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MOD Exam 1 > Cellular Response and Adaptation > Flashcards

Cellular Response and Adaptation Flashcards

Ch 1

1
Q

Neoplasm

A

Any new or abnormal growth, specifically a new growth of tissue in which the growth is uncontrolled and progressive

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2
Q

Hyperplasia and it’s mechanism

A

The increase in the number of cells in a tissue or organ in response to a stimulus

Mechanism: growth factor-driven proliferation of mature cells

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3
Q

Karyorrhexis

A

A pyknotic nucleus undergoes fragmentation

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4
Q

Disorder

A

derrangement or abnormality of function

-a morbid physical or mental state/condition

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5
Q

Common causes of atrophy

A
  1. Decreased workload
  2. loss of innervation (denervation)
  3. diminished blood supply
  4. inadequate nutrition
  5. loss of endocrine stimulation
  6. pressure
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6
Q

What morphological changes are see in dystrophic calcification?

A

calcium salt deposits have a basophilic, amorphous granular appearance; sometimes can clump together

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7
Q

Pyroptosis involves what cytokine?

A

IL-1

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8
Q

What cell type is responsible for phagocytosis of apoptotic bodies?

A

Macrophages

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9
Q

What transcription factor promotes new blood vessel formation, stimulates cell survival pathways, and enhances anaerobic glycolysis in attempt to deal with hypoxic stress?

A

Hypoxia-inducible factor-1

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10
Q

What pathway is thought to be the most important in physiologic hypertrophy?

A

AKT pathway

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11
Q

Morphologic changes

A

structural alterations in cells/tissues that are either characteristic of a disease or diagnostic of an etiologic process

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12
Q

What factors lead to physiologic hyperplasia

A

the actions of hormones or growth factors

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13
Q

Where do anti-apoptotic proteins reside?

A

in the outer mitochondrial membrane, cytosol, and ER

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14
Q

What pathway is the major mechanism of apoptosis in mammalian cells?

A

The intrinsic mitochondrial pathway

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15
Q

What is the function of pro-apoptotic proteins?

A

Once activated, BAK and BAX oligomerize and promote permeability of the outer mitochondrial membrane, allowing cytochrome C to leak out

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16
Q

Gangrenous necrosis

A

Used in clinical practice, describing a limb that has lost blood supply and has undergone necrosis

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17
Q

What is the function of the p16 tumor suppressor gene?

A

protection of cells from uncontrolled signals and promotes senescence

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18
Q

How is the extrinsic pathway of apoptosis initiated?

A

FasL binds to Fas receptors which recruit FADD adaptor protein

FADD binds to procaspase-8, bringing other procaspase-8 molecules together

Procaspase-8 is cleaved into active caspase-8 which then activated caspases 3 and 6, similar to the mitochondrial pathway

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19
Q

Granulomatous inflammation

A

A form of chronic inflammation characterized by collections of macrophages, T lymphocyes and sometimes associated with a central caseating necrosis

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20
Q

What tissues are predisposed to metastatic calcification and why?

A

gastric mucosa, kidneys, lungs, systemic arteries, pulmonary veins; they contain an internal alkaline compartment and excrete acid

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21
Q

Morphological changes associated with irreversible injury

A

Severe swelling of mitochondria

extensive damage to plasma membranes leading to the production of myelin figures

Swelling of lysosomes

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22
Q

Cellular response to injury is dependent on:

A

nature of the injury, duration, and severity

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23
Q

cells unable to maintain ionic and fluid homeostasis d/t failure of energy-dependent ion pumps in the membrane undergo what change?

A

Cellular swelling

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24
Q

Pathologic calcification and the types

A

deposition of calcium salts into tissues

Dystrophic calcification

Metastatic calcification

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25
Q

Metaplasia

A

Reversible change in which one differentiated cell type is replaced by another cell type

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26
Q

What initiates the necroptotic pathway?

A

TNF binding to TNFR1

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27
Q

ischemia-reperfusion injury results from:

A

restoration of blood flow to ischemic tissues, resulting in loss of cells in addition to those cells that underwent irreversible injury

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28
Q

Infarct

A

Localized area of coagulative necrosis

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29
Q

Connective tissue metaplasia

A

Formation of cartilage, bone, or adipose tissue within tissues that do not normally contain these elements

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30
Q

What is the conquence of shortening of telomeres in somatic cells?

A

Somatic cells lack telomerase, therefore with each replication, the telomeres shorten.

Telomere shortening signals cell cycle arrest.

