Immunology Flashcards

1
Q

What is transplantation?

A

The process of taking cells, tissue, or organs and placing them in another person.

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2
Q

What is an Allograft?

A

Transplantation from one person to another.

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3
Q

What is an Autograft?

A

Transplantation from the same person to the same person.

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4
Q

What is a major complication of transplantation?

A

Graft rejection.

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5
Q

What must the host’s immune system do for a transplant to succeed?

A

Recognize the transplant as ‘self’.

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6
Q

Which immune cells help in recognizing foreign antigens during transplantation?

A

T-lymphocytes.

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7
Q

What guides T-lymphocytes in distinguishing self from non-self?

A

HLA proteins on cell surfaces.

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8
Q

What happens when B and T lymphocytes encounter unfamiliar peptides?

A

They attack the cells.

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9
Q

How does the risk of rejection change with HLA similarity?

A

It decreases with greater HLA similarity between donor and recipient.

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10
Q

What are primary immunodeficiency disorders (PIDDS)?

A

Abnormalities in the immune system that are inherited or congenital.

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11
Q

What causes most PIDDS?

A

Deficiencies in the signaling pathway affecting cytokines, receptors, and metabolic pathways.

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12
Q

What are secondary immunodeficiency disorders?

A

Disorders that are acquired later in life.

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13
Q

What is often associated with PIDDS?

A

Autoimmunity.

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14
Q

Name an example of a primary immunodeficiency disorder.

A

Selective deficiency of IgG, IgA, and IgM.

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15
Q

What is DiGeorge syndrome?

A

Congenital thymic aplasia.

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16
Q

What is a hereditary deficiency of complement proteins?

A

An example of a primary immunodeficiency disorder.

17
Q

What are hypersensitivity disorders?

A

Excessive or elevated responses from an active immune system that causes injury to the host tissue.

18
Q

How many types of hypersensitivity disorders are there?

A

Four types (Type I-IV).

19
Q

What are the four hypersensitivity reactions or types

A

Type 1 (IgE) mediated hypersensitivity disorders

Type 2 Antibody-Mediated disorders

Type 3 Immune complement mediated disorders

Type 4 T- Cell mediated hypersensitivity disorder

20
Q

What are autoimmune diseases?

A

Autoimmune diseases occur when the body cannot distinguish its own cells from foreign cells, leading to attacks on normal cells.

21
Q

What causes autoimmune diseases?

A

The exact cause is unknown, but both genetic and environmental factors play a role.

22
Q

Does gender affect autoimmune diseases?

A

Yes, Gender can have an effect on the type of autoimmune disorder.

23
Q

What is the pathophysiology of autoimmune diseases?

A

Autoimmune diseases involve the immune system mistakenly attacking the body’s own tissues, causing chronic inflammation and tissue damage.

24
Q

What are autoantibodies?

A

Autoantibodies are antibodies produced by the immune system that target and attack a person’s own tissues and antigens.

25
What are common elements in autoimmune pathophysiology?
Common elements include autoantibodies, T-cell dysfunction, and molecular mimicry.
26
How are autoimmune diseases diagnosed?
Diagnosis is based on evidence of autoimmunity indicated by history, physical, and serologic findings.
27
What are typical symptoms of autoimmune diseases?
Typical symptoms include fatigue, joint pain and swelling, skin problems, abdominal pain or digestive issues, recurring fever, and swollen glands.
28
What causes Type I hypersensitivity?
It is an IgE-mediated allergic reaction to harmless antigens (e.g., pollen, dust, food). Mast cells and basophils release histamine, leading to symptoms.
29
What are the phases and symptoms of Type I hypersensitivity?
Initial phase (5–60 min): Vasodilation, vascular leakage, smooth muscle contraction. Secondary phase (2–8 hrs): Eosinophil infiltration. Symptoms: Hives, runny nose, asthma, atopic dermatitis, or life-threatening anaphylaxis.
30
What are the main mechanisms of Type II hypersensitivity?
Complement-activated cell destruction (e.g., MAC). ADCC: Natural killer cells destroy targets via IgG. Complement-mediated inflammation (e.g., neutrophil degranulation). Receptor modulation: Antibodies alter receptor function (e.g., Graves' disease).
31
What characterizes Type II hypersensitivity?
IgG/IgM antibodies attack antigens on host cells, leading to cell destruction or dysfunction. Seen in conditions like pemphigus vulgaris and Graves' disease.
32
What causes Type III hypersensitivity?
Immune complexes (antigen-antibody) form in the bloodstream, deposit in tissues, activate complement, and trigger inflammation.
33
What are the clinical effects of Type III hypersensitivity?
Causes vasculitis in autoimmune diseases like SLE and glomerulonephritis, affecting organs like kidneys, skin, lungs, and joints.
34
What are the subcategories of Type IV hypersensitivity?
IVa: Macrophage activation (e.g., eczema). IVb: Eosinophil activation (e.g., delayed hypersensitivity). IVc: Cytotoxic T-cell response (e.g., hepatitis). IVd: Neutrophil activation (e.g., AGEP).
35
What defines Type IV hypersensitivity, and what are the symptoms?
T-cell-mediated tissue damage, with symptoms like skin reactions (contact dermatitis), organ-specific inflammation, and tuberculin test responses.