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SP14 Microbiology > EX2 Hypersensitivity - Stiner > Flashcards

EX2 Hypersensitivity - Stiner Flashcards

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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
Q

How would you treat anaphylaxis

A

with epinephrine (vasoconstrictor and bronchodilator) and antihistamine

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26
Q

What events occur as a result of mast cell activation

A

mast cell degranulation
synthesis and secretion of lipid mediators
cytokine release (late phase)

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27
Q

This is when antibodies produced by the immune response bind to antigens on our own cell surfaces
primarilay IgG and IgM

A

type II hypersensitivity

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28
Q

True or False

In type II hypersensitivity, host antibodies bind foreign Ag on cell surfaces or binds self Ag

A

True

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29
Q

What is the result of type II hypersensitivity

A

it can activate complement resulting in MAC formation

leading to the destruction of cells, inflammation, or interference with normal cell function

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30
Q

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

A

autoimmune hemolytic anemia

autoimmune thrombocytopenic purpura

31
Q

The target antigen of this disease is the acetylcholine receptor which inhibits acetylcholine binding causing muscle weakness and paralysis

A

myasthenia gravis

32
Q

The target antigen of this disease is thyroid stimulation hormone (TSH), causing stimulation of TSH receptors causing hyperthyroidism

A

Grave’s disease

33
Q

Type II hypersensitivity is also known as

A

cytotoxic hypersensitivity

34
Q

In this disease, maternal antibodies target fetal RBCs for destruction

A

hemolytic disease of the newborn (erythoblastosis fetalis) (Rh factor)

35
Q

In this disease, host anti-blood group antibodies, target transfused RBCs for destruction

A

blood transfusion reactions

36
Q 
What are the therapeutic strategies for
autoimmune hemolytic anemia
HDNB
Grave's disease
myasthenia gravis
A

prednisone or blood transfusion
anti-Rh antibodies
radioactive iodine, anti-thyriod drugs, thyroid removal
cholinesterase inhibitors or corticosteriods

37
Q

This is when Ag-Ab complexes (immune complex) clump and deposit in blood vessels or tissues attract an acute inflammatory response

A

type III hypersensitivity

38
Q

What happens when immune complexes are large, and are small?

A

large ones fix complement and are cleared from circulation by phagocytes
small complexes formed in Ag excess deposit in vessel or tissue

39
Q

What are some examples of type III hypersensitivity

A

lupus, arthus reaction, serum sickness, and rheumatoid arthritis

40
Q

When does type III hypersensitivity occur

A

3-10 hours after exposure

can be caused by exogenous or endogenous Ag (foreign/self)

41
Q

Where does the immune complex accumulate

A

at the sites where antigen is localized or at sites of turbulence and/or high pressure (vessel branches, kidneys, etc.)

42
Q

Type III hypersensitivity manifest as

A

vasculitis, arthritis, or nephritis

43
Q

What are the three mechanisms of which immune complexes trigger inflammation

A
  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
Q

What is the Arthus reaction triggered by and what does it form

A

triggered in the skin by IgG, forms immune complexes of which bind to Fc receptors on mast cells and other leukocytes

45
Q

Where does the Arthus reaction occur and as a result of what

A

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
Q

What are the symptoms of an Arthus reaction

A

swelling, induration, pain, edema, hemorrhage, and occasionally necrosis
occurs a couple hours after exposure

47
Q

What is the treatment for Arthus reaction

A

anti-inflammatory

48
Q

This is a classic example of transient systemic immune complex mediated syndrome

A

serum sickness

49
Q

What causes serum sickness and what are the symptoms

A

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
Q

What can specifically cause serum sickness

A

antivenum
anti-lymphoyte globulin (immunosuppressant)
antibiotics
streptokinase (bacterial enzyme)

51
Q

What is the mechanism behind SLE

A

IgG antibodies against self antigen in all nucleated cells

large amounts of small complexes deposit in blood vessels, kidneys, joints, and other tissues

52
Q

What happen in SLE due to the immune cells

A

phagocytosis activated by Fc receptors
auto-reactive T cells become involved
damage can lead to death

53
Q

What are the therapeutic strategies for
Arthus reaction
serum sickness
lupus

A

avoidance and anti-inflammatories
drug avoidance, antihistamines, corticosteriods, etc.
NSAIDs, corticosteroids, immunosuppressive drugs, etc.

54
Q

What is the overview of type III hypersensitivity

A

Ag-Ab complexes clump and aggregate attractive an inflammatory response
primarily IgG
immune complex

55
Q

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

A

type IV hypersensitivity

56
Q

How long does it take for type IV hypersensitivity to take place

A

2-3 days; due to it taking longer than antibody mediated

57
Q

Turburculin type hypersensitivity is mediated by which type of cells (TB test)

A

Th1

58
Q

contact dermatitis is mediated by which type of cells

A

Th1 and/or CTLs

59
Q

chronic asthma is mediated by which type of cells

A

Th2

60
Q

gluten-sensitive enteropathy is mediated by which type of cells

A

Th1 and Th2, but still poorly understood

61
Q

graft rejection is mediated by which type of cells

A

T cells

62
Q

Type IV hypersensitivity is also called what

A

delayed type hypersensitivity (DSH)

63
Q

True or False

Type IV hypersensitivity is antibody mediated

A

False; it is cell mediated, mostly Th cells

64
Q

What are the important cells in DTH response

A

macrophages
CD8 T cells
NK cells

65
Q

Type IV hypersensitivity is generally initiated by what

A

haptens (small molecules)
Ag presented by APCs activate Th cells
Th cells secrete cytokines which activate macrophages

66
Q

contact dermatitis involve this complexing with skin proteins and activating this

A

haptens (itching can push these further in skin)

elicited by CD4 and CD8

67
Q

What are the two phases of contact hypersensitivity

A

sensitization and elicitation

68
Q

When/Where does sensitization occur during type IV hypersensitivity

A

first exposure; 10-14 days

in the Langerhans cells, creation of CD4 memory T cells

69
Q

When/Where does elicitation occur during type IV hypersensitivity

A

upon re-exposure, 24-48 hours
presentation to memory T cells
release of IFN-γ and pro-inflammartory cytokines
inflammation

70
Q

What is the mechanism of chronic asthma

A

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
Q

Granulomatous inflammation/Crohn’s disease are which type of hypersensitivity

A

Type IV; thought to be due to unresolved DTH

initially presents in oral cavity

72
Q 
What are the therapeutic strategies for 
TB test
contact hypersensitivity
chronic asthma
Crohn's disease
A

self-limiting
limit exposure, corticosteroids, antihistamines, etc
corticosteriods, bronchodilators, etc.
corticosteriods, immunosuppressants, etc.

73
Q

What is the overview of type IV hypersensitivity

A

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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