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31
Q

Pathogenesis

A

sequence of biochemical and molecular events that follow the exposure of cells/tissue to injurious agent

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32
Q

Coagulative necrosis

A

Ischemia caused by obstruction in a vessel

Injury denatures structural proteins and enzymes, blocking proteolysis of dead cells

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33
Q

What is the end result of progressive cell injury and is the most crucial event in the evolution of disease?

A

Cell death

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34
Q

What factor separates the mechanism of necroptosis from the mechanism of apoptosis?

A

Necroptosis does not result in the activation of caspases

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35
Q

What is a consistent feature of most forms of cell injury, except for apoptosis?

A

early loss of selective membrane permability, leading to overt membrane damage

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36
Q

What is the strongest independent risk factor for chronic illnesses?

A

Cellular aging

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37
Q

What stimulates production of anti-apoptotic proteins?

A

growth factors

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38
Q

What is the first manifestation of injury in almost all cell forms?

A

cellular swelling

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39
Q

Mechanisms of chemically induced cell injury

A

Direct toxicity

Conversion to toxic metabolites

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40
Q

What tumor suppressor genes does the CDKN2A locus encode?

A

p16

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41
Q

What is the underlying purpose for which a cell type might undergo metaplasia?

A

a change in phenotype of a cell can make the cell better able to withstand stress

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42
Q

Physiologic hyperplasia occurs when?

A

When there is a need to increase the functional capacity of hormone sensitive organs.

When there is a need for compensatory increase after damage or resection (i.e. kidney transplant)

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43
Q

What is the main role of BCL2 anti-apoptotic proteins

A

Keep the outer mitochondrial membrane impermeable, preventing the release of cytochrome C into the cytosol

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44
Q

Apoptosis

A

When the cell’s DNA or proteins are damaged beyond repair, the cell kills itself by nuclear dissolution, fragmentation of the cell and rapid removal of cellular debris.

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45
Q

What happens to myelin figures after they are formed during cell injury?

A

they are phagocytosed by leukocytes or degraded further into fatty acids (can form calcium soaps)

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46
Q

In the process of autophagy, what assists in the elongation of the membrane?

A

Microtubule-associated protein light chain 3 (LC3)

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47
Q

What receptor associated kinases are attracted to TNFR1 after activation?

A

receptor associated kinase 1 and 3 (RIP1 and RIP3)

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48
Q

The extrinsic pathway of apoptosis is inhibited by what protein?

Through what mechanism?

A

FLIP

Binds to pro-caspase 8 and prevents its cleavage, thus preventing apoptosis

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49
Q

What does pathologic hyperplasia provide?

A

A ground for which malginant proliferations can arise

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50
Q

Through what mechanisms has caloric restrictions been shown to increase longevity?

A

reducing signaling intensity of the IGF-1 pathway and increasing sirtuins.

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51
Q

What is the function of sensors in the intrinsic mitochondrial pathway?

A

They sense the loss of growth factors, DNA damage and ER stress, and activate BAK and BAX

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52
Q

Pyknosis

A

nuclear shrinkage and increased basophilia

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53
Q

Cell injury

A

limits of adaptation are exceeded or cells are exposed to severe injurious agents/stress

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54
Q

Karyolysis

A

loss of DNA because of enzymatic degradation by endonucleases

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55
Q

What is the cause behind the common bruise?

A

Local excess of iron 2/2 the breakdown of hemoglobin

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56
Q

What is often deposited at sites of cell death, and what is it classified as?

A

Calcium.

Pathologic calcification

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57
Q

What disorders are associated with an increase in apoptotic cell death?

A

Neurodegenerative diseases including Alzheimer’s dz, Parkinson dz and Huntington dz

Ichemic injury, such as MI

Death of a virally infected cell

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58
Q

Attenuation of IGF-1 signaling leads to

A

Lower rates of cell growth and metabolism

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59
Q

what are the downstream targets of IGF-1

A

AKT and mTOR (mammalian target of Rapamycin)

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60
Q

Depletion of ATP to 5-10% of normal levels causes:

A
  1. decreased activity of Na-K pump leading to cell swelling and dilation of the ER
  2. Cellular energy metabolism is altered: switch to anaerobic glycolysis (LA build-up)
  3. Reduction of protein synthesis 2/2 detachment of ribosomes from the ER and dissociation of polysomes
  4. Unfolded protein response
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61
Q

What protein responds to DNA damage and what is its role?

What happens if it cannot perform its role?

