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Extras > Stiner: Hypersensitivity > Flashcards

Stiner: Hypersensitivity Flashcards

1
Q

_____:exaggerated or aberrant immune response to an antigen resulting in inflammation and tissue damage

A

Hypersensitivity

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2
Q

_____ _____:disorders that are caused by aberrant immune responses

A

Hypersensitivity Diseases

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3
Q

Type __: (immediate)

  • immune reactant= IgE
  • antigen= soluble antigen
  • effector mechanism= mast cell activation
  • ex= allergic rhinitis, asthma, systemic anaphylaxis
A

I

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4
Q

Type __:

  • immune reactant= IgG
  • antigen= cell or matrix associated antigen
  • effector mechanism= complement, FcR+ cells (phagocytes, NK cells)
  • ex= some drugs allergies (penicillin)
A

II

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5
Q

Type __:

  • immune reactant= IgG
  • antigen= cell surface receptor
  • effector mechanism= antibody alters signaling
  • ex= chronic urticaria (antibody against FCeR1a)
A

II

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6
Q

Type __:

  • immune reactant= IgG
  • antigen= soluble antigen
  • effector mechanism= complement, phagocytes
  • ex= serum sickness, arthus rxn
A

III

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7
Q

Type __:

  • immune reactant= TH1 cells
  • antigen= soluble antigen
  • effector mechanism= macrophage activation
  • ex= contact dermatitis, tuberculin rxn
A

IV

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8
Q

Type __:

  • immune reactant=TH2 cells
  • antigen= soluble antigen
  • effector mechanism= IgE production, eosinophil activation, mastocytosis
  • ex= chronic asthma, chronic allergic rhinitis
A

IV

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9
Q

Type __:

  • immune reactant= CTL
  • antigen= cell associated antigen
  • effector mechanism= cytotoxicity
  • ex= contact dermatitis
A

IV

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10
Q 
Type I:
-systemic anaphylaxis (most severe)
Route of Entry: \_\_\_\_\_\_\_
Response:
-e\_\_\_\_\_\_
-increase vascular \_\_\_\_\_\_\_
-tracheal occlusion
-\_\_\_\_\_\_\_ collapse
-death
A 
intravenous
edema
increase vascular permeability
tracheal occlusion
circulatory collapse
death
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11
Q 
Type 1:
-acute urticaria (\_\_\_\_\_and \_\_\_\_\_)
Route of Entry: \_\_\_\_\_\_\_
Response:
-local increase in \_\_\_\_\_ flow and \_\_\_\_\_ permeability
A

wheal and flare
through skin
increase in blood flow and vascular permeability

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12
Q 
Type 1:
-allergic rhinitis (seasonal allergies)
Route of Entry:
Response:
-edema of \_\_\_\_\_ mucosa
-irritation of \_\_\_\_ mucosa
A

inhalation

nasal mucosa

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13
Q 
Type 1:
-asthma (most common)
Route of Entry:
Response:
-bronchial \_\_\_\_\_\_
-increased \_\_\_\_\_\_ production
-airway \_\_\_\_\_\_\_\_\_\_
A

inhalation
bronchial constriction
increased mucus production
airway inflammation

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14
Q 
Type 1:
-food allergy
Route of Entry:
Response:
-v\_\_\_\_\_\_
-d\_\_\_\_\_\_
-p\_\_\_\_\_\_(itching)
-u\_\_\_\_\_\_(hives)
-a\_\_\_\_\_\_(rarely)
A 
oral
vomiting
diarrhea
pruritis
urticaria
anaphylaxis
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15
Q

Immediate hypersensitivity is what type?

  • allergy
  • atopy
A

Type I

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16
Q

Occurs w/in minutes after RE-EXPOSURE to antigen/allergen:

A

Type 1

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17
Q

Rapid ____ and ____ cell mediated vascular and smooth mm rxn that is often followed by inflammation:

A

Type 1

IgE and mast cell

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18
Q

Most common disorder of immune system is what?

