Cell Injury and Cell Death Vocabulary

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Vocabulary flashcards covering key concepts, mechanisms, and examples of cellular adaptation, cell injury, necrosis, and apoptosis based on the lecture notes.

Last updated 3:44 PM on 9/30/26
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22 Terms

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Pathology

The study of disease through the changes it causes in cells, tissues, and organs, explaining why and how diseases occur and guiding patient care.

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Hypertrophy

An increase in the size of cells or tissue without cell division, resulting in organ enlargement without an increase in cell number.

<p>An increase in the size of cells or tissue without cell division, resulting in organ enlargement without an increase in cell number.</p>
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Hyperplasia

An increase in the number of cells in a tissue as a consequence of cell division without an increase in individual cell size.

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Erythroid Hyperplasia

An adaptive increase in red blood cell production in bone marrow, stimulated by increased erythropoietin release in response to hypoxia.

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Atrophy

The decrease in the size of an organ or cell resulting from a reduction in cell size or cell number via reduced proliferation or increased apoptosis.

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Metaplasia

The reversible adaptive replacement of one mature differentiated cell type with another mature differentiated cell type in response to chronic insult or injury.

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Reversible Cell Injury

Early cellular damage characterized by reduced oxidative phosphorylation, ATP depletion, and cellular swelling due to altered ion concentrations and water influx.

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Acute Hydropic Change

A morphological manifestation of reversible cell injury showing cellular swelling, surface blebs, intracytoplasmic vacuoles, and increased cytoplasmic eosinophilia, commonly seen in kidney tubules during acute injury.

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Hepatic Steatosis (NAFLD)

Non-alcoholic fatty liver disease, representing a spectrum ranging from fat accumulation in hepatocytes without inflammation to steatohepatitis, fibrosis, and cirrhosis.

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Necrosis

Uncontrolled, catastrophic cell death resulting from severe injury, characterized by plasma membrane disruption, cell swelling, organelle breakdown, and release of cellular contents triggering inflammation.

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Apoptosis

An energy-dependent, programmed cell death process in which activated intracellular enzymes degrade nuclear and cytoplasmic proteins, producing membrane-bound fragments that are phagocytosed without inciting inflammation.

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Coagulative Necrosis

The most common pattern of necrosis, typically caused by ischemia (infarction), in which basic cellular outlines are preserved for several days while nuclei are lost and cytoplasm becomes eosinophilic.

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Colliquative Necrosis

Also known as liquefactive necrosis; a pattern of tissue necrosis unique to the brain due to its lack of a supporting tissue stroma, where dead brain tissue liquefies into a fluid-filled cavity or cyst.

<p>Also known as liquefactive necrosis; a pattern of tissue necrosis unique to the brain due to its lack of a supporting tissue stroma, where dead brain tissue liquefies into a fluid-filled cavity or cyst.</p>
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Caseous Necrosis

A distinctive pattern of necrosis associated with tuberculosis, where dead tissue converts into a soft, friable, cheese-like material lacking cellular outlines microspopically.

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Fat Necrosis

A form of tissue destruction resulting from lipase release (e.g., in acute pancreatitis), causing lipid breakdown, fatty acid release, and saponification forming white chalky calcium soap deposits.

<p>A form of tissue destruction resulting from lipase release (e.g., in acute pancreatitis), causing lipid breakdown, fatty acid release, and saponification forming white chalky calcium soap deposits.</p>
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Fibrinoid Necrosis

A pattern of vascular necrosis seen in immune-mediated reactions (vasculitis), characterized by bright pink deposition of fibrin and immune complexes within damaged arterial walls.

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Civatte Bodies

Eosinophilic, apoptotic keratinocytes found in the skin (also referred to as colloid bodies) resulting from programmed cell death.

<p>Eosinophilic, apoptotic keratinocytes found in the skin (also referred to as colloid bodies) resulting from programmed cell death.</p>
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Intrinsic Pathway of Apoptosis

The mitochondrial pathway of apoptosis triggered by internal stress or DNA damage, regulated by Bcl-2 family proteins, leading to cytochrome c release and Caspase-9 activation.

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Extrinsic Pathway of Apoptosis

The death-receptor pathway of apoptosis triggered by external ligand signals binding to membrane receptors (such as Fas/CD95 or TNF receptors), leading to Caspase-8 activation.

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Necroptosis

A regulated form of necrosis mediated through TNF receptor pathways that combines mechanisms of programmed cell death with plasma membrane rupture and pro-inflammatory signaling.

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Psoriasis

A chronic skin condition characterized pathologically by excessive proliferation and abnormal differentiation of keratinocytes (pathological epidermal hyperplasia) alongside inflammatory cell infiltration.

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Infarct

A localized area of tissue necrosis resulting from ischemia caused by an interruption or reduction of arterial blood supply.