Pathophys Exam 2 (1 Of 3) - Alterations Of The Immune System (Sans Aids)

Front 1

What are the 4 classifications of hypersenitivity?

Back 1

Type I - IgE mediated (allergy)
Type II - antibody-mediated (ABO, Rh, Haptens (drugs))
Type III - immune-complex mediated (IgG/antigen)
Type IV - cell-mediated (autoimmune)

Front 2

What type of antibody is involved in Type I hypersensitivity? and to what receptors on the mast cell or basophil does it bind?

Back 2

Immunoglobulin E (IgE)

bind to the Fc epsilonRI (FceRI)

Front 3

What mediators are involved in the Type I primary inflammatory response (i.e., early phase) and where do they originate in the mast cell?

Back 3

Mast cell / Basophil Granules release:

chemokines
TNF-alpha
Histamine

Front 4

Name the secondary mediators of the Type I response and how are they formed?

Back 4

AA derived Leukotrienes, Prostoglandins, Thromboxanes, and IL-1

Front 5

Why is it postulated that atopic allergy has a genetic component?

Back 5

if 2 parents allergic = 2x more likely
Neither parent allergic = 0.5x as likely

Front 6

How do atopic persons react to common environmental substances (i.e., what is produced by their immune system) that is not seen in non-atopic persons?

Back 6

higher IgE than non-atopic person

Front 7

Describe a positive result when allergy testing using the prick or scratch test.

Back 7

the skin will become raised, red and appear itchy.

timeframe: min/days
results: record on wheel and flair response chart

Front 8

Describe a positive result when allergy testing using a RAST (radioallergosorbent test) test.

Back 8

1. allergen+insoluble material
2. blood added
3. IgE bind to allergen/insoluble material
4. radiolabeled anti-human IgE added
5. sticks to IgE/allergen, then mixture is washed
6. radioactivity is proportional to IgE in blood

Front 9

Is there a common property of antigens (allergens) that stimulate an IgE response in atopic persons?

Back 9

No common property

(common allergens: pollens, food, drugs, insect products, animal hair)

Front 10

Differentiate between localized Type I anaphylaxis and systemic anaphylaxis in terms of life threatening manifestations.

Back 10

Localized: unpleasant/annoying
ex: rhinitis, hives, bronchoconstriction

Systemic: potentially fatal
-symptoms:
low BP
edema
bronchiole constriction
Inflammation: lips, tongue, throat
-cause:
systemic release of vasoactive mediators:
vasocontriction
smooth muscle contraction

Front 11

Using drug induced type II hypersensitivity
Differentiate Type I / Type II hypersensitivity
When considering mode of action (i.e., mast cells, complement system)

Back 11

Type 1:
-allergen stimulates IgE antibody on mast cell/basophil

Type 2 (drug induced):
-hapten binds to RBC
-humoral response (IgG/IgM)
-activates complement system
-causes hemolysis

Front 12

What are three examples of Type II hypersensitivity? What role do haptens play?

Back 12

ABO blood group incompatibility
Rh incompatibility
Drug induced:

-Haptens (the drug) binds to RBC
-together looks foreign
-humoral response

Front 13

What are two types of Type III hypersensitivities?

give example

Back 13

Systemic:
"serum sickness"
ex: Systemic Lupus Erythromatosis

Localized:
Arthus Reaction
ex: farmer's lung

Front 14

What commonality does Type I and Type III hypersensitivity have?

Back 14

Both involve Mast cells / Basophils

Front 15

In Type III hypersensitivity:

What part of the antibody-antigen (Ab-Ag) complex fits into the receptor on the mast cell?

What is the receptor called?

Back 15

IgG Fc end;

Binds to Mast cell low affinity FcgammaRIII (FcγRIII)

causes granules to release inflammatory mediators

Front 16

In Type III hypersensitivity:

What types of cells are attracted to the area once the mast cells are activated?

Back 16

PMNs (neutrophils and eosinophils)

Front 17

In Type III hypersensitivity:

How are PMN (neutrophils and eosinophils) cells activated?

Back 17

Fc end of the IgG antibodies stimulates the PMNs

Front 18

Historically, what were the most common causes of serum sickness? Why?

Back 18

Type III hypersensitivity:
IgG-antibodies developed against horse serum during antitoxins (rabies, tetanus) injections

Front 19

The term “serum sickness” is presently used to describe syndromes that occur after what medical events?

Back 19

Any Type III / immune complex Hypersensitivity

ex: Systemic Lupus Erythematosus

Front 20

Symptoms of “serum sickness” are very similar to a type I systemic allergic reaction.

