1 Immune, Cardiovascular, and Lymphatic Systems Review

Comprehensive vocabulary flashcards covering the cardiovascular, lymphatic, innate, and adaptive immune systems based on lecture briefing notes.

Continuous Capillaries

The most abundant type of capillary in the body, serving as the primary site for simple diffusion, gas, nutrient, and waste exchange between blood and tissues.

Lymph Nodes

Primary lymph-filtering organs structured with several afferent lymphatic vessels entering and a single efferent vessel exiting at the hilum, slowing fluid flow for thorough filtration through reticular fibers.

Spleen

A primary lymphatic organ that filters blood rather than lymph, removing worn-out blood cells, foreign matter, and pathogens from circulation.

First Line of Defense

External, non-specific innate barriers consisting of physical structures (skin, mucous membranes), chemical secretions (lysozyme, gastric acid, saliva), and mechanical actions (coughing, sneezing)

Second Line of Defense

Internal, Leukocyte Recruitment , Release of Inflammatory Mediators (Histamine, Kinins, Complement), Phagocytosis by Macrophages & Neutrophils, Systemic Thermoregulation Adjustment (Fever via Hypothalamus)

Margination

Cell Adhesion Molecules (CAMs) expressed on endothelial walls cause circulating leukocytes (white blood cells) to group together and adhere to the vessel inner wal

Diapedesis

The process by which leukocytes change shape and squeeze through gaps between capillary endothelial cells to enter injured or infected tissue.

Chemotaxis

The directed migration of exuded leukocytes along a chemical gradient toward molecules released by damaged cells, toxins, or pathogens.

Kinins

produced by the liver; they stimulate local pain receptors, increase capillary permeability, and boost CAM production.

Rubor (Redness)

A cardinal sign of inflammation caused by localized vasodilation and increased blood flow carrying oxygenated hemoglobin to the damaged tissue.

Calor (Heat)

A cardinal sign of inflammation produced by elevated local blood volume coupled with heightened tissue metabolic activity.

Tumor (Swelling)

A cardinal sign of inflammation is fluid accumulation (edema) moving from permeable capillaries into the interstitial space (forming exudate).

Dolor (Pain)

A cardinal sign of inflammation caused by direct stimulation of pain receptors (nociceptors) by tissue compression (fluid accumulation) and chemical secretions.

Loss of Function

A cardinal sign of inflammation caused by severe localized swelling and pain preventing normal anatomical movement.

Pyrogens

Circulating fever-inducing molecules released by immune cells that signal the hypothalamus to produce prostaglandins, resetting the internal thermostat to a higher set point.

Stadium

elevated set point is maintained. Metabolic rates increase to accelerate defense mechanisms. The liver and spleen sequester zinc and iron to deprive bacteria of minerals essential for their reproduction.

Defervescence

Fever breaks as pyrogen levels fall. Prostaglandin release decreases, and the hypothalamus triggers heat-loss mechanisms, including widespread cutaneous vasodilation and sweating

Antigen

Any foreign substance perceived by the host as non-self that elicits an immune response.

Epitope

Antigenic determinant: the precise structural site on an antigen molecule recognized by lymphocytes or antibodies. A single pathogen often possesses multiple distinct epitopes on its surface.

Hapten

Small, non-immunogenic molecules that cannot trigger an immune response on their own. However, when bound to a host carrier protein, they trigger hypersensitivity or allergic responses (e.g., toxins in poison ivy, penicillin, pollen/ragweed).

Cell-Mediated Immunity (CMI)

The branch of adaptive immunity executed by T-lymphocytes that directly targets intracellular pathogens, infected host cells, and mutated tumor cells.

Cytotoxic T-Cells

Effector T-lymphocytes that execute direct cell-to-cell destruction by releasing perforins and lymphotoxins.

Perforin

protein released by cytotoxic T-cells that insert into the pathogen's cell membrane, forming physical pores (holes) that cause osmotic lysis

Lymphotoxin

secretion of cytoxic T-cells that enter the target cell and destroy its nuclear DNA, preventing replication and protein synthesis.

Helper T-Cells

Master regulators of adaptive immunity. They secrete interleukins, which stimulate rapid cell division and proliferation of both T-cells and B-cells. Also enhance the ability of other immune cells to respond to pathogens, playing a crucial role in orchestrating the immune response.

