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
Q

What are common elements in autoimmune pathophysiology?

A

Common elements include autoantibodies, T-cell dysfunction, and molecular mimicry.

26
Q

How are autoimmune diseases diagnosed?

A

Diagnosis is based on evidence of autoimmunity indicated by history, physical, and serologic findings.

27
Q

What are typical symptoms of autoimmune diseases?

A

Typical symptoms include fatigue, joint pain and swelling, skin problems, abdominal pain or digestive issues, recurring fever, and swollen glands.

28
Q

What causes Type I hypersensitivity?

A

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
Q

What are the phases and symptoms of Type I hypersensitivity?

A

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
Q

What are the main mechanisms of Type II hypersensitivity?

A

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
Q

What characterizes Type II hypersensitivity?

A

IgG/IgM antibodies attack antigens on host cells, leading to cell destruction or dysfunction. Seen in conditions like pemphigus vulgaris and Graves’ disease.

32
Q

What causes Type III hypersensitivity?

A

Immune complexes (antigen-antibody) form in the bloodstream, deposit in tissues, activate complement, and trigger inflammation.

33
Q

What are the clinical effects of Type III hypersensitivity?

A

Causes vasculitis in autoimmune diseases like SLE and glomerulonephritis, affecting organs like kidneys, skin, lungs, and joints.

34
Q

What are the subcategories of Type IV hypersensitivity?

A

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
Q

What defines Type IV hypersensitivity, and what are the symptoms?

A

T-cell-mediated tissue damage, with symptoms like skin reactions (contact dermatitis), organ-specific inflammation, and tuberculin test responses.