adaptations 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
Physiologic adaptations
Pathologic adaptations

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2
Q

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

A

cell injury

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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

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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

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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

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6
Q

Hypertrophy

A

◦ Physiologic Cellular
Hypertrophy
- Pathologic Cellular
Hypertrophy

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7
Q

 Enlargement of the uterus
during pregnancy
 Increased work load the
striated muscle cells in
both skeletal and heart

A

Physiologic Cellular
Hypertrophy

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8
Q

– removed for postpartum
bleeding.
- large, plump hypertrophied
smooth muscle cells from a
__

A
  • a gravid uterus
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9
Q
  • B, Small spindle-shaped
    uterine smooth muscle cells
    from a __
A

normal uterus.

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10
Q

 Cardiac enlargement that
occurs with hypertension
or aortic valve disease

A

Pathologic Cellular
Hypertrophy

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11
Q

The type of reversible injury is __, and the irreversible
injury is _

A

ischemia
ischemic coagulative necrosis

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12
Q
A
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13
Q

In__ , the left ventricular wall is
thicker than 2 cm (normal, _)

A

myocardial hypertrophy
- 1–1.5 cm

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14
Q

an enzyme substrate that
colors viable myocardium _. Failure to stain is due
to enzyme loss after cell death

A

triphenyltetrazolium chloride
- magenta

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15
Q

Two types of physiologic hyperplasia:

A

hormonal hyperplasia
compensatory hyperplasia

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16
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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17
Q

 in which residual tissue grows after removal or lossof part of an organ

A

compensatory hyperplasia

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18
Q
  • Occurs due to an abnormal stressor
A

Pathologic Hyperplasia
 Excessive hormonal or growth factor stimulation
 Endometrial hyperplasia
 Benign prostatic hyperplasia
 Papillomavirus

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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

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20
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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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

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22
Q

types of atrophy

A

PHYSIOLOGIC ATROPHY
SENILE ATROPHY
PATHOLOGIC ATROPHY

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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

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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

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25
Q

 -refers to a decrease in size of tissues or
organs
◦ outside the range of normal variability
◦ usually as a consequence of disease

A

pATHOLOGIC ATROPHY

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26
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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27
Q

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

A

Metaplasia

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28
Q

metaplasia

A

EPITHELIAL METAPLASIA
MESENCHYMAL METAPLASIA

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29
Q

◦ -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 _

A

EPITHELIAL METAPLASIA
- ◦ prolonged vitamin A deficiency
- respiratory passages, linings of gland ducts and
mucosal lining of endocervix

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30
Q

◦ -occurring in connective tissues whereby fibroblasts are
transformed into more highly differentiated forms such
as_,__,_

A

MESENCHYMAL METAPLASIA
- osteoblasts, fat cells or tissue macrophages

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31
Q

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:

A

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

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32
Q

Inadequate removal of a normal substance secondary to
defects in _ and _
>__

A

mechanisms of packaging and transport
- ◦ fatty change in the liver

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33
Q

◦ as a result of genetic or acquired defects in its folding,
◦ packaging, transport, or secretion, as with certain mutated
forms of _

A

Accumulation of an abnormal endogenous substance
- α1-antitrypsin

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34
Q

◦ due to inherited-enzyme deficiencies

 The resulting disorders are called

A

failure to degrade a metabolite
- storage diseases

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35
Q

Deposition and accumulation of an abnormal exogenous substance
◦ Accumulation of _ or _

A

carbon or silica particle

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36
Q

abnormal intracellular accumulations

A
  • Fatty Change (Steatosis)
     Accumulation of proteins
     Pigmen
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37
Q

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 ,,_

A

fatty change / steatosis
- liver
- heart, skeletal muscle, kidney, and other organs.

