adaptations Flashcards
(97 cards)
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
Physiologic adaptations
Pathologic adaptations
2
Q
An adaptation to stress can progress to functionally significant__
if the stress is not relieved
A
cell injury
3
Q
◦ Represent responses of cells to normal stimulation by _ or _
_–induced enlargement of the breast
and uterus during pregnancy
Demand of _
A
physiologic Adaptations
- hormones or endogenous chemical mediators.
- Hormone
- mechanical stress
4
Q
◦ Responses to stress that allow cells to modulate their structure and function.
eg_
A
pathologic Adaptations
- Squamous metaplasia of bronchial epithelium in smoker
5
Q
- is an increase in the size of cells
resulting in increase in the size of the organ.
◦ No new cells, just bigger cells, enlarged by an
increased amount of _ and _
◦ Occurs in tissues incapable of cell division
A
Hypertrophy
- structural proteins and organelles
6
Q
Hypertrophy
A
◦ Physiologic Cellular
Hypertrophy
- Pathologic Cellular
Hypertrophy
7
Q
Enlargement of the uterus
during pregnancy
Increased work load the
striated muscle cells in
both skeletal and heart
A
Physiologic Cellular
Hypertrophy
8
Q
– removed for postpartum
bleeding.
- large, plump hypertrophied
smooth muscle cells from a
__
A
- a gravid uterus
9
Q
- B, Small spindle-shaped
uterine smooth muscle cells
from a __
A
normal uterus.
10
Q
Cardiac enlargement that
occurs with hypertension
or aortic valve disease
A
Pathologic Cellular
Hypertrophy
11
Q
The type of reversible injury is __, and the irreversible
injury is _
A
ischemia
ischemic coagulative necrosis
12
Q
A
13
Q
In__ , the left ventricular wall is
thicker than 2 cm (normal, _)
A
myocardial hypertrophy
- 1–1.5 cm
14
Q
an enzyme substrate that
colors viable myocardium _. Failure to stain is due
to enzyme loss after cell death
A
triphenyltetrazolium chloride
- magenta
15
Q
Two types of physiologic hyperplasia:
A
hormonal hyperplasia
compensatory hyperplasia
16
Q
exemplified by the proliferation of the glandular epithelium of the female breast at puberty and during pregnancy
A
hormonal hyperplasia,
17
Q
in which residual tissue grows after removal or lossof part of an organ
A
compensatory hyperplasia
18
Q
- Occurs due to an abnormal stressor
A
Pathologic Hyperplasia
Excessive hormonal or growth factor stimulation
Endometrial hyperplasia
Benign prostatic hyperplasia
Papillomavirus
19
Q
shrinkage in the size of the cell by the loss of cell
substance
◦ Decreased cell and organ size as a result of decreased
nutrient supply or disuse
◦ Associated with decreased synthesis and increased proteolytic
breakdown of cellular organelle
A
atrophy
20
Q
causes of atrophy
A
Decreased Workload
Loss of Innervation,
Diminished Blood Supply,
Inadequate Nutrition,
Loss of Endocrine Stimulation,
Aging (Senile Atrophy)
21
Q
combination of decreased Protein synthesis because of reduced metabolic and increased protein degradation in cells occurs
mainly by the _
◦ increased __
A
MECH OF ATROPHYY
ubiquitin-proteasome pathway.
autophagy
22
Q
types of atrophy
A
PHYSIOLOGIC ATROPHY
SENILE ATROPHY
PATHOLOGIC ATROPHY
23
Q
-occurs as a natural consequence of maturation
◦ __ and __ during
puberty.
