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Pathology > CELLULAR INJURY, CELL DEATH, AND ADAPTATIONS > Flashcards

CELLULAR INJURY, CELL DEATH, AND ADAPTATIONS Flashcards

1
Q

cell can go back to its normal state after the cellular injury is identified

A

Reversible

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2
Q

There is persistence of the injury and the cells can no longer cope up with the stress

A

Irreversible

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3
Q

In hypertension, there is ______ in workload

A

increase

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4
Q

In AMI, there is ______ blood flow to the heart

A

decreased

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5
Q

The major and important cause of cell injury

A

Oxygen deprivation

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6
Q

causes of oxygen deprivation

A

reduced blood flow
cardiorespiratory failure
decreased oxygen-carrying capacity of blood

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7
Q

Causes of cell injury: PHYSICAL AGENTS

A

Mechanical trauma, extremes of temperature, sudden changes in atmospheric pressure, Radiation, Electric shock

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8
Q

serves an essential function in defense against infectious pathogens, but immune reactions may also cause cell injury.

A

Immune system

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9
Q

A functional and structural alteration in early stages or mild forms of injury

A

Reversible cell injury

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10
Q

FEATURES OF REVERSIBLE CELL INJURY

A

Generalized swelling of the cell and its organelles
Blebbing of the plasma membrane
Detachment of ribosomes
Clumping of nuclear chromatin

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11
Q

Ultrastructural changes visible by electron microscopy:

PLASMA MEMBRANE

A

Blebbing
Blunting
Loss of microvilli

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12
Q

Ultrastructural changes visible by electron microscopy:

Mitochondria

A

Swelling

small densities

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13
Q

reversible functional and structural responses to changes in physiologic states and some pathologic stimuli

A

Adaptations

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14
Q

increase in size

A

hypertrophy

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15
Q

increase in cell number

A

hyperplasia

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16
Q

decrease in size and metabolic activity of cells

A

atrophy

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17
Q

change in the phenotype of cells

A

metaplasia

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18
Q

Calcium may be deposited at sites of cell death, resulting in __________

A

Pathological classification

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19
Q

On microscopic examination, small clear vacuoles may be seen within cytoplasm; this pattern of nonlethal injury is sometimes called________

A

Hydropic change or vacuolar degeneration

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20
Q

the cytoplasm of injured cells appear __ when stained w hematoxylin and eosin

A

red

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21
Q

Ultrastructural changes visible by electron microscopy:

Myelin figures in the cytoplasm

A

Derived from phospholipids of damaged membranes

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22
Q

Ultrastructural changes visible by electron microscopy:

Nuclear alterations

A

Disaggregation of granular and fibrillar elements.

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23
Q

Causes of necrosis

A
  • Ischemia
  • Exposure to microbial toxins
  • Burns and other forms of chemical and physical injury
  • unusual situations in which active proteases leak out of the cells and damage surrounding tissues.
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24
Q

basophilia of the chromatin
may fade; presumably reflects loss of
DNA because of enzymatic degradation
by endonucleases

A

Karyolysis

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25
Q 
characterized by nuclear
shrinkage and increased basophilia,
chromatin condenses into a dense,
shrunken basophilic mass (also seen in
apoptotic cell death)
A

Pyknosis

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26
Q

pyknotic nucleus

undergoes fragmentation

A

Karyorrhexis

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27
Q

● Architecture of dead tissue is preserved for a
span of at least some days only with loss of
Nuclei
● Affected tissue has a firm texture

A

COAGULATIVE NECROSIS

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28
Q

Coagulative necrosis is commonly seen in _____in any tissue
EXCEPT the brain which undergo liquefactive
necrosis

A

Ischemia

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29
Q

Localized area of coagulative necrosis is called

an _______

A

infarct

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30
Q

● Digestion of the dead cells, resulting in
transformation of the tissue into a viscous liquid
● Seen in focal bacterial or, occasionally, fungal
infections

A

LIQUEFACTIVE NECROSIS

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31
Q

● Accumulation of leukocytes (predominantly
neutrophils) and the liberation of enzymes from
these cells known as

A

pus

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32
Q

● not a specific pattern of cell death, but the term
is commonly used in clinical practice, usually
applied to a limb

A

GANGRENOUS NECROSIS

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33
Q

this term is derived from the

friable white appearance of the area of necrosis

A

caseous

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34
Q

Necrotic area appears as a structureless
collection of fragmented or lysed cells and
amorphous granular debris enclosed within a
distinctive inflammatory border

