What does hypoxia refer to?
Oxygen deficiency.
What happens to the function of atrophic cells?
They may have diminished function, but they are not dead.
1/573
p.7
Causes of Cell Injury

What does hypoxia refer to?

Oxygen deficiency.

p.99
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What happens to the function of atrophic cells?

They may have diminished function, but they are not dead.

p.105
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is epithelial metaplasia?

A process where one type of epithelium is replaced by another, often in response to chronic irritation.

p.7
Causes of Cell Injury

What are the most common causes of cell injury?

Hypoxia and ischemia.

p.117
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What does the presence of brown pigment in tissue indicate?

It indicates brown atrophy when present in large amounts.

p.127
Clinical Significance of Cell Death and Aging

What effect does calorie restriction have on aging?

It slows down aging and prolongs life.

p.105
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What type of metaplasia often coexists with lung cancers?

Squamous metaplasia of the respiratory epithelium.

p.70
Overview of Cellular Responses to Stress

What is the Warburg effect?

The reliance of rapidly proliferating normal cells and cancer cells on aerobic glycolysis to produce energy.

p.42
Causes of Cell Injury

In which abdominal emergency does fat necrosis commonly occur?

Acute pancreatitis.

p.42
Mechanisms of Cell Death: Necrosis and Apoptosis

What do pancreatic enzymes digest during fat necrosis?

Peritoneal fat cells, including stored triglycerides.

p.125
Aging and Cellular Alterations

How do chronic diseases affect aging?

They exacerbate aging, especially those associated with prolonged inflammation.

p.95
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is an example of pathologic cellular hypertrophy?

Cardiac enlargement due to hypertension or aortic valve disease.

p.52
Mechanisms of Cell Death: Necrosis and Apoptosis

How does pathologic apoptosis differ from physiologic apoptosis?

Pathologic apoptosis occurs as a response to cellular damage or lack of growth factors, while physiologic apoptosis is a normal process.

p.125
Aging and Cellular Alterations

What is one major cause of aging at the cellular level?

Accumulation of DNA damage and mutations.

p.107
Endoplasmic Reticulum Stress and Protein Misfolding

What causes alterations in protein folding and transport leading to intracellular accumulation?

Mutations.

p.118
Overview of Cellular Responses to Stress

Where are melanocytes located?

In the epidermis.

p.68
Role of Hypoxia and Ischemia in Cell Injury

What is the role of HIF-1 in cells under stress?

It stimulates the synthesis of several proteins that help the cell survive.

p.26
Overview of Cellular Responses to Stress

Where are the enzymes responsible for digestion derived from?

Lysosomes of dying cells or leukocytes recruited during inflammation.

p.93
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Can hypertrophy and hyperplasia occur together?

Yes, both can occur together and result in an enlarged organ.

p.92
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What occurs in pure hypertrophy?

There are no new cells, just bigger cells containing increased amounts of structural proteins and organelles.

p.110
Reversible vs. Irreversible Cell Injury

Is fatty liver reversible?

Yes, with lifestyle changes and treatment of underlying conditions.

p.23
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necrosis?

A rapid and uncontrollable form of cell death caused by severe disturbances such as loss of oxygen and nutrient supply or toxins.

p.43
Mechanisms of Cell Death: Necrosis and Apoptosis

What is observed in histologic examination of necrosis?

Foci of necrosis contain shadowy outlines of necrotic fat cells.

p.37
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the appearance of material in liquefactive necrosis initiated by acute inflammation?

Frequently creamy yellow and is called pus.

p.62
Overview of Cellular Responses to Stress

What is formed when the autophagic vacuole fuses with lysosomes?

An autophagolysosome.

p.121
Causes of Cell Injury

What is metastatic calcification?

Deposition of calcium salts in normal tissues, usually secondary to hypercalcemia.

p.5
Reversible vs. Irreversible Cell Injury

What results from severe, persistent, and rapid onset stress on cells?

Irreversible injury and death of the affected cells.

p.65
Mechanisms of Cell Death: Necrosis and Apoptosis

What triggers apoptosis in cells?

Damage to proteins and DNA.

p.108
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are some examples of pigments that can accumulate in cells?

Carbon, lipofuscin, melanin, and hemosiderin.

p.18
Reversible vs. Irreversible Cell Injury

What happens to organ weight during reversible cell injury?

It increases.

p.124
Clinical Significance of Cell Death and Aging

How does cellular aging affect individuals?

It contributes to the aging of individuals.

p.85
Endoplasmic Reticulum Stress and Protein Misfolding

What condition can result from the accumulation of improperly folded proteins in extracellular tissues?

Amyloidosis.

p.119
Causes of Cell Injury

When does hemosiderin accumulate in tissues?

When there is a local or systemic excess of iron.

p.118
Overview of Cellular Responses to Stress

What is melanin?

An endogenous, brown-black pigment synthesized by melanocytes.

p.110
Causes of Cell Injury

What is fatty change in the liver commonly referred to as?

Fatty liver.

p.124
Clinical Significance of Cell Death and Aging

What is one of the strongest independent risk factors for chronic diseases?

Age.

p.85
Endoplasmic Reticulum Stress and Protein Misfolding

How can protein misfolding within cells cause disease?

By creating a deficiency of an essential protein or by inducing apoptosis.

p.111
Causes of Cell Injury

What types of lipids can accumulate in phagocytic cells?

Triglycerides, cholesterol, and cholesteryl esters.

p.127
Clinical Significance of Cell Death and Aging

What are the potential benefits of reduced insulin-like growth factor receptor signaling?

Lower rates of cell growth, metabolism, reduced errors in DNA replication, better DNA repair, and improved protein homeostasis.

p.91
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are the distinct forms of pathologic adaptations?

Hypertrophy, Hyperplasia, Atrophy, Metaplasia.

p.126
Clinical Significance of Cell Death and Aging

What is one of the primary factors thought to contribute to cellular aging?

Several mechanisms are involved.

p.124
Clinical Significance of Cell Death and Aging

What is cellular aging a result of?

A progressive decline in the life span and functional capacity of cells.

p.91
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are physiologic adaptations in cellular responses to stress?

Responses of cells to normal stimulation by hormones or endogenous chemical mediators.

p.116
Overview of Cellular Responses to Stress

What color is lipofuscin?

Brownish-yellow.

p.110
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is a primary characteristic of fatty liver?

Accumulation of fat in liver cells.

p.93
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is hypertrophy?

Occurs when cells have a limited capacity to divide.

p.68
Role of Hypoxia and Ischemia in Cell Injury

What protein does HIF-1 stimulate that promotes new blood vessel growth?

Vascular endothelial growth factor (VEGF).

p.87
Mechanisms of Cell Death: Necrosis and Apoptosis

What can result from DNA damage in cells lacking functional p53?

Mutations or DNA rearrangements, such as translocations.

p.8
Causes of Cell Injury

What are some examples of potentially toxic agents encountered daily?

Air pollutants, insecticides, carbon monoxide (CO), asbestos, cigarette smoke, ethanol, and drugs.

p.21
Irreversible vs. Irreversible Cell Injury

What is a key characteristic of irreversible cell injury?

