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
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
3
Q
2 types of adaptations
A
◆ Physiologic adaptations
◆ Pathologic adaptations
4
Q
An adaptation to stress can progress
to functionally significant __
if the stress is not relieved
A
cell injury
5
Q
Represent responses of cells to normal stimulation by hormones or endogenous chemical mediators.
A
Physiologic Adaptations
6
Q
a physiologic adaptation that induced enlargement of the breast and uterus during pregnancy, this is mainly because of ___
A
Hormone
7
Q
Responses to stress that allow cells to modulate their structure and function.
A
Pathologic Adaptations
8
Q
is an increase in the size of cells
resulting in increase in the size of the organ
A
Hypertrophy
9
Q
form of adaptation wherein there’s increased cell and organ size
A
Hypertrophy
10
Q
Hypertrophy
induced by growth factors produced in response to ___ or ___
A
mechanical stress or other stimuli
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
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
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
14
Q
a lot of number of genes that will stimulate the number of growth factors
A
transduction pathway
15
Q
the causes of the increase in number of cells in Physiologic Cellular Hypertrophy
A
induced by growth factors that stimulates cell protein
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
17
Q
what is the common pathologic cellular hypertrophy __
A
cardiac enlargement
18
Q
what are the mechanical stressors causing cardiac enlargement
A
hypertension
19
Q
The type of reversible injury is
A
ischemia
20
Q
the type of irreversible injury is ___.
A
ischemic coagulative necrosis
21
Q
the normal ventricular wall’s thickness is ___ cm
A
1-1.5
22
Q
to confirm myocardial hypertrophy, we will use an enzyme substrate that colors viable myocardium.
A
Triphenyltetrazolium chloride
23
Q
Triphenyltetrazolium chloride will color the myocardium as colored ____ signifying viable cells
A
magenta
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.
25
➔ Increased cell numbers in response to hormones
and other growth factors
HYPERPLASIA
26
2 causes of HYPERPLASIA
hormones
growth factors
27
occurs in tissues whose
cells are able to divide or contain abundant tissue
STEM CELLS
HYPERPLASIA
28
TWO TYPES OF PHYSIOLOGIC HYPERPLA
HORMONAL HYPERPLASIA
COMPENSATORY HYPERPLASIA
29
exemplified by the proliferation of the
glandular epithelium of the female breast at puberty and during pregnancy
HORMONAL HYPERPLASIA
30
residual tissue grows after removal
or loss of part of an organ.
COMPENSATORY HYPERPLASIA
31
COMPENSATORY HYPERPLASIA is usually happens in what organ
liver
32
weight of liver
1200-1500 grams. 2% of the body mass
33
a type of hyperplasia that has Excessive hormonal or growth factor
stimulation
PATHOLOGIC HYPERPLASIA
34
example of PATHOLOGIC HYPERPLASIA
● Endometrial hyperplasia - causes bleeding
● Benign prostatic hyperplasia - thickening
● Papillomaviruses - growth factor causing warth
35
Shrinkage in the size of the cell by the loss of cell substance
ATROPHY
36
ATROPHY
Decreased cell and organ size as a result of ___ and ___
decreased nutrient supply or disuse
37
Associated with decreased synthesis and
increased proteolytic breakdown of cellular
organelles.
ATROPHY
38
CAUSES OF ATROPHY
➔ Decreased Workload
➔ Loss of Innervation,
➔ Diminished Blood Supply,
➔ Inadequate Nutrition,
➔ Loss of Endocrine Stimulation,
➔ Aging (Senile Atrophy)
39
MECHANISMS OF ATROPHY
combination of decreased protein synthesis and increased protein degradation in cells.
40
in the increase degradation of the cell during the atrophy.
The degradation of cellular proteins occurs mainly by the _____
ubiquitin-proteasome
pathway.
41
a fragmentation of the protein in the cytosol
ubiquitin-proteasome pathway.
42
why do decreasing of protein syntheis and increase of protein degradation happens in atrophy?
◦ Protein synthesis decreases because of reduced metabolic activity.
