Brainscape's Knowledge GenomeTM

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


See full index

Immunology > Ch 15: Allergies, Hypersensitivities, and Chronic Inflammation > Flashcards

Ch 15: Allergies, Hypersensitivities, and Chronic Inflammation Flashcards

1
Q

What is the word origin, or etymology, for the word “allergy”?

A 
Allos = "other"
ergon = "reaction"
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What antibodies are involved in Type I Hypersensitivities?

A

IgE

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

Why was is so hard to research Type I hypersensitivities at first?

A

Free circulating IgE is usually very, very low in concentration in blood serum

Researchers discovered IgE-producing myeloma that released enough IgE to study efficiently (1967)

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

Most antigens that cause T1Hs are which biological macromolecule?

A

Proteins or glycoproteins, which possess many antigen sites per molecule (epitopes)

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

List some of the allergens responsible for type I hypersensitivities.

A 
Pollens
Drugs
Foods
Mold spores
Animal dander
Latex
Insect products
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some characteristics of T1H allergens?

A
  1. Intrinsic enzymatic proteins
  2. PAMPs
  3. Induced IgE-stimulating TH2 responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are intrinsic enzymatic proteins and how do they illicit a T1H response?

A

Proteins found in the Ags that have proteases and can break down epithelial layers, making it easier to introduce the antigen into the body

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

Type I hypersensitivity antigens can also be PAMPs. How does this effect one’s immune response?

A

The antigen that is a PAMP can stimulate innate immunity by binding to a cell’s PRR

The binding of these PAMPs can lead to TH2 responses (IgE production)

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

What is a Type I Hypersensitivity?

A

An immediate, vigorous response to antigen that is mediated by IgE antibodies (pollen & dust allergies)

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

What is a Type II Hypersensitivity?

A

An immediate, vigorous response to antigen that is mediated by IgG or IgM binding to host cells – followed by complement & cell-mediated destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a Type III Hypersensitivity?

A

An immediate, vigorous response to antigen that is mediated by antibody-antigen complexes – followed by complement

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

What is a Type IV Hypersensitivity?

A

A delayed, vigorous to antigen that is mediated by inappropriate T cell activation

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

What is the difference between immediate and delayed hypersensitivities?

A

Immediate - Happens within a very short time period
Generally, result of antibody-antigen interactions

Delayed - Takes hours/days to develop & manifest
Generally, result of T-cell reactions

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

Explain the mechanism behind the development of T1H.

A
  1. Person is exposed to antigen, antigen is expressed on B cell surface, TH2 cells are activated, which then tells B cells to become IgE plasma cells
  2. IgE Abs are secreted and bind to FCERs (receptors on granulocytes for IgE C region)
  3. Allergen is introduced a second time, binds to FCER/IgE complex, inducing degranulation (histamine, heparin, proteases)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the signs a symptoms of T1H?

A

Increase vasodilation to promote recruitment of immune cells to the site

Directly damage parasite through release of reactive compounds

We see inflammation and smooth muscle spasms, with resulting edema, rashes, difficulty breathing, etc.

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

What molecule is a primary inflammatory mediator?

A

Histamine

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

What molecules are secondary inflammatory mediators?

A

Prostaglandins and leukotrienes

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

How does histamine contribute to the signs and symptoms of T1H?

A

First, histamine binds to histamine receptors on mast cells (H1-H4), and each site had a different response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens when histamine binds with H1 receptor?

A

H1 binding = most biological effects (intestinal & bronchial smooth m. constriction, vasodilation, mucous secretion)

20
Q

What happens when histamine binds with H4 receptor?

A

H4 binding = promotes chemotaxis to site of infection, so it induces inflammation at sites of infection/allergy

21
Q

How do prostaglandins and leukotrienes contribute to the signs and symptoms of T1H?

A

Leukotrienes and prostaglandins are synthesized AFTER histamine release, produced by mast cell degranulation.

They are the major causes of bronchospasms and mucus build-up in asthma sufferers.

22
Q

List the cytokines released during a T1H response.

A 
IL-4
IL-3,
IL-5
IL-8
GM-CSF
23
Q

What are the functions of IL-4 and IL-3 in T1Hs?

A

Stimulate TH2 responses to increase IgE production by B cells

24
Q

What is the function of IL-5 in T1Hs?

A

Recruits and activates eosinophils

25
Q

What is the function of IL-8 in T1Hs?

A

Acts as chemotactic factor, attracting other cells

26
Q

What is the function of GM-CSF in T1Hs?

A

Stimulates production and activation of more myeloid cells, including more granulocytes

27
Q

What happens in Early (phase I) T1H response?

A

Early T1H occurs within minutes to allergen. In early, we see mast cell contents heavily involved due to dengranulation (histamine, leukotrienes, prostaglandins)

28
Q

What happens in Late (phase II) T1H response?