Inability to restore mitochondrial function.

p.26
Overview of Cellular Responses to Stress

What are lysosomes?

Organelles that contain digestive enzymes, derived from dying cells.

p.72
Overview of Cellular Responses to Stress

What is the role of cellular enzymes?

Cellular enzymes catalyze biochemical reactions within cells, facilitating metabolic processes.

p.75
Oxidative Stress and Free Radicals in Cell Damage

What are free radicals?

Chemical species with a single unpaired electron in an outer orbital.

p.5
Reversible vs. Irreversible Cell Injury

Is cell injury reversible?

Within certain limits, yes; cells can return to a stable baseline.

p.112
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What condition is associated with protein accumulation in the proximal tubules?

Nephrotic syndrome.

p.99
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is atrophy?

Reduced size of an organ or tissue caused by a reduction in the size and number of cells.

p.91
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are pathologic adaptations?

Responses to stress that allow cells to modulate their structure and function to escape injury.

p.119
Causes of Cell Injury

What is hereditary hemochromatosis?

A condition characterized by more extensive accumulations of iron.

p.104
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the process called when normal columnar epithelium is replaced by squamous epithelium?

Metaplasia.

p.42
Mechanisms of Cell Death: Necrosis and Apoptosis

What is produced when released fatty acids combine with calcium?

Grossly visible chalky white areas (fat saponification).

p.92
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

How does hypertrophy differ from hyperplasia?

Hypertrophy is an increase in cell size, while hyperplasia is characterized by an increase in cell number due to proliferation.

p.38
Mechanisms of Cell Death: Necrosis and Apoptosis

What type of necrosis is often associated with hypoxic death of cells in the central nervous system?

Liquefactive necrosis.

p.48
Mechanisms of Cell Death: Necrosis and Apoptosis

What is apoptosis?

A pathway of cell death where cells activate enzymes to degrade their own nuclear DNA and proteins.

p.75
Oxidative Stress and Free Radicals in Cell Damage

What does oxidative stress refer to?

Cellular abnormalities induced by ROS (free radicals).

p.37
Mechanisms of Cell Death: Necrosis and Apoptosis

What causes liquefactive necrosis?

The accumulation of inflammatory cells and enzymes from leukocytes that digest the tissue.

p.60
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to the cells undergoing apoptosis?

They become shrunken and form cytoplasmic fragments.

p.74
Mechanisms of Cell Death: Necrosis and Apoptosis

What is one mechanism that exacerbates cell injury during reperfusion into ischemic tissues?

Increased Reactive Oxygen Species (ROS) production.

p.88
Inflammation

What types of cells are involved in the inflammatory response?

Neutrophils, macrophages, lymphocytes, and other leukocytes.

p.122
Causes of Cell Injury

What are some causes of dystrophic calcification?

Necrosis of any type, aging or damaged heart valves, indicating past cell injury.

p.8
Causes of Cell Injury

What is a common source of daily environmental toxins?

Air pollutants.

p.115
Impact of Toxins and Infectious Agents on Cells

What happens to inhaled carbon in the lungs?

It is phagocytosed by alveolar macrophages.

p.122
Causes of Cell Injury

What are some causes of metastatic calcification?

Increased secretion of parathyroid hormone, destruction of bone, vitamin D-related disorders, renal failure.

p.33
Mechanisms of Cell Death: Necrosis and Apoptosis

What can replace dead cells in necrosis?

Myelin figures.

p.112
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is 'alcoholic hyaline'?

A type of protein accumulation found in the liver.

p.98
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What triggers pathologic hyperplasia?

Excessive hormonal or growth factor stimulation.

p.11
Causes of Cell Injury

How does trauma affect cells?

It can cause direct damage and disrupt cellular function.

p.122
Causes of Cell Injury

What is a significant consequence of calcification of the aortic valves?

It is an important cause of aortic stenosis in elderly persons.

p.2
Mechanisms of Cell Death: Necrosis and Apoptosis

What types of responses do cells and tissues have to destructive factors?

Responses that include various mechanisms associated with clinical examples.

p.44
Mechanisms of Cell Death: Necrosis and Apoptosis

What appearance does fibrinoid necrosis have on H&E preparations?

A bright pink, amorphous appearance.

p.52
Mechanisms of Cell Death: Necrosis and Apoptosis

What is physiologic apoptosis?

Apoptosis that occurs in many normal situations to eliminate cells that are no longer needed.

p.127
Clinical Significance of Cell Death and Aging

How does calorie restriction influence aging?

By altering signaling pathways.

p.105
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What can chronic gastric reflux cause in the lower esophagus?

Metaplastic transformation of normal stratified squamous epithelium to gastric or intestinal-type columnar epithelium.

p.116
Overview of Cellular Responses to Stress

Where does lipofuscin accumulate in the body?

In a variety of tissues, particularly the heart, liver, and brain.

p.125
Aging and Cellular Alterations

What happens to protein homeostasis during aging?

There is a loss of normal proteins and accumulation of misfolded proteins.

p.116
Overview of Cellular Responses to Stress

Is lipofuscin injurious to cells?

No, it is not injurious to the cell.

p.104
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What protective mechanisms are lost due to metaplasia in the bronchus?

Mucus secretion and ciliary clearance of particulate matter.

p.60
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the stages of chromatin changes in apoptotic cells as seen in H & E-stained tissue sections?

Chromatin condensation, aggregation, and ultimately karyorrhexis.

p.13
Causes of Cell Injury

What is a consequence of cellular senescence?

Diminished ability to respond to damage.

p.28
Necrosis morphological changes

What causes the glassy, homogeneous appearance of necrotic cells?

Loss of glycogen particles.

p.114
Overview of Cellular Responses to Stress

What are endogenous pigments?

Pigments synthesized within the body, such as lipofuscin, melanin, and certain derivatives of hemoglobin.

p.28
Necrosis morphological changes

What happens to the cytoplasm of necrotic cells?

It becomes vacuolated and appears 'motheaten' due to enzyme digestion of organelles.

p.62
Overview of Cellular Responses to Stress

What initiates the formation of the autophagic vacuole?

Cytosolic proteins that sense nutrient deprivation.

p.54
Mechanisms of Cell Death: Necrosis and Apoptosis

What regulates apoptosis?

Biochemical pathways that control the balance of death and survival signals.

p.8
Causes of Cell Injury

Can innocuous substances be toxic?

Yes, substances like glucose, salt, water, and oxygen can be toxic.

p.71
Role of Hypoxia and Ischemia in Cell Injury

How does ATP depletion affect protein synthesis?

It causes detachment of ribosomes from the rough ER, reducing protein synthesis.

p.98
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is hormonal hyperplasia?

Proliferation of glandular epithelium, such as in the female breast at puberty and during pregnancy.

p.12
Causes of Cell Injury

What is a cause of cell injury related to nutrition?

Nutritional imbalances.

p.102
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are the mechanisms of atrophy?