◦ The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway.
◦ increased autophagy
43
is a reversible change in which one
adult cell type (epithelial or mesenchymal) is
replaced by another adult cell type.
METAPLASIA
44
response to chronic irritation that makes cells better able to withstand the stress
METAPLASIA
45
usually induced by altered differentiation pathway
of tissue stem cells
METAPLASIA
46
METAPLASIA may result to
reduce functions
increase propensity for malignant transformation
47
2 types of METAPLASIA
EPITHELIAL METAPLASIA and MESENCHYMAL METAPLASIA
48
occurs in epithelium exposed to mechanical
trauma or chronic irritation of prolonged
inflammation
EPITHELIAL METAPLASIA
49
EPITHELIAL METAPLASIA causes
mechanical trauma
chronic irritation of prolonged inflammation
prolonged vitamin A deficiency
50
EPITHELIAL METAPLASIA
prolonged vitamin A deficiency
most commonly leading to replacement of
columnar cells by ___
stratified squamous
epithelium
51
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
respiratory passages,
linings of gland ducts
mucosal lining of endocervix
52
what are being replaced in mesenchymal metaplasia?
fibroblast
53
occurring in connective tissues whereby fibroblasts
are transformed into more highly differentiated
forms
MESENCHYMAL METAPLASI
54
MESENCHYMAL METAPLASIA
➔ occurring in connective tissues whereby fibroblasts
are transformed into more highly differentiated
forms such as __
osteoblasts,
fat cells
tissue macrophages
55
according to the table
hypertrophy is an increased in cell and organ size which often a response to _____
increase workload,
induced by growth factors in response to mechanical stress or other stimuli
56
according to the table, hyperplasia results in response to
growth factors and hormones
57
The intracellular accumulations may be located in
-Cytoplasm
-Within organelles (typically lysosomes) -In the nucleus,
-May be synthesized by the affected cells or may be produced elsewhere.
58
MECHANISM / PATHWAYS OF ABNORMAL INTRACELLULAR ACCUMULATIONS
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
as a result of genetic or acquired defects in its folding,
Accumulation of an abnormal endogenous substance
60
causes of Accumulation of an abnormal endogenous
substance
defects in folding, packaging, transport, or secretion
61
the defect in protein folding, packaging, transport, or secretion results to what type of mutation
α1-antitrypsin
62
Failure to degrade a metabolite is due to ___
due to inherited enzyme deficiencies
63
Failure to degrade a metabolite
The resulting disorders are called ___
storage diseases
64
Accumulation of carbon or silica particles
Deposition and accumulation of an abnormal exogenous substance
65
Deposition and accumulation of an abnormal
exogenous substance
what might be the cause
ingestion of indigestible food due to carbon or silica particles
66
ABNORMAL INTRACELLULAR ACCUMULATION
➔ Fatty Change (Steatosis)
➔ Accumulation of proteins
➔ Pigments
67
refers to any abnormal accumulation of
triglycerides within parenchymal cells
Fatty change
68
FATTY CHANGE (STEATOSIS) may also occur in ___ aside from liver
heart, skeletal muscle, kidney,
and other organs.
69
Causes of Steatosis
toxins, protein malnutrition, diabetes mellitus, obesity, or anoxia
70
Common causes of fatty change in the liver (fatty liver)
Alcohol abuse and diabetes
71
alter mitochondrial and SER function
HEPATOTOXINS (ALCOHOL)
72
inhibit fatty acid oxidation
HEPATOTOXINS (ALCOHOL)
73
decrease the synthesis of apoproteins
CCl4 AND PROTEIN MALNUTRITION
74
ANOXIA
inhibits fatty acid oxidation
75
increases fatty acid mobilization
STARVATION
76
what are the factors or conditions that can affect fatty change
HEPATOTOXINS (ALCOHOL)
CCl4 AND PROTEIN MALNUTRITION
ANOXIA
STARVATION
ACCUMULATION OF FAT IN THE HEPATOCYTE
CHOLESTEROL AND CHOLESTERYL ESTER
77
ACCUMULATION OF FAT IN THE HEPATOCYTES causes
➔ Increased uptake of triglycerides
➔ Decreased use of fat by cells.