-affecting ~20% of pop

A

Type 1

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19
Q

1st time exposure to allergen= sensitivity

2nd time exposure to allergen= _______

A

hypersensitivity

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20
Q

Type 1 Hypersensitivity:

1) initial exposure to antigen and production of ___ antibodies (Ab)= ________
- TH2 cells secrete IL’s (causing class switching)
- TH2 cell _____ binds to B Cell _____ (activating B Cell)

A

IgE
sensitization
CD40L
CD40

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21
Q

Type 1 Hypersensitivity:

2) binding of ____ Ab to ___ receptors on ____ cells (activation of mast cells causing degranulation)

A

IgE binds to Fc receptors on mast cells

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22
Q

Type 1 Hypersensitivity:

3) cross linking of bound _____ upon reexposture to allergen

A

IgE

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23
Q

Type 1 Hypersensitivity:

4) release of ___ cell mediators

A

mast

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24
Q

Type 1 Hypersensitivity: biphasic response

5) ______ effects: dilation of blood vessels, increased vascular permeability, smooth mm contraction

A

immediate

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25
Q

Type 1 Hypersensitivity: biphasic response

6) _____ response: inflammation by cytokines (need time to be produced)

A

late

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26
Q

Type 1 Hypersensitivity:
Mast cell degranulation-
-immediate response= _____ _____ (histamine and serotonin ) and _____–> initiate tissue damage
–synthesis and secretion of _____ mediators (prostaglandins and leukotrienes made from arachidonic acids)

A

vasoactive amines
proteases
lipid

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27
Q

Type 1 Hypersensitivity:
Lipid Mediators of Immediate Response=
________:
-vascoconstriction in lungs or dilation in vascular smooth mm (depends on receptor)
-constriction or dilation of bronchioles
-cause aggregation or disaggregation of platelets

A

prostanglandins

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28
Q

Type 1 Hypersensitivity:
Lipid Mediators of Immediate Response=
_______:
-powerful inducers of bronchoconstriction, increased vascular permeability
-refereed to as slow reacting substance of anaphylaxis (SRS-A)

A

leukotrienes

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29
Q

Type 1 Hypersensitivity:
Mast cell degranulation-
-late phase rxn= synthesis and secretion of cytokines (___ _, ___ ___, ____ ____, ____-____)
and chemokines (_____-___)
-infiltration of eosinophils (release ROS/major basic proteins), monocytes, neutrophils

A

TNF alpha
IL 4
IL 5
GM-CSF

MIP-1 alpha

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30
Q

-
-

A

coughing
wheezing
shortness of breath

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31
Q

Common asthma triggers:

  • a
  • r
  • p
  • c
  • a
A 
air allergens
respiratory infections
physical activity
cold air
air pollutants/irritants
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32
Q

Response Triggered By Dust Mite Allergens:

  • ____ jnx seal the barrier of airway epithelium
  • enzyme ___ _ _ cleves occuldins in jxn
  • enzyme is taken up by _____ cells for antigen presentation and TH2 priming
  • enzyme specific _____ binds to mast cell; enzyme triggers MAST CELL DEGRANULATION=INFLAMMATORY RESPONCE
A

tight
Der p 1
dendritic cells
IgE

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33
Q

Treatment Strategies for Asthma:

-long term control medications= inhaled ________ and ______ modifiers

A

corticosteroids

leukotriene

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34
Q

Dose and Rts of Entry of Allergens determine the Type of IgE mediated Allergic Rxn that Results:

A

….

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35
Q

Type 1 Hypersensitivity: Key Pts

-all clinical and pathologic features of immediate hypersensitivity rxns are driven by mediators produced by _____ cells

A

mast

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36
Q

Type 1 Hypersensitivity: Key Pts
-mediators produced in different amounts and in different tissues are responsible for ______ immediate hypersensitivity syndromes

A

different

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37
Q

Type 1 Hypersensitivity: Key Pts

-the most severe form of immediate hypersensitivity is ______

A

anaphlaxis

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38
Q

_______: response driven by the systemic release of vasoactive amines and lipid mediators from mast cells

A

anaphylaxis

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39
Q

______: causes life threatening drop in BP accompanied by severe bronchoconstriction

A

anaphylaxis

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40
Q

_____: treated w/ epinephrine (vasoconstrictor and bronchodilator) and antihistamine

A

anayphylaxis

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41
Q

Type ___ Summary:
-sensitization
-events that occur as a result of mast cell activation
1. mast cell degranulation
2. synthesis and secretion of lipid mediators
delayed-last phase response
3. cytokine release- leads to recruitment of neutrophils and eosinophils to the sire of inflammation

