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SP14 Microbiology > EX2 Hypersensitivity - Stiner > Flashcards

EX2 Hypersensitivity - Stiner Flashcards

1
Q

This is an exaggerated or aberrant immune response to an antigen resulting in inflammation and tissue damage

A

hypersensitivity

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2
Q

This is caused by an intravenous route of entry (oral absorption) and results in edema, increased vascular permeability, tracheal occlusion, circulatory collapse, and death

A

systemic anaphylaxis

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3
Q

This is caused by through skin route of entry and results in local increase in blood flow and vascular permeability

A

acute urticaria (wheal-and-flare)

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4
Q

This is caused by inhalation and results in edema and irritation of the nasal mucosa

A

allergic rhinitis (hay fever)

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5
Q

This is caused by inhalation and results in bronchial constriction, increased mucous production, and airway inflammation

A

asthma

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6
Q

This is caused by oral aborption and results in vomiting, diarrhea, pruritis, urticaria, and anaphylaxis (rarely)

A

food allergy

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7
Q

This is often referred to as allergy, atopy, or immediate hypersensitivity

A

Type 1 hypersensitivity

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8
Q

Type 1 hypersensitivity occurs when

A

within minutes of RE-EXPOSURE to antigen/allergen

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9
Q

What is the immune response during a type 1 hypersensitivity reaction

A

rapid IgE and mast cell mediated vascular and smooth muscle reaction that is often followed by inflammation

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10
Q

True or False

The reaction of type 1 hypersensitivity depends on the route of allergen entry

A

True

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11
Q

True or False

Type 1 hypersensitivity is the most common disorder of the immune system, affecting 20% of the population

A

True

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12
Q

What is the sensitization step during type 1 hypersensitivity

A

it is the initial exposure to antigen and production of IgE antibodies
TH2 cells secrete ILs
TH2 cell CD40L binds to B cell CD40 (B cell activation)

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13
Q

What are the 6 steps to type 1 hypersensitivity

A
  1. sensitization
  2. binding of IgE Ab to Fc receptors on mast cells
  3. cross-linkning of bound IgE upon re-exposure (degranulation)
  4. release of mast cell mediators
  5. immediate effects (dilation of bv, etc.)
  6. late response (inflammation)
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14
Q

The release of mast cell mediators triggers what

A

a biphasic response

  1. immediate effects
  2. late response
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15
Q

During the immediate response of mast cell degranulation what is secreted/occurs

A 
vasoactive amines (histamine/serotonin) and proteases
synthesis and secretion of lipid mediators (prostaglandins and leukotrienes)
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16
Q

What three things do prostaglandins stimulate

A

vasoconstriction in the lungs (or dilation in vascular smooth muscle)
constriction or dilation of bronchioles
aggregation or disaggregation of platelets

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17
Q

During the late phase response of mast cell degranulation what is secreted/occurs

A

synthesis and secretion of cytokines and chemokines

leading to infiltration and eosinophils, monocytes, and neutrophils; leading to inflammation and tissue damage

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18
Q

What is the overview of type 1 hypersensitivity

A

IgE on surface of the cell with allergen triggers activation and production of cyotkines, histamines, and lipid mediators

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19
Q

What are some common triggers for asthma

A 
airborne allergens (pollen, dust mites, etc)
respiratory infections
physical activity
cold air
air pollutants
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20
Q

How many people suffer from asthma worldwide

A

235 million (22 million adults and 7 million children in the USA)

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21
Q

The dust mite allergen triggers asthma via which enzyme

A

Der p 1, it occludes tight junctions and triggers mast degranulation

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22
Q

What are some treatment strategies for asthma

A

inhaled corticosteroids

leukotriene modifiers

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23
Q

The dose and route of entry of allergens determine what

A

the type of IgE-mediated allergic reaction that results

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24
Q

This is a response riven by the systemic release of vasoactive amines and lipid mediators from mast cells causing a life-threating drop in blood pressure accompanied by severe bronchoconstriction

