Pathophysiology Immune System Flashcards

1
Q

Benefits of the Immune System

A

Elimination of pathogens, toxins, and tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Detriments of the Immune System

A

Immediate/delayed hypersensitivities

Autoimmune diseases

Inherited and acquired immunodeficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Normal function of the Immune System

A

Discrimination: Self vs Non-self

Memory: Able to recall exposures to previous foreign antigens

Specificity: Ability to discern between different foreign antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Innate Immune System

A

1st line of defense

Nonspecific arm, pattern recognition of antigens

Controls/contains pathogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Adaptive immune system

A

Antigen specific arm, focused recognition
- Discrimination, specificity, and memory

Less rapid, but more specific response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Physical barriers of the Innate Immune System

A

Skin, mucosal membranes, ciliary action in bronchi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Chemical barriers of the Innate Immune System

A

Intestinal and vaginal pH

Enzymes: Secretions, tears, and saliva

Complement: Alternative pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Cellular defense of the Innate Immune System

A

Dendritic cells

Monocytes/macrophages

Polymorphonuclear leukocytes

NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Adaptive Immunity

A

Attacks specific pathogen after exposure to an antigen from a pathogen

Includes humoral and cell mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Humoral immunity

A

B-lymphocytes and antibodies

Primarily extracellular pathogens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cell-mediated immunity

A

T-lymphocytes

Primarily for intracellular antigens (Viruses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Principle Adaptive Immunity Cells

A

Lymphocytes: B-cells, T helper (CD4), and Cytotoxic T (CD8) cells

Antigen presenting cells: Macrophages and dendritic cells

Effector cells: Activated cytotoxic T cells, B cells, and Leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Major Histocompatibility Complexes (MHC)

A

Two classes: MHC 1 and 2

Help with intracellular antigen recognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MHC Class 1 antigens

A

On all nucleated cells of the body

Recognize intracellular antigens

Viral peptide complex with MHC-1 on surface, complex signal target for cytotoxic T-cell mediated death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MHC Class 2 antigens

A

On phagocytic cells

Engulfed fragments complex with MHC-2 on surface

T-helper cells recognize complex and become activated

Secrete cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Typical Kinetics of an Immune Response

A

Innate Mostly: Phagocytes, inflammatory cytokines, interferons, and cytokines

Adaptive mostly: T cells and antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Innate vs Adaptive Immunity

A

Innate: Physical barriers, phagocytes, complements, and NK cells

Adaptive immunity: B lymphocytes, T lymphocytes, and Effector T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Antibody Effector Functions

A

Neutralization

Opsonization

Antibody dependent cell-mediated cytotoxicity

Complement activation (fixation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Antibody Neutralization Function

A

Toxins, viruses, bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Antibody Opsonization Function

A

Coating of antigen by Ig increases efficiency of phagocytosis via Fc receptors on the phagocytic cells

20
Q

Antibody Cytotoxicity Function

A

Increases efficiency of NK lysis of target cell; IgE-mediated helminth destruction by eosinophils

21
Q

Complement Activation

A

Recruitment of inflammatory cells

Opsonization of pathogens

Killing of pathogens via membrane attack complex

22
Q

Lymphoid Tissue

A

Central organs: Bone marrow and thymus
- Cell production and maturation

Peripheral organs: Spleen, lymph nodes, tonsils, Peyer’s patches, appendix, and submucosal layers
- Trap and process antigens

23
Q

Human Immunoglobulins

A

IgA: Mucosal immunity, prevents antigens from entering

IgD: Found on B-cells, antigen receptor

IgE: Found on mast cells, immediate hypersensitivity, parasite immunity, inflammation reactions

IgG: Opsonization, neutralization, complement activation

IgM: Receptor - B cells, complement activation

24
Q

Immune system regulation

A

Inadequate response: Immunodeficiency

Excessive response: Hypersensitivity, autoimmune diseases

Increased tolerance to foreign antigens: Infections

Immune privileged tissues: Maternal-fetal tissues, brain, testes, ovaries, eyes

25
Q

Type 1 Hypersensitivity

A

IgE mediated allergies

Typical allergens: Pollen, dust mites, animal dander, foods, drugs

Cells involved: Mast cells and CD4 T-helper cells

Examples: Hay fever, asthma, and anaphylaxis reaction

26
Q

Systemic Type 1 Hypersensitivity reactions

A

Anaphylactic shock: Can be stopped with epinephrine injection

27
Q

Local (Atopic) Type 1 Hypersensitivity reactions

A

Allergic rhinitis

Hives

Asthma

Dermatitis

GI distress

28
Q

Type 2: Antibody-mediated

A

IgG or IgM mediated

Directed against cell surface antigens

  • Endogenous: ABO/Rh mismatch
  • Exogenous: Drug=cell interaction
29
Q

Type 3: Immune-complex mediated

A

Insoluble Ag-AB complexes
- Vessel wall = vasculitis
- Glomeruli = Glomerulonephritis
- Joint synovium

Inflammation and tissue damage

Systemic reactions
- Lupus erythematosus
- Serum sickness

Local reactions
- Arthus reaction
— Local skin necrosis and red, raised lesion with vasculitis

30
Q

Type 4: Cell-mediated

A

Mediated with sensitized T-cells

Direct cytotoxicity
- Primed Th cells activate Tc cells
- Self-antigen = autoimmunity

Delayed type (DTH)
- Activated Th secrete cytokines
- Recruit, activate other cells
- Cytokine synthesis = 24-74 hours