Memory T-Cells

Long-lived, antigen-experienced T-lymphocytes that persist for decades to rapidly expand into effector cells upon re-encountering the same antigen.

Antibody Mediated (Humoral) Immunity

The adaptive immune pathway driven by B-lymphocytes and circulating antibodies that targets extracellular pathogens present in body fluids (blood, lymph, interstitial fluid)

Plasma Cells

Fully differentiated, antibody-producing B-lymphocytes that synthesize and secrete large quantities of immunoglobulins directed against a specific epitope.

Antibodies

Soluble Y-shaped immunoglobulin proteins possessing antigen-binding sites tailored to lock onto matching epitopes, marking targets for phagocytosis, agglutination, or complement destruction.

First Line of Defense: Primary Components

Skin, mucous membranes, secretions (lysozyme, gastric acid, saliva, tears).

Second Line of Defense: Cellular and Molecular Components

Innate internal leukocytes (neutrophils, monocytes, and macrophages) alongside antimicrobial plasma proteins (interferons, complement proteins, and kinins).

Second Line of Defense: Operational Mechanisms

Acute inflammatory recruitment (margination, diapedesis, chemotaxis), phagocytosis of foreign debris, and hypothalamic resetting to induce fever.

Third Line of Defense (CMI): Key Cells and Maturation Site

T-lymphocytes (including cytotoxic T-cells, helper T-cells, and memory T-cells) that achieve immunocompetence and mature in the thymus.

Third Line of Defense (Humoral) Immunity: Key Cellular and Molecular Components

B-lymphocytes, differentiated plasma cells, and secreted Y-shaped immunoglobulins (antibodies).

Humoral Immunity: Operational Mechanism

Specific recognition and binding of extracellular antigens within blood, lymph, and interstitial fluid, marking them for neutralization, agglutination, or complement destruction.

Innate Immunity

The body's first line of defense against pathogens, consisting of physical barriers (like skin), chemical barriers (like saliva), and immune cells (like macrophages and neutrophils) that respond quickly to infections.

Adaptive Immunity

The body's second line of defense that develops over time, involving specific responses to pathogens through the action of lymphocytes, including B and T cells, and the formation of immunological memory.

Mechanisms of Inflammation

vascular changes, leukocyte recruitment & migration, plasma protein delivery

Third Line of Defense

Adaptive Immunity

Interferon

A group of signaling proteins produced by host cells in response to viral infections, which help inhibit viral replication and modulate the immune response.

Complement Protein

A set of proteins that enhances the ability of antibodies and phagocytic cells to clear pathogens from an organism, also involved in inflammation and cellular lysis.

Acute Inflammation

lasts 8 to 10 days. Within 72 hours, the process slows, tissue repair begins, and fibroblasts build new connective tissue.

Cardinal Signs of Inflammation

Rubor, calor, tumor, dolor, loss of function

Pus

A thick fluid composed of dead white blood cells, bacteria, and tissue debris that forms at the site of infection or inflammation.

Chronic Inflammation

dominated by macrophages and lymphocytes, which can lead to severe tissue destruction and scar tissue formation.

Prostaglandins

are lipid compounds that have diverse effects, including promoting inflammation, regulating blood flow, and facilitating pain transmission.

Stages of fever

onset, stadium, defervescence

Fever benefits

include enhancing immune response, inhibiting pathogen growth, and promoting tissue repair.

Fever Risks

can include dehydration, increased metabolic demand, and protein denaturation & potential brain damage in extreme cases.

Immunogen

Any substance that induces an immune response, often through antibody production. Immunogens can be proteins, polysaccharides, or other molecules recognized by the immune system.

Immunogenicity

degree to which an antigen triggers that response, influenced by the antigen's degree of foreignness, molecular size, structural complexity, and overall quantity present.

Adaptive Immunity Types

CMI, Humoral

Major T-Lymphocytes Types

Cytotoxic, helper, & memory T-cells

B-Lymphocyte Actions

directly recognize extracellular foreign antigens without requiring complex antigen-presenting cell processing. They differentiate into plasma cells that produce antibodies and memory B cells for future immune responses.