Pathophysiology of the Immune System ch6,7,8

100 vocabulary-style flashcards derived from the lecture notes on immune pathophysiology.

Innate immunity

Born-with, non-specific defense system that provides immediate protection against pathogens.

First line of defense

Barriers that prevent entry of pathogens: physical, mechanical, and biochemical.

Physical barriers

Structural defenses such as skin and mucosal surfaces that block pathogens.

Skin

Outer protective barrier composed of keratinized epithelium; part of the first line of defense.

Mucosal linings

Mucous membranes in GI, GU, and respiratory tracts that trap and remove pathogens.

Sloughing off cells

Regular shedding of cells helps remove attached microbes.

Coughing

Mechanical clearance of inhaled or trapped pathogens from the airways.

Sneezing

Expulsion of air and mucus to remove irritants from the nasal passages.

Flushing

Urine flow that mechanically washes out microbes from the urinary tract.

Vomiting

Expulsion of stomach contents to remove ingested toxins or pathogens.

Mucus

Thick secretion that traps pathogens on mucosal surfaces.

Mucous (adj)

Describes cells that produce mucus; related to mucous membranes.

Lysozyme

Antimicrobial enzyme found in secretions (e.g., tears, saliva) that helps kill bacteria.

Antimicrobial peptides

Small proteins produced by epithelial cells that inhibit microbial growth.

Microbiome

Community of microorganisms living in and on the body; many are non-harmful or beneficial.

Symbiotic relationship

Mutually beneficial association between host and microbes.

Pseudomembranous colitis

Antibiotic-associated overgrowth of Clostridium difficile in the gut.

Clostridium difficile

Bacterium that overgrows after antibiotics, causing colitis.

Antibiotics

Drugs that kill or inhibit bacteria; can disrupt normal gut flora.

Vaginal candidiasis

Fungal overgrowth in the vagina due to imbalance; typically caused by Candida albicans.

Candida albicans

Fungal organism responsible for yeast infections including vaginal candidiasis.

Inflammation

Vascular and cellular response to injury intended to contain damage and promote healing.

Acute inflammation

Immediate, short-duration inflammatory response; non-specific.

Chronic inflammation

Inflammation of prolonged duration; ongoing tissue injury and repair.

Ischemia

Reduced blood flow leading to hypoxia and cellular injury.

Necrosis

Cell or tissue death due to injury or lack of blood supply.

Foreign bodies

Non-self materials that can provoke an inflammatory response.

Inappropriate immune reaction

Immune response against self or harmless antigens (e.g., autoimmunity, allergy).

Cardinal signs of inflammation

Pain, heat, redness, swelling, and loss of function indicating inflammation.

Pain

Discomfort or aching associated with inflammation; a cardinal sign.

Heat

Increased tissue temperature due to vasodilation in inflammation.

Redness

Erythema caused by increased blood flow during inflammation.

Swelling

Edema from vascular permeability during inflammation.

Loss of function

Impaired function as a result of inflammation and tissue damage.

Endothelial cells

Cells lining blood vessels; regulate vascular permeability and leukocyte migration.

Endothelial activation

Endothelial cells respond to inflammatory signals by increasing permeability and adhesion molecule expression.

Margination

Leukocytes accumulate along the vascular endothelium in preparation for transmigration.

Diapedesis

Leukocytes transmigrate through the endothelium into tissue.

Chemotaxis

Directed movement of leukocytes toward chemical signals at the injury site.

Neutrophils

First-responder white blood cells; phagocytose pathogens and release reactive species.

Macrophages

Phagocytes that engulf debris and pathogens; orchestrate repair and antigen presentation.

Mast cells

Cells that release histamine and other mediators, promoting vasodilation and permeability.

Dendritic cells

Professional antigen-presenting cells; bridge innate and adaptive immunity.

Cytokines

Signaling proteins (e.g., TNF, IL-1) that modulate inflammation and immune responses.

Complement system

Cascade of proteolytic serine proteases enhancing inflammation and pathogen clearance.

Clotting factors

Proteins that promote blood clotting to limit bleeding and spread of infection.

Bradykinin

Kinin peptide that increases vascular permeability and pain.

Kinin system

Pathway producing bradykinin, contributing to inflammation.

Histamine

Vasodilator released by mast cells and basophils; increases permeability.

5-Lipoxygenase (5-LOX)

Enzyme producing leukotrienes, promoting inflammation and leukocyte chemotaxis.