30
Q

Mechanisms of Autoimmunity

A

Largely unknown

  • Genetic factors - but relatively few
  • Environmental factors:
  1. Decreased anergy - Promotes responsiveness to self-antigens
    1a. Anergy = Prolonged unresponsiveness to self-antigens
  2. Release of normally sequestered antigens
    2a. Sperm + ocular antigens via trauma
  3. Molecular mimicry
    3a. Mistaken identity
    3b. Pathogens with same amino acid sequence as self antigens
  4. Superantigens
    4a. Exotoxins that inappropriately activate T-helper cells
31
Q

Autoimmune diseases

A

Loss of self-tolerance
- APC presents antigen + MHC-2 to CD4 cells

Mechanisms of tolerance
- Eliminate self-reactive B-cells in:
— Bone marrow
— Spleen + lymph nodes
- Eliminate self-reactive T-cells in:
— Thymus gland

Failure of tolerance results in:
- Autoimmune diseases

32
Q

Graves Disease

A

B-cells produce thyroid stimulating IgG
1. IgG mimics TSH; Greater T3/T4 from thyroid

Symptoms:
1. Hyperthyroidism
2. Goiter

33
Q

Myasthenia gravis disease

A

Auto-antibodies against nicotinic receptors in neuromuscular junction

Symptoms:
1. Ptosis
2. Diplopia
3. Difficulty swallowing and chewing
4. Weakness in the extremities
5. Breathing difficulties

34
Q

Rheumatoid arthritis

A

Pathogenesis:
1. Activated macrophages –> inflammation
2. Activated B-cells –> Complement activation –> damage
3. Pannus –> granulation tissue

Results:
1. Immune-mediated inflammation: Synovitis
2. Destruction of articular cartilage and underlying bone

Signs/Symptoms: Stiff achy joints, enlarged joints, extreme stiffness, ankylosis

Variable progression
50% chronic remitting-relapsing course
25% stabilize
25% recover, near normal function

Treatment:
1. NSAIDS
2. Immunosuppression (methotrexate) and steroids
3. Biologicals: anti-TNF’s - recent advance in therapy

35
Q

Systemic Lupus Erythematosus

A

Chronic, systemic inflammatory disease
- Effects all organ systems

Etiology: Largely unknown

Pathogenesis:
1. B-cell hyperactivity - polyclonal autoantibodies
a. Against RBCs, platelets
b. Anti-nuclear (DNA) antibodies

Factors:
1. Genetics: Class 2 HLA-DR, HLA-DQ, twins
2. Hormonal: Exacerbation during menses, pregnancy
3. Environmental: Some drugs, UV light

36
Q

Systemic Lupus Symptoms and Treatment

A

Disease course (exacerbations and remissions):
1. Joints, kidney, musculoskeletal, CV/lungs, skin, RBCs, platelets

Treatment:
1. Steroids
2. Immunosuppression

37
Q

Primary Immunodeficiency Disorders

A

Congenital or inherited
a. Humoral deficiencies
b. Cellular deficiencies
c. Severe combined immunodeficiency syndrome

38
Q

Humoral Disorder Examples

A

Genetically deceased/absent B-cell function and antibody production
a. Prone to —- pathogens

Hypogammaglobulinemia or agammaglobulinemia
(IgG, IgA, IgM, IgE, and IgD) or selective (IgA or IgG)
a. Intracellular bacteria and viral pathogens —-

38
Q

Secondary Immunodeficiency Disorders

A

Usually acquired later in life
a. HIV/AIDS

39
Q

Cellular Disorder Examples

A

DiGeorge syndrome:
a. Chromosome 22 defect: Incomplete thymus development
b. Decreased T-cell maturation
c. Decreased T-helpers = No adaptive immune system
d. Result: Prone to reinfection

Treatment: Thymus transplant, bone marrow transplant

Severe combined immunodeficiency syndrome: SCIDS
a. Absence of all immune function
b. Resembles AIDS: Cancers, disease, death by 2 years old
c. Can be treated with bone marrow or stem cell transplants

40
Q

Obligate Intracellular Bacteria

A

Chlamydia: Most common STD
Rickettsia: Typhus
Mycobacterium leprae: Leprosy

41
Q

Facultative Bacteria

A

Bartonella henselae: Cat-scratch disease

Salmonella typhi: Typhoid

Legionella: Legionnaires’ disease

Mycobacterium: Tuberculosis

Neisseria: Meningitis and gonorrhea

S. aureus: Sinusitis, food poisoning

42
Q

Acquired Immunodeficiency Syndrome (AIDS)

A

HIV infection

Transmission:
a. Unprotected sexual contact
b. Blood-blood contact
c. Occupational
d. Breast feeding

43
Q

AIDS Cellular Pathophysiology

A

Infects CD4 cells, macrophages, and dendritic cells

Sequence of infection:
1. Binding/attachment to CD4 cells
2. Internalization and uncoating
3. DNA synthesis
4. Integration
5. Transcription
6. Translation
7. Cleavage
8. Assembly and release

44
Q

AIDS Treatment Options

A

Reverse transcriptase inhibitors

Protease inhibitors

Attachment inhibitors

Integrase inhibitors

45
Q

Diseases that are more common with HIV

A

Respiratory tract: Pneumonia, TB

GI tract: Chronic gastroenteritis, esophagitis

CNS infections: Dementia, lethargy, demyelination, and ataxia

Malignancies: Kaposi’s sarcoma, non-Hodgkin’s Lymphoma

General wasting syndrome