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PHYT 6311: Clinical Pathology > Test 1: Module 2 (Immune System) > Flashcards

Test 1: Module 2 (Immune System) Flashcards

1
Q

Immune system

A

the bodily system that protects the body from foreign substances, cells, and tissues by producing the immune response and that includes ….. macrophages, lymphocytes including the B cells and T cells,
and antibodies.

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2
Q

Phases of the adaptive immune response

A
  1. Recognition phase: APC to Naive T and B lymphocytes (day 0)
  • Clonal expansion and differentiation
  1. Amplification phase: Antibody producing cells and effector T lymphocytes (~7 days)
  2. Effector phase: Elimation of antigens, cell mediated immunity, humoral immunity (~7-14 days)
  3. Termination phase: Apoptosis (~14-30 days)
  4. Memory: Surviving memory cells (>30 days)
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3
Q

Antibodies

A

proteins produced by the body (predominantly plasma B cells) that helps fight foreign pathogens

They bind to antigens

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4
Q

Major functions of immunoglobulins/Antibodies

A
  1. Directly attack antigens, destroying or neutralizing them through the process of agglutination, precipitating the toxins out of solution, neutralizing antigenic substances, and lysing the organism’s cell wall
  2. Activate the complement system
  3. Activate anaphylaxis by releasing histamine in tissue and blood
  4. Stimulate antibody-mediated hypersensitivity
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5
Q

Antigens

A

Any substance foreign to the body that evokes an immune response either alone or after forming a complex with a larger molecule (such as a protein) and that is capable of binding with a product (such as an antibody or T cell) of the immune response

Substance that is capable of stimulating an immune response,
specifically activating lymphocytes, which are the body’s infection-fighting white
blood cells.

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6
Q

MHC/HLA

A

Major Histocompatibility Complex: membrane proteins that function to present antigenic peptides for recognition by T cells.

  • MHC proteins found in humans are known as human leukocyte
    antigens (HLAs)
  • MHC I & MHC II
  • All nucleated proteins present MHC I (self-antigens)
  • Antigen presenting cells (APC) contain MHC II.
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7
Q

Granulocytes

A

Basophil
Neutrophil
Eosinophil

Apart of innate (non-specific) immune system

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8
Q

Antigen-presenting cells (APCs)

A

B lymphocyte - adaptive
Macrophage - innate
Dendritic cells - innate

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9
Q

Basophil and mast cell function

A

Release chemicals that mediate inflammation and allergic responses

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10
Q

Neutrophils function

A

Ingest and destroy invaders

Most abundant. Make up 50-70% of WBCs in blood.

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11
Q

Eosinophils function

A

Destroy invaders, particularly parasites

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12
Q

Monocytes and Macrophages function

A

Ingest and destroy invaders. Antigen presentation

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13
Q

Lymphocytes and Plasma cell function

A

Specific responses to invaders, including antibody production

Second most abundant. Make up 20-35% of WBCs in blood.

B and T lymphocytes, NKCs

APCs

Specific/Adaptive Immune System

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14
Q

Dendritic cell function

A

Recognize pathogens and activate other immune cells by antigen presentation.

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15
Q

Role of antigen-presenting cells in the innate immune system (Macrophage and Dendritic cells)

A
  1. Phagocytosis of enemy cell (antigen)
  2. Fusion of lysosome and phagosome
  3. Enzymes start to degrade enemy cell
  4. Enemy cell broken into small fragments
  5. Fragments of antigen presented on APC surface
  6. Leftover fragments released by exocytosis
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16
Q

Natural Killer Cells – Innate

A

Kills tumors & infected cells
* Need activating ligands
* And absence of inhibitory signal (MHC I)

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17
Q

T Helper cells

A

CD4

Naiive helper T cell binds to the antigen on an antigen presenting cell. The antigen is presented on the MHC class 2 complex

The T helper cell becomes activated and clonal proliferation and differentiation occurs. (The T helper cells “call for help”)

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18
Q

Cytotoxic T Cells

A

CD8

An infected cell presents an antigen on the MHC class 1 complex. The CTL (cytotoxic T cell) becomes activated.

The CTL releases perforin and granzymes that invade the infected cell and induce controlled destruction (apoptosis) of the infected cell.

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19
Q

Activation of T cells

A
  1. Antigen is taken into APC (macrophage, dendritic cell). The antigen is processed and presented on the surface of the APC, via the MHC class 2 complex.
  2. Helper T cell binds to the antigen on the APC and calls for help.
  3. Cytotoxic T cells bind to the antigen on the APC and become activated
  4. Activated cytotoxic T cells bind to infected cells that present the processed antigen on MHC class 1 complex.
  5. The cytotoxic T cells release granzymes and perforins for controlled cell death of the infected cell (apoptosis).
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20
Q

B cell – humoral immunity

A
  1. An antigen on a bacteria is presented to the B cell.
  2. The B cell begins undergoing clonal selection and presents the antigen to the T helper cell on an MHC class 2 complex. The T helper cell releases cytokines.
  3. Clonal expansion occurs due to cell proliferation
  4. Memory B cells, to recognize the same antigen, and plasma cells arise.
21
Q