A

p53

accumulates within the cell, arresting the cell in the cycle cycle at G1 phase to allow for DNA repair

If damage is too great, then p53 triggers apoptosis by activating pro-apoptotic proteins

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62
Q

Cause of pathological hyperplasia?

A

excessive or inappropriate actions of hormones or growth factors on target cells.

Ex: increased proliferation of endometrial tissue 2/2 increased levels of estrogen, BPH

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63
Q

What are the morphological characteristics of necroptosis?

A

Loss of ATP, cell swelling, generation of ROS, release of lysosomal enzymes and rupture of plasma membrane (charateristic of necrosis)

Triggered by a programmed signal transduction, resembling the hallmark of apoptosis

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64
Q

Mechanisms of perfusion injury include?

A

oxidative stress

intracellular Ca overload

Inflammation

complement system activation

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65
Q

Syndrome

A

Set of symptoms that occur together; the sum of signs of any morbid state

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66
Q

Pyroptosis involves which caspase?

What does this caspase do?

A

Caspase-1

Cleaves the precursor form of IL-1 into biologically active, fever inducing, IL-1

Caspase-1 works with Caspase-11 to induce cell death

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67
Q

Dysregulation of autophagy occurs in many disease states including

A

CA

Neurodegenerative disorders

IBD

Infectious

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68
Q

What is released from necrotic cardiac muscle cells that can be detected within the blood as soon as 2 hrs post-cell death?

A

Cardiac specific enzymes and proteins (Biomarkers- CRP and troponin)

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69
Q

Muscle atrophy can be accompanied by what other condition?

A

Osteoporosis

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70
Q

What is the critical initiator caspase and how is it activated?

A

Caspase-9

Activated by the apoptosome

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71
Q

Adaptations

A

Reversible functional and structural responses to changes in physiologic states and some pathologic stimuli; a new steady state is achieved

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72
Q

Hemosiderin is the major storage form of

A

Iron

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73
Q

Liquefactive necrosis

A

Characterized by digestion of dead cells, resulting in transformation of tissue into a liquid viscous mass

  • Commonly seen in the brain
  • Seen in focal bacteria because microbes stimulate accumulation of leukocytes
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74
Q

Disease

A

any deviation from or interruption from the normal structure or function of a part, an organ or system.

-manifested by characteristic signs and symptoms

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75
Q

Necrotic cells show what in an H&E stain?

A

increased eosinophila d/t loss of cytoplasmic RNA and denaturation of cytoplasmic proteins

76
Q

Systemic overload of iron leads to what condition?

A

Hemosiderosis

The accumulation of hemosiderin in organs and tissues

77
Q

What is the most common stimulus for hypertrophy of muscle?

A

increased work load

78
Q

What is the first response to the accumulation of misfolded proteins in the ER?

What happens if this response fails?

A

Unfolded protein response: protein production halts, increasing production of chaperones which facilitate protein folding

If cell is unable to cope with the increase in misfolded proteins, the ER becomes stressed which triggers the activation of caspases and induces apoptosis

79
Q

Consequences of cell injury depend on:

A

the type, state, and adaptability of the injured cell

80
Q

Metastatic calcification

A

Occurs in normal tissues whenever there is hypercalcemia

81
Q

What is a fundamental cause of necrotic cell death?

A

Reduction in ATP levels

82
Q

To what family do death receptors belong to?

A

TNF receptor family

83
Q

Physiologic apoptosis occurs during?

A

Embryogenesis

Menstruation (endometrium)

Elimination of self-reactive T-cells

84
Q

Cells undergo a fixed number of divisions before they halt in a terminally nondividing state, these cells have undergone what process?

A

Replicative (cellular) senscence

85
Q

What are the main pro-apoptotic proteins?

What family do they belong to?

A

BAX and BAK

BCL2 family

86
Q

Process of autophagy includes?

A
  1. Formation of an isolation membrane, usually derived from ER
  2. Elongation of vesicle
  3. Maturation of the autophagosome
  4. Fusion with endosome and eventually lysosome
  5. Degradation of cell’s own contents within the lysosme
87
Q

Autophagy

A

the process in which starved cells eat their own components in an attempt to reduce nutrient demand

88
Q

Provide examples of lipid accumulation

A

Steatosis

Atherosclerosis

Xanthomas

Cholesterolosis

Niemann-Pick Disease

89
Q

What is the most important sites of membrane damage during cell injury?

A

Mitochondrial membrane

Plasma membrane

Membrane of lysosomes

90
Q

What is produced in large amounts by activated leukocytes (neutrophils and macrophages) during an inflammatory reaction?