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38
Q

 Causes of Steatosis

A

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

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39
Q

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

A

Alcohol abuse and diabetes

40
Q
  • alter mitochondrial and SER
    function
A

Hepatotoxins (alcohol)

41
Q

 decrease the synthesis of
apoproteins

A

CCl4 and Protein Malnutrition

42
Q

inhibits fatty acid oxidation

A

Hepatotoxins (alcohol)
Anoxia

43
Q

increases fatty acid
mobilization

A

Starvation

44
Q

The possible mechanisms leading
to accumulation of _ in _
Defects in any of the steps of
uptake, catabolism, or secretion
can lead to_

A

triglycerides in fatty liver
lipid accumulation

45
Q

accumulation of fat in the hepatocyte

A
  • Increased uptake of triglycerides
    ◦ Decreased use of fat by cells.
    ◦ Overproduction of fat in cells.
    ◦ Decreased secretion of fat from the cells
46
Q

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

A

Cellular cholesterol metabolism
- lipid (triglycerides, cholesterol, and cholesteryl esters)

47
Q

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

A

Eosinophilic Russel
bodies
- tumors

48
Q

◦ Is an eosinophilic cytoplasmic
inclusion in liver cells that is highly
characteristic of alcoholic liver disease.
◦ Damaged_
within the hepatocytes

A

Mallory Body, or “Alcoholic
Hyalin,”
- intermediate filaments

49
Q

 Are aggregates of hyperphosphorylated
tau protein (proteins that stabilize
microtubules) that are most commonly known as a primary marker of __ aggregated protein inclusions

A

neurofibrillary tangle (NFTs)
- Alzheimer’s disease.

50
Q

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 _

A

Glycogen
glucose or glycogen
- renal tubular epithelium,
cardiac myocytes, and β cells of the islets of Langerhans
- glycogen storage diseases, or
glycogenoses

51
Q

can occur in normal or in pathological conditions.

A

Pigments
- Endogenous pigments
- Exogenous pigments

52
Q

are produced within the tissue
to serve a physiological function, or may be by- products of normal metabolism.

A
  • Endogenous pigments
53
Q

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

A
  • Exogenous pigments
54
Q
  • Endogenous pigments
A
  • hematogenous or blood-derived
    pigments
  • nonhematogenous
  • endogenous minerals
55
Q

hematogenous or blood-derived
pigments

A

◦ (hemosiderin, hemoglobin, bile pigment)

56
Q

nonhematogenous

A

(such as melanin, lipofuscin and
chromaffin)

57
Q

endogenous minerals

A

◦ (such as iron, calcium and copper)

58
Q

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 _

A
  • Exogenous pigments
    -jet black pigments
  • lymph nodes and pulmonary parenchyma ( anthracosis)
  • coal workers’ pneumoconiosis
59
Q

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

60
Q

are the only source of melanin
◦ _in the skin can accumulate the
pigment (e.g., in _)

A

melanocytes
- basal keratinocytes
- freckles

61
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
of iron.
◦ Identified by its staining reaction _

A

hemosiderin
- (blue color) with the Prussian blue dye

62
Q

two types of hemosiderin

A

Hemosiderosis
Hereditary Hemochromatosis

63
Q

◦ accumulation is primarily within tissue macrophages & is not associated with tissue
damage

A

Hemosiderosis

64
Q

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

A

Hereditary Hemochromatosis

65
Q

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

lipofuscin or wear and tear pigment
- heart, liver, and brain

66
Q

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

A

brown atrophy

67
Q

Pathologic Calcification

A
  1. Metastatic Calcification
  2. Dystrophic Calcification
68
Q

abnormal deposition of calcium salts,
together with smaller amounts of iron,
magnesium, and other minerals

A

Pathologic Calcification

69
Q

When the deposition occurs in dead or dying tissues,

it occurs in the absence of __ in calcium metabolism ( with normal serum levels of calcium)

A

Dystrophic
- calcium metabolic derangements

70
Q

◦ deposition of calcium salts in normal tissues

always reflects some derangement in calcium metabolism (__)

A

Metastatic
- hypercalcemia

71
Q

is encountered in
areas of necrosis of any type.
 It is virtually inevitable in the __

A

Dystrophic calcification
- atheromas of
advanced atherosclerosclerosis

72
Q

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

A

Initiation (or nucleation)