Complement system

A
  1. Opsonization for phagocytosis: a process that helps the immune system identify and destroy pathogens by coating them with opsonins, which are substances that help phagocytes find, attach to, and engulf the pathogens
  2. Cell lysis by membrane attack
    complex (MAC): a complex of proteins that forms pores in the membranes of microbes and other target cells, leading to cell lysis and death
  3. Chemotactic factors (C3a, C5a): attract immune cells to sites of infection and injury, where they help eliminate pathogens
22
Q

Hypersensitivity Type 1 Mechanism of activation and Examples

A

An allergen specific IgE antibodies bind to mast cells via Fc receptor. When the specific antigen binds to the IgE, crosslinking of IgE induces degranulation (release of inflammatory chemicals, or mediators) of mast cells.

The release of primary and secondary mediators causes smooth muscle spasms, edema, mucus secretion, epithelial damage, and leukocyte infiltration

Examples:

Local and systemic anaphylaxis
Seasonal hay fever
Food allergies
Drug allergies

23
Q

Hypersensitivity Type 1 - Allergy

A

Stimulus: exogenous

  • Immune response: allergic,
    inflammatory response
  • Mediator process: IgE
    antibodies
  • Timing: immediate
  • Previous exposure increases B
    cell sensitivity & may worsen
    response
  • Epinephrine: opposite effect
24
Q

Hypersensitivity Type 2 Mechanism of activation and Examples

A

Cytotoxic reaction to self

IgG or IgM antibody bind to cellular antigen, leading to complement activation and cell lysis.

IgG can also mediate Antibody-dependent cell cytotoxicity (ADCC) with cytotoxic T cells, NKCs, macrophages, and neutrophils

Examples:
RBC destruction after transfusion with mismatched blood types during hemolytic disease of the newborn

25
Q

Type II: myasthenia gravis

A
  • Voluntary muscle weakness & fatigue
  • Disruption in the normal communication between nerves and muscles
  • No cure for MG
  • PT for safe mobility and function.
26
Q

Hypersensitivity Type 3 Mechanism of activation and Examples

A

Stimulus: Exogenous or Endogenous
Immune Response: Excessive antibody complex, complement system
Mediator process: IgG an IgM antibodies, complement system

Immune complex disease

  1. Antigen-antibody complexes (IgG and IgM with antigens attached) are deposited in tissues.
  2. Complement activation provides inflammatory mediators and recruits neutrophils.
  3. Neutrophil chemotaxis and adherence (stick to endothelial wall)
  4. Degranulation (enzymes released from neutrophils damage tissue)
  5. Outcome: Cell lysis

***Examples:

Post-streptococcal glomerulonephritis

Rheumatoid Arthritis

Systemic Lupus Erythematosus

27
Q

Type III: Rheumatoid arthritis

A
  • chronic inflammatory disorder
  • May affect joints, skin, eyes, lungs, heart and blood vessels.
  • No cure for RA
  • PT to maintain function & mobility
28
Q

Hypersensitivity Type 4 Mechanism of activation and Examples

A

Delayed cell-mediated

T Helper cells secrete cytokines which activate macrophages and cytotoxic T cells, resulting in tissue injury and cell killing.

Type 1 can develop into Type 4

Examples:
Contact dermatitis
Type 1 diabetes mellitus
Multiple sclerosis

29
Q

Type IV: type I diabetes

A
  • Chronic condition in which the
    pancreas produces little or no
    insulin
  • the body’s own immune system
    mistakenly destroys the insulin-
    producing (islet, or islets of
    Langerhans) cells in the pancreas.
  • No cure for t1dm
  • No prevention method
  • Exercise help improve glucose
    control.
30
Q

Immunodeficiency (primary and secondary)

A

the immune response is absent or depressed as a result
of a primary or secondary disorder

Primary immunodeficiency reflects a defect involving T cells, B cells, or lymphoid tissues
- Genetic defect

Secondary immunodeficiency results from an underlying disease or factor that depresses or blocks the immune response.

 - HIV, malnutrition, alcoholism, 
   aging, diabetes, autoimmune 
   disease, cancer
31
Q

HIV

A

Initially, HIV-1 infects T cells and macrophages directly

Viral replication in both T cells and macrophages continues unabated.

A gradual erosion of CD4+cells by productive infection

Ultimately, CD4+cell numbers decline, and the patient develops clinical symptoms of full-blown AIDS

32
Q

Systemic Lupus Erythematosus (SLE)

A

Causes: Autoimmune disorder triggered by genetics, hormones, and environmental factors (e.g., sunlight, infections).

Presentation: Butterfly-shaped rash on face, joint pain, fatigue, fever, sensitivity to sunlight, multi-organ involvement (kidneys, heart, lungs).

Type 3 hypersensitivity

33
Q

Rheumatoid Arthritis (RA)

A

Causes: Autoimmune disorder triggered by genetics, smoking, and hormonal factors.

Presentation: Symmetrical joint pain, morning stiffness, joint swelling, fatigue, joint deformities, and rheumatoid nodules.