A

Reactive oxygen species (ROS)

91
Q

What anti-apoptotic proteins help to control the release of pro-apoptotic proteins from the mitochondria?

What family do they belong to?

A

BCL2, BCL-XL, MCL1

BCL2 family

92
Q

Dystrophic calcification can be distinguished from metastatic calcification by what factor?

A

Serum calcium is normal in dystrophic calcification

93
Q

Generation of free radicals occurs in what ways?

A
  1. redox rxns that occur during normal metabolic processes
  2. absorption of radiant energy
  3. Bursts of ROS produced during inflammation by leukocytes
  4. Transition metals: Fenton reaction
  5. Nitric oxide
94
Q

Why does apoptosis not elicit an inflammatory reaction in the host?

A

Unlike necrosis, the plasma membrane of apoptotic cells remains intact and the dead cell fragments are rapidly devoured.

Cell fragments do not get a chance to leak out and therefore do not have the opportunity to elicit an inflammatory response.

95
Q

Fenton reaction

A

H202 + Fe2+ –> Fe3+ + .OH + -OH

Iron must be in the ferrous form (Fe2+) to participate in the Fention rxn

96
Q

Wet-gangrene

A

results when a bacterial infection is superimposed onto coagulative necrosis causing more liquefactive necrosis

97
Q

What is the most common cause of fatty change in the liver?

A

Alcohol abuse

Nonalcoholic fatty liver disease as a result of DM and obesity

98
Q

What is the hallmark of cardiac metabolism before birth?

A

The use of carbohydrates for energy

99
Q

Fat necrosis

A

Refers to a focal area of fat destruction resulting from the release of activated pancreatic lipases

100
Q

In what circumstance would pyroptosis be activated?

A

In cells that have been infected by microbes

101
Q

Why does necrosis elicit a host reaction (inflammation)?

A

Cellular contents leak through damaged plasma membrane into EC space

102
Q

What is the mechanism of atrophy?

A

Decreased protein production (2/2 reduced metabolic activity) and increased protein degradation in cells

103
Q

Necrosis

A

accidental and unregulated form of cell death resulting from damage to cell membranes and loss of ion homeostasis

104
Q

Major causes of ATP depletion?

A
  1. Reduced oxygen supply
  2. Reduced nutrient supply
  3. Mitochondrial damage
  4. Actions of some toxins (cyanide)
105
Q

What causes the increase in cell size encountered in hypertrophy?

A

synthesis and assembly of additional intracellular structural components, including proteins and myofilaments

106
Q

What causes a more rapid and severe cell and tissue injury than hypoxia?

A

Ischemia

107
Q

Through which pathway does degradation of cellular proteins typically occur in atrophy?

A

Ubiquitin-proteosome pathway

108
Q

When is autophagy employed by a cell?

A

Under various stress conditions, including states of nutrient deprivation

109
Q

Does cell death by apoptosis elicit an inflammatory reaction?

A

No

110
Q

What morphological changes are seen in cells undergoing apoptosis?

A

Cell shrinkage (pyknosis)

Chromatin condensation and fragmentation (karyorrhexis)

Production of cellular blebs and apoptotic bodies

Phagocytosis

111
Q

Clinical manifestation

A

signs and symptoms of a disease 2/2 alterations is cells or tissues

112
Q

What types of cell injury tend to induce apoptosis?

A

Growth factor withdrawal

DNA damage

Protein misfolding

113
Q

Mechanism of Ischemic cell injury

is this reversible?

A
  1. Oxygen depletion
  2. decreased ATP production
  3. failure in Na-K pump, allowing efflux of K and influx of Na and water, ultimately leading to cell swelling
  4. Loss of glycogen and protein synthesis

If oxygen is restored, these disturbances are reversible

114
Q

Pathways of cell death

A

necrosis, apoptosis

115
Q

Is apoptosis always associated with cell death?

A

No, it serves many normal functions as well

116
Q

What type of metaplasia occurs in Barret’s esophagus?

A

Squamous to columnar type

117
Q

How does the accumulation of misfolded proteins lead to apoptosis?

A

Proteins accumulate within the endoplasmic reticulum, resulting in ER stress

This ER stress culminates in apoptotic cell death.

118
Q

Oxidative stress

A

increased production or decreased scavenging of ROS leading to an excess of free radicals

119
Q

Function of sirtuins

A

promote the expression of gene products that increase longevity

120
Q

What protein forms hemosiderin granules and under what circumstance does this occur?