◦ Sexual organs and brain begin to undergo at about _ of age
A
PHYSIOLOGIC ATROPHY
- atrophy of the thymus and lymphoid tissues
- 50 years
24
Q
-occurs in old age characterized by dry, lusterless,
wrinkled skin due to atrophy of sweat and
sebaceous glands and loss of fat, gray hair, atrophy
of the ligaments, brittle bones which easily break
A
SENILE ATROPHY
25
-refers to a decrease in size of tissues or
organs
◦ outside the range of normal variability
◦ usually as a consequence of disease
pATHOLOGIC ATROPHY
26
is a reversible
change in which one adult
cell type (epithelial or
mesenchymal) is replaced
by another adult cell type
Metaplasia
27
response to chronic
irritation that makes cells
better able to withstand
the stress
Metaplasia
28
metaplasia
EPITHELIAL METAPLASIA
MESENCHYMAL METAPLASIA
29
◦ -occurs in epithelium exposed to mechanical trauma or
chronic irritation of prolonged inflammation
__ most commonly leading to replacement of columnar cells by
stratified squamous epithelium
(seen in r_,_ and _
EPITHELIAL METAPLASIA
- ◦ prolonged vitamin A deficiency
- respiratory passages, linings of gland ducts and
mucosal lining of endocervix
30
◦ -occurring in connective tissues whereby fibroblasts are
transformed into more highly differentiated forms such
as_,__,_
MESENCHYMAL METAPLASIA
- osteoblasts, fat cells or tissue macrophages
31
Under some circumstances cells may accumulate abnormal amounts of various substances may be harmless or associated
with varying degrees of injury.
The substance may be located:
intracellular accumulations
Cytoplasm
Within organelles (typically lysosomes)
In the nucleus,
May be synthesized by the affected cells or may be
produced elsewhere
32
Inadequate removal of a normal substance secondary to
defects in _ and _
>__
mechanisms of packaging and transport
- ◦ fatty change in the liver
33
◦ as a result of genetic or acquired defects in its folding,
◦ packaging, transport, or secretion, as with certain mutated
forms of _
Accumulation of an abnormal endogenous substance
- α1-antitrypsin
34
◦ due to inherited-enzyme deficiencies
The resulting disorders are called
failure to degrade a metabolite
- storage diseases
35
Deposition and accumulation of an abnormal exogenous substance
◦ Accumulation of _ or _
carbon or silica particle
36
abnormal intracellular accumulations
- Fatty Change (Steatosis)
Accumulation of proteins
Pigmen
37
refers to any abnormal accumulation of triglycerides within parenchymal cells.
It is most often seen in the _
> major organ involved in fat metabolism,
> may also occur in _,_,_
fatty change / steatosis
- liver
- heart, skeletal muscle, kidney, and other organs.
38
Causes of Steatosis
◦ toxins, protein malnutrition, diabetes mellitus, obesity, or
anoxia.
39
Common causes of fatty change in the liver (fatty liver)
Alcohol abuse and diabetes
40
- alter mitochondrial and SER
function
Hepatotoxins (alcohol)
41
decrease the synthesis of
apoproteins
CCl4 and Protein Malnutrition
42
inhibits fatty acid oxidation
Hepatotoxins (alcohol)
Anoxia
43
increases fatty acid
mobilization
Starvation
44
The possible mechanisms leading
to accumulation of _ in _
Defects in any of the steps of
uptake, catabolism, or secretion
can lead to_
triglycerides in fatty liver
lipid accumulation
45
accumulation of fat in the hepatocyte
- Increased uptake of triglycerides
◦ Decreased use of fat by cells.
◦ Overproduction of fat in cells.
◦ Decreased secretion of fat from the cells
46
is tightly regulated to ensure normal cell membrane
synthesis without significant intracellular accumulation.
However, phagocytic cells may become overloaded with__ in several different pathologic processes
Cellular cholesterol metabolism
- lipid (triglycerides, cholesterol, and cholesteryl esters)
47
Immunoglobulins that
may occurs in the
RER of some plasma
cells
found in the
peripheral areas of
_
Eosinophilic Russel
bodies
- tumors
48
◦ Is an eosinophilic cytoplasmic
inclusion in liver cells that is highly
characteristic of alcoholic liver disease.
