Immunology and Stress Management Overview

Objectives

• PowerPoint review covering stress management (Chapter 7), inflammation (Chapter 12), normal immune response, Type I IgE-mediated reactions & allergic disorders (Chapter 14), hematological assessment (Chapter 33), and hematological problems (Chapter 34)
• In-class application activities
• Group nutrition presentation on anemia

Immune Responses & Inflammation

• Slides display a microscopic image of blood cells
• Basic functions of the immune system: defense (protects, prevents attacks), homeostasis (digests, removes), and surveillance (recognizes, destroys)
• Antigens are foreign substances triggering an immune response. All cells have surface antigens for self-recognition, avoiding self-response.

Antigens

• Foreign substances initiating immune responses
• All cells have surface antigens for unique self-identification.
• Enables the body to differentiate between self and non-self.

Types of Immunity

• Innate: present at birth, first line of defense, non-antigen-specific, immediate response (natural WBC response), primarily neutrophils and monocytes
• Active (long-lived): invasion of a foreign antigen, antibody production (e.g., disease, immunization), reinvasion leads to a quicker response, memory cells
• Passive (short-lived): receives antibodies from a source (e.g., mother to fetus, serum antibodies), no memory cells

Hematopoiesis

• Process of blood cell formation.
• Hematopoietic stem cell is the origin of all blood cells.
• Stem cells differentiate into: Lymphoid (B-cells, T-cells, NK cells), Myeloid (Neutrophils, Basophils, Mast cells, Eosinophils, Dendritic cells, Macrophages), and Erythroid (RBC, Megakaryocytes, Platelets) lineages

Lymphoid Organs

• Central lymphoid organs: thymus gland (T cells), bone marrow (B cells)
• Peripheral lymphoid organs: lymph nodes, tonsils, spleen, gut-associated lymphoid tissue, genital-associated lymphoid tissue, bronchial-associated lymphoid tissue, skin-associated lymphoid tissue

Inflammatory & Immune Response

• B-lymphocytes: mature in bone marrow, differentiate into plasma cells, produce antibodies (immunoglobulins), last to arrive at the injury site.
• T-lymphocytes: migrate and mature in the thymus, responsible for immunity against viruses, tumor cells, and fungi.

Antibody Immunity

• B-lymphocytes: first exposure to antigen triggers antibody production (IgG, IgA, IgM, IgD, IgE); first exposure
• 2nd exposure to antigen: Memory B-lymphocytes recognize the antigen resulting in rapid antibody production.

Cell-Mediated Immunity

• T-lymphocytes differentiate into cytotoxic T cells (CD8) and helper T cells (CD4).
• CD8 T-cells: attack and destroy antigens by releasing cytolytic substances and become memory T cells.
• CD4 T-cells: regulate cell-mediated immunity, antibody response, cytokines, NK cells, T dendritic cells

Cytokines

• Cell messengers instructing cells on proliferation, differentiation, secretion, or cellular activity.
• Types include interleukins, interferons, tumor necrosis factor (TNF), colony-stimulating factors, and erythropoietin.

Autoimmune Diseases

• Body's inability to recognize self.
• Cause is unknown.
• Loss of self-tolerance for the body's own DNA antigens.

Altered Immune Response

• Type I (IgE-mediated): immediate onset (e.g., asthma, hives) caused by histamine, leukotrienes, mast cells, and prostaglandins.
• Type II (Cytotoxic): minutes to hours onset (e.g., transfusions, ITP, Graves disease) from IgG & IgM antibodies binding to antigens.
• Type III (Immune Complex): hours to days onset (e.g., RA, SLE), caused by monocytes, macrophages, and neutrophils.
• Type IV (Delayed Hypersensitivity): several days onset (e.g. contact dermatitis), caused by T cytotoxic cells and cytokines.

Stress on the Immune Response

• Acute/chronic stress leads to immunosuppression.
• It decreases the number of NK cells and lymphocytes proliferation.
• It alters cytokine production and decreases phagocytosis by neutrophils/monocytes.

Allergic Disorders

• Assessment includes personal and family history of allergies, social/environmental factors.
• Diagnostic studies include skin testing (scratch/prick, intradermal, patch).
• Treatment includes treatment for anaphylaxis (ABCs), seasonal/chronic allergy recognition and control (medications, immunotherapy).

Inflammatory & Immune Response (detailed)

• Vascular Response: Facilitates fluid movement from capillaries to tissue spaces (vasodilation).
• Cellular Response (WBCs with Differential):
  • Neutrophils: (6-12 hrs) 1st responders, phagocytize bacteria, foreign material, damaged and dead cells, and tissue debris creating pus.
  • Monocytes (macrophages): phagocytize bacteria and present antigens to T or B lymphocytes, triggering cell-mediated immunity.

Inflammation (continued)

• Lymphocytes: differentiate into B and T cells, responsible for long-term immunity.
• Eosinophils: associated with allergic responses and atopic disorders.
• Basophils: release histamine for inflammatory responses.
• Chemical mediators: prostaglandins, leukotrienes, complements

Clinical Manifestations

• Signs of inflammation: fever (antipyretics, hydration), inflammation (anti-inflammatory, vitamins, RICE), erythema, increased WBC count, green/yellow colored sputum, purulent exudate (pus), odor, cloudy/discolored urine

CBC - Shifts

• Left Shift (Bacterial): increased WBC count, increased neutrophils, presence of bands (immature neutrophils).
• Right Shift (Viral): decreased or normal WBC count, decreased neutrophils, increased lymphocytes.