A

CASEOUS NECROSIS

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35
Q

Focal areas of fat destruction, typically resulting
from release of activated pancreatic lipases into
the substance of the pancreas and the
peritoneal cavity

A

FAT NECROSIS

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36
Q

Fatty acids are generated that combine with
______to produce grossly visible chalky-white
areas

A

calcium

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37
Q

Special form of vascular damage usually seen in
immune reactions involving blood vessels

-Occurs when complexes of antigens and
antibodies are deposited in the walls of arteries
called “fibrinoid” (fibrin-like)

A

FIBRINOID NECROSIS

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38
Q

● Basically cell shrinkage or reduce size

● Induced by tightly regulated suicide program

A

APOPTOSIS

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39
Q

this pathway is responsible for apoptosis in

most physiologic and pathologic situations

A

Mitochondrial

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40
Q

presence of active
_____ is therefore a marker for cells
undergoing apoptosis

A

caspases

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41
Q

A phase wherein caspases become active

A

Initiation phase

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42
Q

The mitochondrial pathway is initiated by____

A

Capsase 9

Intrinsic pathway

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43
Q 
When \_\_\_\_\_\_\_ is
released into the
cytoplasm, it initiates a
suicide program of
apoptosis
A

cytochrome c

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44
Q 
Release of cytochrome c is determined
by integrity of the outer
mitochondrial
membrane, which is
tightly controlled by
\_\_\_\_\_\_
A

BCL2 family of proteins

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45
Q

Death receptor pathway is initiated by

A

CASPASE 8,10

Extrinsic activity

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46
Q

Extrinsic pathway is Initiated by engagement
of plasma membrane
death receptors that are
members of the ___________

A

TNF
receptor family [TNFR1,
fas (CD95)]

47
Q

In this phase, Capsapses trigger cellular

fragmentation

A

Execution phase

48
Q 
Apoptotic bodies may also
become coated with natural
antibodies and proteins of the
complement system, notably
\_\_\_\_, which are recognized by
phagocytes
A

C1q

49
Q

Acts as a backup mechanism in host defense
against certain viruses that encode caspase
inhibitors (e.g., cytomegalovirus)

A

NECROPTOSIS

50
Q

Physiologic necroptotsis occurs during

A

the formation of the

mammalian bone growth plate

51
Q

Form of apoptosis that is accompanied by the

release of the fever-inducing cytokine IL-1

A

PYROPTOSIS

52
Q

Triggered when excessive intracellular levels of
iron or reactive oxygen species overwhelm the
glutathione-dependent antioxidant defenses to
cause unchecked membrane lipid peroxidation

A

FERROPTOSIS

53
Q

● process in which a cell eats its own contents

A

AUTOPHAGY

54
Q 
Nucleation and formation of
an isolation membrane, also called a
\_\_\_\_\_ derived from the ER and other
membrane sources such as the plasma
membrane and mitochondria.
A

phagophore

55
Q

The elongation and closure of
the initiation membrane require the coordinated
action of two ubiquitin-like conjugation systems
that result in the covalent linkage of the lipid
_______ to
microtubule-associated protein light chain 3
(LC3)

A

phosphatidylethanolamine (PE)

56
Q 
characterized by impaired
autophagosome maturation, and
in mouse models of the disease
genetic defects in autophagy
accelerate neurodegeneration.
A

Alzheimer disease

57
Q

Macrophage-specific deletion of
_____ increases susceptibility to
tuberculosis

A

Atg5

58
Q 
Genome-wide association
studies have linked both \_\_\_\_\_\_to
single-nucleotide
polymorphisms (SNPs) in the
autophagy-related gene
ATG16L1.
A

Crohn

disease and ulcerative colitis

59
Q

Decreased ATP synthesis and
ATP depletion are frequently associated with
both hypoxic and chemical (toxic) injury. It
produces ______

A

ATP utilizing oxidative phosphorylation

and glycolytic pathway

60
Q

Mitochondrial damage often results in the
formation of a high-conductance channel in the
mitochondrial membrane, called the__________

A

mitochondrial permeability transition pore

61
Q

Cellular energy metabolism is altered: If the
supply of oxygen to cells is reduced, as in
ischemia, oxidative phosphorylation ceases,
resulting in a _____in cellular ATP and
associated increase in AMP.

