization occur? how long does it take? which cells play a pivotal role?

A

1) Occurs during first exposure to Ag
2) Takes 10-14 days (delayed response) to develop.
3) Langerhans’ cells in skin
- (APC of the skin) take up Ag and present to T cells.
4) Formation of CD4+ memory T cells specific for the Ag

47
Q

when does Elicitation occur? which cells produce cytokines?

A

Upon reexposure to Ag

Develops within 24-48 h.

Involves LC Ag presentation to memory T cells at site of Ag entry.

T cells release IFN-gamma & pro-inflammatory cytokines

48
Q

what is poison ivy an example of?

A

contact dermatitis

49
Q

chronic asthma- type 4 hypersensitivity

A

1) Mast cell degranulation leads to Th2 (IL-5) and eosinophil influx
2) Eosinophils activate and degranulate
3) Chronic inflammation can cause irreversible damage and death

50
Q

Granulomatous Inflammation/Crohn’s

Disease

A
  • type 4 reaction
  • Type of Inflammatory Bowel Disease (IBD) of the terminal ileum
  • Initial presentation may be in oral cavity and pharynx
51
Q

therapeutic treatments for type 4 hypersensitivity

A

TB Test injection
-Self limiting
Contact hypersensitivity
-Limit exposure, corticosteroids, antihistamines, etc..
Chronic Asthma
-Corticosteroids, bronchodilators, cromolyn, etc ..
Crohn’s Disease
-Corticosteroids, immunosuppressants, etc..

52
Q

type 4 hypersensitivity overview

A

-mediated by Ag specific T cells which induce macrophage infiltration in a sensitized individual.
-DTH response to injected or absorbed Ab
2-3 days
-Ex. TB test, contact dermatitis, chronic asthma, Crohn’s

immuno/micro exam 2 (7 decks)

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