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Hpct > LEC3 - CELLULAR ADAPTATION > Flashcards

LEC3 - CELLULAR ADAPTATION Flashcards

1
Q

are reversible changes in the number,
size, phenotype, metabolic activity or functions of cells in response to changes in their environment.

A

Adaptations

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2
Q

Adaptations are reversible changes in the _______ of
cells in response to changes in their environment.

A

number,
size,
phenotype,
metabolic activity or functions

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3
Q

2 types of adaptations

A

◆ Physiologic adaptations
◆ Pathologic adaptations

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4
Q

An adaptation to stress can progress
to functionally significant __
if the stress is not relieved

A

cell injury

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5
Q

Represent responses of cells to normal stimulation by hormones or endogenous chemical mediators.

A

Physiologic Adaptations

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6
Q

a physiologic adaptation that induced enlargement of the breast and uterus during pregnancy, this is mainly because of ___

A

Hormone

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7
Q

Responses to stress that allow cells to modulate their structure and function.

A

 Pathologic Adaptations

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8
Q

is an increase in the size of cells
resulting in increase in the size of the organ

A

Hypertrophy

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9
Q

form of adaptation wherein there’s increased cell and organ size

A

Hypertrophy

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10
Q

Hypertrophy

induced by growth factors produced in response to ___ or ___

A

mechanical stress or other stimuli

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11
Q

what are the causes of increase of the size of the cell or known as hypertrophy

A

PHYSIOLOGIC CELLULAR HYPERTROPHY
PATHOLOGIC CELLULAR HYPERTROPHY

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12
Q

the type of hypertrophy which is one of the example is

the Increased workload in the striated muscle cells in both skeletal and heart

A

Physiologic Cellular Hypertrophy

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13
Q

the type of hypertrophy which is one of the example is

Cardiac enlargement that occurs with hypertension or aortic valve disease

A

Pathologic Cellular Hypertrophy

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14
Q

a lot of number of genes that will stimulate the number of growth factors

A

transduction pathway

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15
Q

the causes of the increase in number of cells in Physiologic Cellular Hypertrophy

A

induced by growth factors that stimulates cell protein

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16
Q

Hypertrophy can be physiologic or pathologic and is
caused either by ____or ____

A

increased functional demand or by growth factor or hormonal stimulation

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17
Q

what is the common pathologic cellular hypertrophy __

A

cardiac enlargement

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18
Q

what are the mechanical stressors causing cardiac enlargement

A

hypertension

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19
Q

The type of reversible injury is

A

ischemia

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20
Q

the type of irreversible injury is ___.

A

ischemic coagulative necrosis

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21
Q

the normal ventricular wall’s thickness is ___ cm

A

1-1.5

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22
Q

to confirm myocardial hypertrophy, we will use an enzyme substrate that colors viable myocardium.

A

Triphenyltetrazolium chloride

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23
Q

Triphenyltetrazolium chloride will color the myocardium as colored ____ signifying viable cells

A

magenta

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24
Q

using Triphenyltetrazolium chloride enzyme substrate, how will you know if the cells are already dead

A

Failure to stain is due to enzyme loss after cell
death.

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25
Q

➔ Increased cell numbers in response to hormones
and other growth factors

A

HYPERPLASIA

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26
Q

2 causes of HYPERPLASIA

A

hormones
growth factors

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27
Q

occurs in tissues whose
cells are able to divide or contain abundant tissue
STEM CELLS

A

HYPERPLASIA

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28
Q

TWO TYPES OF PHYSIOLOGIC HYPERPLA

A

HORMONAL HYPERPLASIA
COMPENSATORY HYPERPLASIA

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29
Q

exemplified by the proliferation of the
glandular epithelium of the female breast at puberty and during pregnancy

A

HORMONAL HYPERPLASIA

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30
Q

residual tissue grows after removal
or loss of part of an organ.

