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Botany > GPHT LEC - Cell Adaptation > Flashcards

GPHT LEC - Cell Adaptation Flashcards

1
Q

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

A

CELL ADAPTATION

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2
Q

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

A

 Genetic programs of metabolism  Differentiation

 Specialization

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3
Q

TYPES OF CELLULAR ADAPTATION

5

A

Atrophy Hypertrophy Hyperplasia Metaplasia Dysplasia

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4
Q

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

A

ATROPHY

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5
Q

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

A

physiologic

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6
Q

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

A

pathologic

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7
Q

Cause by increased functional demand or specific hormonal stimulation

A

hypertrophy

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8
Q

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

A

hypertrophy

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9
Q

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

A

HYPERTROPHY

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10
Q

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

A

hyperplasia

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11
Q

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

A

physiologic

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12
Q

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

A

pathologic

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13
Q

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

A

HYPERTHYROIDISM (GRAVES DISEASE)

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14
Q

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

A

HYPERTHYROIDISM (GRAVES DISEASE)

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15
Q

pathology of HYPERTHYROIDISM (GRAVES DISEASE)

A

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

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16
Q

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

A

NODULAR HYPERPLASIA, PROSTATE GLAND

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17
Q

pathogenesis of NODULAR HYPERPLASIA, PROSTATE GLAND

A

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

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18
Q

gross manifestation of NODULAR HYPERPLASIA, PROSTATE GLAND

A

Gross: nodular, enlarged, rubbery

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19
Q

micro manifestation of NODULAR HYPERPLASIA, PROSTATE GLAND

A

Micro: fibromuscular & glandular hyperplasia

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20
Q

Usually secondary to chronic stimulation by corticotropin

A

ADRENAL CORTICAL HYPERPLASIA

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21
Q

chronic stimulation by corticotropin due to

2

A

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

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22
Q

Bilateral diffuse or nodular hyperplasia of

adrenal glands

A

ADRENAL CORTICAL HYPERPLASIA

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23
Q

clinical manifestations (2) of ADRENAL CORTICAL HYPERPLASIA

A 
Cushing syndrome (obesity, moon facies, osteoporosis, HPN, amenorrhea, virilization)
 Primary aldosteronism (Conn syndrome)
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24
Q

Primary aldosteronism

A

conn syndrome

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25
Q

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

A

Cushing syndrome

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26
Q

what syndrome: hypersecretion of corticotropin

A

Cushing syndrome

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27
Q

roliferative lesions of the endometrium usually resulting from hyperestrinism

A

endometrial hyperplasia

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28
Q

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

A

METAPLASIA

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29
Q

 Thought to arise from reprogramming of stem or

undifferentiated cells that are present in adult tissue.

A

METAPLASIA

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30
Q

most common metaplasia

A

columnar to squamous

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31
Q

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

A

METAPLASIA

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32
Q

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

A

DYSPLASIA

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33
Q

apreneoplasticlesion(astageinthecellular evolution to cancer)

A

DYSPLASIA

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34
Q

type of cellular adaptation

minor degrees are associated with chronic irritation or inflammation.

A

DYSPLASIA

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35
Q

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

A

DYSPLASIA

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36
Q

strongly implicated as a precursor of cancer.

A

DYSPLASIA

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37
Q

 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).

A

CELL INJURY

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38
Q

screening test for cervical cancer

A

Pap smear

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39
Q

CIN meaning

A

cervical intraepithelial neoplasia

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40
Q

CIN lower 1/3

A

CIN 1

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41
Q

CIN lower 2/3

A

CIN 2

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42
Q

CIN full thickness

A

CIN 3

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43
Q

ETHANOL in pap smear is for

A

preserving/preservative

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44
Q

features of reversible cell injury [2]

A

Cellular swelling and vacuoles formation (Hydropic changes)

 Fatty changes

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45
Q

Ultratructural changes of reversible cell injury

A

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

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46
Q

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

what type of cell injury

A

irreversible/necrosis

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47
Q

cytoplasm of necrotic cell

A

increased eosinophilia

48
Q

3 things that happen to the nucleus of a necrotic cell

A

pyknosis
karyolysis
karyorrhexis

49
Q

also known as shrinkage (nucleus)

50
Q

also known as fading(nucleus)

A

karyolysis

51
Q

also known as fragmentation (nucleus)

A

karyorrhexis

52
Q

intracellular inclusions found in a chronic cell injury (3)

A

Mallory body
Lewy body
Neurofibrillary tangles

53
Q

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

A

chronic cell injury

54
Q

changes that occur in chronic cell injury (2)

A
  1. Changes in mitochondria

2. Cytoskeletal changes

55
Q

Death of cells occurs in two ways:

A

necrosis

apoptosis

56
Q

changes produced by enzymatic digestion of dead cellular
elements

what type of cell death

57
Q

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

58
Q

Patterns of Necrosis In Tissues or Organs

 the outline of the dead cells are maintained and the tissue is
somewhat firm.