A

Type 1

42
Q

Type II Hypersensitivity:

  • antibodies produced by the immune response that bind to antigens on our own cell surfaces
  • -primarily ____ and ____ isotypes
A

IgG (own)

IgM

43
Q

Type II Hypersensitivity:

-host Ab binds foreign Ab on cell surfaces or binds ____ ___

A

self Ag

44
Q

Type II Hypersensitivity:

  • can activate ______ resulting in membrane attack complex formation
  • -leads to _______ of cells, inflammation, or interfere with normal cellular fnx
A

complement

destruction

45
Q

Type II Hypersensitivity or _______ hypersensitivity

A

cytotoxic

46
Q

Type II Hypersensitivity:
______ ____ of the Newborn (Erythroblastosis fetalis)
–maternal Ab’s target fetal RBC’s for destruction
(Rh positive or negative)

A

Hemolytic Disease of the Newborn

47
Q

Type II Hypersensitivity:
________ _____-
-auto antibodies are produced against self Ag’s on the surface of RBC’s
-this triggers the rapid destruction of RBC’s leading to anemia

A

Hemolytic anemia

48
Q

Type II Hypersensitivity:
____ ____ _____-
-host anti blood grp Ab’s target transfused RBC’s for destruction

A

blood transfusion rxn

49
Q

Type II Hypersensitivity:
_____ _____-
-TSH receptor Ab’s stimulate TSH receptor to over produce thyroid hormone

A

Graves Disease

50
Q

Type II Hypersensitivity:
_______ _______-
-Ach receptor Ab’s bind to and block the Ach receptor

A

Myasthenia Gravis

51
Q

Therapeutic Strategies:
Autoimmune Hemolytic Anemia-
______ or _____ _______

A

prednisone

blood transfusion

52
Q

Therapeutic Strategies:
HDNB-
_____-_____ ___

A

anti-Rh Ab

53
Q

Therapeutic Strategies:
Graves disease-
radioactive _____, anti-____ drugs, or ____ removal

A

iodine
anti thyroid drugs
thyroid removal

54
Q

Therapeutic Strategies:
Myasthenia Gravis-
________ inhibitors and _________

A

cholinesterase

corticosteroids

55
Q

Type ___ Summary:

  • host Ab binds foreign AG on cell surfaces or binds self Ag
  • IgG (some IgM)
A

2

56
Q

Type III Hypersensitivity: (____-____ mediated)

-Ag-Ab complexes ___ and deposit in blood vvs or tissues attracting an _____ inflammatory rxn

A

immune- complex mediated
clump
acute

57
Q

Type III Hypersensitivity:

-an ____ _____ consists of an Ag (allergen) binding to its specific Ab (IgG/IgM)

A

immune complex

58
Q

Type III Hypersensitivity:

  • larger aggregates fix _____ and are cleared from circulation by _______
  • small complexes formed in Ag ____ deposit in vvs or tissues (ligate ___ receptors on leukocytes, leading to activation and tissue damage)
A

complement
phagocytes
excess
Fc

59
Q

Type III Hypersensitivity:

-how long does it occur after activation?

A

3-10 hrs

60
Q

Type III Hypersensitivity:

-can be caused by exogenous (____) or endogenous (____) Ag

A

foreign

self

61
Q

Type III Hypersensitivity:
-deposits tend to accumulate at sites where antigens are ______ or at sites of turbulence (_______) or high pressure (_______)

A

localized
vessel brs
kidneys

–vasculitis, arthritis, nephritis

62
Q

Type III Hypersensitivity:
Mechanisms- immune complexes trigger inflammation via 3 mechanisms:
1. ___ ___ ____

A

mast cell activation

63
Q

Type III Hypersensitivity:
Mechanisms- immune complexes trigger inflammation via 3 mechanisms:
2. macrophages release _____-___ and ____-___ that induces the inflammatory ______

A

TNF-alpha
IL-1
inflammatory cascade

64
Q

Type III Hypersensitivity:
Mechanisms- immune complexes trigger inflammation via 3 mechanisms:
3. ____, ____, ____=stimulate mast cells to release more histamines, serotonin, and chemotactic facts
=attracts monocytes, neutrophils, leukocytes

