Hypersensitives (Final) Flashcards

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

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2
Q

Hypersensitivity is a normal immune response that is:

A

-Inappropriately trigger

or

-Excessive

or

-Produces undesirable effects on the body

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3
Q

Hypersensitivity: Basic trigger

A

-Specific antigen antibody reaction or a specific antigen lymphocyte interaction

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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

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5
Q

B cells

A

Are antibodies

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6
Q

T cells

A

Long term immunity

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7
Q

Type 1: IgE mediated Reaction

A

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

-Pet dander - Nuts - Pollen

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8
Q

Type 1 hypersensitivity: Key characterisitics

A

Immediate reaction (15-20 min)

This reaction occurs after being sensitized to an antigen

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9
Q

Type 1 Hyper Sensitivity: Antigens

A

-Environmental (bee sting - Pet dander)

-Foods (Nuts - Shellfish)

-Medications (Penicillin - Contrast Dye)

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10
Q

Type 1 Hypersensitivity: Etiology

A

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

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11
Q

Key cells involved in Type 1

A

-B lymphocytes

-igE (antibody)

-Mast cells (granulocyte)

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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

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13
Q

Type 1 Response

A

Histamines

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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)

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15
Q

Type 1: Atopic reactions (Local)

A

-Allergic Rhinitis

-Asthma

-Urticaria (hives)

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16
Q

Type 1: Anaphylaxis Reaction (Systemic)

A

-Systemic release of chemical mediators

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

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17
Q

What are most common triggers of anaphylaxis?

A

-Medications

-Bee stings

-Foods

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18
Q

Type II hypersensitivity: Cytotoxic reaction

A

What would happen if….

A patient received the wrong blood type?

Incompatible blood

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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

A
24
Q

Type II response: Example disorders

A

-Blood transfusion

-Rg incompatibility in pregnancy birth

-Autoimmune disorders

-Certain drug reactions

25
Q

RH parents slide

A

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
Q

Type II manifestations: transfusion Reaction

A

-Fever - Chills - Flushing (first sign)

-Increase HR

-Decrease BP

-Chest pain or back pain

-N/V

-Restlessness and anxiety

-Headache

27
Q

Type III hypersensitivity: Immune Complex Reaction

A

What happens when you have rheumatoid arthritis?

Inflammation of tissue that causes the damage

28
Q

Type III: Key Charactersitics

A
  1. Antigen anitbody complexes form (IgG and IgM)
  2. There are deposited into tissues
  3. Inflammatory response cause tissue damage
29
Q

Type III: Etiology

A

-Autoimmune attack

-Low grade infection

-Inhaled antigens from molds or contaminated plants

29
Q

Type III: Possible offending antigens

A

-Inhaled from antigens from molds or contaminated plants

-Body’s own response

-Bacteria and viruses

30
Q

Type III: Key immune cells involved

A

-Antibodies IgG and IgM taht clump with antigens

-Complement

-Neutrophils and mast cells

31
Q

Type III: Pathogenesis

A

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
Q

Type III: Clinical Manifestations

A

-Manifestations depend on where the complexes are deposited in the tissue

Rheumatoid arthritis = Joints

Glomerulonephritis = Kidney Failure

Systemic lupus erythematosus = skin and organs

33
Q

Type II vs Type III

A

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
Q

Type IV: Delayed Hypersensitivity

A
  • Have you ever had poison ivy? Postive TB skin test? Jellyfish sting? Allergic reaction to jewelry? Chron’s disease?
34
Q

Type IV hypersensitivity: Key characteristics

A

-Delayed response

-No antibody involvement

35
Q

Type IV: Key Immune cells

A

-T cells (NO B CELLS)

-Cytokines

-Mast cells and Macrophages

36
Q

Type IV: Etiology

A

Delayed cellular reaction to antigen. Because it takes time for the T cells to make their journey to the site

37
Q

Type IV: Possible Antigens

A

-Plant oil

-Cosmetics and clothings

-Nickel alloys

-Tuberculin antigen (TB test)

-Organ transplant or skin graft

-Gluten

38
Q

Type IV: Pathogenesis

A

-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
Q

Type IV: Clincial Maifestiations

A

-Peak 49-72 hours

-Contact dermatitis: Redness, edema, itching, blisters

-Tuberculin hypersensitivity: Redness, induration and inflammation

40
Q

Hypersinsitivity Reaction: Pharmacotherapy Options

A

Immunosuppressants (transplant patients) (Lower the immune response)

Antihistamines (reduces symptoms) (do not stop reaction)

Epinephrine (Important with anaphlyic reaction)

41
Q

People on immune suppressants we need to watch for what?

A

Infections

42
Q

Antihistamines

A

not stoping reaction just suppressing symptoms

43
Q

Organ transplatn and drug therapy options (know slide)

A