A
  1. Coagulative necrosis
59
Q

Patterns of Necrosis In Tissues or Organs

E.g. myocardial infarction

A
  1. Coagulative necrosis
60
Q

Patterns of Necrosis In Tissues or Organs

 the dead cells undergo disintegration and affected tissue is
liquified.
 E.g. cerebral infarction.

A
  1. Liquefactive necrosis
61
Q

 a form of coagulative necrosis (cheese-like).

 E.g. tuberculosis lesions.

A

Caseous necrosis

62
Q

 enzymatic digestion of fat.

 E.g. necrosis of fat by pancreatic enzymes.

A
  1. Fat necrosis
63
Q

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

A
  1. Gangrenous necrosis
64
Q

molecular events in apoptosis (3)

A

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

65
Q

inhibitory gene which regulate apoptosis

66
Q

stimulatory gene which regulate apoptosis

67
Q

The final phase of apoptosis?

A

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

68
Q

 a manifestation of metabolic derangement

 accumulation of substances in various amounts

A

INTRACELLULAR ACCUMULATIONS

69
Q

3 categories of

INTRACELLULAR ACCUMULATIONS

A 
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
70
Q

pathways of intracellular accumulations

A
  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.
71
Q

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

A

Steatosis (Fatty Change)

72
Q

causes of steatosis

A

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

73
Q

accumulation of cholesterol or cholesterol esters

A

atherosclerosis

74
Q

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)

A

atherosclerosis

75
Q

accumulation of cholesterol within macrophages

76
Q

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

77
Q

what intracellular accumulation

 appear as rounded, eosinophilic droplets, vacuoles or aggregates seen in the cytoplasm

78
Q

causes of protein accumulation (3)

A

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

79
Q

what intracellular accumulation
 seen in patients with derangement in glucose or glycogen metabolism

 appears as clear vacuoles within the cytoplasm

80
Q

diseases associated with glycogen accumulation

A

 Diabetes mellitus, glycogen storage diseases

81
Q

colored substances; may be exogenous or endogenous

what type of intracellular accumulation

82
Q

exogenous pigments (4)

A

carbon, coal dust, tattoo

83
Q

type of pigment

does not evoke an inflammatory reaction

84
Q

endogenous pigments (3)

A

lipofuscin
hemosiderin
melanin

85
Q

 Brown, wear and tear, aging pigment

A

lipofuscin

86
Q

 Golden yellow to brown, Iron excess

A

hemosiderin

87
Q

 Brown-black

 Alkaptonuria, Onchronosis

88
Q

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

A

PATHOLOGIC CALCIFICATION

89
Q

type of pathologic calcification

 occurs locally in dying tissues
 normal serum calcium level
 no abnormality in calcium metabolism

A

Dystrophic calcification

90
Q

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


A

Metastatic calcification

91
Q

type of virus that can cause hyperplasia

A

papilloma virus

92
Q

classification of physiologic hyperplasia

A

hormonal

compensatory

93
Q

endometrial hyperplasia results from

A

hyperestrinism

94
Q

causes of endometrial hyperplasia

A

polycystic ovarian syndrome
estrogen-producing syndrome
obesity
anovulatory cycles

95
Q

carcinoma constitutes of morphologic and biologic continuum

A

endometrial hyperplasia

96
Q

Barrett esophagitis type of cell adaptation

A

metaplasia

97
Q

respiratory tract of smokers type of cell adaptation

A

metaplasia

98
Q

chronic infection of endocervix type of cell adaptation

A

metaplasia

99
Q

Type of cell adaptation

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

100
Q

hydropic changes in reversible cellular injury

A

cellular swelling

vacuole formation

101
Q

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

A 
ATP depletion
Loss of calcium homeostasis and free cytosolic calcium
Free radicals
Defective Membrane permeability
Mitochondrial damage
Cytoskeletal damage
102
Q

free radicals involved in necrosis

A

Superoxide anion
Hydroxyl radicals
hydrogen peroxide

103
Q

necrosis pattern secondary to ischemia

A

gangrenous necrosis

104
Q

morphologic changes in apoptosis

A

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

105
Q

examples of apoptosis

A

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

106
Q

this allows escape of cytochrome-c into the cytosol

A

abnormal mitochondrial membrane permeability

107
Q

escape of cytochrom-c causes

A

caspases activation

108
Q

what intracellular accumulation

rounded eosinophilic droplets

109
Q

what intracellular accumulation

clear vacuoles w/in cytoplasm

110
Q

which intracellular accumulations look similar under the microscope

A

lipid and glycogen deposits

111
Q

blackening of the tissues in the lungs

A

anthracosis

112
Q

anthracosis is due to what pigment

113
Q

major storage forms of iron what pigment

A

hemosiderin

114
Q

causes of metastatic calcification (major) [4]

A

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

115
Q

lesser causes of metastatic calcification [3]

A

aluminum intoxication
milk-alkali syndrome
chronic renal dialysis

Botany (324 decks)

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