Type 3 hypersensitivity

34
Q

Reiter Syndrome (Reactive Arthritis)

A

Causes: Triggered by an infection, often following a gastrointestinal or genitourinary infection (e.g., Salmonella, Chlamydia).

Presentation: Joint pain, inflammation of the eyes (conjunctivitis), and urethritis (“can’t see, can’t pee, can’t climb a tree”).

Type 3 hypersensitivity

35
Q

Sjögren Syndrome

A

Causes: Autoimmune disorder where the immune system attacks moisture-producing glands, often associated with other autoimmune diseases like RA.

Presentation: Dry eyes, dry mouth, difficulty swallowing, joint pain, fatigue, and sometimes involvement of internal organs (kidneys, lungs).

Type 4 hypersensitivity

36
Q

Release chemicals that mediate inflammation and allergic responses

A

Basophil and mast cell function

37
Q

Ingest and destroy invaders

Most abundant. Make up 50-70% of WBCs in blood.

A

Neutrophils function

38
Q

Destroy invaders, particularly parasites

A

Eosinophils function

39
Q

Ingest and destroy invaders. Antigen presentation

A

Monocytes and Macrophages function

40
Q

Specific responses to invaders, including antibody production

Second most abundant. Make up 20-35% of WBCs in blood.

B and T lymphocytes, NKCs

APCs

Specific/Adaptive Immune System

A

Lymphocytes and Plasma cell function

41
Q

Recognize pathogens and activate other immune cells by antigen presentation.

A

Dendritic cell function

42
Q

An allergen specific IgE antibodies bind to mast cells via Fc receptor. When the specific antigen binds to the IgE, crosslinking of IgE induces degranulation (release of inflammatory chemicals, or mediators) of mast cells.

The release of primary and secondary mediators causes smooth muscle spasms, edema, mucus secretion, epithelial damage, and leukocyte infiltration

Examples:

Local and systemic anaphylaxis
Seasonal hay fever
Food allergies
Drug allergies

A

Hypersensitivity Type 1 Mechanism of activation and Examples

43
Q

Cytotoxic reaction to self

IgG or IgM antibody bind to cellular antigen, leading to complement activation and cell lysis.

IgG can also mediate Antibody-dependent cell cytotoxicity (ADCC) with cytotoxic T cells, NKCs, macrophages, and neutrophils

Examples:
RBC destruction after transfusion with mismatched blood types during hemolytic disease of the newborn

A

Hypersensitivity Type 2 Mechanism of activation and Examples

44
Q

Stimulus: Exogenous or Endogenous
Immune Response: Excessive antibody complex, complement system
Mediator process: IgG an IgM antibodies, complement system

Immune complex disease

  1. Antigen-antibody complexes (IgG and IgM with antigens attached) are deposited in tissues.
  2. Complement activation provides inflammatory mediators and recruits neutrophils.
  3. Neutrophil chemotaxis and adherence (stick to endothelial wall)
  4. Degranulation (enzymes released from neutrophils damage tissue)
  5. Outcome: Cell lysis

***Examples:

Post-streptococcal glomerulonephritis

Rheumatoid Arthritis

Systemic Lupus Erythematosus

A

Hypersensitivity Type 3 Mechanism of activation and Examples

45
Q

Delayed cell-mediated

T Helper cells secrete cytokines which activate macrophages and cytotoxic T cells, resulting in tissue injury and cell killing.

Type 1 can develop into Type 4

Examples:
Contact dermatitis
Type 1 diabetes mellitus
Multiple sclerosis

A

Hypersensitivity Type 4 Mechanism of activation and Examples

46
Q

Causes: Autoimmune disorder triggered by genetics, hormones, and environmental factors (e.g., sunlight, infections).

Presentation: Butterfly-shaped rash on face, joint pain, fatigue, fever, sensitivity to sunlight, multi-organ involvement (kidneys, heart, lungs).

Type 3 hypersensitivity

A

Systemic Lupus Erythematosus (SLE)

47
Q

Causes: Autoimmune disorder triggered by genetics, smoking, and hormonal factors.

Presentation: Symmetrical joint pain, morning stiffness, joint swelling, fatigue, joint deformities, and rheumatoid nodules.

Type 3 hypersensitivity

A

Rheumatoid Arthritis (RA)

48
Q

Causes: Triggered by an infection, often following a gastrointestinal or genitourinary infection (e.g., Salmonella, Chlamydia).

Presentation: Joint pain, inflammation of the eyes (conjunctivitis), and urethritis (“can’t see, can’t pee, can’t climb a tree”).

Type 3 hypersensitivity

A

Reiter Syndrome (Reactive Arthritis)

49
Q

Causes: Autoimmune disorder where the immune system attacks moisture-producing glands, often associated with other autoimmune diseases like RA.

Presentation: Dry eyes, dry mouth, difficulty swallowing, joint pain, fatigue, and sometimes involvement of internal organs (kidneys, lungs).

Type 4 hypersensitivity

A

Sjögren Syndrome

PHYT 6311: Clinical Pathology (10 decks)

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