A

Responses occur hours later, a result of recruited cells

Often inflammatory cell types such as neutrophils

29
Q

List the 3 types of Type I hypersensitivity.

A
  1. Systemic anaphylaxis
  2. Localized reactions
  3. Food allergies
30
Q

What are the allergens and symptoms of systemic anaphylaxis in T1Hs?

A

Allergens= Injected or gut-absorbed; insect venom, drugs (penicillin), foods (peanuts, shellfish)

Symptoms= Anaphylactic shock (drop in BP), smooth muscle contraction (defecation, urination, bronchiolar constriction)

31
Q

What are the allergens and symptoms of localized reaction in T1Hs?

A

Allergens= Pollen, pet dander, dust, feathers; causing allergic rhinitis, allergic asthma, atopic dermatitis

Symptoms= Tearing, runny nose, sneezing, coughing

32
Q

What are the allergens and symptoms of food allergies in T1Hs?

A

Allergens: Water soluble glycoproteins that can withstand internal environment; milk, eggs, peanuts, soy, wheat, fish, shellfish, etc.

Symptoms: Vomiting, diarrhea (smooth m. constriction), oral hypersensitivity (tingling, angioedema of lips, palate, & throat), anaphylaxis if mast-cell degranulation makes it into the blood.

33
Q

Why does an EpiPen work to halt anaphylaxis?

A

It counteracts the effects of histamine and leukotrienes by increasing sympathetic outflow. It diminishes smooth muscle contraction, increases airway (bronchodilation), reduces vascular permeability, increases HR.

34
Q

What types of gene products are implicated in a genetic cause of type I hypersensitivities?

A

Proteins of:

  1. Immune responsiveness
  2. Epithelial barrier integrity
  3. Activating allergic responses
35
Q

How does over-expression of proteins involved in immune responsiveness lead to allergies?

A

When over-expressed, these proteins can cause allergic reactions due to the HIGH immune response or cytokine release

Innate immunity and cell communication is working overtime, and not to our benefit

36
Q

How does under-expression of proteins involved in maintenance of epithelial barrier integrity lead to allergies?

A

If we don’t have a good barrier, more Ags can get through and cause immune response

We lack growth factor and proteolytic enzymes to strengthen the barrier and break down allergens

37
Q

How does over-expression of proteins involved in activating allergic responses lead to allergies?

A

More GFs and more FCER binding mean more genes that code and transcribe into allergy responding proteins.

38
Q

What types of environmental triggers can increase or decrease an individual’s risk for developing allergies?

A
  1. Air pollution and early exposure of antibiotics (increase risk)
  2. Diet (increase risk)
  3. Bacterial/diverse microbe exposure (decrease allergy risk from early exposure)
    o Stonger and balanced TH responses
39
Q

Summarize the principle behind skin testing in allergy identification.

A

The test is performed by injecting very small amounts of different allergens on a patient’s back or forearm to observe swelling and redness. If these two results appear, it’s indicative of an allergic response to those allergens. The swelling is caused by local mast cell degranulation.

40
Q

How do antihistamines, leukotriene antagonists, inhalation corticosteroids treat allergic reactions?

A

Antihistamines – bind and block H1 receptors on target cells

Leukotriene antagonists – similar to antihistamines

Inhalation corticosteroids – Inhibit innate immune cell activity in airways (Tx for asthma)

41
Q

How do medications that reduce allergic asthma and anaphylaxis treat allergic reactions?

A

By using epinephrine or epinephrine antagonists (albuterol)

i. Block degranulation of mast cells (anaphylaxis)
ii. Counter bronchoconstriction (asthma)

42
Q

How do immunotherapeutics treat allergic reactions?

A

Anti-IgE antibodies bind to IgE and inhibit IgE binding to FCR

43
Q

How does Desensitization/Immunotherapy treat allergic reactions?

A

Tx by repeated exposure of gradually increasing doses of allergen (up to 3 years Tx)

i. Via injections, skin/tongue application

44
Q

Explain what makes up human blood groups.

A

Human blood groups are determined based on the carbohydrate antigens they have on their blood cells.

Also, humans produce Abs to the blood type they do NOT have.

45
Q

Why do we make antibodies for blood groups that are not our own, even if we haven’t been exposed to blood belonging to those groups at some point in our lives?

A

These antibodies are similar to carb antigens on microbes. As we are exposed to those bacteria with the similar carb antigens, we develop those anti-B or anti-A antibodies bc those bacteria antigen are seen as foreign.

46
Q

True or False:

Type II Hypersensitivities are mediated by antigens.

A

False; they are antibody-mediated

47
Q

What is an example of type II hypersensitivity?

A

Blood transfusion reactions

Immunology (5 decks)

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