A

C3a
C4a
C5a

65
Q

Type III Hypersensitivity:
Mechanisms-
= cells bearing ____ receptors for IgG/IgM/IgE may be crucial for antibody complex mediated hypersensitivity

A

Fc receptors

66
Q

Type III Hypersensitivity: Arthus Rxn

  • triggered in the ____ by Ig___
  • immune complexes form
  • complexes bind to ___ receptors on ____ cells/leukocytes
  • -local ____ rxn w/ vascular permeability
  • -fluid and cells enter site
  • -____ activates leukocytes once they arrive
A

skin IgG
Fc mast
inflammatory
C5a

67
Q

Type III Hypersensitivity: Arthus Rxn

  • typically occurs in _____ walls, pleura, pericardium, synovium, glomeruli
  • at repeated subcutaneous infection sites
  • local
A

vessel

68
Q

Type III Hypersensitivity: Arthus Rxn

  • symptoms:
  • swelling/pain/edema
  • treatment:
  • ________
A

anti-inflammatory agents

69
Q

Type III Hypersensitivity: Serum Sickness

-ex of ____ ____ immune complex mediated syndrom

A

transient systemic

70
Q

Type III Hypersensitivity: Serum Sickness

  • caused by an injection of ____ protein leading to an Ab response
  • -Ab form immune complexes with prot.–>deposit in small blood vvs–>activate complement and phagocytes
A

foreign

71
Q

Type III Hypersensitivity: Serum Sickness

  • symptoms occur w/in ___ or ____
  • -chills, fever, rash ect.
  • -rash= mast cell degranulation caused by immune complex ligation of ______
A

days or weeks

FcRy

72
Q

Type III Hypersensitivity: Serum Sickness
Causes:
_______: (serum from horses immunized w/ snake venoms)- source of neutralizing Ab to treat ppl w/ poisonous snake bites

A

antivenin

73
Q

Type III Hypersensitivity: Serum Sickness
Causes:
______: immunosuppressive agent used for transplant recipients

A

anti-lymphocyte globulin

74
Q

Type III Hypersensitivity: Serum Sickness
Causes:
____: penicillin, cephalosporin

A

anti-biotic

75
Q

Type III Hypersensitivity: Serum Sickness
Causes:
_____: (a bacterial enzyme(- used as thrombolytic agent to treat heart attack pts

A

streptokinase

76
Q

Type III Hypersensitivity and Autoimmune: SLE (Lupus)

  • Ig___ Ab against ubiquitous ____ Ag in all nucleated cells
  • large amounts of small complexes deposits
  • phagocytes activated by ____ receptors
  • auto reactive T cells involved = more Ab produced, effector fnx destroys cells–>death
A

IgG
self
Fc

77
Q

Type III Hypersensitivity: Ther. Strag- Athus Rxn

A

avoidance or anti inflammatory agents

78
Q

Type III Hypersensitivity: Ther. Strag- Serum Sickness

A

drug avoidance, antihistamines, corticosteroids

79
Q

Type III Hypersensitivity: Ther. Strag- Lupus

A

NSAID’s, corticosteroids, immunosuppressive agents

80
Q

Type _____ Summary:

  • Ag-Ab complexes clump and aggregate in or near blood vessels attracting an acute inflammatory rxn
  • -primarily IgG (IgM/IgE)
  • -immune complex
  • -ex. arthus rxn, serum sickness, SLE
A

III

81
Q

Type IV Hypersensitivity: Delayed Time

  • Cell mediated rxn:
  • mediated by Ag specific ___ Cells which induce macrophage infiltration in a ____ individual
  • _____ response to injected or absorbed Ag
  • occurs w/in ___-___ days
A

T cells
sensitized
DTH= delayed time hypersensitivity
2-3 days

82
Q

Type IV Hypersensitivity:
-tuburculin type hypersensitivity (_____ into the skin)
=mediated by ____ ____

A

injected into the skin

TH1 cells

83
Q

Type IV Hypersensitivity:
-contact dermatitis (_____ by the skin)
=mediated by ____ ___ and or _____

A

absorbed

TH1 cells and or CTL’s

84
Q

Type IV Hypersensitivity:
-chronic asthma (______)
=mediated by _____ ______

A

inhaled

TH2 cells

85
Q

Type IV Hypersensitivity:
- gluten-sensitive enteropathy (_______)
=still poorly understood but evidence suggests response involves ___ and ___