A combination of decreased protein synthesis and increased protein degradation in cells.

p.74
Mechanisms of Cell Death: Necrosis and Apoptosis

How does inflammation change with reperfusion after ischemic injury?

It increases due to the influx and activation of leukocytes.

p.88
Causes of Cell Injury

In what conditions can dysregulated immune responses occur?

In autoimmune diseases and allergies.

p.115
Impact of Toxins and Infectious Agents on Cells

How is inhaled carbon transported in the body?

Through lymphatic channels to the regional tracheobronchial lymph nodes.

p.9
Causes of Cell Injury

What is the largest type of infectious agent mentioned that can cause cell injury?

Meter-long tapeworms.

p.4
Overview of Cellular Responses to Stress

What happens to cells when they encounter physiologic stresses or injurious conditions?

They can undergo adaptation, achieving a new steady state.

p.72
Overview of Cellular Responses to Stress

What is the significance of enzyme activity in cellular metabolism?

Enzyme activity is crucial for maintaining metabolic pathways and overall cellular function.

p.16
Reversible vs. Irreversible Cell Injury

What causes cells to swell during reversible injury?

Failure of energy-dependent ion pumps in the plasma membrane.

p.74
Mechanisms of Cell Death: Necrosis and Apoptosis

What system's activation may contribute to ischemia reperfusion injury?

The complement system.

p.123
Overview of Cellular Responses to Stress

How does calcification appear on histologic examination?

As basophilic deposits.

p.105
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is a potential risk of persistent metaplastic changes in epithelium?

They may predispose to malignant transformation.

p.116
Overview of Cellular Responses to Stress

What is lipofuscin commonly referred to as?

Wear-and-tear pigment.

p.119
Reversible vs. Irreversible Cell Injury

What is the condition called when there is excessive deposition of hemosiderin?

Hemosiderosis.

p.104
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What type of epithelium replaces normal ciliated columnar cells in habitual cigarette smokers?

Stratified squamous epithelial cells.

p.92
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is hypertrophy?

An increase in the size of cells resulting in an increase in the size of the organ.

p.96
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is an example of physiologic hypertrophy?

The massive enlargement of the uterus during pregnancy due to estrogen stimulation.

p.41
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the characteristic appearance of a focus of inflammation known as a granuloma?

An area of caseous necrosis enclosed within a distinctive inflammatory border.

p.110
Reversible vs. Irreversible Cell Injury

What can untreated fatty liver lead to?

Liver inflammation, fibrosis, or cirrhosis.

p.71
Role of Hypoxia and Ischemia in Cell Injury

What happens to sodium and potassium levels due to reduced activity of ATP-dependent sodium pumps?

Intracellular sodium accumulates and potassium effluxes, causing cell swelling and dilation of the ER.

p.5
Causes of Cell Injury

What happens when the adaptive capability of a cell is exceeded?

Cell injury develops.

p.121
Causes of Cell Injury

What is pathologic calcification?

The abnormal deposition of calcium salts in tissues.

p.114
Overview of Cellular Responses to Stress

Give an example of an endogenous pigment.

Lipofuscin, melanin, or certain derivatives of hemoglobin.

p.38
Mechanisms of Cell Death: Necrosis and Apoptosis

How is the liquid mass formed from dead cells eventually removed?

By phagocytes.

p.94
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Give an example of pathologic hypertrophy.

Left ventricular hypertrophy in hypertension.

p.43
Mechanisms of Cell Death: Necrosis and Apoptosis

What surrounds the necrotic fat cells in histologic examination?

An inflammatory reaction.

p.38
Mechanisms of Cell Death: Necrosis and Apoptosis

What is ischemic necrosis?

Hypoxic death of cells.

p.62
Overview of Cellular Responses to Stress

What role do lysosomal enzymes play in autophagy?

They digest the cellular components within the autophagolysosome.

p.36
Mechanisms of Cell Death: Necrosis and Apoptosis

What texture do affected tissues exhibit in necrosis?

A firm texture.

p.76
Oxidative Stress and Free Radicals in Cell Damage

How can ionizing radiation contribute to free radical generation?

It can hydrolyze water into hydroxyl (•OH) and hydrogen (H•) free radicals.

p.65
Causes of Cell Injury

Can the same injurious agent trigger multiple biochemical pathways?

Yes, the same injurious agent may trigger multiple and overlapping biochemical pathways.

p.36
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to structural proteins and enzymes during necrosis?

They are denatured.

p.54
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the end result of apoptotic cell death?

The clearance of apoptotic bodies by phagocytes.

p.97
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

When does hyperplasia occur?

When the tissue contains cell populations capable of replication.

p.90
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What factors can trigger cellular adaptations?

Changes in the environment.

p.102
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is autophagy?

The process in which a starved cell eats its own components to survive.

p.109
Causes of Cell Injury

What are the most common causes of fatty change in the liver?

Alcohol abuse and diabetes associated with obesity.

p.73
Mechanisms of Cell Death: Necrosis and Apoptosis

Under what circumstances does ischemia-reperfusion injury occur?

When blood flow is restored to ischemic but viable tissues.

p.117
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the appearance called when brown pigment is present in large amounts in tissue?

Brown atrophy.

p.120
Overview of Cellular Responses to Stress

How can iron be identified in histochemical analysis?

By the Prussian blue histochemical reaction.

p.123
Overview of Cellular Responses to Stress

What do calcium salts appear as on gross examination?

Fine white granules.

p.124
Clinical Significance of Cell Death and Aging

What chronic diseases are associated with aging?

Cancer, Alzheimer disease, and ischemic heart disease.

p.111
Causes of Cell Injury

What can happen to phagocytic cells in pathological processes?

They may become overloaded with lipids such as triglycerides, cholesterol, and cholesteryl esters.

p.111
Causes of Cell Injury

What is the most important pathological process associated with lipid overload in phagocytic cells?

Atherosclerosis.

p.52
Mechanisms of Cell Death: Necrosis and Apoptosis

What triggers pathologic apoptosis?

Deprivation of growth factors or damage to the cell's DNA or proteins beyond repair.

p.85
Endoplasmic Reticulum Stress and Protein Misfolding

What is a recognized feature of cell death related to protein misfolding?

It is associated with neurodegenerative disorders, including Alzheimer's disease.

p.127
Clinical Significance of Cell Death and Aging

What signaling pathway is reduced by calorie restriction?

Insulin-like growth factor receptor signaling.

p.10
Causes of Cell Injury

What is a potential negative effect of the immune system?

Immune reactions can result in cell injury.

p.119
Overview of Cellular Responses to Stress

What is hemosiderin?

A hemoglobin-derived granular pigment that is yellow to brown.

p.91
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Give an example of a physiologic adaptation.

Hormone-induced enlargement of the breast and uterus during pregnancy.

p.42
Mechanisms of Cell Death: Necrosis and Apoptosis

What is fat necrosis?

Focal areas of fat destruction typically resulting from activated pancreatic enzymes.

p.41
Mechanisms of Cell Death: Necrosis and Apoptosis

What does a necrotic focus appear as under microscopic examination?

A collection of cellular debris with an amorphous granular pink appearance in H&E-stained tissue.

p.125
Aging and Cellular Alterations

What is replicative senescence?