A

anaphylaxis

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25
How would you treat anaphylaxis
with epinephrine (vasoconstrictor and bronchodilator) and antihistamine
26
What events occur as a result of mast cell activation
mast cell degranulation synthesis and secretion of lipid mediators cytokine release (late phase)
27
This is when antibodies produced by the immune response bind to antigens on our own cell surfaces primarilay IgG and IgM
type II hypersensitivity
28
True or False | In type II hypersensitivity, host antibodies bind foreign Ag on cell surfaces or binds self Ag
True
29
What is the result of type II hypersensitivity
it can activate complement resulting in MAC formation | leading to the destruction of cells, inflammation, or interference with normal cell function
30
The target antigens of this disease are erythrocyte membrane proteins and platelet membrane proteins, of which causes opsonization/phagocytosis of them, and results in hemolysis, anemia, and bleeding
autoimmune hemolytic anemia | autoimmune thrombocytopenic purpura
31
The target antigen of this disease is the acetylcholine receptor which inhibits acetylcholine binding causing muscle weakness and paralysis
myasthenia gravis
32
The target antigen of this disease is thyroid stimulation hormone (TSH), causing stimulation of TSH receptors causing hyperthyroidism
Grave's disease
33
Type II hypersensitivity is also known as
cytotoxic hypersensitivity
34
In this disease, maternal antibodies target fetal RBCs for destruction
hemolytic disease of the newborn (erythoblastosis fetalis) (Rh factor)
35
In this disease, host anti-blood group antibodies, target transfused RBCs for destruction
blood transfusion reactions
36
``` What are the therapeutic strategies for autoimmune hemolytic anemia HDNB Grave's disease myasthenia gravis ```
prednisone or blood transfusion anti-Rh antibodies radioactive iodine, anti-thyriod drugs, thyroid removal cholinesterase inhibitors or corticosteriods
37
This is when Ag-Ab complexes (immune complex) clump and deposit in blood vessels or tissues attract an acute inflammatory response
type III hypersensitivity
38
What happens when immune complexes are large, and are small?
large ones fix complement and are cleared from circulation by phagocytes small complexes formed in Ag excess deposit in vessel or tissue
39
What are some examples of type III hypersensitivity
lupus, arthus reaction, serum sickness, and rheumatoid arthritis
40
When does type III hypersensitivity occur
3-10 hours after exposure | can be caused by exogenous or endogenous Ag (foreign/self)
41
Where does the immune complex accumulate
at the sites where antigen is localized or at sites of turbulence and/or high pressure (vessel branches, kidneys, etc.)
42
Type III hypersensitivity manifest as
vasculitis, arthritis, or nephritis
43
What are the three mechanisms of which immune complexes trigger inflammation
1. mast cell activation 2. macrophages release TNF-α and IL-1 which induces the inflammatory cascade 3. cells bearing Fc receptors for IgG/IgM/IgE
44
What is the Arthus reaction triggered by and what does it form
triggered in the skin by IgG, forms immune complexes of which bind to Fc receptors on mast cells and other leukocytes
45
Where does the Arthus reaction occur and as a result of what
occurs in vessel walls, pleura, pericardium, synovium, or glomeruli can occur as a result of repeated subQ inject of tetanus toxoid containing or dipthetia toxoid containing (rare) and upon subsequent exposure to an Ag for which a person has high circulating levels of IgG, complexes can be found in localized vasculature
46
What are the symptoms of an Arthus reaction
swelling, induration, pain, edema, hemorrhage, and occasionally necrosis occurs a couple hours after exposure
47
What is the treatment for Arthus reaction
anti-inflammatory
48
This is a classic example of transient systemic immune complex mediated syndrome
serum sickness
49
What causes serum sickness and what are the symptoms
an injection of a foreign protein or proteins which leads to an antibody response symptoms occur within days or weeks after injection; chills, fever, rash, etc.
50
What can specifically cause serum sickness
antivenum anti-lymphoyte globulin (immunosuppressant) antibiotics streptokinase (bacterial enzyme)
51
What is the mechanism behind SLE
IgG antibodies against self antigen in all nucleated cells | large amounts of small complexes deposit in blood vessels, kidneys, joints, and other tissues
52
What happen in SLE due to the immune cells
phagocytosis activated by Fc receptors auto-reactive T cells become involved damage can lead to death
53
What are the therapeutic strategies for Arthus reaction serum sickness lupus
avoidance and anti-inflammatories drug avoidance, antihistamines, corticosteriods, etc. NSAIDs, corticosteroids, immunosuppressive drugs, etc.
54
What is the overview of type III hypersensitivity
Ag-Ab complexes clump and aggregate attractive an inflammatory response primarily IgG immune complex
55
This is mediated by Ag specific T cells which induce macrophage infiltration in a sensitized individual
type IV hypersensitivity
56
How long does it take for type IV hypersensitivity to take place
2-3 days; due to it taking longer than antibody mediated
57
Turburculin type hypersensitivity is mediated by which type of cells (TB test)
Th1
58
contact dermatitis is mediated by which type of cells
Th1 and/or CTLs
59
chronic asthma is mediated by which type of cells
Th2
60
gluten-sensitive enteropathy is mediated by which type of cells
Th1 and Th2, but still poorly understood
61
graft rejection is mediated by which type of cells
T cells
62
Type IV hypersensitivity is also called what
delayed type hypersensitivity (DSH)
63
True or False | Type IV hypersensitivity is antibody mediated
False; it is cell mediated, mostly Th cells
64
What are the important cells in DTH response
macrophages CD8 T cells NK cells
65
Type IV hypersensitivity is generally initiated by what
haptens (small molecules) Ag presented by APCs activate Th cells Th cells secrete cytokines which activate macrophages
66
contact dermatitis involve this complexing with skin proteins and activating this
haptens (itching can push these further in skin) | elicited by CD4 and CD8
67
What are the two phases of contact hypersensitivity
sensitization and elicitation
68
When/Where does sensitization occur during type IV hypersensitivity
first exposure; 10-14 days | in the Langerhans cells, creation of CD4 memory T cells
69
When/Where does elicitation occur during type IV hypersensitivity
upon re-exposure, 24-48 hours presentation to memory T cells release of IFN-γ and pro-inflammartory cytokines inflammation
70
What is the mechanism of chronic asthma
mast cell degranulation leads to Th2 and eosinophil influx eosinophils activate and degranulate resulting in more eosinophils and tissue damage can cause irreversible damage and death
71
Granulomatous inflammation/Crohn's disease are which type of hypersensitivity
Type IV; thought to be due to unresolved DTH | initially presents in oral cavity
72
``` What are the therapeutic strategies for TB test contact hypersensitivity chronic asthma Crohn's disease ```
self-limiting limit exposure, corticosteroids, antihistamines, etc corticosteriods, bronchodilators, etc. corticosteriods, immunosuppressants, etc.
73
What is the overview of type IV hypersensitivity
cell mediated by Ag specific T cells which induce macrophage infiltration DTH response to injected or absorbed Ab 2-3 days

SP14 Microbiology (31 decks)

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