A

COMPENSATORY HYPERPLASIA

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31
Q

COMPENSATORY HYPERPLASIA is usually happens in what organ

A

liver

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32
Q

weight of liver

A

1200-1500 grams. 2% of the body mass

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33
Q

a type of hyperplasia that has Excessive hormonal or growth factor
stimulation

A

PATHOLOGIC HYPERPLASIA

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34
Q

example of PATHOLOGIC HYPERPLASIA

A

● Endometrial hyperplasia - causes bleeding
● Benign prostatic hyperplasia - thickening
● Papillomaviruses - growth factor causing warth

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35
Q

Shrinkage in the size of the cell by the loss of cell substance

A

ATROPHY

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36
Q

ATROPHY

Decreased cell and organ size as a result of ___ and ___

A

decreased nutrient supply or disuse

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37
Q

Associated with decreased synthesis and
increased proteolytic breakdown of cellular
organelles.

A

ATROPHY

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38
Q

CAUSES OF ATROPHY

A

➔ Decreased Workload
➔ Loss of Innervation,
➔ Diminished Blood Supply,
➔ Inadequate Nutrition,
➔ Loss of Endocrine Stimulation,
➔ Aging (Senile Atrophy)

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39
Q

MECHANISMS OF ATROPHY

A

combination of decreased protein synthesis and increased protein degradation in cells.

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40
Q

in the increase degradation of the cell during the atrophy.

The degradation of cellular proteins occurs mainly by the _____

A

ubiquitin-proteasome
pathway.

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41
Q

a fragmentation of the protein in the cytosol

A

ubiquitin-proteasome pathway.

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42
Q

why do decreasing of protein syntheis and increase of protein degradation happens in atrophy?

A

◦ Protein synthesis decreases because of reduced metabolic activity.

◦ The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway.

◦ increased autophagy

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43
Q

is a reversible change in which one
adult cell type (epithelial or mesenchymal) is
replaced by another adult cell type.

A

METAPLASIA

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44
Q

response to chronic irritation that makes cells better able to withstand the stress

A

METAPLASIA

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45
Q

usually induced by altered differentiation pathway
of tissue stem cells

A

METAPLASIA

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46
Q

METAPLASIA may result to

A

reduce functions

increase propensity for malignant transformation

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47
Q

2 types of METAPLASIA

A

EPITHELIAL METAPLASIA and MESENCHYMAL METAPLASIA

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48
Q

occurs in epithelium exposed to mechanical
trauma or chronic irritation of prolonged
inflammation

A

EPITHELIAL METAPLASIA

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49
Q

EPITHELIAL METAPLASIA causes

A

mechanical trauma
chronic irritation of prolonged inflammation
prolonged vitamin A deficiency

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50
Q

EPITHELIAL METAPLASIA

prolonged vitamin A deficiency

most commonly leading to replacement of
columnar cells by ___

A

stratified squamous
epithelium

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51
Q

the epithelial metaplasia that occurs upon the lack of vitamin A causing the replacement of columnar cells by stratified squamous epithelium are usually seen in what part of the body

A

respiratory passages,
linings of gland ducts
mucosal lining of endocervix

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52
Q

what are being replaced in mesenchymal metaplasia?

A

fibroblast

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53
Q

occurring in connective tissues whereby fibroblasts
are transformed into more highly differentiated
forms

A

MESENCHYMAL METAPLASI

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54
Q

MESENCHYMAL METAPLASIA

➔ occurring in connective tissues whereby fibroblasts
are transformed into more highly differentiated
forms such as __

A

osteoblasts,
fat cells
tissue macrophages

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55
Q

according to the table

hypertrophy is an increased in cell and organ size which often a response to _____

A

increase workload,

induced by growth factors in response to mechanical stress or other stimuli

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56
Q

according to the table, hyperplasia results in response to

A

growth factors and hormones

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57
Q

The intracellular accumulations may be located in

A

-Cytoplasm
-Within organelles (typically lysosomes) -In the nucleus,
-May be synthesized by the affected cells or may be produced elsewhere.

