Cellular Adaptation, Injury, and Death Flashcards

Vocabulary practice flashcards covering cellular adaptations, mechanisms of cell injury, calcification, intracellular accumulations, apoptosis, and necrosis types.

Cellular Adaptation

Cells adapt to changes in the internal environment due to increased work demands by changing in size, number, or form.

Cellular Adaptation Overview Diagram

A conceptual illustration depicting normal epithelial cells alongside adaptive changes including atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia.

Atrophy

A decrease in cell size.

Muscle Atrophy

Cells revert to a smaller size and a lower and more efficient level of functioning compatible with survival. Cell size is mediated by insulin and insulin-like growth factor (IGF-1).

Insulin and $\text{IGF}-1$

Hormones that mediate cellular signaling pathways responsible for regulating cell size and atrophy.

General Causes of Atrophy

Includes disuse, denervation, lack of endocrine stimulation, inadequate nutrition, and ischemia or decreased blood flow.

Disuse Atrophy

Reduction in cell and tissue size caused by a lack of muscle activity or reduced physical workload.

Denervation Atrophy

Atrophy occurring in skeletal muscle tissue following the loss of nerve supply and neural stimulation.

Endocrine Atrophy

Shrinkage of tissue or organ size resulting from the loss of normal hormonal stimulation.

Ischemic Atrophy

Cellular shrinkage occurring when tissue blood flow and oxygen delivery are chronically reduced.

Hypertrophy

An increase in individual cell size and overall tissue mass in response to increased workload of an organ or body part. Common in cardiac and skeletal muscle tissue. May be normal or pathologic.

Pathologic Left Ventricular Hypertrophy

Gross cardiac structural enlargement and wall thickening of the left ventricle resulting from persistent hypertension.

Compensatory Hypertrophy

The enlargement of a remaining organ or tissue to offset the loss or removal of a portion of that organ, such as a solitary kidney expanding after nephrectomy.

Exercise-Induced Hypertrophy

A normal physiologic increase in skeletal muscle cell size resulting from repeated weightlifting or resistance training.

Hyperplasia

An increase in the total number of cells in an organ or tissue as a response to a stimulus and ceases after the stimulus is removed. It can occur in two types: compensatory and hormonal hyperplasia. Also common in skin, intestinal epithelium, and glandular tissue.

Hormonal Hyperplasia

An increase in cell number driven by hormone exposure, such as estrogen-induced expansion of breast and uterine tissues during pregnancy.

Compensatory Hyperplasia

Tissue regeneration involving increased cell division in response to injury or partial organ resection, such as blood vessel growth during wound repair.

Precancerous Hyperplasia

A condition characterized by an abnormal increase in the number of cells in a tissue, such as excess hormone production, that may lead to cancer if left untreated.

Hypertrophy vs Hyperplasia Comparison

Visual and cellular distinction showing an increase in individual cell size versus an increase in total cell number.

Metaplasia

A reversible change (if irritant is removed) in which one adult cell type is replaced by another cell type better able to withstand environmental stress in response to chronic irritation and inflammation.

Airway Metaplasia in Smokers

Cellular replacement of respiratory ciliated columnar epithelium with stratified squamous epithelium due to chronic cigarette smoke irritation because stratified squamous cells are more resistant to chemical irritation, but they lose cilia, which increases risk of infection.

Epithelial Metaplasia Diagram

Diagram showing columnar epithelium being replaced by reserve cells giving rise to stratified squamous epithelium.

Dysplasia

Deranged cell growth of a specific tissue resulting in cells that vary in size, shape, and cellular organization. Can be associated with inflammation/irritation, is potentially reversible, and may progress to cancer, but it is an adaptive process and does not always lead to cancer.

Cervical Dysplasia

Precancerous transformation of cervical epithelial cells characterized by marked variation in size, shape, and nucleus structure.

Intracellular Accumulations

The progressive buildup of substances within cells that cannot be immediately processed, used, or eliminated.

Normal Body Substance Accumulation

Intracellular storage of excessive components such as lipids, proteins, carbohydrates, or melanin, as seen in excess adipose tissue.

Abnormal Endogenous Accumulation

Cellular retention of metabolic byproducts resulting from inborn errors of metabolism, such as bilirubin retention causing jaundice.

Exogenous Product Accumulation

Cellular uptake and storage of indigestible environmental pigments or toxic particles, such as coal dust causing black lung disease.

Pathologic Calcification

The abnormal tissue deposition of calcium salts along with small amounts of iron, magnesium, and other minerals.

Dystrophic Calcification

Microscopic calcium salt deposition that occurs specifically in dead, dying, or ischemic tissues, such as atherosclerosis.

Atherosclerosis

A chronic disease characterized by the buildup of plaques in the arterial walls, leading to narrowing and potential blockage of blood flow, often associated with high cholesterol and hypertension.

Metastatic Calcification

The abnormal deposition of calcium salts in normal tissues, leading to accumulation in blood vessels and renal tubules caused by overdose of vitamin D or cancers.

Mechanical Force Injury

Physical cell trauma caused by impact or pressure that splits or tears tissue, breaks bone, or disrupts blood flow.

Extremes of Temperature

Refers to the damage caused to cells and tissues due to burns, heat strokes, or cold exposure.

Alternating Current (AC) Electrical Injury

Electrical shock hazard that is more dangerous than direct current ($\text{DC}$) because it easily triggers ventricular fibrillation and muscular tetany.

Ionizing Radiation Injury

High-energy radiation damage, such as from cancer radiotherapy, that disrupts molecular bonds and causes cell death.

Ultraviolet (UV) Radiation Injury

Sunlight, heart, or curing lamp radiation that creates thermal energy and induces direct nuclear $\text{DNA}$ damage/changes in exposed cells.