Leukotrienes

Inflammatory mediators that increase vascular permeability and cause bronchoconstriction.

Cyclooxygenase (COX)

Enzyme that forms prostaglandins and thromboxanes; key inflammatory mediators.

Prostaglandins

Eicosanoids that promote vasodilation, permeability, pain, and fever.

PGE2

Prostaglandin involved in fever and pain; produced by COX pathways.

Pyrogen

Substance that induces fever via hypothalamic temperature set point.

Interleukin-1 (IL-1)

Pro-inflammatory cytokine; activates endothelium and induces fever.

TNF-α (Tumor necrosis factor alpha)

Pro-inflammatory cytokine; promotes inflammation and leukocytosis.

Interferons (IFN)

Cytokines with antiviral activity; activate antiviral proteins in neighboring cells.

Opsonization

Tagging of pathogens by molecules (e.g., antibodies, C3b) to enhance phagocytosis.

Membrane Attack Complex (MAC)

C5b-C9 complex that lyses certain bacteria by forming pores in membranes.

C3b

Opsonin that promotes phagocytosis of pathogens.

C5a

Chemotactic anaphylatoxin that recruits neutrophils to sites of inflammation.

C3a

Anaphylatoxin that stimulates histamine release and inflammation.

Hypoxia

Low oxygen condition resulting from ischemia or inflammation.

Leukocytosis

Elevated white blood cell count in response to inflammation.

Acute-phase reactants

Liver-produced proteins (e.g., CRP) elevated during inflammation.

C-reactive protein (CRP)

Acute-phase protein used as a clinical marker of inflammation.

Abscess

Localized collection of pus within tissue due to infection.

Scarring (fibrosis)

Formation of fibrous tissue during chronic inflammation and healing.

Granulomatous inflammation

Chronic inflammatory pattern with organized macrophages and lymphocytes.

Caseating granuloma

Granuloma with central necrosis, typical of TB or certain fungi.

Non-caseating granuloma

Granuloma without central necrosis; seen in sarcoidosis, Crohn’s, or foreign body reactions.

MHC Class I

Molecule on all nucleated cells presenting endogenous antigens to CD8+ T cells.

MHC Class II

Molecule on APCs presenting exogenous antigens to CD4+ T helper cells.

Antigen

Molecule recognized specifically by B or T cell receptors.

Antigen-presenting cells (APCs)

Cells (e.g., dendritic cells, macrophages, B cells) that present antigens via MHC to T cells.

Dendritic cell antigen presentation

Dendritic cells process and present antigens to naive T cells in lymph nodes.

T cell receptor (TCR)

Receptor on T cells that recognizes peptide-MHC complexes.

CD4+ T helper cells

T cells that recognize antigens via MHC II and orchestrate immune responses.

CD8+ cytotoxic T cells

T cells that recognize antigens via MHC I and kill infected or abnormal cells.

B lymphocytes

Lymphocytes that can differentiate into plasma cells to produce antibodies.

Plasma cells

Differentiated B cells that secrete antibodies.

Antibody (Immunoglobulin)

B cell–derived protein that binds antigen and mediates neutralization, opsonization, and complement activation.

IgM

First antibody isotype produced; pentameric; strong at activating complement.

IgG

Most abundant antibody in serum; mediates opsonization, neutralization, complement; transfers placenta.

IgA

Antibody isotype protecting mucosal surfaces and secretions.

IgE

Antibody involved in allergic responses and defense against helminths; binds mast cells/basophils.

Class switching

B cells switch from IgM to other isotypes (IgG/IgA/IgE) to tailor responses.

Clonal expansion

Proliferation of antigen-specific B or T cells after antigen recognition.

Memory cells

Long-lived lymphocytes that provide rapid responses on re-exposure to antigen.

Primary immune response

Initial exposure to antigen; slower lag and predominance of IgM before switching.

Secondary immune response

Faster, higher-titer response due to memory cells; mainly IgG/IgA/IgE.

Affinity maturation

Increased antibody affinity for antigen over time during the immune response.

Antibody isotypes

Different classes of antibodies (IgM, IgG, IgA, IgE) with distinct roles.

Pattern Recognition Receptors (PRRs)

Receptors on innate immune cells that recognize common microbial patterns (PAMPs) or damage signals (DAMPs).

PAMPs

Pathogen-associated molecular patterns recognized by PRRs (e.g., LPS in Gram-negative bacteria).

DAMPs

Damage-associated molecular patterns released by injured cells that activate PRRs.