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58
Q

MECHANISM / PATHWAYS OF ABNORMAL INTRACELLULAR ACCUMULATIONS

A

Inadequate removal of a normal substance secondary to defects in mechanisms of packaging and transport

Accumulation of an abnormal endogenous substance

Failure to degrade a metabolite

Deposition and accumulation of an abnormal exogenous substance

59
Q

as a result of genetic or acquired defects in its folding,

A

Accumulation of an abnormal endogenous substance

60
Q

causes of Accumulation of an abnormal endogenous
substance

A

defects in folding, packaging, transport, or secretion

61
Q

the defect in protein folding, packaging, transport, or secretion results to what type of mutation

A

α1-antitrypsin

62
Q

Failure to degrade a metabolite is due to ___

A

due to inherited enzyme deficiencies

63
Q

Failure to degrade a metabolite

The resulting disorders are called ___

A

storage diseases

64
Q

Accumulation of carbon or silica particles

A

Deposition and accumulation of an abnormal exogenous substance

65
Q

Deposition and accumulation of an abnormal
exogenous substance

what might be the cause

A

ingestion of indigestible food due to carbon or silica particles

66
Q

ABNORMAL INTRACELLULAR ACCUMULATION

A

➔ Fatty Change (Steatosis)
➔ Accumulation of proteins
➔ Pigments

67
Q

refers to any abnormal accumulation of
triglycerides within parenchymal cells

A

Fatty change

68
Q

FATTY CHANGE (STEATOSIS) may also occur in ___ aside from liver

A

heart, skeletal muscle, kidney,
and other organs.

69
Q

Causes of Steatosis

A

toxins, protein malnutrition, diabetes mellitus, obesity, or anoxia

70
Q

Common causes of fatty change in the liver (fatty liver)

A

Alcohol abuse and diabetes

71
Q

alter mitochondrial and SER function

A

HEPATOTOXINS (ALCOHOL)

72
Q

inhibit fatty acid oxidation

A

HEPATOTOXINS (ALCOHOL)

73
Q

decrease the synthesis of apoproteins

A

CCl4 AND PROTEIN MALNUTRITION

74
Q

ANOXIA

A

inhibits fatty acid oxidation

75
Q

increases fatty acid mobilization

A

STARVATION

76
Q

what are the factors or conditions that can affect fatty change

A

HEPATOTOXINS (ALCOHOL)
CCl4 AND PROTEIN MALNUTRITION
ANOXIA
STARVATION
ACCUMULATION OF FAT IN THE HEPATOCYTE
CHOLESTEROL AND CHOLESTERYL ESTER

77
Q

ACCUMULATION OF FAT IN THE HEPATOCYTES causes

A

➔ Increased uptake of triglycerides
➔ Decreased use of fat by cells.
➔ Overproduction of fat in cells.
➔ Decreased secretion of fat from the cells

78
Q

INTRACELLULAR PROTEIN

A

Mallory Body, or “Alcoholic Hyalin
Neurofibrillary tangle (NFTs)
Eosinophilic Russel bodies

79
Q

Is an eosinophilic cytoplasmic inclusion in liver
cells that is highly characteristic of alcoholic liver
disease

A

Mallory Body, or “Alcoholic Hyalin,”

80
Q

what is the effect of mallory body

A

Damaged intermediate filaments within the
hepatocytes

81
Q

Are aggregates of hyperphosphorylated tau
protein (proteins that stabilize microtubules) that
are most commonly known as a primary marker
of Alzheimer’s disease.

A

Neurofibrillary tangle (NFTs)

82
Q

Neurofibrillary tangle (NFTs) are found in what patients

A

Found in the brain in Alzheimer disease aggregated protein inclusion.