A

Ferritin

When there is a local or systemic excess of iron

121
Q

What is the stimulus for hypertrophy in cardiac muscle?

A

chronic hemodynamic overload 2/2 HTN or valve defects

122
Q

What occurs if hormonal stimulation is reduced?

A

Hyperplasia regresses

123
Q

Most common epithelial metaplasia

A

Columnar to squamous

ex: respiratory tract

124
Q

What signals the reprogramming seen in metaplasia?

A

cytokines, growth factors, EC matrix components

125
Q

What are the mechanisms of membrane damage?

A
  1. Reactive oxygen species
  2. decreased phospholipid synthesis
  3. increased phospholipid breakdown
  4. cytoskeletal abnormalities
126
Q

What constitutes an apoptosome?

When does one form?

A

Cytochrome C + APAF-1

When cytochrome C leaks into cytosol

127
Q

Dystrophic calcification is commonly seen in what conditions?

A

advanced atherosclerosis, damaged heart valves

128
Q

In what types of cells can hyperplasia occur?

A

In cells that are capable of dividing

129
Q

After birth, energy provision is achieved through which mechanism?

A

Oxidation of fatty acids

130
Q

What type of cancers are apt to develop psammoma bodies?

A

Papillary (i.e. thyroid)

131
Q

What cytokine is thought to be responsible for appetite suppression and lipid depletion, culminating in muscle atrophy?

A

Tumor necrosis factor (TNF)

132
Q

An increase in sirtuins, including Sirtuin-6 results in

A

adaptation of caloric restriction, promotion of genomic integrity by activating DNA repair enzymes through deacylation

133
Q

Cell injury induced by what is an important mechanism of cell damage in many pathological conditions?

A

Free radicals, specifically reactive oxygen species (ROS)

134
Q

Hypertrophy

A

increase in size of cells, results in increase in size of specific organ

135
Q

What mechanisms are believed to underie the process of cellular senescence?

A

Telomere attrition (shortening)

Activation of tumor suppressor genes

136
Q

How do cells die after injury to lysosomal membranes?

A

lysosomes leak their contents into the intraceullar space, including: RNases, DNases, proteases, phosphatases, glucosidases

Activation of these enzymes leads to degradation of proteins, the cells die by necrosis

137
Q
A
138
Q

What do the pancreatic lipases do to contribute to fat necrosis?

A

Split the triglyceride esters contained within fat cells; these FA combine with calcium to create calcium soaps

139
Q

Necrosis is encountered typically in what kind of injuries?

A

ischemia, exposure to toxins, infections, trauma

140
Q

Dystrophic calcification occurs in what tissue types?

A

Necrotic, damaged, or aging tissues

141
Q

Fibrinoid necrosis

A

Seen in immune reactions involving blood vessels, when Ag-Ab complexes are deposited within walls of arteries

-Result in bright pink amorphous appearance on histological imaging

142
Q

What locus seems to be involved in controlling cell senescence?

A

CDKN2A

143
Q

Types of adaptations

A
  1. Hypertrophy
  2. Hyperplasia
  3. Atrophy
  4. Metaplasia
144
Q

The influences that predispose to metaplasia, if persistent, lead to what?

A

Malignant transformation

145
Q

What is the most common genetic abnormality found in human cancers?

A

Mutation in TP53

146
Q

Caseous necrosis

A

A structureless collection of fragmented or lysed cells and amorphous granular debris enclosed within a distinct inflammatory border (granuloma)

147
Q

Causes of cell injury

A
  1. oxygen deprivation
  2. physical agents
  3. chemical agents and drugs
  4. infectious agents
  5. genetic derangement
  6. nutritional imbalances
148
Q

What is the most common type of cell injury in clinical medicine?

What does it result from?

A

Ischemia

hypoxia induced by reduced blood flow, most commonly d/t mechanical arterial obstruction

149
Q

What are the main causes of hemosiderosis?

A

Increased absoprtion of dietary iron as seen in Hemochromatosis

Hemolytic anemias

Repeated blood transfusion

150
Q

Mechanism of metaplasia

A

reprogramming of stem cells in normal tissues, or of undifferentiated mesenchymal cells present in CT

151
Q

What factors are present in apoptotic body cell membranes that make them better targets for phagocytes?

A

Phosphatidylserine

Thrombospondin

C1q

152
Q

Hyperplasia is a characteristic response to what types of infection?

A

Viral (i.e. papillomaviruses)

153
Q

On what cell type is FasL typically found?

