Cellular Adaptation and Pathology

<p>Increase in cell number resulting in an increase in organ size (C)</p> Signup and view all the answers

<p>All of the above (D)</p> Signup and view all the answers

<p>Both A and B (D)</p> Signup and view all the answers

<p>The growth of the endometrial lining of the uterus in response to excessive estrogen stimulation (B)</p> Signup and view all the answers

<p>Increase in cell size resulting in an increase in organ size (D)</p> Signup and view all the answers

<p>The growth of skeletal muscle in response to exercise (C)</p> Signup and view all the answers

<p>True (A)</p> Signup and view all the answers

<p>All of the above (E)</p> Signup and view all the answers

<p>All of the above. (D)</p> Signup and view all the answers

A reversible change in cells in response to changes in their environment (stress/stimulation), affecting size, number, phenotype, metabolic activity or function.

An increase in cell number resulting in increased organ size, common in cells capable of replication.

Physiological hyperplasia stimulated by hormonal changes like puberty, pregnancy, and lactation.

Physiological hyperplasia where remaining tissue grows after a portion is removed, like after liver resection.

Pathological hyperplasia caused by excessive or uncontrolled hormonal/growth factor stimulation, often due to estrogen.

An increase in cell size resulting in increased organ size due to more structural proteins and organelles.

Physiological hypertrophy caused by increased functional demand like weightlifting or hormonal changes during pregnancy.

Pathological hypertrophy where stressed cells reach their limit of enlargement and can no longer compensate, leading to complications like heart failure.

Shrinkage in cell size by loss of cell substance, resulting in a decrease in tissue/organ size, meaning the cells are not dead but have diminished function.

Physiological atrophy caused by loss of endocrine stimulation, like uterine atrophy after menopause, or natural aging of tissues.

Pathological atrophy caused by decreased workload, loss of innervation, reduced blood supply, or inadequate nutrition.

A change of one mature (differentiated) cell type to another mature (differentiated) cell type, an adaptive response to better tolerate a specific environmental change.

Physiological metaplasia caused by hormonal changes, such as the replacement of columnar epithelium in the cervix by squamous epithelium during reproductive age.

Pathological metaplasia caused by chronic irritation from smoking or gastric reflux, like squamous metaplasia in the bronchi or Barrett's esophagus.

The accumulation of substances produced by the cell itself or elsewhere, primarily in the cytoplasm, organelles (like lysosomes), or nucleus.

Any accumulation of triglycerides within parenchymal cells, often in the liver due to alcohol abuse, diabetes, or other causes.

Macrophages engulf LDL lipoprotein, overloading with cholesterol and cholesterol esters, leading to the formation of 'foam cells' in atherosclerosis.

Less common than lipid accumulation, this occurs due to excess protein synthesis, uptake, or misfolding.

Excessive intracellular glycogen deposits associated with abnormalities in glucose or glycogen metabolism, like in uncontrolled diabetes mellitus or glycogen storage diseases.

Colored substances that are either exogenous (derived from outside the body) or endogenous (synthesized by the body).

Most common exogenous pigment derived from soot, diesel exhaust, coal, cigarette smoke, and air pollution, causing blackening of lung parenchyma and draining lymph nodes.

An insoluble brownish-yellow granular intracellular material, aka ‘wear-and-tear pigment,’ that accumulates in various tissues due to aging or atrophy.

An endogenous brown-black pigment synthesized by melanocytes in the epidermis, acting as a screen against harmful UV radiation.

Hemoglobin-derived granular pigment (iron) that accumulates in tissues when there is a local or systemic excess of iron, appearing golden yellow to brown.

Abnormal deposition of calcium salts, iron, magnesium, and other minerals, commonly occurring in various disease states.

Calcification occurs in injured/degenerated tissues, dead/necrotic tissues at normal calcium levels, possibly causing organ dysfunction.

Calcification occurs in any tissues, including normal ones, associated with hypercalcemia (high blood calcium levels), potentially impacting organ function.

Cells age due to a progressive decline in their lifespan and functional activity, caused by factors like DNA mutations, decreased replication, and protein imbalances.

Cells accumulate mutations in their DNA, primarily caused by reactive oxygen species (ROS) due to toxins or radiation, leading to functional deficiencies and eventual cell death.

Normal cells have a limited replication capacity, eventually entering a non-dividing state (replicative senescence) due to telomere shortening, leading to cell cycle arrest and aging.

Cells lose their ability to maintain normal protein homeostasis, leading to decreased synthesis, increased turnover, and accumulation of misfolded proteins, triggering apoptosis.

Cellular damage, accumulation of lipids, and endogenous substances activate the inflammasome pathway, contributing to persistent inflammation and exacerbating aging.