83
Q

Immunoglobulins that may occurs in the RER of
some plasma cells found in the peripheral areas
of tumor

A

Eosinophilic Russel bodies

84
Q

Glycogen accumulates in ___

A

renal tubular epithelium,
cardiac myocytes,
β cells of the islets of Langerhans

85
Q

Excessive intracellular deposits of glycogen are associated with abnormalities in the metabolism of
either ___ or ___

A

glucose or glycogen

86
Q

Glycogen also accumulates within cells in a group of
closely related genetic disorders collectively referred
to as _______, or glycogenoses

A

glycogen storage diseases

87
Q

2 types of PIGMENTS

A

Endogenous pigments
Exogenous pigments

88
Q

a pigment that are produced within the tissue to serve a physiological function, or may be byproducts of normal metabolism.

A

Endogenous pigments

89
Q

a pigment that are consist of foreign
materials, usually minerals introduced to the body thru air, food, medication and injections

A

Exogenous pigments

90
Q

3 category of endogenous pigments

A

hematogenous or blood-derived pigments
nonhematogenous
endogenous minerals

91
Q

hematogenous or blood-derived pigment

examples

A

hemosiderin, hemoglobin, bile pigment

92
Q

nonhematogenous examples

A

such as melanin, lipofuscin and chromaffin

93
Q

endogenous minerals\

exampls

A

(such as iron, calcium and copper

94
Q

a exogenous pigment that is appearing as jet black pigments in lung
sections and bronchial glands of chronic smokers

A

Carbon

95
Q

Aggregates of the pigment blacken the draining
lymph nodes and pulmonary parenchyma
(_____)

A

anthracosis

96
Q

EXOGENOUS PIGMENT

Heavy accumulations may induce emphysema or a
fibroblastic reaction that can result in a serious lung
disease called

A

coal workers’ pneumoconiosis

97
Q

an endogenous, brown-black pigment that is
synthesized by melanocytes located in the epidermis
and acts as a screen against harmful ultraviolet
radiation.

A

MELANIN

98
Q

are the only source of melanin

A

melanocytes

99
Q

basal keratinocytes in the skin can accumulate
the pigment (e.g., in -_____)

A

freckles

100
Q

is a hemoglobin-derived granular pigment that is
golden yellow to brown and accumulates in tissues
when there is a local or systemic excess

A

HEMOSIDERIN

101
Q

a lack of melanin is called as

A

vitiligo

102
Q

s a hemoglobin-derived granular pigment that is
golden yellow to brown and accumulates in tissues
when there is a local or systemic excess of iron.

A

HEMOSIDERIN

103
Q

hemosiderin is Identified by its staining reaction (blue color) with the
_____

A

Prussian blue dye

104
Q

2 types of hemosiderin

A

HEMOSIDEROSIS
HEREDITARY HEMOCHROMATOS

105
Q

a type of hemosiderin wherein there’s an accumulation of iron primarily within tissue
macrophages & is NOT associated with
tissue damage

A

HEMOSIDEROSIS

106
Q

hemosiderin

extensive accumulation within
parenchymal cells, which leads to tissue
damage, scarring & organ dysfunction

A

HEREDITARY HEMOCHROMATOSIS

107
Q

HEREDITARY HEMOCHROMATOSIS

extensive accumulation within
parenchymal cells, which leads to ________

A

tissue damage, scarring & organ dysfunction

108
Q

WEAR AND TEAR PIGMENT

A

LIPOFUSCIN

109
Q

is an insoluble brownish-yellow granular intracellular
material that accumulates in a variety of tissues
(particularly the heart, liver, and brain) as a function
of age or atrophy

A

LIPOFUSCIN OR “WEAR AND TEAR PIGMENT”

110
Q

LIPOFUSCIN OR “WEAR AND TEAR PIGMENT”

is an insoluble brownish-yellow granular intracellular
material that accumulates in a variety of tissues
(particularly the ___, ___ , ______) as a function
of age or atrophy

A

heart, liver, and brain

111
Q

➔ It is not injurious to the cell but is a marker of past
free radical injury.

A

LIPOFUSCIN OR “WEAR AND TEAR PIGMENT”

112
Q

lipofuscin

The brown pigment , when present in large amounts,
imparts an appearance to the tissue that is called
____.