A

digested

TH1 and TH2

86
Q

Type IV Hypersensitivity:
-graft rejection
=mediated by ___ ____

A

T cell

87
Q

Type IV Hypersensitivity:

-what are the effector cells in the DTH response? (3)

A

macrophages
CD8T cells
NK cells

88
Q

Type IV Hypersensitivity:

  • initiated by ______ (antigens that usually do not initiated responses)
  • small molecules that must become bound to a larger carrier molecule in order to illicit an immune or inflammatory response
A

haptens

89
Q

Type IV Hypersensitivity:

  • Ag presented by APC’s activates ____ cells after the initiation of haptens
  • -these cells then secrete cytokines which will activate macrophages
A

TH

90
Q

Type IV Hypersensitivity: TB Test
Tuberculin Test (Mantoux PPD test)
-test to determine previous exposure/infection w/ ______ ______
-small amounts injected intradermally
-w/in ___-___ hrs a local t cell mediated inflammatory rxn evolves in individuals previously exposed to M. TB
==response mediated by ____ cells

A

mycobacterium tuberculosis
24-72 hrs
TH1

91
Q

Type IV Hypersensitivity:
Major DTH Mechanism= Ag Presentation
-Antigen is processed by _____ and stimulates by ____ cells

A

macrophages

TH1

92
Q

Type IV Hypersensitivity: Contact Dermatitis

  • highly reactive small molecules (____) complexed w/ skin _____ and internalized by _____ in the skin
  • elicited by ____ or ____ T cells
  • inflammation occurs by inflammatory response initiated by T cells
  • 2 phages of contact: _____ and ______
A 
hapens
proteins
APC's
CD4 or CD8 t cells
sensitization and elicitation
93
Q

Type IV Hypersensitivity:
_________
-occurs during 1st exposure to Ag
-takes ___-___ days to develop
-langerhan’s cells in skin
-APC of skin take up Ag and present to T cells
-formation of CD4+ memory t cells specific for the AG

A

Sensitization

10-14

94
Q

Type IV Hypersensitivity:
________
-upon reexposure to Ag
-develops w/in ___ - ___ hrs
-involves LC Ag presentation to memory T cells at site of Ag entry
-T cells release IFNgamma and pro inflammatory cytokines
-cytokines recruit macrophages, CTL, NK, and other effectory cells (inflammatory response continues)

A

Elicitation

24-48 hrs

95
Q

Type IV Hypersensitivity: Poison Ivy

  • example of ____ ____
  • response requires a sensitization period and elicitation of the allergic response on subsequent interactions w/
A

contact dermatitis

96
Q

Type IV Hypersensitivity: Chronis Asthma

  • mast cell degranulation leads to ____ (IL-5) and esosinophil influx
  • eosinophils active and degranulate
  • -damaging tissue/recruiting more cells
  • chronic inflammation can cause irreversible damage and death

–ppl can have type 1 and type 4 (leads to tissue damage)

A

TH2

97
Q

Type IV Hypersensitivity: Crohn’s Disease

  • type of IBD in terminal ileum
  • chronic _______ of the bowel mucosa or submucosa
  • symptoms due to unresolved ____
  • initial presentation may be in ____ cavity (6%)
A

inflammation
DTH
oral

98
Q

Type IV Hypersensitivity: Ther. Str.
__ ____ _____
-self limiting= will pass/not long

A

TB Test Injection

99
Q

Type IV Hypersensitivity: Ther. Str.
____ _____
-limit exposure, corticosteroids, antihistamines

A

Contact hypersensitivy

100
Q

Type IV Hypersensitivity: Ther. Str.
_____ _____
-corticosteroids, bronchodilates, cromolyn

A

Chronic Asthma

101
Q

Type IV Hypersensitivity: Ther. Str.
_____ _____
corticosteroids, immunosuppressants

A

Crohn’s Disease

102
Q

Type ___ Summary:
-cell mediated rxn
-by Ag specific ___ cells which induce macrophage infiltration in a sensitized individual
–DTH response to injected or absorbed AB
-2-3 days
ex TB test, contact dermatitis, chronic asthma, crohn’s

A

4

T

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