Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PDAT4 > 14 - Hypersensitivity > Flashcards

14 - Hypersensitivity Flashcards

1
Q

Initial Exposure to Allergen

Type 1 Hypersensitivity:
ALLERGIC REACTION

A

Allergen –> ATOPIC individual
VVV
IgE Antibody
that recognizes that allergen is produces
VVV
Mast Cell Receptors
bind to the IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Subsequent Exposure to Allergen
Type 1 Hypersensitivity:
ALLERGIC REACTION

A

Allergen –> MAST CELL (in mucosa)
VVV
Allergen CROSS LINKS IgE-Fc receptors
VVV
Triggers Mast cell to Degranulate
VVV
Mediators Released
Histamine / Prostaglandins / Leukotrienes / TNF-a / IL-4
&
Basophils are recruited from blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

LATE PHASE REACTION
Type 1 Hypersensitivity:
ALLERGIC REACTION

A

Caused by the MEDIATORS released from mast cell degranulation
Histamines / Prostaglandins / Leukotriens / TNF-Aa / IL-4

the RECRUIT Inflammatory cells such as:
EOSINOPHILS + NEUTROPHILS

take ~6 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

WHICH MEDIATOR?
rom the granules of MAST CELLS
Type 1 HYPERsensitivity

Vasodilation

INCREASED Capillary Permeability

Smooth Muscle Contraction** = **BronchoSpasm

A

HISTAMINE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

WHICH MEDIATOR?
from the granules of MAST CELLS
Type 1 HYPERsensitivity

BronchoCONSTRICTION

A

PROSTAGLANDINS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

WHICH MEDIATOR?
from the granules of MAST CELLS
Type 1 HYPERsensitivity

Capillary PERMEABILITY

A

LEUKOTRIENES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

WHICH MEDIATOR?
from the granules of MAST CELLS
Type 1 HYPERsensitivity

Inflammation

Cytokine Release

Stimulate Th2

A

TNF-A

IL-4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What makes an EFFECTIVE ALLERGEN?

A

Small inhaled proteins that stimulate
IgE production in atopic individuals

Small / Highly Soluble

Low Dose

Carried on DRY PARTICLES (Pollen)

Ex.
Mold Spores / Dust Mites / Pets / Cockroaches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why do ATOPIC INDIVIDUALS have
IgE ALLERGY PRODUCTION?

A

MORE TH2
allergen-specific cells

IL-4

IL-5

IL-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

HOW does MORE TH2-allergen-specific cells in atopic individuals
result in
MORE IgE Production?

A

IL-4
induce CLASS SWITCHING –> B-cell produces IgE

IL-5
produce EOSINOPHILS

  • *IL-10**
  • INHIBIT production of* TH1 cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is there more TH2 vs Th1 in atopic individuals?

4 Reasons

A

FETUS + PLACENTA
express freign paternal AG, must be protected from maternal CTL+NKcells
TNF-A –> stimulates NK/CTL –> Th2 Bias
Placenta secretes IL-4 & IL-10 –> more Th2 bias

CHILDHOOD INFECTION
Th1 response –> memory cells remember allergen & TH1 response
Hygiene Hypothesis

HEREDITY
Genes / Mutant IgE receptors / Mutation in Il-4 Promotor gene

TREG CELLS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

FETUS

Why is there more TH2 vs Th1 in atopic individuals?

A

Placenta & Fetus express FOREIGN Paternal Ag
must be protected from the MATERNAL CTL & NK cells

Th1 –> TNF-a –> stimulates NK & CTL
Th2 Bias Preferred

  • *Placenta** secretes IL-4 & IL10
  • *Th2 Bias** in mother & fetus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Childhood Infection

Why is there more TH2 vs Th1 in atopic individuals?

A

Childhood infection = TH1 RESPONSE

  • *Memory cells** remember:
  • *Allergen & Th1 Response** to allergen

HYGIENE HYPOTHESIS
early microbial infections important
Higher Hygiene = lower infections = Higher Allergies
>3 older siblings or < 6mo at daycare = protection vs allergies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HEREDITY
Why is there more TH2 vs Th1 in atopic individuals?

A

Certain Genes have been linked with certain allergic disease
(bias towards Th2)
Asthma & Atopic Dermatitis

  • *Mutant IgE receptors**
  • *CROSS-LINKING** = STRONG signal –> IL-4 Release

Mutation in IL_4 Promoter Gene
Increase IL-4 Production
TH2 stimulated IL-4 –> B-cell produces IgE instead

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

T-REG CELLS
Why is there more TH2 vs Th1 in atopic individuals?

A

Repeat stimulation of T-helper Cells –> TREG production

TREGS suppress immune response to allergen by producing:

  • *IL-10**
  • inhibits* pro-inflammatory Th1 cells

TGF-B
bias towards IgG / IgA production
AWAY from IgE production!

In Atopic Individuals:
their T-REGS are DEFECTIVE in supressing Th2 cytokine production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which Treatment for Allergies?

Treats BRONCHOCONSTRICTION

A

BRONCHODIALATORS

B- Agonist

Albuterol

Xanthine Derivatives = Theophylline

17
Q

​Which Treatment for Allergies?

Block CYTOKINE production by HELPER T-CELLS
↓B-cell activation = ↓AB production

A

CORTICOSTEROIDS

18
Q

What Treatment for Allergies?

  • *ANTIBODY** which grasps Fc Region of IgE Ab
  • blocking binding to* Mast Cells

Reliieves allergic symptoms & ↓severity of asthma attack

A

OMALIZUMAB

19
Q

What Treatment for Allergies?