The reduced capacity of cells to divide due to progressive shortening of telomeres.

p.70
Overview of Cellular Responses to Stress

Why do rapidly proliferating cells rely on glycolysis?

Because glycolysis generates metabolites needed for cell growth and division, such as proteins, lipids, and nucleic acids.

p.41
Mechanisms of Cell Death: Necrosis and Apoptosis

How does caseous necrosis differ from coagulative necrosis?

In caseous necrosis, the tissue architecture is completely obliterated and cellular outlines cannot be discerned.

p.70
Overview of Cellular Responses to Stress

What types of cells exhibit the Warburg effect?

Rapidly proliferating normal cells and cancer cells.

p.61
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What does autophagy refer to?

Lysosomal digestion of the cell’s own components.

p.52
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the main purpose of physiologic apoptosis?

To eliminate unnecessary cells.

p.10
Causes of Cell Injury

What is an example of an autoimmune reaction?

Autoimmune reactions against one’s own tissues.

p.10
Causes of Cell Injury

What type of reactions can cause cell injury in genetically susceptible individuals?

Allergic reactions against environmental substances.

p.116
Overview of Cellular Responses to Stress

What causes the accumulation of lipofuscin?

As a function of age or atrophy.

p.107
Causes of Cell Injury

What results from a deficiency of critical enzymes in lysosomal storage diseases?

Accumulation of substrates in lysosomes.

p.110
Causes of Cell Injury

What are common causes of fatty liver?

Alcohol consumption, obesity, diabetes, and certain medications.

p.94
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is physiologic hypertrophy?

Hypertrophy that occurs in response to normal physiological demands, such as skeletal muscles in athletes or uterine muscles during pregnancy.

p.37
Mechanisms of Cell Death: Necrosis and Apoptosis

What is liquefactive necrosis?

A type of necrosis seen in focal bacterial or fungal infections.

p.19
Reversible vs. Irreversible Cell Injury

What do small clear vacuoles in the cytoplasm represent?

Distended cisternae of the endoplasmic reticulum (ER).

p.79
Causes of Cell Injury

What is one way ROS causes cell injury?

Peroxidation of membrane lipids.

p.19
Reversible vs. Irreversible Cell Injury

What is a key morphological change observed in reversible cell injury?

Cellular swelling.

p.48
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to the fragments of apoptotic cells?

They break off, giving the appearance that is responsible for the name 'apoptosis'.

p.49
Mechanisms of Cell Death: Necrosis and Apoptosis

How does apoptosis differ from necrosis regarding the plasma membrane?

In apoptosis, the plasma membrane remains intact.

p.2
Overview of Cellular Responses to Stress

What is the primary focus of cellular responses to stress?

The response of cells to various types of stress and noxious stimuli.

p.115
Impact of Toxins and Infectious Agents on Cells

What is the most common exogenous pigment?

Carbon, with coal dust as an example.

p.23
Reversible vs. Irreversible Cell Injury

How does necrosis differ from other forms of cell death?

Necrosis happens accidentally due to severe injury that cannot be repaired, leading to the failure of cellular constituents.

p.39
Mechanisms of Cell Death: Necrosis and Apoptosis

What is gangrenous necrosis?

A term commonly used in clinical practice, though not a distinctive pattern of cell death.

p.9
Causes of Cell Injury

What are the smallest infectious agents that can cause cell injury?

Viruses.

p.103
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is metaplasia?

A reversible change in which one adult cell type is replaced by another adult cell type.

p.3
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

How do cells typically respond to stress?

By undergoing adaptations such as hypertrophy, hyperplasia, atrophy, or metaplasia.

p.84
Endoplasmic Reticulum Stress and Protein Misfolding

How does aging affect protein folding?

Aging decreases the capacity to correct misfolding.

p.77
Oxidative Stress and Free Radicals in Cell Damage

What are Reactive Oxygen Species (ROS)?

Chemically reactive molecules containing oxygen that can lead to cellular damage.

p.112
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are neurofibrillary tangles?

Intracellular accumulations of proteins in neurons.

p.86
Mechanisms of Cell Death: Necrosis and Apoptosis

What can induce DNA damage in cells?

Exposure to radiation, chemotherapeutic agents, intracellular generation of ROS, and mutations.

p.50
Mechanisms of Cell Death: Necrosis and Apoptosis

What is apoptosis?

A programmed and controlled process of cell death that occurs naturally in the body.

p.33
Mechanisms of Cell Death: Necrosis and Apoptosis

What do fatty acids bind to after necrosis?

Calcium salts.

p.16
Reversible vs. Irreversible Cell Injury

What is the consequence of failing ion pumps in injured cells?

Inability to maintain ionic and fluid homeostasis.

p.45
Clinical Significance of Cell Death and Aging

What contractile protein is specific to cardiac muscle?

Troponin.

p.67
Overview of Cellular Responses to Stress

How much ATP do the cells of a healthy human burn every day?

50 to 75 kg.

p.58
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens after caspase-9 or caspase-8 is activated in apoptosis?

They activate additional caspases that degrade the cells' proteins and nucleus.

p.61
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the primary function of autophagy?

It serves as a survival mechanism during nutrient deprivation.

p.28
Necrosis morphological changes

What is a key cytoplasmic change observed in necrotic cells?

Increased eosinophilia due to denatured proteins and loss of RNA.

p.79
Causes of Cell Injury

What are Reactive Oxygen Species (ROS) known to cause in cells?

Cell injury by damaging multiple components.

p.107
Causes of Cell Injury

What is an example of abnormal metabolism leading to intracellular accumulation?

Fatty change in the liver.

p.94
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is pathologic hypertrophy?

Hypertrophy that occurs due to abnormal conditions, such as left ventricular hypertrophy in hypertension.

p.87
Mechanisms of Cell Death: Necrosis and Apoptosis

What is a potential consequence of DNA mutations or rearrangements in cells with damaged DNA?

Neoplastic transformation.

p.8
Causes of Cell Injury

How can therapeutic drugs lead to cell injury?

They can cause cell injury in susceptible patients or if used excessively.

p.65
Causes of Cell Injury

How do different insults affect cells?

They typically affect different cellular organelles and biochemical pathways.

p.17
Reversible vs. Irreversible Cell Injury

What is the primary mechanism involved in reversible cell injury related to sodium?

Failure of the sodium pump.

p.21
Irreversible vs. Irreversible Cell Injury

What structural integrity is lost during irreversible cell injury?

Loss of DNA and chromatin structural integrity.

p.74
Mechanisms of Cell Death: Necrosis and Apoptosis

Who generates some of the Reactive Oxygen Species (ROS) during reperfusion?

Injured cells and infiltrating leukocytes.

p.54
Mechanisms of Cell Death: Necrosis and Apoptosis

What enzyme system is ultimately activated during apoptosis?

Caspase.

p.3
Causes of Cell Injury

What types of stimuli can lead to cellular stress?

Injurious stimuli such as toxins, hypoxia, and physical damage.

p.71
Role of Hypoxia and Ischemia in Cell Injury

What is the effect of failing ATP-dependent Ca2+ pumps?