A

decrease ; increase

62
Q

These changes
stimulate phosphorylase and
phosphofructokinase activities, leading to
increased rates of____

A

glycogenolysis and glycolysis.

63
Q

Leakage of mitochondrial proteins due to
__________is the initial step in apoptosis by the
intrinsic pathway

A

channel formation by pro-apoptotic BAX and BAK

64
Q

Oxygen free radicals cause injury to cell

membranes by lipid peroxidation

A

ROS

65
Q

With _______ there is Decreased
phospholipid synthesis which may affect all
cellular membranes, including those of
mitochondria

A

lipid peroxidation

66
Q

Damage to nuclear DNA activates sensors that
trigger p53-dependent pathways which arrests
cells in the _____of the cell cycle and
activates DNA repair mechanisms (important in
development of tumors)

A

G1 phase

67
Q

are chemical species that have a
single unpaired electron in an outer orbit which
are highly reactive and “attack” and modify
adjacent molecules, such as inorganic or
organic chemicals—proteins, lipids,
carbohydrates, nucleic acids—many of which
are key components of cell membranes and
nuclei.

A

Free radicals

68
Q

ROS are produced normally in cells during
__________,
but they are degraded and removed by
intracellular ROS scavengers

A

mitochondrial respiration and energy generation

69
Q

Increased production or decreased scavenging
of ROS may lead to an excess of free radicals, a
condition called ___

A

oxidative stress

70
Q

Rapid bursts of ROS are produced in

activated ______during inflammation

A

leukocytes

71
Q

Pathologic Effect of Free radicals:

A

○ Lipid peroxidation in membranes
○ Oxidative modification of proteins
○ Lesions in DNA

72
Q

T or F

free radicals can also trigger apoptosis.

A

T

73
Q

normally serve as second
messengers in several signalling pathways but if released into cytoplasm in excessive amounts,
are also an important source of cell injury.

A

Calcium ions

74
Q

T or F
Cytosolic free Ca2+ is normally maintained at
very low concentrations (~0.1µmol)

A

T

75
Q

Accumulation of ____ in mitochondria
result in opening of mitochondrial
permeability transition pore and failure
of ATP generation

A

Ca2+

76
Q

_____ control the proper folding

of newly synthesized proteins

A

Chaperones in the ER

77
Q

Triggered by the accumulation of

unfolded or misfolded proteins in the ER

A

Unfolded Protein response

78
Q 
Occurs when the cytoprotective
response is unable to cope with the
accumulation of misfolded proteins in
the cell leading to the activation of
caspases and induces apoptosis
A

ER Stress

79
Q

is the most common cause of cell

injury in clinical medicine

A

Ischemia

80
Q

Results from hypoxia induced by
reduced blood flow, most often due to a
mechanical arterial obstruction

A

Ischemia

81
Q 
T or F
In ischemic tissues, not only does
aerobic metabolism cease but anaerobic
energy generation also fails after
glycolytic substrates are exhausted or
glycolysis is inhibited by the
accumulation of metabolites
A

T

82
Q 
Blood flow is maintained and during
which energy production by anaerobic
glycolysis can continue, ischemia
compromises the delivery of substrates
for glycolysis
A

Hypoxia

83
Q

Restoration of blood flow to ischemic tissues can

promote recovery of cells in reversible injury

A

ISCHEMIA REPERFUSION INJURY

84
Q

These free radicals may be produced in
reperfused tissue as a result of
__________

A

incomplete reduction of oxygen
leukocytes, and in damaged endothelial
cells and parenchymal cells

85
Q

Intracellular and mitochondrial calcium
overload begins during reperfusion due
to __________

A

influx of calcium resulting from cell
membrane damage and ROS-mediated
injury to sarcoplasmic reticulum

86
Q

some ____
antibodies have propensity to deposit in
ischemic tissues

A

IgM

87
Q

is often the reason for
terminating the therapeutic use or development
of a drug

A

Toxic liver injury

88
Q

Mercury binds to the _________ of cell membrane
proteins, causing increased
membrane permeability and
inhibition of ion transport

A

sulfhydryl

groups

89
Q

○ Most toxic chemicals are not biologically
active in their native form but must be
converted to reactive toxic metabolites,
which then act on target molecules
○ This modification is usually
accomplished by the cytochrome P-450
mixed-function oxidases in the ____ of the liver and other organs