  • intracellular or extracellular
  • crystalline calcium phosphate
  • extracellular sites
  • intracellular calcification
73
Q

After initiation in either location, propagation of_ occurs

A

crystal formation

74
Q

Metastatic calcification can occur in normal tissues whenever there is _

A

hypercalcemia

75
Q

Deposits of calcium salts
in dead and degenerated
tissues
Calcium metabolism
>__
Deranged Serum calcium
level
>_
Reversibility
>_
Causes
>_

A

Dystrophic
- normal
- normal
- Irreversible
- aging or damaged heart
valves

76
Q

Deposits salts in normal
tissues
Calcium metabolism
>__
Deranged Serum calcium
level
>_
Reversibility
>_
Causes
>_

A

Metastatic
- Deranged
- Hypercalcaemia
- Reversible upon
correction of metabolic
disorders
- hypercalcemia

77
Q

Regardless of the site, _ are seen on gross examination as fine white granules or clumps, often felt as gritty deposits

A

calcium salts

78
Q

Dystrophic calcification is
common in areas of __
* Sometimes a tuberculous lymph
node is essentially converted to
__
* On histologic examination,
calcification appears as
_ or _

A

caseous necrosis in tuberculosis
- radiopaque stone
intracellular and/or extracellular
basophilic deposits

79
Q

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.

A

Metastatic calcification
- vasculature, kidneys, lungs, and
gastric mucosa
- nephrocalcinosis

80
Q

Four Major Causes of Hypercalcemia

A

(1) Increased Secretion of Parathyroid Hormone
(2) Destruction if Bone
(3) Vitamin D-related Disorders
(4) Renal Failure

81
Q
  • Due to either primary parathyroid tumors or production of parathyroid hornone-related protein by other malignant tumors;
A

Increased Secretion of Parathyroid Hormone

82
Q

Destruction of Bone

A
  • e.g. Paget disease
  • Tumors
    • (increased bone catabolism associated with multiple myeloma, leukemia, or diffuse skeletal metastases)
83
Q

Vitamin D-related Disorders
_
_ (in which macrophages activate a __)

A
  • Vitamin D intoxication
  • Sarcoidosis (in which macrophages activate a vitamin D precursor)
84
Q
  • Phosphate retention leads to secondary hyperparathyroidism
A

renal Failure

85
Q
  • Abnormal desposits of materials in cells and tissues are the result of __
A

excessive intake or defective transport or catabolism.

86
Q

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

A
  • Depositions of lipids
  • Fatty change:
87
Q

result defective catabolism and excessive intake; in macrophages and smooth muscle cells of vessel walls in atherosclerosis

A
  • Cholesterol deposition:
88
Q

reabsorbed proteins in kidney tubules; immunoglobulins in plasma cells

A

Deposition of proteins:

89
Q

in macrophages of patients with defects in lysosomal enzymes that break down glycogen (glycogen storage diseases)

A

Deposition of glycogen:

90
Q

typically indigestible pigments, such as_,_ (breakdown product of lipid peroxidation), or __ (usually due to overload, as in _)

A

Deposition of pigments
- carbon, lipofuscin
- iron
- hemosiderosis

91
Q
  • Pathologic calcifications
A
  • Dystrophic calcification
    Metastics calcifications:
92
Q

deposition of calcium at sites of cell injury and necrosis

A
  • Dystrophic calcification:
93
Q

deposition of calcium in normal tissues, caused by hypercalcemia (usually a consequence or parathyroid hormone excess)

A
  • Metastics calcifications:
94
Q

Mechanisms of abnormal/intracellular Accumulations

A

1 Abnormal Metabolism
2 Defect in protein folding transport
3 lack of enzyme
4 ingestion of indigestible material

95
Q

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 ___

A

Lipofuscin
past free radical injury

96
Q
  • usually induced by
    altered differentiation
    pathway of tissue stem
    cells
A

metaplasia

97
Q
  • may result in reduced
    functions or increased
    propensity for malignant
    transformation
A

metaplasia