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Immunology final exam > Hypersensitivity > Flashcards

Hypersensitivity 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

IgE is really responsible for a lot of allergic reactions. Check out slide 5 of the lecture for a table to know

A

okay

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3
Q

In order for type I hypersensitivity to occur, what must happen first?

A

A prior exposure to the allergen must have happened for hypersensitivity to occur.

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4
Q

What is the initial exposure to an antigen and subsequent production of IgE called?

A

Sensitization

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5
Q

IgE is made in response to some cytokines. What does IgE bind to that causes the hypersensitive reaction?

A

IgE binds to mast cells, which degranulate and cause a bisphasic response

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6
Q

What are the immediate and late effects of mast cell degranulation (release of mediators)?

A

Immediate effects: dilation of blood vessels, increased vascular permeability, and smooth muscle contraction
Late effects: inflammation

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7
Q

What do prostaglandins do?

A

Vasoconstriction in the lungs

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8
Q

What do leukotrienes do?

A

bronchoconstriction and increased vascular permeability

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9
Q

What is contained in the granules released by eosinophils?

A

ROS
major basic protein
prostaglandins and leukotrienes

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10
Q

What are the most common signs/symptoms of asthma?

A

coughing, wheezing, and shortness of breath

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11
Q

What are some common asthma triggers?

A 
airborne allergens like pollen, animal dander, mold, cockroaches, and DUST MITES
respiratory infections
physical activity
cold air
air pollutants
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12
Q

What do ITAMs do?

A

They activate map kinase

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13
Q

What enzyme do dust mites have that cleaves the tight junctions of respiratory epithelium? Then what happens?

A

It’s called Der p1 and it cleaves the occludin protein

Then the dust mite gets taken up by an APC and the specific IgE binds a mast cell and degranulation takes place

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14
Q

During asthma, mucous is produced and muscles often become thickened, but constricting the airways

A

indeed

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15
Q

What are two treatment strategies for asthma? What do they do?

A

Inhaled corticosteroids- relieve airway inflammation and swelling
Leukotriene modifiers-help block the chain reaction that increases inflammation in the airways

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16
Q

T/F the dose and routes of entry of allergens determine the type of IgE mediated allergic reaction that results

A

true

17
Q

What is an example of a wheel and flare reaction?

A

A hive

18
Q

When a mast cell degranulates, what molecule is responsible for vascular leakage?

A

histamine

19
Q

When a mast cell degranulates, what molecule is responsible for intestinal hypermotility?

A

lipid mediators

20
Q

When a mast cell degranulates, what molecule is responsible for tissue damage?

A

enzymes

21
Q

When a mast cell degranulates, what molecule is responsible for inflammation?

A

cytokines

22
Q

T/F all clinical and pathological features of immediate hypersensitivity reactions are driven by mediators produced by B cells?

A

False- mediators produced by mast cells

23
Q

What is the most severe form of immediate hypersensitivity?

A

Anaphylaxis

24
Q

An anaphylactic reaction is driven by the systemic release of what?

A

vasoactive amines (histamines) and lipid mediators from mast cells

25
Q

Why is anaphylaxis so deadly?

A

It causes a life-threatening drop in BP and is accompanied by severe bronchoconstriction

26
Q

How is anaphylaxis treated?

A

epinephrine and antihistamine injection

27
Q

Cytokine release recruits what to where?

A

eosinophils and neutrophils to the site of inflammation

28
Q

What is type II hypersensitivity?

A

Where antibodies produced by the immune system bind to antigens on our own cell surface or bind self antigens and can activate the complement cascade and kill our cells

29
Q

What happens in hemolytic disease of the new born?

A

Maternal antibodies target fetal RBCs for destruction

30
Q

What happens in hemolytic anemia?

A

Auto-antibodies are produced against self antigens on the surface of RBCs. This triggers the rapid destruction of RBCs, leading to anemia

31
Q

What happens in hemolytic disease of the new born?

A

Maternal antibodies target fetal RBCs for destruction (opsinization of RBC’s)

32
Q

What happens in hemolytic anemia?

A

Auto-antibodies are produced against self antigens on the surface of RBCs. This triggers the rapid destruction of RBCs, leading to anemia (opsinization of RBC’s)

33
Q

What happens in graves disease?

A

TSH receptor antibodies stimulate TSH receptor to over produce thyroid hormone

34
Q

What happens in myasthenia gravis?

A

Ach receptor antibodies bind to and block the Ach receptor

35
Q

What is type III hypersensitivity?

A

Ag-Ab complexes clump and deposit in blood vessels or tissues attracting an acute inflammatory reaction

36
Q

In type III hypersensitivity, what happens to larger and smaller complexes/aggregates?

A

Larger aggregates are cleared from the circulation by phagocytes
Smaller complexes formed in Ag excess are deposited in blood vessels or tissue

37
Q

How quickly does type III hypersensitivity occur?

A

3-10 hours

38
Q

What are the three ways that immune complexes trigger inflammation?

A
  1. Mast cell activation
  2. Macrophages release TNF-alpha and IL-1 that induce the inflammatory cascade
  3. C3a, C4a, and C5a stimulate mast cells to release more histamine, serotonin and chemotactic factors-also attracts monocytes, neutrophils, and other leukocytes

Immunology final exam (7 decks)

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