It leads to an influx of Ca2+, causing damaging effects on numerous cellular components.

p.109
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Where is fatty change most often seen?

In the liver, but also in the heart, skeletal muscle, kidney, and other organs.

p.60
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the morphologic appearance of apoptosis in tissue sections?

Cells show various stages of chromatin condensation and shrunken appearance.

p.45
Clinical Significance of Cell Death and Aging

How are increased serum levels of intracellular proteins used clinically?

To assess damage to tissues.

p.102
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What role does ubiquitin play in cellular protein degradation?

It attaches to cellular proteins and targets them for degradation in proteasomes.

p.9
Causes of Cell Injury

Which types of infectious agents fall between viruses and tapeworms in size?

Rickettsiae, bacteria, fungi, and protozoans.

p.4
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are the principal adaptive responses of cells?

Hypertrophy, Hyperplasia, Atrophy, Metaplasia.

p.27
Mechanisms of Cell Death: Necrosis and Apoptosis

What type of damage occurs to cellular membranes during necrosis?

Damage to plasma and lysosomal membranes, resulting in leakage of cellular contents.

p.115
Impact of Toxins and Infectious Agents on Cells

What effect does carbon have on draining lymph nodes?

It blackens them.

p.78
Oxidative Stress and Free Radicals in Cell Damage

What role does superoxide dismutase (SOD) play in cells?

It converts superoxide into hydrogen peroxide (H2O2).

p.27
Mechanisms of Cell Death: Necrosis and Apoptosis

What causes irreversible damage to cellular components in necrosis?

Reactive oxygen species (ROS) and other factors.

p.77
Oxidative Stress and Free Radicals in Cell Damage

What role do enzymes play in the removal of ROS?

Enzymes like superoxide dismutase and catalase convert ROS into less harmful substances.

p.93
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is hyperplasia?

An adaptive response in cells capable of replication.

p.118
Overview of Cellular Responses to Stress

What is the function of melanin?

Acts as a screen against harmful ultraviolet radiation.

p.125
Aging and Cellular Alterations

What role does stress play in aging?

Stress exacerbates the aging process.

p.71
Role of Hypoxia and Ischemia in Cell Injury

What is the effect of persistent hypoxia and ischemia on ATP levels?

It leads to depletion of ATP.

p.40
Mechanisms of Cell Death: Necrosis and Apoptosis

What does the term 'caseous' refer to in caseous necrosis?

It means 'cheese-like,' describing the friable yellow-white appearance of the necrotic area.

p.68
Role of Hypoxia and Ischemia in Cell Injury

How does HIF-1 affect cellular metabolism during hypoxia?

It stimulates glucose uptake and glycolysis while dampening mitochondrial oxidative phosphorylation.

p.13
Causes of Cell Injury

What ultimately results from the changes caused by cellular senescence?

The death of cells and of the organism.

p.3
Overview of Cellular Responses to Stress

What do cellular responses to stress and injurious stimuli aim to achieve?

A new steady state.

p.68
Role of Hypoxia and Ischemia in Cell Injury

What happens to cells subjected to hypoxia that do not immediately die?

They activate compensatory mechanisms induced by HIF-1.

p.23
Causes of Cell Injury

What causes necrosis?

Severe damage that is beyond salvage, often due to loss of oxygen, nutrient supply, or the actions of toxins.

p.72
Overview of Cellular Responses to Stress

How do enzymes affect the rate of cellular reactions?

Enzymes increase the rate of reactions by lowering the activation energy required.

p.75
Oxidative Stress and Free Radicals in Cell Damage

Why are free radicals considered extremely unstable?

Because they readily react with nucleic acids, proteins, and lipids.

p.33
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to necrotic cells over time?

They may persist for some time or be digested by enzymes and disappear.

p.2
Causes of Cell Injury

What factors contribute to cell injury?

Various factors that have roles in cell injury along with their mechanisms.

p.16
Reversible vs. Irreversible Cell Injury

What happens to injured cells if the damaging stimulus is removed?

Their function and morphology can return to normal.

p.44
Mechanisms of Cell Death: Necrosis and Apoptosis

What is fibrinoid necrosis?

A special form of necrosis visible by light microscopy, usually in immune reactions.

p.17
Reversible vs. Irreversible Cell Injury

What occurs to potassium levels during cell injury?

Potassium is lost from the cell (outflux).

p.12
Causes of Cell Injury

What type of nutritional insufficiency can lead to cell injury?

Protein-calorie insufficiency.

p.44
Mechanisms of Cell Death: Necrosis and Apoptosis

Where are immune complexes deposited in fibrinoid necrosis?

In the walls of arteries.

p.24
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the primary function of apoptosis?

To eliminate cells without eliciting an inflammatory reaction.

p.29
Mechanisms of Cell Death: Necrosis and Apoptosis

What is a characteristic feature of mitochondria in necrotic cells?

Marked dilation with large amorphous intramitochondrial densities.

p.84
Endoplasmic Reticulum Stress and Protein Misfolding

What role do infections play in protein misfolding?

Infections can lead to the synthesis of large amounts of microbial proteins.

p.78
Oxidative Stress and Free Radicals in Cell Damage

What are free radicals?

Inherently unstable molecules that decay spontaneously.

p.97
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Can hyperplasia occur alongside other processes?

Yes, it may occur concurrently with hypertrophy and often in response to the same stimuli.

p.30
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens during karyorrhexis?

The pyknotic nucleus undergoes fragmentation.

p.76
Oxidative Stress and Free Radicals in Cell Damage

What is the effect of reperfusion of ischemic tissues on free radicals?

It can lead to increased generation of free radicals.

p.22
Reversible vs. Irreversible Cell Injury

What is irreversible cell injury?

A type of cell damage that leads to cell death and cannot be reversed.

p.30
Mechanisms of Cell Death: Necrosis and Apoptosis

What is karyolysis?

The fading of basophilia of the chromatin due to digestion of DNA.

p.64
Causes of Cell Injury

What factors determine the consequences of an injurious stimulus?

The type of cell, its metabolic state, adaptability, and genetic makeup.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

What are death receptors?

Surface molecules that trigger apoptosis in many cells.

p.41
Mechanisms of Cell Death: Necrosis and Apoptosis

What is often found enclosing the area of caseous necrosis?

A distinctive inflammatory border.

p.116
Overview of Cellular Responses to Stress

What does the presence of lipofuscin indicate?

It is a marker of past free radical injury.

p.21
Irreversible vs. Irreversible Cell Injury

What happens to injured cells with persistent or excessive noxious exposures?

They pass a 'point of no return' and undergo cell death.

p.122
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the definition of metastatic calcification?

Deposits of calcium salts in normal tissues.

p.96
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What causes smooth muscle hypertrophy in the uterus during pregnancy?

Estrogen stimulation.

p.122
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the serum calcium level in dystrophic calcification?

Normal.

p.38
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to dead cells during liquefactive necrosis?