Decrease or Prevents
MAST CELL DEGRANULATION

A

MAST CELL MEMBRANE STABILIZERS

Cromolyn Sodium

20
Q

What Treatment for Allergies?

Binds to LEUKOTRINE RECEPTORS
or
INHIBITS the formation of Leukotrines

Prevents:
Airway Edema
Bronchoconstriction
Inflammation

A

LEUKOTRIENE MODIFIERS

ZAFIRLUKAST

21
Q

Specific ImmunoTherapy
for
Treatment for Allergies

A

ONLY APPROACH FOR ALLERGY CURE

  • *Several Years of** **maintanence injections
  • -> TOLERANCE**

Can induce the
shift Th1 instead of Th2

IgG:IgE ratio
can increase 100 fold
Repeated injections –> TREGS which produce TGF-B
which suppress IgE Ab production

22
Q

ICU DRUG DESENSITATION

Done when a
Drug NEEDS to to be given to a patient who has that DRUG ALLERGY

A

EVALULATION
indication / ICU BED / plan / IV access

ORDERING
Allergy consult / PRN meds / CRASH CART / Phamacist dilution assist

MONITORING
watch for: HypoTension / TachyCardia / Tightness / Wheezing
Dyspnia / Hives / other allergies

PREPARATION
prepares ALL DILUTION and clearly labeled doses

ADMINISTRATION
each dose given over 30 min via pump @ specific times
30 min after IV dose –> 60 min monitoring after PO dose

23
Q

Which TYPE OF HYPERSENSITIVITY?

Immediate & Anaphylactic

Mediated by IgE

A
  • *TYPE 1**
  • *The Allergic Reaction**

IgE induced by allergen & binds to mast cells + basophils
VVV
Re-Exposure to allergen –> allergen CROSS LINKS bound IgE
VVV
Degranulation & Mediator Release

24
Q

Which TYPE OF HYPERSENSITIVITY?

Mediated by IgG

Antigens on cell-surface combine w/ AB

COMPLEMENT-mediated lysis

PMN-mediated cell dmg

Ab-Ag induced cell dysfunction

A

TYPE 2
CYTOTOXIC

25
Q

Which TYPE OF HYPERSENSITIVITY?

Mediated by IgG

Ag-Ab immune complex deposited in tissue

Complement activated –> PMNs attracted to site
VVV
release LYSOSOMAL ENZYMES
VVV
TISSUE DMG

A

TYPE 3
IMMUNE COMPLEX

26
Q

Which TYPE OF HYPERSENSITIVITY?

CELL MEDIATED

Helper T-Cell sensitized by antigen –> re-exposure to Ag
VVV
Lymphokine Release
VV
Inflammation & MACROPHAGE activation
w/ mediator release

A
  • *TYPE 4**
  • *DELAYED**
27
Q

Type 2: CYTOTOXICITY

3 Mechanisms

A

IgG Mediated Reaction

Complement –> MAC –> LYSE

Complement –> PMN to site** –> **PHAGOCYTOSIS

  • *IgG** binds to Ag on membrane –>
  • *Ab-Ag induced cell DYSFUNCTION**
28
Q

Examples of TYPE 2 HYPERSENSITIVITY:
CYTOTOXICITY

A

RBC CELL:

  • *Hemolytic Anemia** / ABO Transfusion Reactions
  • *Drugs (PLT also) / Rh Hemolytic Disease**

Cardiac Cell
Infections = Rheumatic Fever

Kidney + Lung Cells
Goodpasture’s Syndrome

29
Q

Type 3: IMMUNE COMPLEX

A

FREE FLOATING AG + AB
complexes form in BLOOD
VVV
Deposit into blood vessel = COMPLEX DESPOSITION
VVV
Activate COMPLEMENT = C5a
does not go all the way to MAC
VVV
Attracts NEUTROPHILS –> release enzymes
to DESTROY endothelium

30
Q

Which type of TYPE 4 HYPERSENSITIVITY disease?

Localized Inflammation
immune complexes @ local site

Repeated Ag Admin = HIGH IgG then SC injection of Ag

A

ARTHUS REACTION

31
Q

What disease? Type 3 Hypersensitivity

Immune complexes deposited throughout the body
SYSTEMIC INFLAMMATORY RESPONSE

  • *Foreign Drug serum** injected = SLOW Ag Excretion
  • *AB production** –> Immune complex formation & deposition
A

SERUM SICKNESS

32
Q

What disease? Type 3 Hypersensitivity

Post-Streptococcal Ag-Ab complexes
along the basement membrane of KIDNEY
VV
Complement Active –> Neutrophil recruitment

A

GLOMERULONEPHRITIS

33
Q

What disease? Type 3 Hypersensitivity

Rh Factor binds with AB
VV
Immune complex deposit in Synovial membranes
VV
Complement Activation -> Neutrophil Recruitment

A

RHEUMATOID ARTHRITIS

34
Q

What disease? Type 3 Hypersensitivity

Ab targetted against
DNA of Face/Kidney/Joints

A

Systemic LUPUS ERYTHREMATOUS

35
Q

Type 4: DELAYED

A

only CELL-MEDIATED type of hypersensitivity

Macrophage + Ag (on MHC2) –> IL-1** + **IL-12
^^^
VV
T-HELPER CELL TH1 –> INF-Y
Activates Macrophage

Delayed = Takes hours or days after contact
& lasts for days

36
Q

Examples of
TYPE 4 HYPERSENSITIVITY

A
  • *CONTACT HYPERSENSITIVITY**
  • *POISON OAK**

TUBERCULIN = TB

PDAT4 (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions