Exam 2

What is cellular adaptation?

cells adapt to changes in their environment to avoid injury

What are the five types of cellular adaptation?

Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia

atrophy

A decrease in cell size due to reduced demand or adverse environmental conditions

example of atrophy

muscle atrophy from prolonged bed rest; brain atrophy due to aging

hypertrophy

an increase in cell size due to increased workload or stimulation.

example of hypertrophy

muscle growth from weightlifting

What is the difference between physiologic and pathologic hypertrophy?

Physiologic occurs due to normal stress (e.g., muscle growth from exercise); pathologic occurs due to disease (e.g., left ventricular hypertrophy from hypertension).

hyperplasia

An increase in the number of cells in an organ or tissue due to increased demand.

example of physiologic hyperplasia

Breast enlargement during pregnancy

example of non-physiological hyperplasia

Endometrial hyperplasia due to excessive estrogen

metaplasia

A reversible change where one cell type is replaced by another

example of metaplasia

Columnar to squamous epithelial cells in smokers

dysplasia

Disordered cell growth; considered a precursor to cancer

intracellular accumulations

Buildup of substances that cells cannot immediately use or eliminate

What are the three types of intracellular accumulations?

Normal body substances (lipids, proteins), abnormal endogenous products (genetic disorders), and exogenous products (coal dust, pigments).

dystrophic calcification

Deposition of calcium in injured tissue (ex: atherosclerosis)

metastatic calcification

Deposition of calcium in normal tissues due to high blood calcium levels (e.g., hyperparathyroidism)

What are the two types of cell death?

Necrosis (uncontrolled) and apoptosis (programmed)

What are common causes of cell injury?

Physical agents, radiation, chemicals, biologic agents, nutritional imbalances

How are biologic agents different from injurious agents?

they are able to replicate and can continue to produce their injurious effects

What is free radical injury?

Damage to cells by highly reactive molecules that steal electrons from cellular components.

photon

particle of radiation energy

examples of chemical agents that cause injury

drugs, mercury toxicity, carbon monoxide, insecticides, strong acids

exotoxins

actively secreted by a living bacteria & can be released into the surrounding environment

endotoxins

only released when the cell dies

nonionizing radiation

radiation energy at frequencies below those of visible light

UV radiation

the portion of the spectrum of electromagnetic radiation just above the visible range

ionizing radiation

Radiation energy above the ultraviolet (UV) range where the photons have enough energy to knock electrons off atoms and molecules

What are the cardinal signs of inflammation?

Redness, swelling, heat, pain, and loss of function.

What is the purpose of inflammation?

To eliminate harmful agents, remove damaged tissue, and initiate repair.

What are the two types of inflammation?

Acute and chronic inflammation.

What are the phases of acute inflammation?

Vascular phase and cellular phase.

What happens in the vascular phase of inflammation?

Vasodilation and increased permeability lead to redness, heat, and swelling.

What happens in the cellular phase of inflammation?

White blood cells, mainly neutrophils, migrate to the site of injury for phagocytosis.

chronic inflammation

Long-lasting inflammation that may lead to tissue damage and scarring

What are two patterns of chronic inflammation?

Non-specific chronic inflammation and granulomatous inflammation

granulomatous inflammation

A special type of chronic inflammation characterized by granuloma formation

What are the three phases of wound healing?

Inflammatory phase, proliferative phase, wound contraction/remodeling phase.

What happens in the proliferative phase of wound healing?

Fibroblasts produce collagen, and new blood vessels form.

What happens in the wound contraction and remodeling phase of wound healing?

Collagen is reorganized to strengthen the scar.

What factors affect wound healing?

Malnutrition, oxygen supply, infection, age, and immune response.

epithelialization

epithelial cells at the wound edges proliferate to form a new surface layer that is similar to that which was destroyed by the injury

immunity

body’s ability to defend against specific pathogens and/or foreign substances responsible for the development of disease

fibroblast

a connective tissue cell that synthesizes and secretes the collagen, proteoglycans, and glycoproteins needed for wound healing

What happens in the inflammatory phase of wound healing?

begins at the time of injury with the formation of a blood clot and the migration of phagocytic white blood cells into the wound site

fibrogenesis

the influx of activated fibroblasts

Granulation tissue

a glistening red, moist connective tissue that contains newly formed capillaries, proliferating fibroblasts, and residual inflammatory cells

Body cells are divided into three types according to their ability to undergo regeneration:

labile, stable, or permanent cells

labile cells

cells that divide and replicate throughout life, replacing cells

that are continually being destroyed

stable cells

cells that normally stop dividing when growth

ceases

fixed cells

cells that do not normally regenerate

stromal tissues

consist of the supporting connective tissues, blood vessels, ECM, and nerve fibers

parenchymal tissues

contain the functioning cells of an organ or body part (e.g., hepatocytes, renal tubular cells).

granuloma

a small, 1- to 2-mm lesion in which there is a massing of macrophages surrounded by lymphocytes

What are the two main types of immunity?

innate and adaptive

innate immunity

first line of defense, occurs early and more rapidly

adaptive immunity

usually delayed unless the host has been previously exposed

What are the major components of innate immunity?

Epithelial barriers, phagocytes, natural killer (NK) cells, and complement proteins

epithelial cells

block the entry of infectious agents and secrete antimicrobial enzymes, proteins, and peptides

complement system

A group of proteins that enhance immune responses by promoting inflammation and destroying microbes.

What are the three pathways of complement activation?

Classical, alternative, and lectin pathways.

What are the two branches of adaptive immunity?

Humoral immunity (B cells) and cell-mediated immunity (T cells)

antigens

Substances that trigger an immune response

antibodies

Proteins produced by B cells that bind to specific antigens

What are the five classes of antibodies?

IgG, IgA, IgM, IgE, and IgD

What is the role of IgG?

Provides long-term immunity and crosses the placenta.

What is the function of IgA?

Protects mucosal surfaces

What is the function of IgM?

First antibody produced during an infection.

What is the role of T-helper (CD4) cells?

Activate B cells and other immune cells.

What is the function of cytotoxic T (CD8) cells?

Kill virus-infected and cancerous cells.

What is the difference between active and passive immunity?

Active immunity results from infection or vaccination; passive immunity is acquired through antibody transfer.

What is an example of passive immunity?

Transfer of maternal antibodies to a newborn through the placenta or breast milk

immunization

The process of inducing immunity through vaccination.

cytokines

signals molecules that regulate immune responses

natural killer (NK) cells

Kill virus-infected and cancer cells without prior activation

What is delayed hypersensitivity (Type IV)?

A T-cell-mediated immune response, such as allergic contact dermatitis

alternative pathway in complement system

activated on microbial cell surfaces in the absence of antibody

classical pathway in complement system

activated by certain types of antibodies bound to antigen

lectin pathway in complement system

activated by a plasma lectin that binds to mannose on microbes and activates the classical system pathway in the absence of antibody

C3b

a key opsonin that coats bacteria and allows them to be phagocytized after binding to complement receptor on leukocytes