A

T-cells the recognize self Ags

Some CTLs

154
Q

Distinct patterns of necrosis

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Fat necrosis
  6. Fibrinoid necrosis
155
Q

What is the most common exogenous pigment?

A

Carbon

156
Q

Caseous necrosis is most often seen in what type of infection?

A

Mycobacterium Tuberculosis

157
Q

Nuclear changes appear in three patterns d/t breakdown of DNA

A

karyolysis, pkynosis, karyorrhexis

158
Q

When does cell injury change from reversible to irreversible?

A

If a stimulus persists long enough or if it is severe enough from the beginning, a cell will enter irreversible injury and eventually undergo cell death

159
Q

In what type of cells is autophagy prominent?

A

Atrophic cells which are exposed to nutrient deprived states

160
Q

Microscopic features of reversible cell injury

A
  1. Cellular swelling
  2. Fatty change (i.e. fatty liver 2/2 alcohol use)
161
Q

What does damaging the mitochondrial membrane result in?

What does this lead to?

A

Opening of the mitochondrial permeability transition pore.

Leads to a decrease in ATP production and release of proteins that trigger apoptotic death

162
Q

What enzyme is released from the mitochondria after cell injury which leads to the activation of apoptosis?

A

Cytochrome C

163
Q

What do patients with Werner Syndrome typically show and what is the reason for this manifestation?

A

These pts show premature aging d/t defective helicase.

Defective helicase causes accumulation of chromosomal damage, leading to aging of the cell.

164
Q

In certain pathophysiologic conditions, what occurs in the heart?

A

As an adaptive mechanism, the heart returns to it’s “fetal” gene program

165
Q

In what organ is steatosis typically seen and why?

A

The liver; it is the primary organ responsible for fat metabolism

166
Q

What endogenous pigment is insoluble and known as the wear and tear pigment?

In what organs is this pigment commonly found in aging patients or patients who are malnurished?

A

Lipofuscin

Liver and heart

167
Q

What cellular components are most significantly affected by injurious stimuli?

A

mitochondria, cell membranes, protein synthesis and packaging machinery, DNA

168
Q

Atrophy

A

Reduction in the size of an organ or tissue d/t a decrease in cell size and number

169
Q

What occurs when in response to an increase in hemodynamic load?

A

Heart muscle enlarges (hypertrophies) and can become injured

170
Q

What factor is a frequent problem in clinical medicine, limiting drug therapy

A

chemical (toxic) injury

171
Q

Four aspects of disease process

A
  1. Etiology
  2. Pathogenesis
  3. Morphologic changes
  4. Clinical manifestations
172
Q

What two conditions are associated with mutated genes that are unable to repair double strand breaks?

A

Bloom syndrome, ataxiatelangiectasia

173
Q

What is a common example of CT metaplasia and what occurs?

A

Myositis ossificans

CT within muscle changes to bone during healing s/p trauma

174
Q

What type of cancer can form as a result of dysplasia from Barrett’s esophagus?

A

Adenocarcinoma

175
Q

Hallmark of reversible cell injury

A

Decrease in ATP production

Cellular swelling

176
Q

What is the morphologic hallmark of cell death?

A

Loss of the nucleus

177
Q

Apoptosis occurs in what pathological states?

A

DNA damage

Accumulation of misfolded proteins

Infection, specifically viral

178
Q

Cellular aging is induced by

A

ROS

Telomere shortening

Defective protein homeostasis

179
Q

What factors counteract aging?

A

A decrease in the IGF-1 signaling pathway and an increase in sirtuins leads to altered transcription and an increase in DNA repair and protein homeostasis

180
Q

What is the most characteristic morphological change seen in apoptosis?

A

Condensatio of chromatin, aggregating peripherally

181
Q

An increase in intracellular calcium leads to cell injury in what ways?

A

Opening of the mitochondrial transition pore, resulting in increased permeability and decreased ATP production

Activation of apoptosis through release of caspases from permeable mitochondria

Activation of enzymes at inappropriate times

182
Q

What does the Fenton rxn allow for?

A

Iron to generate ROS

183
Q

Pathologic effects of ROS include?

A

Lipid peroxidation leading to membrane damage

Protein modifications, resulting in the breakdown or misfolding and eventual activation of apoptosis

DNA damage leading to mutations

184
Q

In what diseases is necroptosis a possible mechanism of cell death?

A

steatohepatitis, acute pancreatitis, reperfusion injury, and neurodegenerative dzs like PD

185
Q

Vitamin A deficiency leads to what type of cellular change?

A

Metaplasia

MOD Exam 1 (5 decks)

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