◦ Damaged_
within the hepatocytes
Mallory Body, or “Alcoholic
Hyalin,"
- intermediate filaments
49
Are aggregates of hyperphosphorylated
tau protein (proteins that stabilize
microtubules) that are most commonly known as a primary marker of __ aggregated protein inclusions
neurofibrillary tangle (NFTs)
- Alzheimer's disease.
50
Excessive intracellular deposits of it are associated with abnormalities in the metabolism of
either_ or _
- accumulates in _,_,_
◦ also accumulates within cells in a group of closely related genetic disorders collectively
referred to as _ or _
Glycogen
glucose or glycogen
- renal tubular epithelium,
cardiac myocytes, and β cells of the islets of Langerhans
- glycogen storage diseases, or
glycogenoses
51
can occur in normal or in pathological conditions.
Pigments
- Endogenous pigments
- Exogenous pigments
52
are produced within the tissue
to serve a physiological function, or may be by- products of normal metabolism.
- Endogenous pigments
53
consist of foreign materials,
usually minerals introduced to the body thru air, food,
medication and injections
- Exogenous pigments
54
- Endogenous pigments
- hematogenous or blood-derived
pigments
- nonhematogenous
- endogenous minerals
55
hematogenous or blood-derived
pigments
◦ (hemosiderin, hemoglobin, bile pigment)
56
nonhematogenous
(such as melanin, lipofuscin and
chromaffin)
57
endogenous minerals
◦ (such as iron, calcium and copper)
58
Carbon appearing as _ in lung sections and bronchial glands of chronic smokers.
Aggregates of the pigment blacken the draining_ and _
Heavy accumulations may induce emphysema or a fibroblastic reaction that can result in a
serious lung disease called _
- Exogenous pigments
-jet black pigments
- lymph nodes and pulmonary parenchyma ( anthracosis)
- coal workers' pneumoconiosis
59
an endogenous, brown-black pigment that is
synthesized by melanocytes located in the
epidermis and acts as a screen against
harmful ultraviolet radiation.
melanin
60
are the only source of melanin
◦ _in the skin can accumulate the
pigment (e.g., in _)
melanocytes
- basal keratinocytes
- freckles
61
is 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.
◦ Identified by its staining reaction _
hemosiderin
- (blue color) with the Prussian blue dye
62
two types of hemosiderin
Hemosiderosis
Hereditary Hemochromatosis
63
◦ accumulation is primarily within tissue macrophages & is not associated with tissue
damage
Hemosiderosis
64
◦ extensive accumulation within parenchymal cells,
which leads to tissue damage, scarring & organ
dysfunction
Hereditary Hemochromatosis
65
is an insoluble brownish-yellow granular intracellular
material that accumulates in a variety of tissues
(particularly the_,_,_) as a function
of age or atrophy.
lipofuscin or wear and tear pigment
- heart, liver, and brain
66
The brown pigment , when present in large amounts, imparts an
appearance to the tissue that is called
brown atrophy
67
Pathologic Calcification
1. Metastatic Calcification
2. Dystrophic Calcification
68
abnormal deposition of calcium salts,
together with smaller amounts of iron,
magnesium, and other minerals
Pathologic Calcification
69
When the deposition occurs in dead or dying tissues,
it occurs in the absence of __ in calcium metabolism ( with normal serum levels of calcium)
Dystrophic
- calcium metabolic derangements
70
◦ deposition of calcium salts in normal tissues
◦
always reflects some derangement in calcium metabolism (__)
Metastatic
- hypercalcemia
71
is encountered in
areas of necrosis of any type.
It is virtually inevitable in the __
Dystrophic calcification
- atheromas of
advanced atherosclerosclerosis
72
pathogenesis of dystrophic calcification
>___
Propagation
>both of which may be either _ or _
The ultimate end product is the formation of __
Initiation in __occurs in membrane bound .
