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Flashcards in GPHT LEC - Cell Adaptation Deck (115)
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1

Normally confined to a fairly narrow range of function and structure by

CELL ADAPTATION

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Normally confined to a fairly narrow range of function and structure by:
(3)

 Genetic programs of metabolism  Differentiation
 Specialization

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TYPES OF CELLULAR ADAPTATION
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Atrophy Hypertrophy Hyperplasia Metaplasia Dysplasia

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Shrinkage in the size of the cell by loss of cell substance  May ultimately lead to cell death

ATROPHY

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Atrophy classified as _ due to decreased work load (e.g., decreased size of uterus following child birth, or disease)

physiologic

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Atrophy classified as _ primarily due to denervation of muscle, diminished blood supply, nutritional deficiency

pathologic

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Cause by increased functional demand or specific hormonal stimulation

hypertrophy

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Increase in the size of cells which results in an increase in the size of the organs

hypertrophy

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mostly seen in cells that cannot divide, such as skeletal muscle, and cardiac muscle

HYPERTROPHY

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Increase in the number of cells in an organ or tissue, leading to increased organ or tissue size
 Occurs if the cellular population is capable of synthesizing DNA, permitting mitotic division

hyperplasia

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hyperplasia can be classified as __ if Increased local production of growth factor receptors on the responding cells activating transcription factors and leading to cell proliferation

physiologic

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hyperplasia can be classified as __  Stimulation of growth factors
 Excessive hormonal stimulation
 Viral infection (papilloma viruses)  May give rise to neoplasms

pathologic

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Autoimmune disorder characterized by diffuse goiter, hyperthyroidism, and exophthalmos.

HYPERTHYROIDISM (GRAVES DISEASE)

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Immune mechanism: IgG antibodies vs. TSH receptor (agonists), increasing thyroid hormone secretion.

HYPERTHYROIDISM (GRAVES DISEASE)

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pathology of HYPERTHYROIDISM (GRAVES DISEASE)

dark red, meaty; tall columnar epithelium with intraluminal papillae.

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Proliferation of prostatic glands and stroma resulting in enlargement of the gland with obstruction of urine flow through the bladder outlet.

NODULAR HYPERPLASIA, PROSTATE GLAND

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pathogenesis of NODULAR HYPERPLASIA, PROSTATE GLAND

Pathogenesis: unknown; altered normal ratio of testosterone to estrogen that develops in the elderly.

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gross manifestation of NODULAR HYPERPLASIA, PROSTATE GLAND

Gross: nodular, enlarged, rubbery

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micro manifestation of NODULAR HYPERPLASIA, PROSTATE GLAND

Micro: fibromuscular & glandular hyperplasia

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Usually secondary to chronic stimulation by corticotropin

ADRENAL CORTICAL HYPERPLASIA

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chronic stimulation by corticotropin due to
(2)

 Primary hypersecretion of corticotropin by pituitary
(Cushing disease)
 Ectopic corticotropin production by nonpituitary
tumor

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Bilateral diffuse or nodular hyperplasia of
adrenal glands

ADRENAL CORTICAL HYPERPLASIA

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clinical manifestations (2) of ADRENAL CORTICAL HYPERPLASIA

Cushing syndrome (obesity, moon facies, osteoporosis, HPN, amenorrhea, virilization)
 Primary aldosteronism (Conn syndrome)

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Primary aldosteronism

conn syndrome

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(obesity, moon facies, osteoporosis, HPN, amenorrhea, virilization)

Cushing syndrome

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what syndrome: hypersecretion of corticotropin

Cushing syndrome

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roliferative lesions of the endometrium usually resulting from hyperestrinism

endometrial hyperplasia

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 Transformation or replacement of one adult cell type to another adult cell type
 Reversible

METAPLASIA

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 Thought to arise from reprogramming of stem or
undifferentiated cells that are present in adult tissue.

METAPLASIA

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most common metaplasia

columnar to squamous

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