Hypersensitives (Final) Flashcards

(45 cards)

1
Q

Immune system

A

Complex system in charged of protecting our body from foreign substances

Immune system can identify these antigens to destroy these

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

Hypersensitivity is a normal immune response that is:

A

-Inappropriately trigger

or

-Excessive

or

-Produces undesirable effects on the body

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

Hypersensitivity: Basic trigger

A

-Specific antigen antibody reaction or a specific antigen lymphocyte interaction

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

Four types of hypersensitivity

A

-Type I II II = mediated by antibodies produces by B cells (specifically plasma cells)

-Type IV = Mediated by T cells

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

B cells

A

Are antibodies

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

T cells

A

Long term immunity

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

Type 1: IgE mediated Reaction

A

-How does someone develop an allergy to something this cute?

-Pet dander - Nuts - Pollen

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

Type 1 hypersensitivity: Key characterisitics

A

Immediate reaction (15-20 min)

This reaction occurs after being sensitized to an antigen

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

Type 1 Hyper Sensitivity: Antigens

A

-Environmental (bee sting - Pet dander)

-Foods (Nuts - Shellfish)

-Medications (Penicillin - Contrast Dye)

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

Type 1 Hypersensitivity: Etiology

A

-Genetic link
1 Parent = 30% chance
2 Parent = 50% chance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Key cells involved in Type 1

A

-B lymphocytes

-igE (antibody)

-Mast cells (granulocyte)

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

Type 1: Pathogenesis

A

-Antigen (Ragweed) attaches to B cell during the first time they are exposed

-B cell is triggered to form into a plasma cells. This plasma cells starts producing IgE antibodies

-IgE attach to mast cells and lie and wait

-Next time the person is exposed to allergen. it binds to the IgE antibodies that are attached to the mast cells. This triggers the release of chemical mediators from the mast cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type 1 Response

A

Histamines

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

Type 1 Mediator Activites (know these)

A

Potent vasodilation - Stuffy nose, lower BP, Wheals on skin

Increased vascular permeability - Edema and runny nose

Bronchial smooth muscle contraction - Breathing difficulties and wheezing

Stimulates irritant receptor - Itching (pruritus)

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

Type 1: Atopic reactions (Local)

A

-Allergic Rhinitis

-Asthma

-Urticaria (hives)

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

Type 1: Anaphylaxis Reaction (Systemic)

A

-Systemic release of chemical mediators

-Life threatening because of bronchial constriction - airway obstruction - vascular collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are most common triggers of anaphylaxis?

A

-Medications

-Bee stings

-Foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Type II hypersensitivity: Cytotoxic reaction

A

What would happen if….

A patient received the wrong blood type?

Incompatible blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Type II: Etiology

A

-Exposure to antigen or foreign tissue / cells

-Antigens are located on cell surface

20
Q

Type II: Key Characteristics

A

-Antigen stimulate antibody production

-Antibodies recognize and attach to cell surface antigens

-Direct destruction of targeted cells that contain the antigen (Cell lysis) (Phagocytosis)

-Do this or purpose with transplant patients. Give medication that slow down and decrease immune response so we don’t have this reaction

21
Q

Type II Hypersensitive: Immune Cells involved

A

-Antibodies (IgG and IgM)

-Complement (Fixes to foreign cell and lysis it)

-WBC’s (Phagocytes)

22
Q

Examples of Type II antigens

A

Blood

Some of your bodies own cells (auto immune conditions like diabetes)

Erythroblastosis fetalis (Hemolytic Anemia) (RH factor difference between parent and fetus)

23
Q

Slide for type 2 can go here

24
Q

Type II response: Example disorders

A

-Blood transfusion

-Rg incompatibility in pregnancy birth

-Autoimmune disorders

-Certain drug reactions

25
RH parents slide
RH+ father RH- mother carrying her first RH+ fetus. RH antigens from the developing fetus can enter the mothers blood during delivery In response to the fetal Rh antigens, the moth will produces anti-Rh antibodies IF the woman becomes pregnant with another Rh+ fetus, her antibodies will cross the placenta and damage fetal red blood cells
26
Type II manifestations: transfusion Reaction
-Fever - Chills - Flushing (first sign) -Increase HR -Decrease BP -Chest pain or back pain -N/V -Restlessness and anxiety -Headache
27
Type III hypersensitivity: Immune Complex Reaction
What happens when you have rheumatoid arthritis? Inflammation of tissue that causes the damage
28
Type III: Key Charactersitics
1. Antigen anitbody complexes form (IgG and IgM) 2. There are deposited into tissues 3. Inflammatory response cause tissue damage
29
Type III: Etiology
-Autoimmune attack -Low grade infection -Inhaled antigens from molds or contaminated plants
29
Type III: Possible offending antigens
-Inhaled from antigens from molds or contaminated plants -Body's own response -Bacteria and viruses
30
Type III: Key immune cells involved
-Antibodies IgG and IgM taht clump with antigens -Complement -Neutrophils and mast cells
31
Type III: Pathogenesis
antibody complex formed in blood Deposits in tissue Activation of complement and chemo attraction of neutrophils Release of enzymes and free radicals A ton of inflammation going on
32
Type III: Clinical Manifestations
-Manifestations depend on where the complexes are deposited in the tissue Rheumatoid arthritis = Joints Glomerulonephritis = Kidney Failure Systemic lupus erythematosus = skin and organs
33
Type II vs Type III
Type II: Reacitons occur on the cell surface and result in direct cell death or malfunction Type III: Immune complexes are deposited into tissues and the resulting inflammation destroys the tissue
33
Type IV: Delayed Hypersensitivity
- Have you ever had poison ivy? Postive TB skin test? Jellyfish sting? Allergic reaction to jewelry? Chron's disease?
34
Type IV hypersensitivity: Key characteristics
-Delayed response -No antibody involvement
35
Type IV: Key Immune cells
-T cells (NO B CELLS) -Cytokines -Mast cells and Macrophages
36
Type IV: Etiology
Delayed cellular reaction to antigen. Because it takes time for the T cells to make their journey to the site
37
Type IV: Possible Antigens
-Plant oil -Cosmetics and clothings -Nickel alloys -Tuberculin antigen (TB test) -Organ transplant or skin graft -Gluten
38
Type IV: Pathogenesis
-Small, incomplete antigen, call a hapten penetrates the skin -The hapten combines with human protein to form a complete antigen -T cells become aware of antigen (antigen processing cell) -T cells attack the antigen via: 1. Direst attack from T cells 2. Release of cytokine (inflammation) 3. Macrophages (cell destruction)
39
Type IV: Clincial Maifestiations
-Peak 49-72 hours -Contact dermatitis: Redness, edema, itching, blisters -Tuberculin hypersensitivity: Redness, induration and inflammation
40
Hypersinsitivity Reaction: Pharmacotherapy Options
Immunosuppressants (transplant patients) (Lower the immune response) Antihistamines (reduces symptoms) (do not stop reaction) Epinephrine (Important with anaphlyic reaction)
41
People on immune suppressants we need to watch for what?
Infections
42
Antihistamines
not stoping reaction just suppressing symptoms
43
Organ transplatn and drug therapy options (know slide)