They are completely digested, transforming the tissue into a liquid viscous mass.

p.21
Irreversible vs. Irreversible Cell Injury

What is another phenomenon associated with irreversible cell injury?

Loss of structure and functions of the plasma and intracellular membranes.

p.71
Role of Hypoxia and Ischemia in Cell Injury

What is the consequence of increased anaerobic glycolysis during ATP depletion?

Lactic acid accumulates, leading to decreased intracellular pH and reduced activity of many cellular enzymes.

p.43
Mechanisms of Cell Death: Necrosis and Apoptosis

What type of deposits are found in necrotic fat cells?

Basophilic calcium deposits.

p.65
Reversible vs. Irreversible Cell Injury

What is the primary effect of deprivation of oxygen and nutrients on cells?

It primarily impairs energy-dependent cellular functions, leading to necrosis.

p.4
Overview of Cellular Responses to Stress

What is the steady state that cells normally maintain?

Homeostasis.

p.37
Mechanisms of Cell Death: Necrosis and Apoptosis

In which type of infections is liquefactive necrosis commonly observed?

In focal bacterial or fungal infections.

p.59
Mechanisms of Cell Death: Necrosis and Apoptosis

Where is phosphatidylserine located in normal cells?

On the inner leaflet of the plasma membrane.

p.121
Causes of Cell Injury

What typically causes metastatic calcification?

Hypercalcemia.

p.54
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the two distinct pathways for caspase activation?

The mitochondrial pathway (intrinsic) and the death receptor pathway (extrinsic).

p.97
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is hyperplasia?

An increase in the size of an organ due to increased numbers of component cells.

p.122
Causes of Cell Injury

How can dystrophic calcification affect heart valves?

Calcification can develop in aging or damaged heart valves, compromising valve motion.

p.64
Causes of Cell Injury

What factors influence the cellular response to injurious stimuli?

The type of injury, its duration, and severity.

p.109
Causes of Cell Injury

What are some causes of steatosis?

Toxins, protein malnutrition, diabetes mellitus, obesity, or anoxia.

p.39
Reversible vs. Irreversible Cell Injury

What type of necrosis occurs in the lower leg due to loss of blood supply?

Coagulative necrosis involving multiple tissue layers.

p.36
Mechanisms of Cell Death: Necrosis and Apoptosis

What type of cells may persist at the site of necrosis?

Eosinophilic, anucleate cells.

p.64
Reversible vs. Irreversible Cell Injury

What can low doses of toxins or brief ischemia lead to?

Reversible cell injury.

p.9
Causes of Cell Injury

What is the focus of the discussion regarding infectious agents?

The diverse ways in which infectious pathogens cause injury.

p.80
Oxidative Stress and Free Radicals in Cell Damage

What are some major properties of ROS?

They are highly reactive molecules that can damage cellular components.

p.101
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is one cause of atrophy related to physical activity?

Decreased workload, such as immobilization of a limb to permit healing of a fracture.

p.24
Mechanisms of Cell Death: Necrosis and Apoptosis

What role does apoptosis play during development?

It serves to eliminate unwanted cells.

p.67
Role of Hypoxia and Ischemia in Cell Injury

What do hypoxia and ischemia lead to in cells?

ATP depletion and failure of energy-dependent metabolic pathways.

p.45
Clinical Significance of Cell Death and Aging

Which enzymes are found in hepatocytes?

Transaminases.

p.87
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens when p53 is mutated or absent in cells?

Cells with damaged DNA survive.

p.122
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the definition of dystrophic calcification?

Deposits of calcium salts in dead and degenerated tissues.

p.104
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are the survival advantages of metaplastic squamous epithelium?

It provides better survival in the harsh environment of habitual cigarette smoke.

p.114
Overview of Cellular Responses to Stress

What are exogenous pigments?

Pigments that come from outside the body, such as carbon.

p.7
Causes of Cell Injury

What is a common consequence of both hypoxia and ischemia?

Both deprive oxygen.

p.88
Causes of Cell Injury

What is a common cause of cell injury?

The inflammatory reaction elicited by pathogens, necrotic cells, and dysregulated immune responses.

p.94
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Give an example of physiologic hypertrophy.

Skeletal muscles in athletes.

p.4
Overview of Cellular Responses to Stress

What do cells do in response to changing demands and extracellular stresses?

They adjust their function.

p.59
Mechanisms of Cell Death: Necrosis and Apoptosis

What signals do apoptotic cells produce to facilitate their clearance?

Apoptotic cells produce 'eat-me' signals.

p.18
Reversible vs. Irreversible Cell Injury

What causes pallor in an organ affected by cellular swelling?

Compression of capillaries.

p.109
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is fatty change?

An abnormal accumulation of triglycerides within parenchymal cells.

p.60
Mechanisms of Cell Death: Necrosis and Apoptosis

Can substantial apoptosis be detected histologically?

No, it may be histologically undetectable.

p.98
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is compensatory hyperplasia?

Growth of residual tissue after removal or loss of part of an organ, such as the liver.

p.23
Clinical Significance of Cell Death and Aging

What local reaction does necrosis elicit?

Inflammation.

p.2
Reversible vs. Irreversible Cell Injury

What morphological changes are associated with reversible and irreversible cell injury?

Changes that occur during apoptosis and necrosis.

p.59
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to phosphatidylserine in apoptotic cells?

It flips to the outer leaflet of the plasma membrane.

p.103
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What usually triggers metaplasia?

Abnormal stimuli such as chronic irritation and inflammation.

p.33
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to myelin figures after necrosis?

They are either phagocytosed by other cells or further degraded into fatty acids.

p.59
Mechanisms of Cell Death: Necrosis and Apoptosis

What role do tissue macrophages play in the clearance of apoptotic cells?

They recognize phosphatidylserine on apoptotic cells and lead to their phagocytosis.

p.45
Clinical Significance of Cell Death and Aging

Which unique isoform of enzyme is found in cardiac muscle?

Creatine kinase.

p.24
Mechanisms of Cell Death: Necrosis and Apoptosis

In what situations does apoptosis occur?

When a cell’s DNA or proteins are damaged beyond repair or when deprived of necessary survival signals.

p.39
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens when bacterial infection occurs in gangrenous necrosis?

Coagulative necrosis is modified by the liquefactive action of bacteria and attracted leukocytes, resulting in wet gangrene.

p.77
Oxidative Stress and Free Radicals in Cell Damage

How do antioxidants help in the removal of ROS?

They neutralize ROS, preventing cellular damage.

p.24
Mechanisms of Cell Death: Necrosis and Apoptosis

How does apoptosis differ from necrosis?

Apoptosis can occur in healthy tissues, while necrosis typically occurs in pathological conditions.

p.86
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the role of p53 in response to DNA damage?

p53 arrests the cell cycle at the G1 phase to allow for DNA repair.

p.103
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Is metaplasia a result of transdifferentiation?

No, it arises from reprogramming of stem cells rather than a phenotypic change of already differentiated cells.

p.81
Causes of Cell Injury

What are the two general mechanisms by which toxins induce cell injury?

Direct-acting toxins and latent toxins.

p.58
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the end result of the activation of caspases in apoptosis?