Initiation of _ occurs in the
mitochondria of dead or dying cells that have lost their
ability to regulate intracellular calcium
Initiation (or nucleation)
- intracellular or extracellular
- crystalline calcium phosphate
- extracellular sites
- intracellular calcification
73
After initiation in either location, propagation of_ occurs
crystal formation
74
Metastatic calcification can occur in normal tissues whenever there is _
hypercalcemia
75
Deposits of calcium salts
in dead and degenerated
tissues
Calcium metabolism
>__
Deranged Serum calcium
level
>_
Reversibility
>_
Causes
>_
Dystrophic
- normal
- normal
- Irreversible
- aging or damaged heart
valves
76
Deposits salts in normal
tissues
Calcium metabolism
>__
Deranged Serum calcium
level
>_
Reversibility
>_
Causes
>_
Metastatic
- Deranged
- Hypercalcaemia
- Reversible upon
correction of metabolic
disorders
- hypercalcemia
77
Regardless of the site, _ are seen on gross examination as fine white granules or clumps, often felt as gritty deposits
calcium salts
78
Dystrophic calcification is
common in areas of __
* Sometimes a tuberculous lymph
node is essentially converted to
__
* On histologic examination,
calcification appears as
_ or _
caseous necrosis in tuberculosis
- radiopaque stone
intracellular and/or extracellular
basophilic deposits
79
principally affects the interstitial tissues of the _,_,_,_
* The calcium deposits morphologically
resemble those described in
dystrophic calcification
* The massive deposits in the kidney
(__) can lead to renal
damage.
Metastatic calcification
- vasculature, kidneys, lungs, and
gastric mucosa
- nephrocalcinosis
80
Four Major Causes of Hypercalcemia
(1) Increased Secretion of Parathyroid Hormone
(2) Destruction if Bone
(3) Vitamin D-related Disorders
(4) Renal Failure
81
- Due to either primary parathyroid tumors or production of parathyroid hornone-related protein by other malignant tumors;
Increased Secretion of Parathyroid Hormone
82
Destruction of Bone
- e.g. Paget disease
- Tumors
- (increased bone catabolism associated with multiple myeloma, leukemia, or diffuse skeletal metastases)
83
Vitamin D-related Disorders
_
_ (in which macrophages activate a __)
- Vitamin D intoxication
- Sarcoidosis (in which macrophages activate a vitamin D precursor)
84
- Phosphate retention leads to secondary hyperparathyroidism
renal Failure
85
- Abnormal desposits of materials in cells and tissues are the result of __
excessive intake or defective transport or catabolism.
86
accumulation of free triglycerides in cells, resulting from excessive intake or defective transport (often because of defects in synthesis of transport proteins); manifestation of reversible cell injury
* Depositions of lipids
- Fatty change:
87
result defective catabolism and excessive intake; in macrophages and smooth muscle cells of vessel walls in atherosclerosis
- Cholesterol deposition:
88
reabsorbed proteins in kidney tubules; immunoglobulins in plasma cells
Deposition of proteins:
89
in macrophages of patients with defects in lysosomal enzymes that break down glycogen (glycogen storage diseases)
Deposition of glycogen:
90
typically indigestible pigments, such as_,_ (breakdown product of lipid peroxidation), or __ (usually due to overload, as in _)
Deposition of pigments
- carbon, lipofuscin
- iron
- hemosiderosis
91
* Pathologic calcifications
- Dystrophic calcification
Metastics calcifications:
92
deposition of calcium at sites of cell injury and necrosis
- Dystrophic calcification:
93
deposition of calcium in normal tissues, caused by hypercalcemia (usually a consequence or parathyroid hormone excess)
- Metastics calcifications:
94
Mechanisms of abnormal/intracellular Accumulations
1 Abnormal Metabolism
2 Defect in protein folding transport
3 lack of enzyme
4 ingestion of indigestible material
95
represents complexes of lipid and protein
that derive from the free radical–catalyzed
peroxidation of polyunsaturated lipids of subcellular membranes.
It is not injurious to the cell but is a marker of ___
Lipofuscin
past free radical injury
96
- usually induced by
altered differentiation
pathway of tissue stem
cells
metaplasia
97
- may result in reduced
functions or increased
propensity for malignant
transformation
metaplasia
