Cellular Injury

Vocabulary flashcards covering key terms and concepts related to mechanisms, stages, and consequences of cellular injury.

Cellular Injury

Damage that occurs when homeostasis fails or adaptive changes are exceeded, potentially reversible or leading to cell death.

Hypoxia

Insufficient oxygen supply to tissues, the most common cause of cellular injury.

Ischemia

Reduced blood flow causing localized hypoxia; gradual onset allows some adaptation.

Anoxia

Total absence of oxygen, poorly tolerated by most tissues.

Hypoxic Cell Injury – Early Stage

Low ATP → Na⁺/K⁺ pump failure, Na⁺ and water influx, cellular swelling, ER dilation, ribosome detachment, lactic acidosis, nuclear chromatin clumping; potentially reversible.

Hypoxic Cell Injury – Prolonged Stage

Continued swelling, vacuolation, lysosomal rupture, mitochondrial swelling, Ca²⁺-activated proteases/phospholipases, membrane damage, irreversible cell death.

Na⁺/K⁺ Pump Failure

ATP-dependent transport loss causing intracellular Na⁺ accumulation and osmotic water influx.

Cellular Swelling

First morphologic sign of reversible injury due to water entry following ion pump failure.

Oxidative Stress

Cell injury produced by excess reactive oxygen species overwhelming antioxidant defenses.

Reactive Oxygen Species (ROS)

Chemically reactive oxygen-containing molecules (e.g., superoxide, H₂O₂) that damage lipids, proteins, and DNA.

Free Radical

Uncharged atom or molecule with an unpaired electron, highly unstable and reactive with cellular macromolecules.

Lipid Peroxidation

ROS-mediated breakdown of unsaturated fatty acids in membranes, leading to structural damage.

mtDNA

Mitochondrial DNA inherited maternally; susceptible to ROS damage generated during oxidative phosphorylation.

Chemical Injury

Cell damage produced by toxic chemicals via direct membrane effects, free radical generation, or enzyme/protein alteration.

Carbon Tetrachloride (CCl₄)

Industrial solvent that converts to free radicals in the liver, causing lipid peroxidation and cell necrosis.

Lead Toxicity

Heavy-metal poisoning disrupting heme synthesis, neurologic development, and cell membranes; exemplified by Flint, Michigan water crisis.

Carbon Monoxide Poisoning

Chemical injury where CO binds hemoglobin with high affinity, preventing oxygen delivery to tissues.

Ethanol Metabolism

Alcohol converted to acetaldehyde and free radicals in the liver, causing inflammation, fatty change, membrane damage, and CNS depression.

Mercury Toxicity

Exposure to elemental or organic mercury leading to nervous system and kidney injury via binding sulfhydryl groups.

Reperfusion Injury

Additional cell damage occurring when blood supply returns after ischemia, driven by ROS formation and Ca²⁺ overload.

Xanthine & Hypoxanthine

Purine metabolites that accumulate during ischemia and generate ROS on reperfusion.

Mitochondrial Permeability Transition Pore (MPTP)

Calcium-induced channel in mitochondria that opens during reperfusion, causing loss of ATP and solutes → apoptosis.

abnormal metabolism, defect in protein folding or transport, enzyme defect, cellular uptake of substances

Intracellular build-up of substances (water, lipids, proteins, pigments, calcium, urate) due to metabolic or handling defects. List the 4 types of cellular accumulations.

Abnormal Metabolism (Accumulation Mechanism)

Excess production or inadequate removal of normal substances leading to intracellular storage.

Defect in Protein Folding/Transport

Misfolded proteins accumulate because they cannot be transported or degraded properly.

Enzyme Defect

Inherited or acquired absence of specific lysosomal or metabolic enzymes causing substrate build-up.

Storage Diseases

Genetic lysosomal disorders where missing enzymes lead to accumulation of unmetabolized products in cells and macrophages.

Systemic Manifestations of Cellular Injury

Clinical signs such as fatigue, fever, tachycardia, leukocytosis, pain, and release of tissue enzymes.

Lysosomal Dysfunction

Failure of lysosomal degradation pathways contributing to storage diseases and cellular accumulation toxicity.

Fatty Liver

Reversible accumulation of triglycerides in hepatocytes, commonly due to chronic alcohol intake.