ADVANCED PATHOPHYSIOLOGY NURS 5060 LATEST
REVIEWED STUDY GUIDE: ALTERATIONS IN IMMUNITY,
INFECTION, AND STRESS CHAPTERS 7,8,9,10,11
Chapter 7: Innate Immunity: Inflammation and Wound Healing
First Line of Defense:
• These barriers are always present and include:
o Physical barriers: Intact skin and epithelial linings prevent pathogen entry.
o Mechanical barriers: Coughing, sneezing, vomiting, and mucus trap and expel
microbes.
o Biochemical barriers: Secretions like saliva, tears, and gastric acid contain
enzymes and antimicrobial peptides that destroy invaders.
Second Line of Defense – Inflammation:
• A nonspecific, rapid immune response triggered by tissue injury or infection.
• Cardinal signs: Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of
function.
• Vascular response: Arterioles dilate and capillary permeability increases, allowing
immune cells and proteins to enter the tissue.
• Cellular response: Neutrophils are first responders followed by monocytes that become
macrophages. Mast cells release inflammatory mediators.
Chemical Mediators of Inflammation:
• Histamine: Released by mast cells; causes vasodilation and increased vascular
permeability.
• Prostaglandins: Induce pain, fever, and enhance vascular permeability.
• Leukotrienes: Promote chemotaxis of neutrophils and vascular responses.
• Cytokines (e.g., IL-1, IL-6, TNF-α): Coordinate immune response, fever induction, and
leukocyte activation.
Plasma Protein Systems:
• Complement system: Activates opsonization, cell lysis via MAC (membrane attack
complex).
• Clotting system: Forms fibrin mesh to trap pathogens and stop bleeding.
• Kinin system: Produces bradykinin which causes pain, smooth muscle contraction, and
vascular permeability.
Wound Healing:
• Resolution: Restoration to original structure/function.
• Repair: Scar formation from collagen deposition.
• Phases:
1. Inflammation (up to 3 days)
, 2. Proliferation (3–14 days): Fibroblast activity, angiogenesis, granulation tissue
3. Remodeling (weeks–months): Collagen maturation and tensile strength
improvement
• Impaired healing: Delayed in ischemia, diabetes, infection, nutritional deficits, and
obesity.
Chapter 8: Adaptive Immunity
Third Line of Defense – Adaptive Immunity:
• Targeted and specific, involving memory for faster future response.
• Two branches:
o Humoral immunity: B lymphocytes produce antibodies.
o Cell-mediated immunity: T lymphocytes kill infected or abnormal cells.
Antigens:
• Molecules recognized by immune receptors as foreign, triggering a specific immune
response.
• Have antigenic determinants (epitopes) recognized by antibodies or T cell receptors.
Key Cells:
• B cells: Mature in bone marrow; differentiate into plasma cells that secrete antibodies.
• T cells: Mature in the thymus; include:
o Helper T cells (CD4+): Activate B cells, cytotoxic T cells, and macrophages via
cytokines.
o Cytotoxic T cells (CD8+): Kill virus-infected or cancerous cells.
Antibodies (Immunoglobulins):
• IgG: Most abundant; long-term immunity; crosses placenta.
• IgA: Found in mucosal secretions; protects against pathogens at entry points.
• IgM: First antibody made during primary response.
• IgE: Involved in allergic responses and defense against parasites.
• IgD: Found on immature B cells; uncertain function.
Immune Response Timing:
• Primary response: First exposure; slower; mostly IgM.
• Secondary response: Faster and stronger due to memory B cells; mostly IgG.
MHC Molecules:
REVIEWED STUDY GUIDE: ALTERATIONS IN IMMUNITY,
INFECTION, AND STRESS CHAPTERS 7,8,9,10,11
Chapter 7: Innate Immunity: Inflammation and Wound Healing
First Line of Defense:
• These barriers are always present and include:
o Physical barriers: Intact skin and epithelial linings prevent pathogen entry.
o Mechanical barriers: Coughing, sneezing, vomiting, and mucus trap and expel
microbes.
o Biochemical barriers: Secretions like saliva, tears, and gastric acid contain
enzymes and antimicrobial peptides that destroy invaders.
Second Line of Defense – Inflammation:
• A nonspecific, rapid immune response triggered by tissue injury or infection.
• Cardinal signs: Redness (rubor), heat (calor), swelling (tumor), pain (dolor), and loss of
function.
• Vascular response: Arterioles dilate and capillary permeability increases, allowing
immune cells and proteins to enter the tissue.
• Cellular response: Neutrophils are first responders followed by monocytes that become
macrophages. Mast cells release inflammatory mediators.
Chemical Mediators of Inflammation:
• Histamine: Released by mast cells; causes vasodilation and increased vascular
permeability.
• Prostaglandins: Induce pain, fever, and enhance vascular permeability.
• Leukotrienes: Promote chemotaxis of neutrophils and vascular responses.
• Cytokines (e.g., IL-1, IL-6, TNF-α): Coordinate immune response, fever induction, and
leukocyte activation.
Plasma Protein Systems:
• Complement system: Activates opsonization, cell lysis via MAC (membrane attack
complex).
• Clotting system: Forms fibrin mesh to trap pathogens and stop bleeding.
• Kinin system: Produces bradykinin which causes pain, smooth muscle contraction, and
vascular permeability.
Wound Healing:
• Resolution: Restoration to original structure/function.
• Repair: Scar formation from collagen deposition.
• Phases:
1. Inflammation (up to 3 days)
, 2. Proliferation (3–14 days): Fibroblast activity, angiogenesis, granulation tissue
3. Remodeling (weeks–months): Collagen maturation and tensile strength
improvement
• Impaired healing: Delayed in ischemia, diabetes, infection, nutritional deficits, and
obesity.
Chapter 8: Adaptive Immunity
Third Line of Defense – Adaptive Immunity:
• Targeted and specific, involving memory for faster future response.
• Two branches:
o Humoral immunity: B lymphocytes produce antibodies.
o Cell-mediated immunity: T lymphocytes kill infected or abnormal cells.
Antigens:
• Molecules recognized by immune receptors as foreign, triggering a specific immune
response.
• Have antigenic determinants (epitopes) recognized by antibodies or T cell receptors.
Key Cells:
• B cells: Mature in bone marrow; differentiate into plasma cells that secrete antibodies.
• T cells: Mature in the thymus; include:
o Helper T cells (CD4+): Activate B cells, cytotoxic T cells, and macrophages via
cytokines.
o Cytotoxic T cells (CD8+): Kill virus-infected or cancerous cells.
Antibodies (Immunoglobulins):
• IgG: Most abundant; long-term immunity; crosses placenta.
• IgA: Found in mucosal secretions; protects against pathogens at entry points.
• IgM: First antibody made during primary response.
• IgE: Involved in allergic responses and defense against parasites.
• IgD: Found on immature B cells; uncertain function.
Immune Response Timing:
• Primary response: First exposure; slower; mostly IgM.
• Secondary response: Faster and stronger due to memory B cells; mostly IgG.
MHC Molecules:
