GPHT LEC - Cell Adaptation Flashcards by Carmina Mislang

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

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

 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

what syndrome: hypersecretion of corticotropin

Cushing syndrome

roliferative lesions of the endometrium usually resulting from hyperestrinism

endometrial hyperplasia

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

METAPLASIA

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

METAPLASIA

most common metaplasia

columnar to squamous

also occurs in mesenchymal tissue (e.g., formation of bone in skeletal muscle).

METAPLASIA

 abnormalgrowthanddifferentiation  variations in size and shape of cells  enlargement, irregularity, and hyperchromasia of nuclei  disorderly arrangement of cells within the epithelium

DYSPLASIA

apreneoplasticlesion(astageinthecellular evolution to cancer)

DYSPLASIA

type of cellular adaptation | minor degrees are associated with chronic irritation or inflammation.

DYSPLASIA

 most frequently encountered in metaplastic squamous epithelium of the respiratory tract and uterine cervix.

DYSPLASIA

strongly implicated as a precursor of cancer.

DYSPLASIA

 Term used when the limits of adaptive response are exceeded, or when the cell is exposed to an injurious agent or stress  The affected cells may recover from the injury (reversible) or may die (irreversible).

CELL INJURY

screening test for cervical cancer

Pap smear

CIN meaning

cervical intraepithelial neoplasia

CIN lower 1/3

CIN 1

CIN lower 2/3

CIN 2

CIN full thickness

CIN 3

ETHANOL in pap smear is for

preserving/preservative

features of reversible cell injury [2]

Cellular swelling and vacuoles formation (Hydropic changes)  Fatty changes

Ultratructural changes of reversible cell injury

blebbing of the plasma membrane, swelling of mitochondria and dilatation of ER

The changes are produced by enzymatic digestion of dead cellular elements, denaturation of proteins and autolysis (by lysosomal enzymes) what type of cell injury

irreversible/necrosis

cytoplasm of necrotic cell

increased eosinophilia

3 things that happen to the nucleus of a necrotic cell

pyknosis karyolysis karyorrhexis

also known as shrinkage (nucleus)

pyknosis

also known as fading(nucleus)

karyolysis

also known as fragmentation (nucleus)

karyorrhexis

intracellular inclusions found in a chronic cell injury (3)

Mallory body Lewy body Neurofibrillary tangles

type of cell injury (?) Non-lethal injury may cause subcellular changes some of which are characteristically seen in certain pathologic conditions.

chronic cell injury

changes that occur in chronic cell injury (2)

1. Changes in mitochondria | 2. Cytoskeletal changes

Death of cells occurs in two ways:

necrosis | apoptosis

changes produced by enzymatic digestion of dead cellular elements what type of cell death

necrosis

what type of cell death vital process that helps eliminate unwanted cells an internally programmed series of events effected by dedicated gene products

apoptosis

Patterns of Necrosis In Tissues or Organs  the outline of the dead cells are maintained and the tissue is somewhat firm.

1. Coagulative necrosis

Patterns of Necrosis In Tissues or Organs | E.g. myocardial infarction

1. Coagulative necrosis

Patterns of Necrosis In Tissues or Organs  the dead cells undergo disintegration and affected tissue is liquified.  E.g. cerebral infarction.

2. Liquefactive necrosis

 a form of coagulative necrosis (cheese-like). |  E.g. tuberculosis lesions.

Caseous necrosis

 enzymatic digestion of fat. |  E.g. necrosis of fat by pancreatic enzymes.

4. Fat necrosis

 necrosis (secondary to ischemia) usually with superimposed infection.  E.g. necrosis of distal limbs, usually foot and toes in diabetes.

5. Gangrenous necrosis

molecular events in apoptosis (3)

 protein cleavage by a group of enzymes (caspases)  protein cross-linking  DNA breakdown

inhibitory gene which regulate apoptosis

bcl-2

stimulatory gene which regulate apoptosis

bax

The final phase of apoptosis?

the removal of dead cell fragments by phagocytosis without inflammatory reactions.

 a manifestation of metabolic derangement |  accumulation of substances in various amounts

INTRACELLULAR ACCUMULATIONS

3 categories of | INTRACELLULAR ACCUMULATIONS

``` 1. a normal cellular constituent (water, lipids, proteins, carbohydrates) 2. an abnormal substance (mineral, products of infectious agents, products of abnormal synthesis or metabolism) 3. Pigment ```

pathways of intracellular accumulations

1. Production of a normal endogenous substance at a normal or increased rate, but inadequate rate of metabolism to remove it. 2. Genetic or acquired defects in metabolism, packaging, transport or secretion of a normal or abnormal endogenous substance. 3. Lack of enzyme to degrade the substance or inability of transport the substance to other sites.

 abnormal accumulations of triglycerides within parenchymal cells  involves the liver, heart, muscles, kidneys

Steatosis (Fatty Change)

causes of steatosis

toxins, protein malnutrition, diabetes mellitus, obesity, anoxia, alcohol abuse

accumulation of cholesterol or cholesterol esters

atherosclerosis

lipid vacuoles fills up the smooth muscle cells and macrophages of the intimal layer of the aorta and large arteries giving a foamy appearance (foam cells)

atherosclerosis

accumulation of cholesterol within macrophages

Xanthomas

clusters of foamy cells are deposited in the subepithelial CT of the skin and tendons, manifested as tumorous masses

Xanthomas

what intracellular accumulation |  appear as rounded, eosinophilic droplets, vacuoles or aggregates seen in the cytoplasm

Proteins

causes of protein accumulation (3)

Renal disease (reabsorption droplets in the proximal tubules)  Plasma cells actively secreting immunoglobulins (Russel bodies)  Defects in protein folding

what intracellular accumulation  seen in patients with derangement in glucose or glycogen metabolism  appears as clear vacuoles within the cytoplasm

Glycogen

diseases associated with glycogen accumulation

 Diabetes mellitus, glycogen storage diseases

colored substances; may be exogenous or endogenous what type of intracellular accumulation

pigments

exogenous pigments (4)

carbon, coal dust, tattoo

type of pigment | does not evoke an inflammatory reaction

exogenous

endogenous pigments (3)

lipofuscin hemosiderin melanin

 Brown, wear and tear, aging pigment

lipofuscin

 Golden yellow to brown, Iron excess

hemosiderin

 Brown-black |  Alkaptonuria, Onchronosis

Melanin

 abnormal tissue deposition of calcium salts, iron, magnesium, and other mineral salts

PATHOLOGIC CALCIFICATION

type of pathologic calcification  occurs locally in dying tissues  normal serum calcium level  no abnormality in calcium metabolism

Dystrophic calcification

type of pathologic calcification  deposition of calcium salts in normal tissues  hypercalcemia is present  causes: increased PTH secretion, destruction of bone tissue, vit D-related disorders, renal failure, aluminum intoxication, milk-alkali syndrome, chronic renal dialysis

Metastatic calcification

type of virus that can cause hyperplasia

papilloma virus

classification of physiologic hyperplasia

hormonal | compensatory

endometrial hyperplasia results from

hyperestrinism

causes of endometrial hyperplasia

polycystic ovarian syndrome estrogen-producing syndrome obesity anovulatory cycles

carcinoma constitutes of morphologic and biologic continuum

endometrial hyperplasia

Barrett esophagitis type of cell adaptation

metaplasia

respiratory tract of smokers type of cell adaptation

metaplasia

chronic infection of endocervix type of cell adaptation

metaplasia

Type of cell adaptation | most frequently encountered in metaplastic squamous epithelium of respiratory tract and uterine cervix

dysplasia

hydropic changes in reversible cellular injury

cellular swelling | vacuole formation

Biochemical events seen in the process of cell necrosis (6)

``` ATP depletion Loss of calcium homeostasis and free cytosolic calcium Free radicals Defective Membrane permeability Mitochondrial damage Cytoskeletal damage ```

free radicals involved in necrosis

Superoxide anion Hydroxyl radicals hydrogen peroxide

necrosis pattern secondary to ischemia

gangrenous necrosis

morphologic changes in apoptosis

shrinkage of cells condensation of chromatin formation of apoptotic bodies phagocytosis of apoptotic bodies by adjacent healthy cells or phagocytes

examples of apoptosis

separation of webbed fingers and toes development of neural connections removal of cells from intestinal villa and removal of senescent blood cells

this allows escape of cytochrome-c into the cytosol

abnormal mitochondrial membrane permeability

escape of cytochrom-c causes

caspases activation

what intracellular accumulation | rounded eosinophilic droplets

proteins

what intracellular accumulation | clear vacuoles w/in cytoplasm

glycogen

which intracellular accumulations look similar under the microscope

lipid and glycogen deposits

blackening of the tissues in the lungs

anthracosis

anthracosis is due to what pigment

coal

major storage forms of iron what pigment

hemosiderin

causes of metastatic calcification (major) [4]

increased PTH secretion renal failure bone resorption vit-D related disorders

lesser causes of metastatic calcification [3]

aluminum intoxication milk-alkali syndrome chronic renal dialysis