The characteristic cellular fragmentation of apoptosis.

p.107
Causes of Cell Injury

What is a consequence of an inability to degrade phagocytosed particles?

Accumulation of carbon pigment.

p.118
Overview of Cellular Responses to Stress

What type of pigment is melanin classified as?

An endogenous pigment.

p.61
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

How does autophagy help a starved cell?

By allowing the cell to eat its own contents and recycle them for nutrients and energy.

p.40
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the appearance of tissue affected by caseous necrosis?

Friable yellow-white.

p.98
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is physiological hyperplasia?

A type of hyperplasia that occurs in response to normal physiological stimuli.

p.7
Causes of Cell Injury

What additional effects does ischemia have compared to hypoxia?

It results in a deficiency of essential nutrients and a buildup of toxic metabolites.

p.108
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is fatty change also known as?

Steatosis.

p.48
Mechanisms of Cell Death: Necrosis and Apoptosis

What does the term 'apoptosis' mean in Greek?

'Falling off', similar to the loss of leaves from a tree.

p.108
Overview of Cellular Responses to Stress

What types of substances can accumulate intracellularly?

Fatty change, cholesterol and cholesteryl esters, proteins, glycogen, and pigments.

p.88
Inflammation

What do inflammatory cells secrete?

Products that destroy microbes but may also damage host tissues.

p.48
Reversible vs. Irreversible Cell Injury

Is apoptosis considered a reversible or irreversible cell injury?

Irreversible cell injury.

p.45
Clinical Significance of Cell Death and Aging

What happens to intracellular proteins during cell death?

They leak through the damaged cell membrane.

p.4
Overview of Cellular Responses to Stress

How is the intracellular milieu of cells regulated in homeostasis?

It remains fairly constant and tightly regulated.

p.102
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What activates ubiquitin ligases in the context of atrophy?

Nutrient deficiency and disuse.

p.17
Reversible vs. Irreversible Cell Injury

What is a visible effect of cytoplasmic swelling in cells?

Vacuolation.

p.108
Causes of Cell Injury

What is the impact of protein accumulation in cells?

It can disrupt cellular function and lead to cell injury.

p.30
Mechanisms of Cell Death: Necrosis and Apoptosis

What is pyknosis characterized by?

Nuclear shrinkage and increased basophilia; DNA condenses into a dark shrunken mass.

p.103
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

How does metaplasia help cells in response to stress?

A cell type sensitive to a particular stress is replaced by another cell type better able to withstand the adverse environment.

p.46
Mechanisms of Cell Death: Necrosis and Apoptosis

What is apoptosis?

A programmed form of cell death that occurs in a regulated manner, allowing for the removal of damaged or unnecessary cells.

p.90
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What aspects of cells can be altered during adaptations to stress?

Number, size, phenotype, metabolic activity, and functions.

p.103
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the proposed mechanism behind metaplasia?

Reprogramming of stem cells to differentiate along a new pathway.

p.106
Causes of Cell Injury

Why is understanding intracellular accumulation important?

It helps explain the pathogenesis of related diseases.

p.47
Mechanisms of Cell Death: Necrosis and Apoptosis

What are five morphological differences between necrosis and apoptosis?

1. Cell size: Necrosis involves swelling, while apoptosis involves shrinkage. 2. Membrane integrity: Necrosis shows loss of membrane integrity, apoptosis maintains it. 3. Nuclear changes: Necrosis has random nuclear fragmentation, apoptosis has chromatin condensation. 4. Inflammatory response: Necrosis triggers inflammation, apoptosis does not. 5. Cell death mechanism: Necrosis is passive, apoptosis is active.

p.51
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necrosis?

A form of cell injury that results in the premature death of cells in living tissue.

p.46
Causes of Cell Injury

What are common causes of irreversible cell injury?

Severe hypoxia, toxins, infections, and physical trauma.

p.13
Causes of Cell Injury

What is cellular senescence?

A process that leads to alterations in replicative and repair abilities of individual cells and tissues.

p.19
Reversible vs. Irreversible Cell Injury

What do cells look like under light microscopy during reversible cell injury?

Cells are swollen, and the cytoplasm is pale, granular, vacuolated, or clear.

p.7
Causes of Cell Injury

What does ischemia mean?

Reduced blood supply.

p.62
Overview of Cellular Responses to Stress

What is autophagy?

A process of 'self-eating' where intracellular organelles and portions of cytosol are degraded.

p.93
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the outcome of both hypertrophy and hyperplasia?

An enlarged organ.

p.18
Reversible vs. Irreversible Cell Injury

What is reversible cell injury often referred to as?

Hydropic change or vacuolar degeneration.

p.122
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the serum calcium level in metastatic calcification?

Hypercalcemia.

p.79
Causes of Cell Injury

How do ROS affect proteins in cells?

They cause crosslinking and other changes, leading to degradation or loss of enzymatic activity.

p.121
Causes of Cell Injury

What is dystrophic calcification?

Deposition of calcium salts in dead tissues with normal serum levels of calcium.

p.60
Mechanisms of Cell Death: Necrosis and Apoptosis

How are the cytoplasmic fragments from apoptotic cells handled by the body?

They are quickly shed and phagocytosed without eliciting an inflammatory response.

p.49
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to the cell during apoptosis?

The cell is divided into small pieces called apoptotic bodies.

p.76
Oxidative Stress and Free Radicals in Cell Damage

What can increase the generation of free radicals?

Absorption of radiant energy, such as ultraviolet (UV) light and x-rays.

p.90
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are cellular adaptations to stress?

Reversible changes in the number, size, phenotype, metabolic activity, and functions of cells in response to environmental changes.

p.79
Causes of Cell Injury

What type of damage can ROS cause to DNA?

DNA damage.

p.106
Causes of Cell Injury

What are intracellular accumulations?

The buildup of substances within cells that can lead to cellular dysfunction.

p.46
Reversible vs. Irreversible Cell Injury

What is irreversible cell injury?

A type of cell damage that leads to cell death and cannot be reversed.

p.108
Causes of Cell Injury

What is the significance of intracellular accumulation of cholesterol?

It can lead to cellular dysfunction and disease.

p.74
Mechanisms of Cell Death: Necrosis and Apoptosis

What role do leukocytes play in reperfusion injury?

They produce products that cause additional tissue injury.

p.23
Overview of Cellular Responses to Stress

What does the term 'necros' mean in Greek?

Death.

p.27
Mechanisms of Cell Death: Necrosis and Apoptosis

What is one of the biochemical mechanisms of necrosis related to energy generation?

Failure of energy generation in the form of ATP due to reduced oxygen supply or mitochondrial damage.

p.77
Oxidative Stress and Free Radicals in Cell Damage

What are common sources of ROS generation in cells?

Mitochondrial respiration, inflammation, and exposure to environmental toxins.

p.108
Causes of Cell Injury

What is glycogen accumulation associated with?

Metabolic disorders and certain diseases.

p.86
Mechanisms of Cell Death: Necrosis and Apoptosis

How do cells sense DNA damage?

