EX2 Hypersensitivity - Stiner Flashcards Preview

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Flashcards in EX2 Hypersensitivity - Stiner Deck (73):
1

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

hypersensitivity

2

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

systemic anaphylaxis

3

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

acute urticaria (wheal-and-flare)

4

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

allergic rhinitis (hay fever)

5

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

asthma

6

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

food allergy

7

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

Type 1 hypersensitivity

8

Type 1 hypersensitivity occurs when

within minutes of RE-EXPOSURE to antigen/allergen

9

What is the immune response during a type 1 hypersensitivity reaction

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

10

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

True

11

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

True

12

What is the sensitization step during type 1 hypersensitivity

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)

13

What are the 6 steps to type 1 hypersensitivity

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)

14

The release of mast cell mediators triggers what

a biphasic response
1. immediate effects
2. late response

15

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

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

16

What three things do prostaglandins stimulate

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

17

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

synthesis and secretion of cytokines and chemokines
leading to infiltration and eosinophils, monocytes, and neutrophils; leading to inflammation and tissue damage

18

What is the overview of type 1 hypersensitivity

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

19

What are some common triggers for asthma

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

20

How many people suffer from asthma worldwide

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

21

The dust mite allergen triggers asthma via which enzyme

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

22

What are some treatment strategies for asthma

inhaled corticosteroids
leukotriene modifiers

23

The dose and route of entry of allergens determine what

the type of IgE-mediated allergic reaction that results

24

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

anaphylaxis

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