➔ Overproduction of fat in cells.
➔ Decreased secretion of fat from the cells
78
INTRACELLULAR PROTEIN
Mallory Body, or “Alcoholic Hyalin
Neurofibrillary tangle (NFTs)
Eosinophilic Russel bodies
79
Is an eosinophilic cytoplasmic inclusion in liver
cells that is highly characteristic of alcoholic liver
disease
Mallory Body, or “Alcoholic Hyalin,"
80
what is the effect of mallory body
Damaged intermediate filaments within the
hepatocytes
81
Are aggregates of hyperphosphorylated tau
protein (proteins that stabilize microtubules) that
are most commonly known as a primary marker
of Alzheimer's disease.
Neurofibrillary tangle (NFTs)
82
Neurofibrillary tangle (NFTs) are found in what patients
Found in the brain in Alzheimer disease aggregated protein inclusion.
83
Immunoglobulins that may occurs in the RER of
some plasma cells found in the peripheral areas
of tumor
Eosinophilic Russel bodies
84
Glycogen accumulates in ___
renal tubular epithelium,
cardiac myocytes,
β cells of the islets of Langerhans
85
Excessive intracellular deposits of glycogen are associated with abnormalities in the metabolism of
either ___ or ___
glucose or glycogen
86
Glycogen also accumulates within cells in a group of
closely related genetic disorders collectively referred
to as _______, or glycogenoses
glycogen storage diseases
87
2 types of PIGMENTS
Endogenous pigments
Exogenous pigments
88
a pigment that are produced within the tissue to serve a physiological function, or may be byproducts of normal metabolism.
Endogenous pigments
89
a pigment that are consist of foreign
materials, usually minerals introduced to the body thru air, food, medication and injections
Exogenous pigments
90
3 category of endogenous pigments
hematogenous or blood-derived pigments
nonhematogenous
endogenous minerals
91
hematogenous or blood-derived pigment
examples
hemosiderin, hemoglobin, bile pigment
92
nonhematogenous examples
such as melanin, lipofuscin and chromaffin
93
endogenous minerals\
exampls
(such as iron, calcium and copper
94
a exogenous pigment that is appearing as jet black pigments in lung
sections and bronchial glands of chronic smokers
Carbon
95
Aggregates of the pigment blacken the draining
lymph nodes and pulmonary parenchyma
(_____)
anthracosis
96
EXOGENOUS PIGMENT
Heavy accumulations may induce emphysema or a
fibroblastic reaction that can result in a serious lung
disease called
coal workers' pneumoconiosis
97
an endogenous, brown-black pigment that is
synthesized by melanocytes located in the epidermis
and acts as a screen against harmful ultraviolet
radiation.
MELANIN
98
are the only source of melanin
melanocytes
99
basal keratinocytes in the skin can accumulate
the pigment (e.g., in -_____)
freckles
100
is a hemoglobin-derived granular pigment that is
golden yellow to brown and accumulates in tissues
when there is a local or systemic excess
HEMOSIDERIN
101
a lack of melanin is called as
vitiligo
102
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.
HEMOSIDERIN
103
hemosiderin is Identified by its staining reaction (blue color) with the
_____
Prussian blue dye
104
2 types of hemosiderin
HEMOSIDEROSIS
HEREDITARY HEMOCHROMATOS
105
a type of hemosiderin wherein there's an accumulation of iron primarily within tissue
macrophages & is NOT associated with
tissue damage
HEMOSIDEROSIS
106
hemosiderin
extensive accumulation within
parenchymal cells, which leads to tissue
damage, scarring & organ dysfunction
HEREDITARY HEMOCHROMATOSIS
107
HEREDITARY HEMOCHROMATOSIS
extensive accumulation within
parenchymal cells, which leads to ________
tissue damage, scarring & organ dysfunction
108
WEAR AND TEAR PIGMENT
LIPOFUSCIN
109
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
LIPOFUSCIN OR “WEAR AND TEAR PIGMENT”
110
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
heart, liver, and brain
111
➔ It is not injurious to the cell but is a marker of past
free radical injury.