A

brown atrophy

113
Q

Lipofuscin is a function of

A

age or atrophy

114
Q

Lipofuscin, where it came from?

A

from the free radical that catalyzed peroxidation of polyunsaturated lipids

115
Q

CALCIFICATION

Abnormal deposition of calcium salts, together with smaller amounts of ___,___, and other
minerals

A

iron, magnesium

116
Q

types of CALCIFICATION

A
  1. Metastatic Calcification
  2. Dystrophic Calcification
117
Q

a calcification where the deposition occurs in dead or dying tissues

A

DYSTROPHIC

118
Q

it occurs in the absence of calcium metabolic derangements in calcium metabolism

(with normal serum levels of calcium).

A

DYSTROPHIC

119
Q

deposition of calcium salts in normal tissues
➔ always reflects some derangement in calcium
metabolism (hypercalcemia)

A

METASTATIC

120
Q

Dystrophic calcification is encountered in areas of
_____ of any type

A

necrosis

121
Q

DYSTROPHIC CALCIFICATION
It is virtually inevitable in the atheromas of advanced
___

A

atherosclerosis

122
Q

2 type of mechanism of THE PATHOGENESIS OF DYSTROPHIC
CALCIFICATION

A

➔ Initiation (or nucleation)
➔ Propagation

123
Q

The ultimate end product of calcification is the formation of

A

crystalline calcium phosphate

124
Q

Initiation of calcification in extracellular sites occurs in

A

membrane
bound

125
Q

Initiation of intracellular calcification occurs in the ____of dead or dying cells that have lost
their ability to regulate intracellular calcium

A

mitochondria

126
Q

FOUR MAJOR CAUSES OF HYPERCALCEMIA

A

INCREASED SECRETION OF PARATHYROID HORMONE

DESTRUCTION OF BONE

VITAMIN D RELATED DISORDER

RENAL FAILURE

127
Q

Due to either primary parathyroid tumors
or production of parathyroid
hormone-related protein by other
malignant tumors

A

INCREASED SECRETION OF PARATHYROID
HORMONE

128
Q

example of DESTRUCTION OF BONE disease

A

Paget disease

129
Q

Tumors in the destruction of bone are seen in what conditions

A

Increased bone catabolism
associated with multiple myeloma,
leukemia, or diffuse skeletal
metastases

130
Q

VITAMIN D RELATED DISORDERS

A

➔ Vitamin D intoxication
➔ Sarcoidosis (in which macrophages
activate a vitamin D precursor)

131
Q

the most common reason of hypercalcemia

A

Phosphate retention leads to secondary hyperparathyroidism

132
Q

among the type of metastatic calcification, which one is irreversible

A

dystrophic

133
Q

causes of dystrohpc

A

aging or damaged heart valves (atrophy )

134
Q

cause of metastatic

A

hypercalcemia

135
Q

Regardless of the site, calcium salts are seen on gross examination as ___,
often felt as gritty deposits.

A

fine white granules or clumps

136
Q

dystrophic calcification is common in areas of

A

caseous necrosis in tuberculosis

137
Q

in dystrophic, sometimes a tuberculous lymph node is essentially converted to +____

A

radiopaque stone

138
Q

on histologic examination, the dystrophic calcification appears as

A

intracellular and or extracellular basophilic deposits

139
Q

metastatic calcification principally affects which organs

A

interstitial tissues of the vasculature, kidneys, lungs, and gastric mucosa

140
Q

the massive deosite of calcium salts in metastatic calcification in the kidney is called as

A

nephrocalcinosis

141
Q

what depositions of of materials in cells which are being the result of excessive intake or defective transport or catabolism

A

depositions of lipids
depositions of cholesterol
depositions of proteins
depositions of glycogen
depositions of pigments

142
Q

depositions of protein is caused by

A

reabsorbed proteins in the kidney
presence of immunoglobulin in plasma cells

143
Q

cause of depositions of glycogen

A

due to the break down of glycogen caused by lysosomal enzymes (glycogen storage disease)

144
Q
A

Hpct (15 decks)

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