Abnormal Immune Responses Flashcards

1
Q

What are the three types of abnormal immune response?

A
  1. Immunodeficiency
  2. Hypersensitivities
  3. Autoimmunity
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2
Q

What is an immunodificiency?

A

Immunodificiency is when the body can only mount a partial Immune Response or cannot mount a full normal immune response.

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3
Q

Explain Primary Immunodificiency?

A

A primary immunodificiency is genetic or congenital. You are born (pre-natal) with the condition.

Ex - Developmental failure of an organ (Thymus) therefore you have no mature T-cells.

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4
Q

Explain Secondary Immunodificency?

A

Secondary immunodificiency is aquired after birth (post-natal), due to another disease or condition.

Ex: Infection with AIDS, CA treatment, Immunosuppressive drugs (steriods).

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5
Q

What are the 5 types of Immunodeficiencies?

A
  1. B-Cell Disorders (Impared Ab production)
  2. T-Cell Disorders (Impared T-cell Function)
  3. T & B Cell Disorders (Impared Immune Fucntion)
  4. Complement disorders
  5. Disorders of Phagocytosis
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6
Q

What is a B-Cell Disorder?

A

B-cell disorders occur when the body has impared Antibody (Ab) production. Thus, the inability to produce antibodies to defend against microorganisims and toxins that circulate in the body.

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7
Q

What is a T-Cell Disorder?

A

T-Cell disorders are denoted by impared T-Cell function. T-cells orchestrate the immune response to protect against fungal, viral and intracllular infections. Those with T-cell disorders are at a higher risk of certain types of cancer.

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8
Q

What are T & B Cell Disorders?

A

This type of disorder results in a total breakdown of the immune function. The body has no defense at all.

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9
Q

What is a complement disorder?

A

Complement disorders is an alteration in normal complement or the absence of a complement component which leads to enhanced susceptibility to infectious diseases and immune-mediated disorders.

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10
Q

What is a Disorder of Phagocytosis?

A

The body lacks the ability to perform Phagocytosis, leaving an individual prone to bacterial infections.

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11
Q

What are the treatment options for Immunodeficiencies?

A
  1. Replacement Therapy (Synthetic Antibodies - Gamma Globulins).
  2. Marro/Thymus Transplant (Limited success, not often used).
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12
Q

What is a Hypersensitivity?

A

When the immune response is exaggerated or inappropriate. Inflammation and tissue damage results.

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13
Q

What are the 4 types of Hypersensitivity
(ACID)

A

A - Allergy or IgE Mediated Hypersensitivity
C - Cytotoxic Hypersensitivity (Bad Blood)
I - Immune Complex Hypersensitivity
D - Delayed Hypersensitivity

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14
Q

Which types of Hypersensitivity B-cell reactions?

A

Types I, II, & III
i. Allergy
ii. Cytotoxic
iii. Immune Complex

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15
Q

What cells are involved in delayed hypersensitivity?

What is not involved because of this?

A

T-Cells

Ther are no antibodies involved in type IV Delayed Hypersensitivity.

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16
Q

What Antibody mediates an Allegy hypersensitivity?

A

IgE mediated = Immunoglobulin E

17
Q

Explain IgE Mediated Hypersensitivity

A

Initial Exposure: When an allergen is first present to the body the Antigen is taken up by a Type 2 Helper T-cell. The helper cell then secretes Cytokines to stimulate differentiation of B-cells into Antibody-IgE producing plasma cells. IgE then sensitizes and binds to the mast cells (tissue cells). Secondary Exposure: The allergen binds to the IgE on the mast cells. Binding causes degranulation of the mast cells and the release of mdiators (i.e - histamine) which triggers the primary early allergice response (vasodilation, vascular damage, smooth muscle spasm). The mast cell also releases cytokines which recruit inflammatory cells and lead to the late secondary response (mucosal edema, bronchospasm -ANAPHYLACTIC SHOCK!).

18
Q

What anitbodies mediate a Cytotoxic Hypersensitivity?

A

Immunogloublin M & Immunoglobulin G

19
Q

What is a common example of Cytotoxici Hypersensitivity?

A

An incompatiable blood transfusion

20
Q

Explain the Cytotoxic Hypersensitivity reaction?

A

Mediated by IgM & IgG.
This occurs when Antibodies miss target cell surface Antigens

Abs + Ags results in the destruction of the Ag bearing cell via complement, phagocytosis (of itself), or inflammation.
Ex - incompatible blood transfusion

21
Q

What is the Type III Hypersensitivity?

A

Immune Complex (Also known as clumping)

22
Q

Explain Type III Immune Complex (Clumping)

A

Clumping occurs when antigens and antibodies form insoluble immune complexes. These complexes circulate through the blood and get deposited in the body (endothlium tissue). The complexes then react and activate complement which cause Basophil and Neutrophils to degranulate causing vasodilation and enzyme release causing tissue damage, scar tissue formation, and inflammation.
Eg. Rheumatoid arthritis - Complexes depositied in joints, IR defense cells try to remove them, resulting in inflm, tissue damage.

23
Q

What is Type IV Hypersensitivity?

A

Delayed or T-Cell Mediated Hypersensitivity.

24
Q

Explain Type IV Hypersensitivity?

A

Type IV hypersensitivity is different because there is no involvement of Antibodies.

There are two types:
1. Direct (Stat) - Involves a cell destroying antigen bearing cell. Lymphocytes directly kill antigen presenting target cells.
2. Delayed (Days) - Lymphokines need to be produced and then they destroy al antigen bearing cells.

Macrophage presents an Antigen to the T-cell causing it to become sensitized. Upon second contact, the T-cells interact with the Antigen and release cytokines that attracts more macrophages, followed by inflammation and skin leisons.

25
Q

What is an Autoimmune disorder?

A

A disorder where our “self-antigens” are no longer tolerated and considered foreign. Our own antibodies target our self antigens resulting in inflammation and necrosis.

Self tolerace can be lost in 3 ways:
1. Abnormal T-cell activity
2. Molecular mimicry
3. Previously Masked Self-Antigens (Hidden)

26
Q

What is molecular mimicry?

A

Molecular Mimicry is a type of autoimmune disorder when our own cells have a similar molecular protein structure to a foreign antigen. Our body mistakes the identity of a similar epitope and attacks our own self-antigens.

27
Q

Explain what happens when previously masked self-antigen are exposed?

A

The body believes the self-anitgens are foreign because they do not recongnize them. This causes the immune system to destroy our self-antigens.

28
Q

How does abnormal T-cell activity affect an autoimmune disorder?

A

Normally at the end of an infection suppressor T-cells signal the stoppage of the immune response. However, when we have abnormal T-cell autoimunne disorders, the suppressor T-cells no longer signal the T-cells to stop. This results in the T-cells staying and destroy the bodies own cells because of the absence of bacteria.

29
Q

What is MCH/HLA?

A

MHC: Major Histocompatibility Complex (MHC) - it is a set of cell surface molecules when controls a major part of the immune system. Each molecule displays a molecular fraction of a protein called an epitope.

HLA: Human Leukocyte Antigen

MHC/HLA is the tissue-antigen that allows the immune system (T-cells specifically) to bind to, recongnize, and tolerate itself.