What are the differences between these two reactions in terms of onset of symptoms?

Back 20

Type I:
-seconds-minutes-hours

Type III:
-8-14 days

(b/c the humoral IgG response time)

Front 21

Why does the Arthus reaction occur at the site of introduction?

(using example: Farmer’s Lung disease)

Back 21

Inhalation of spores cause primary/secondary humoral response (IgG antibodies)

large IgG/antigen complexs (Ag-Ab) bind to FcGammaRIII on Mast cells

Degranulation ->
Chemotaxis ->
basophil/neutrophil activation ->
inflammation of alveoli

Front 22

What characteristic separates Type IV hypersensitivity from the other three?

Back 22

Type IV is a cytotoxic reaction:

Type I-III:
humoral response
(Th2, IgG, IgE, IgM)

Front 23

What specific T cell is activated in a Type IV hypersensitvity?

and how does this cell illicit the response?

3 examples

Back 23

Th1 clones -->> macrophages
(via cytokines)

ex: atopic dermatitis, latex allergy, manatoux TB test

Front 24

Why is the term delay-type hypersensitivity (DTH) used to describe type IV hypersensitivity?

Back 24

Type IV: 1 or 2 days later
understood first, therefore called DTH

Type III: 8-14 days (longer delay, but was understood later)

Front 25

What two cells are involved in the sensitization phase of type IV hypersensitivity?

Back 25

Macrophages (APCs) on skin

Th1 cells (naive)

Front 26

Which of the two cells involved in the SENSITIZATION phase of Type IV hypersensitivity is stimulated into differentiation and clonal expansion?

Back 26

Th1 cells (activated)

Front 27

What two cells are involved in the EFFECTOR phase of type IV hypersensitivity and how do they interact?

Back 27

Th1 clones secrete cytokines
attract activated Macrophages

Macrophages secrete inflammatory mediators
skin erupts with inflammation

Front 28

Define immunologic tolerance/immunologic homeostasis.

Back 28

Host does NOT react to self-antigens
MHC Class I and II

Front 29

When and how does immunologic tolerance / immunologic homeostasis develops?

Back 29

Develops during the embryonic period

Eliminate/Suppress: Autoreactive lymphocytes (Th)
(those that react to self MHC class I / II cell)

Front 30

There are three models for autoimmune reactions, explain each and give an example.

Back 30

1. mimicry:
MYASTHENIA GRAVIS (NOT ankylosing spondolitus)
muscle acetylcholin receptors destroyed?

2. autoreactive lymphocytes:
type 1 diabetes:
lymphocytes destroy beta cells in pancrease islet of langerhanns
(HLA DR3 and DR4 alleles)

3. Release of Sequestered Antigen
trauma or infection expose sequestered antigens (not ordinarly available to immune system for self recognition

ex. eye damage releases "lens proteins", cataracts

Front 31

Historically, why was the term “lupus” used in the condition of Systemic Lupus Erythematosus (SLE)?

Back 31

butterfly rash on the face of the people with it, looked like the bite of a wolf

Front 32

What is the most characteristic autoantibody produced in SLE?

Back 32

Antinuclear antibodies (ANA)

Front 33

What type hypersensitivity is incited by SLE?

Back 33

Type III serum sickness reaction because you are making antibodies against proteins

Front 34

What areas of the body does SLE Type III hypersensitivites involve?

Back 34

Joints, Kidney, skin, brain, sereosa, lung, heart and GI tract

Front 35

Are the symptoms of SLE constant present from onset or can they “wax and wane”?

Back 35

You have periods of flares alternating with remission, causing it to be unpredictable

Front 36

What gender is chiefly affected by SLE?

Back 36

female; child bearing age

Front 37

What is the mainstay of serologic testing for lupus?

When is it positive?

Back 37

Fluorescent antinuclear antibody test (FANA).

patients serum w/ antinuclear antibodies
add a fluorescent nuclear antibody to it.
When it hooks on it glows = positive test

Front 38

What is the conservative approach to the treatment of SLE?

Back 38

NSAIDs: Ibuprofen (motrin, advil); naproxen or antimalarial drugs Hydroxychoroquine

Front 39

Why would a conservative approach to treating SLE be changed to a more aggressive approach?

Back 39

flare ups with the skin - OK

damage to internal organs - go aggressive

Front 40

What type of medications would be used in the more aggressive SLE treatement approach?

What are their side effects?

Back 40

High dose corticosteroids:
-prednisone
-other immunosuppressive drugs:
-cyclosporine (chemo treatment)

Side effects:
-suppress immune system
-susceptible to fungal and bacterial infections