I - Cell Injury, Cell Death and Adaptations Flashcards
Increase in size of cells resulting in increased size of organ.
Hypertrophy
Robbins Basic Pathology, 9th ed. p. 34
Increase in number of cells.
Hyperplasia
Robbins Basic Pathology, 9th ed. p.35
Hypertrophy of hyperplasia?Uterus during pregnancy
Both (Estrogen stimulated)
Robbins Basic Pathology, 9th ed. p.34
Hypertrophy or hyperplasia?Wound healing
Hyperplasia
Robbins Basic Pathology, 8th ed. p.4
Hypertrophy or hyperplasia?
Female breast at puberty
Both
Robbins Basic Pathology 9th ed., p 36
Cellular adaptation of non-dividing cells such as myocardial fibers.
Hypertrophy
A 50 y/o male has untreated hypertension for several years. What cellular alteration will be most likely seen in the myocardium?
Hypertrophy
A 40 y/o male underwent partial hepatectomy. What cellular adaptation will the liver most likely undergo?
Hyperplasia
The most common stimulus for hypertrophy of muscle
Increased workload
Robbins Basic Pathology, 9th ed., p.34
A 65 y/o male presents with 3-month history of weak stream, straining, and hesitancy. There is no history of prostate cancer. Prostate was severely enlarged without nodules. PSA level is 3 mcg. What cellular adaptation does the prostate most likely undergo?
Hyperplasia (Case of BPH)
Stimulus for hyperplasia in BPH
Hormonal stimulation by androgens
Robbins Basic Pathology, 9th ed., p. 36
Cellular adaptation in papilloma virus infection
Hyperplasia
Robbins Basic Pathology, 9th ed., p. 36
Reduction in the size of an organ or tissue due to decrease in cell size and number
Atrophy
Robbins Basic Pathology, 9th ed., p. 35
A 60 y/o female has been experiencing hot flushes and irritability. Her uterine epithelium will most likely reveal what type of cellular adaptation?
Atrophy (in menopause)
Chronic production of this cytokine is thought to be responsible for appetite suppression and lipid depletion, culminating in muscle atrophy and marked muscle wasting (cachexia)
Tumor necrosis factor (TNF)
Robbins Basic Pathology, 9th ed., p. 35
A reversible change in which one differentiated cell type is replaced by another cell type.
Metaplasia
Robbins Basic Pathology, 9th ed., p. 37
A 49 y/o female had a chronic history of heartburn. Biopsy done showed glandular changes in the distal epithelium of the esophagus. What cellular adaptation is present?
Metaplasia
This is a case of Barret’s esophagus (squamous to glandular epithelium)
The basal cell changes seen in reflux esophagitis is an example of this adaptive change
Metaplasia
Most common epithelial metaplasia
Columnar to squamous
Robbins Basic Pathology, 9th ed., p. 37
Type of metaplasia in trachea and bronchi in habitual cigarette smoking
Columnar to squamous
Robbins Basic Pathology, 9th ed., p. 37
Its hallmarks are reduced oxidative phosphorylation with resultant depletion of energy stores in the form of ATP and cellular swelling
Reversible injury
Robbins Basic Pathology, 9th ed., p. 38
Type of cell death characterized by nuclear dissolution, without complete loss of membrane integrity.
Apoptosis
Robbins Basic Pathology, 8th ed. p.7
Type of cell death which is energy-dependent, tightly regulated, and associated with normal cellular functions.
Apoptosis
Robbins Basic Pathology, 8th ed. p.7
Type of cell death which results from a pathologic cell injury.
Necrosis
Robbins Basic Pathology, 8th ed. p.9
Type of cell death associated with inflammation.
Necrosis
Robbins Basic Pathology, 8th ed. p.10
It is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is characterized by nuclear shrinkage and increased basophilia.
Pyknosis
Robbins Basic Pathology, 9th ed. p.42
It is the destructive fragmentation of the nucleus of a dying cell.
Karyorrhexis
Robbins Basic Pathology, 8th ed. p.10
It is the complete dissolution of the chromatin of a dying cell.
Karyolysis
Robbins Basic Pathology, 8th ed. p.10
This is the first manifestation of almost all forms of injury to cells.
Cellular swelling
Robbins Basic Pathology, 8th ed. p.8
Small clear vacuoles within the cytoplasm, representing pinched-off segments of the endoplasmic reticulum.
Hydropic change or Vacuolar degeneration
Robbins Basic Pathology, 8th ed. p.23
Appearance of lipid vacuoles in the cytoplasm.
Fatty Change
Robbins Basic Pathology, 8th ed. p.23
Surface blebs, increased eosinophilia of the cytoplasm, cellular swelling.
Reversible/ Early Ischemic Injury
Robbins Basic Pathology, 8th ed. p.18
Cell injury with loss of nuclei, cellular fragmentation and leakage of cellular contents.
Irreversible/ Necrotic cellular injury
Robbins Basic Pathology, 8th ed. p.18
Cell injury with loss of microvilli, blunting, appearance of smal amorphous densities, ER dilation and disaggregation of granular and fibrillar elements.
Reversible/ Early Ischemic Injury
Robbins Basic Pathology, 9th ed., p.41
A form of tissue necrosis in which the component cells are dead but the basic tissue architecture is preserved. The affected tissues take on a firm texture.
Coagulative necrosis
Robbins Basic Pathology, 9th ed. p.43
Characterized by digestion of dead cells, resulting in transformation of the tissue into a liquid viscous mass.
Liquefactive necrosis
Robbins Basic Pathology , 9th ed. p.43
Refers to focal areas of fat destruction, typically resulting from release of activated pancreatic lipases into the substance of the pancreas and the peritoneal cavity. The foci of necrosis contain shadowy outlines of necrotic fat cells with basophilic calcium deposits, surrounded by an inflammatory reaction.
Fat necrosis
Robbins Basic Pathology, 9th ed., p. 44
A special form of necrosis usually seen in immune reactions involving blood vessels. Deposits of immune complexes, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like) by pathologists.
Fibrinoid necrosis
Robbins Basic Pathology, 9th ed., p. 44
Seen in focal bacterial or, occasionally, fungal infections, because microbes stimulate the accumulation of inflammatory cells and the enzymes of leukocytes digest the tissue.
Liquefactive necrosis
Robbins Basic Pathology, 8th ed. p.10
This term is usually applied to a limb, generally the lower leg, that has lost its blood supply and has undergone coagulative necrosis involving multiple tissue layers.
Gangrenous necrosis
Robbins Basic Pathology, 9th ed. p.43
Friable, white appearance of necoris. It appears as a structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinctive inflammatory border.
Caseous necrosis
Robbins Basic Pathology, 9th ed. p.43
Obstruction of the blood supply would lead to which type of pathologic process in the brain parenchyma?
Liquefactive necrosis