Nonionizing Radiation Injury

Low-frequency electromagnetic radiation (microwaves, TV signals) that causes thermal cellular injury.

Drugs

Chemical substances that alter physiological functions in the body, potentially leading to cellular injury or death.

Carbon Tetrachloride Toxicity

A chemical exposure to carbon tetrachloride that leads to liver damage and necrosis, typically through free radical formation and lipid peroxidation.

Lead Toxicity

Heavy metal poisoning from ingestion or inhalation of contaminated paint, dust, or pipes, manifesting as severe abdominal pain and cognitive deficits.

Mercury Toxicity

Toxic metal exposure linked to fish consumption, dental work, or thimerosal preservative, causing neurotoxic cellular damage.

Injury from Biologic Agents

Damage to tissues caused by pathogens such as bacteria, viruses, or parasites, leading to inflammation, apoptosis, or necrosis.

Injury from Nutritional Imbalances

Damage to tissues resulting from deficiencies or excesses of essential nutrients, leading to conditions such as anemia or scurvy.

Free Radical Formation (Oxidative Stress)

Generation of highly reactive oxygen species ($\text{ROS}$) caused by radiation, toxins, inflammation, or ischemia reperfusion that damage cell lipids, proteins, and DNA.

Membrane Lipid Peroxidation

Process in which reactive oxygen species attack double bonds in membrane phospholipids, causing severe cell membrane damage and rupture.

Amyotrophic Lateral Sclerosis (ALS)

Progressive neurodegenerative disease implicated with free radical formation and ongoing oxidative stress.

Hypoxia

A state of cellular oxygen deprivation that impairs mitochondrial respiration and halts ATP production, leading to cell injury or death.

Causes of Hypoxia

Includes inadequate oxygen supply, respiratory disease, inability of the cells to use oxygen, edema, or ischemia.

$\text{Na}^+/\text{K}^+$ ATPase Pump Failure

Primary ion pump failure during hypoxia that causes cellular accumulation of sodium and loss of potassium, leading to cellular swelling and dysfunction.

Cellular Lactic Acidosis

Intracellular pH drop caused by anaerobic glycolysis activation during severe oxygen starvation, disrupting cell functions.

Cytosolic Calcium Homeostasis Disruption

Injury mechanism where cellular damage allows uncontrolled calcium entry into the cytoplasm, inappropriate enzyme activation, and cell destruction.

Phospholipase Activation

Enzymatic pathway triggered by elevated intracellular calcium that degrades membrane phospholipids and destroys membrane integrity.

Protease Activation

Intracellular calcium-dependent enzyme activation that breaks down cytoskeletal proteins and disrupts structural cell framework.

Endonuclease Activation

Calcium-dependent enzymatic activity that induces nuclear chromatin fragmentation and DNA breakdown.

Reversible Cell Injury

Cellular stress or damage that can be reversed if the stimulus is removed. Caused by hypoxia, toxins, or mild oxidative stress.

Hydropic Change

Reversible morphologic alteration where affected cells swell due to intracellular water accumulation secondary to sodium pump failure.

Fatty Change

Intracellular accumulation of lipid vacuoles within organs such as the liver or heart following reversible metabolic injury.

Mild Membrane Blebbing

A reversible change where protrusions called blebs form on the cell membrane, often due to cellular stress or injury.

Apoptosis

Energy-dependent, programmed cell destruction that systematically eliminates unwanted or damaged cells without eliciting an inflammatory response by DNA fragmentation and cell shrinkage.

Apoptotic Bodies

Membrane-bound vesicles containing organelle and nuclear fragments formed during apoptosis that are cleanly phagocytosed by macrophages.

Necrosis

Uncontrolled, accidental cell death resulting from irreversible lethal injury or disease, typically accompanied by cellular rupture and inflammation.

Coagulative Necrosis

Pattern of cell death where cell proteins denaturation, yielding firm, pale tissue typical of ischemic solid organs (heart, kidney).

Liquefactive Necrosis

Pattern of cell death where tissue becomes soft/liquid due to enzymatic digestion, characteristic of brain infarcts and bacterial abscess (pus formation).

Caseous Necrosis

Distinct form of cell death characterized by a cheese-like tissue appearance, classic in tuberculosis granulomas.

Gangrene

A considerable mass of tissue undergoes necrosis resulting from loss of blood supply (ischemia) and infection, often in the extremities in diabetes or peripheral vascular disease. Common forms include dry, wet, and gas gangrene.

Abscess

A localized collection of pus that forms within tissue due to bacterial infection, often resulting from the body’s immune response to bacteria.

Cellular Angina

A temporary reversible ischemia injury without death due to reduced blood flow, such as myocardial angina.

Myocardial Angina

A type of chest pain caused by reduced blood flow to the heart muscle, often triggered by physical activity or stress.

Dry Gangrene

An ischemic tissue necrosis where the affected tissue becomes dark, shriveled, and wrinkled. The color changes to dark brown or black. The spread or progression is slow.

Wet Gangrene

Rapidly spreading, life-threatening necrosis of ischemic tissue from a bacterial infection (usually anaerobic) that can lead to sepsis. The affected area is cold, swollen, foul-smelling, and pulseless. The skin is moist, dark red or black, and under tension. Blebs form on the surface with liquefaction occurring.

Common Locations of Wet Gangrene

Includes extremities, fingers, toes, and internal organs (after obstruction).

Gas Gangrene

A rapid, life-threatening tissue necrosis caused by anaerobic Clostridium bacteria that can produce toxins and shock. Characterized by swollen, tense, pale or bronze then dark appearance, gas bubble accumulation in tissues, crepitus on palpation, and severe pain.

Common Locations of Gas Gangrene

Includes deep wounds, traumatic injuries, and surgical wounds.