LIPOFUSCIN OR “WEAR AND TEAR PIGMENT”
112
lipofuscin
The brown pigment , when present in large amounts,
imparts an appearance to the tissue that is called
____.
brown atrophy
113
Lipofuscin is a function of
age or atrophy
114
Lipofuscin, where it came from?
from the free radical that catalyzed peroxidation of polyunsaturated lipids
115
CALCIFICATION
Abnormal deposition of calcium salts, together with smaller amounts of ___,___, and other
minerals
iron, magnesium
116
types of CALCIFICATION
1. Metastatic Calcification
2. Dystrophic Calcification
117
a calcification where the deposition occurs in dead or dying tissues
DYSTROPHIC
118
it occurs in the absence of calcium metabolic derangements in calcium metabolism
(with normal serum levels of calcium).
DYSTROPHIC
119
deposition of calcium salts in normal tissues
➔ always reflects some derangement in calcium
metabolism (hypercalcemia)
METASTATIC
120
Dystrophic calcification is encountered in areas of
_____ of any type
necrosis
121
DYSTROPHIC CALCIFICATION
It is virtually inevitable in the atheromas of advanced
___
atherosclerosis
122
2 type of mechanism of THE PATHOGENESIS OF DYSTROPHIC
CALCIFICATION
➔ Initiation (or nucleation)
➔ Propagation
123
The ultimate end product of calcification is the formation of
crystalline calcium phosphate
124
Initiation of calcification in extracellular sites occurs in
membrane
bound
125
Initiation of intracellular calcification occurs in the ____of dead or dying cells that have lost
their ability to regulate intracellular calcium
mitochondria
126
FOUR MAJOR CAUSES OF HYPERCALCEMIA
INCREASED SECRETION OF PARATHYROID HORMONE
DESTRUCTION OF BONE
VITAMIN D RELATED DISORDER
RENAL FAILURE
127
Due to either primary parathyroid tumors
or production of parathyroid
hormone-related protein by other
malignant tumors
INCREASED SECRETION OF PARATHYROID
HORMONE
128
example of DESTRUCTION OF BONE disease
Paget disease
129
Tumors in the destruction of bone are seen in what conditions
Increased bone catabolism
associated with multiple myeloma,
leukemia, or diffuse skeletal
metastases
130
VITAMIN D RELATED DISORDERS
➔ Vitamin D intoxication
➔ Sarcoidosis (in which macrophages
activate a vitamin D precursor)
131
the most common reason of hypercalcemia
Phosphate retention leads to secondary hyperparathyroidism
132
among the type of metastatic calcification, which one is irreversible
dystrophic
133
causes of dystrohpc
aging or damaged heart valves (atrophy )
134
cause of metastatic
hypercalcemia
135
Regardless of the site, calcium salts are seen on gross examination as ___,
often felt as gritty deposits.
fine white granules or clumps
136
dystrophic calcification is common in areas of
caseous necrosis in tuberculosis
137
in dystrophic, sometimes a tuberculous lymph node is essentially converted to +____
radiopaque stone
138
on histologic examination, the dystrophic calcification appears as
intracellular and or extracellular basophilic deposits
139
metastatic calcification principally affects which organs
interstitial tissues of the vasculature, kidneys, lungs, and gastric mucosa
140
the massive deosite of calcium salts in metastatic calcification in the kidney is called as
nephrocalcinosis
141
what depositions of of materials in cells which are being the result of excessive intake or defective transport or catabolism
depositions of lipids
depositions of cholesterol
depositions of proteins
depositions of glycogen
depositions of pigments
142
depositions of protein is caused by
reabsorbed proteins in the kidney
presence of immunoglobulin in plasma cells
143
cause of depositions of glycogen
due to the break down of glycogen caused by lysosomal enzymes (glycogen storage disease)
144