A

smooth

ER

90
Q

● Increased functional demand (body builders)

● Stimulation by hormones and growth factors

A

PHYSIOLOGIC HYPERTROPHY

91
Q

● Common to permanent cells - nondividing cells
(skeletal muscles, myocytes, brain cells)
● Increased workload
● Synthesis of more protein by increasing the
number of myofilaments per cell, increase the
amount of force, more strength and work
capacity

A

PATHOLOGIC HYPERTROPHY

92
Q

MECHANISM OF HYPERTROPHY

A

Mechanical sensors detect the increased load ->
activate a complex downstream web of signaling
pathways, including PI3K/AKT pathway
(physiologic) and G-protein-coupled
receptor-initiated pathways (pathologic) ->
stimulate increased production of growth factors
and vasoactive agents -> activate transcription
factors [GATA4, NFAT, MEF2] which increase
the expression of genes that encode muscle
proteins

93
Q

Increase in number of cells and (consequently)

organ

A

HYPERPLASIA

94
Q

● Action of hormones or growth factors
● Increase functional capacity of the organ
● Compensatory increase after damage or
resection

A

PHYSIOLOGIC HYPERPLASIA

95
Q

● Excessive or inappropriate action of hormones
and growth factors on target cells
● Usually benign but it can initiate cancer
● Constitutes a fertile soil in which cancerous
proliferations may eventually arise

A

PATHOLOGIC HYPERPLASIA

96
Q

Prostatic hyperplasia

A

there is significant amount of stroma in

between the glands (normal)

97
Q

there is significant amount of stroma in

between the glands (normal)

A

there are more glands and are seen in a

haphazard/random fashion

98
Q

Result of growth factor-driven proliferation of
mature cells and, in some cases, by increased
output of new cells from tissue stem cells

A

MECHANISM OF HYPERPLASIA

99
Q

● Reduction in size of organ or tissue

● Decrease in cell size and number

A

ATROPHY

100
Q

● Regression of the uterus after pregnancy
● Regression of the breast after pregnancy and
lactation
● Regression of the thyroglossal duct - (during
development) originates at the base of the
tongue and transports the thyroid to the anterior
neck; this duct normally regress
● Common during normal development

A

PHYSIOLOGIC ATROPHY

101
Q

In _____, there is a decrease in blood supply because
of atherosclerotic cerebrovascular disease -> widened
sulci because of the thinning of some of the gyri

A

atrophy

102
Q

Degradation of proteins occurs mainly by the
_________. Nutrient
deficiency and disuse may activate ubiquitin
ligases.

A

ubiquitin-proteasome pathway.

103
Q

Reversible change in which one differentiated
cell type is replaced by another cell type
(change should be from a stronger or more
stable type of cell)

A

METAPLASIA

104
Q

● Reprogramming of local tissue stem cells (there
is transition of the cells to a more durable cells
depending on the condition that stimulated the
metaplastic reaction)
● Colonization by differentiated cell population
from adjacent sites (extension of squamous
epithelium going into the endocervical region
and replacing glandular epithelium)

A

METAPLASIA

105
Q

*Squamous metaplasia of cervix

A

the glandular

epithelium is replaced by squamous epithelium

106
Q

BARRETT’S METAPLASIA

A

Esophagus - squamous epithelium; gastric - glandular
epithelium -> glandular epithelium is starting to replace
your squamous epithelium because glandular epithelium
is more resistant to acid

107
Q

● Manifestations of metabolic derangements
● Harless or can cause injury
● Location- cytoplasm, organelles, or nucleus
● Endogenous or exogenous

A

INTRACELLULAR ACCUMULATIONS

108
Q

(abnormal
accumulations of triglycerides within
parenchymal cells)

A

steatosis

109
Q

Cholesterol and cholesterol esters

A

atherosclerosis, xanthomas, cholesterolosis, and

niemann pick disease type c

110
Q

) there is deposition of
cholesterol esters in the wall; sometimes there is
corresponding fibrosis

A

Atheroma

111
Q

yellow bright color in the mucosa because

of the deposition of your cholesterol esters

A

*gallbladder

112
Q

intracellular accumulations of __________ usually
appear as rounded, eosinophilic droplets,
vacuoles, or aggregates in the cytoplasm.

A

proteins

113
Q

T or F
Proteins can be amorphous, fibrillar, or crystalline in
appearance under electron microscopy.

A

T

Pathology (31 decks)

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