Through intracellular sentinel proteins that transmit signals leading to p53 accumulation.

p.47
Clinical Significance of Cell Death and Aging

What is the clinical significance of apoptosis?

Apoptosis plays a crucial role in maintaining tissue homeostasis and eliminating damaged cells.

p.33
Mechanisms of Cell Death: Necrosis and Apoptosis

What can occur to dead cells as a result of fatty acid binding?

They may ultimately become calcified.

p.69
Role of Hypoxia and Ischemia in Cell Injury

What is the primary substrate for anaerobic glycolysis?

Glucose.

p.11
Causes of Cell Injury

How can electric shock lead to cell injury?

It can disrupt electrical activity and cause thermal damage.

p.73
Mechanisms of Cell Death: Necrosis and Apoptosis

What types of ischemia are particularly affected by ischemia-reperfusion injury?

Myocardial and cerebral ischemia.

p.101
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

How can loss of innervation lead to atrophy?

It results in a lack of stimulation to the affected muscles or tissues.

p.51
Mechanisms of Cell Death: Necrosis and Apoptosis

What is apoptosis?

A programmed cell death process that is a normal part of growth and development.

p.40
Mechanisms of Cell Death: Necrosis and Apoptosis

What is caseous necrosis most often associated with?

Foci of tuberculous infection.

p.114
Overview of Cellular Responses to Stress

What are pigments in the context of intracellular accumulations?

Colored substances that can be either exogenous or endogenous.

p.26
Overview of Cellular Responses to Stress

What role do leukocytes play in digestion?

They are recruited as part of the inflammatory reaction to provide digestive enzymes.

p.65
Causes of Cell Injury

What typically causes cell injury?

Functional and biochemical abnormalities of essential cellular components.

p.96
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is an example of physiologic hyperplasia?

The increase in smooth muscle cells in the uterus during pregnancy.

p.18
Reversible vs. Irreversible Cell Injury

What are the gross morphological changes associated with cellular swelling?

Pallor, increased turgor, and an increase in organ weight.

p.3
Overview of Cellular Responses to Stress

What is the significance of achieving a new steady state in cells?

It allows cells to adapt to stress and maintain function despite adverse conditions.

p.79
Causes of Cell Injury

What can happen to damaged proteins due to ROS?

They may fail to fold properly, triggering the unfolded protein response.

p.112
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are Russell bodies?

Intracellular accumulations of proteins.

p.84
Endoplasmic Reticulum Stress and Protein Misfolding

What can cause the intracellular accumulation of misfolded proteins?

Gene mutations that lead to the production of proteins that cannot fold properly.

p.49
Mechanisms of Cell Death: Necrosis and Apoptosis

What is unique about the membrane of apoptotic bodies?

The membrane is altered and becomes highly 'edible' for phagocytes.

p.5
Clinical Significance of Cell Death and Aging

Why is cell death significant in the context of disease?

It is one of the most crucial events in the evolution of disease in any tissue or organ.

p.39
Causes of Cell Injury

What part of the body is commonly affected by gangrenous necrosis?

The lower leg that has lost its blood supply.

p.16
Reversible vs. Irreversible Cell Injury

What is a characteristic of reversible injury in cells?

Cells and intracellular organelles become swollen due to water intake.

p.5
Causes of Cell Injury

What leads to cell death?

Diverse causes.

p.46
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necrosis?

A form of cell death characterized by the uncontrolled breakdown of cell structures, often due to injury or disease.

p.73
Mechanisms of Cell Death: Necrosis and Apoptosis

What is ischemia-reperfusion injury?

Increased cell injury that occurs when blood flow is restored to ischemic but viable tissues.

p.80
Oxidative Stress and Free Radicals in Cell Damage

What does ROS stand for?

Reactive Oxygen Species.

p.106
Causes of Cell Injury

What can result from intracellular accumulation of substances?

Pathogenesis and diseases.

p.84
Endoplasmic Reticulum Stress and Protein Misfolding

What is a consequence of increased demand for secretory proteins?

Increased demand for secretory proteins, such as insulin, can lead to misfolding in insulin-resistant states.

p.44
Mechanisms of Cell Death: Necrosis and Apoptosis

What contributes to the appearance of fibrinoid necrosis?

Deposited immune complexes and fibrin that has leaked out of vessels.

p.63
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the mechanisms of necrosis?

Necrosis involves cell injury due to factors like ischemia, hypoxia, and chemical injury.

p.36
Mechanisms of Cell Death: Necrosis and Apoptosis

How is cellular debris removed after necrosis?

By phagocytosis.

p.27
Mechanisms of Cell Death: Necrosis and Apoptosis

What cellular contents leak out due to membrane damage in necrosis?

Cellular contents including enzymes.

p.34
Mechanisms of Cell Death: Necrosis and Apoptosis

What characterizes liquefactive necrosis?

The transformation of tissue into a liquid viscous mass.

p.20
Reversible vs. Irreversible Cell Injury

What does electron microscopy reveal about the endoplasmic reticulum during reversible cell injury?

Swelling of the endoplasmic reticulum (ER).

p.17
Reversible vs. Irreversible Cell Injury

What happens to sodium and water during cell injury?

There is an influx of Na and H2O.

p.72
Overview of Cellular Responses to Stress

What factors can influence the activity of cellular enzymes?

Factors include temperature, pH, substrate concentration, and the presence of inhibitors or activators.

p.75
Oxidative Stress and Free Radicals in Cell Damage

What happens to molecules attacked by free radicals?

They are often converted into other types of free radicals, propagating the chain of damage.

p.11
Causes of Cell Injury

What are some physical agents that can cause cell injury?

Trauma, extremes of temperature, radiation, electric shock, and sudden changes in atmospheric pressure.

p.8
Causes of Cell Injury

What role do drugs play in cell injury?

They can cause injury at therapeutic doses in susceptible individuals or excessive use.

p.72
Overview of Cellular Responses to Stress

What is enzyme inhibition?

Enzyme inhibition is the process by which a molecule decreases the activity of an enzyme.

p.49
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the inflammatory response associated with apoptotic cell death?

Apoptotic cell death does not elicit an inflammatory reaction.

p.106
Causes of Cell Injury

Name one important type of accumulating substance in the cell.

Lipids.

p.115
Impact of Toxins and Infectious Agents on Cells

What condition is caused by the accumulation of carbon in lymph nodes and pulmonary parenchyma?

Anthracosis.

p.11
Causes of Cell Injury

What impact do extremes of temperature have on cells?

They can lead to cellular damage or death.

p.17
Reversible vs. Irreversible Cell Injury

What disturbance occurs in the Na/K pump during cell injury?

Disturbance of the Na/K pump leads to cellular dysfunction.

p.69
Role of Hypoxia and Ischemia in Cell Injury

What process generates ATP in the absence of oxygen?

Anaerobic glycolysis.

p.102
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is often increased alongside atrophy?

Autophagy, resulting in more autophagic vacuoles.

p.109
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is another term for fatty change in the liver?

Fatty liver.

p.39
Mechanisms of Cell Death: Necrosis and Apoptosis

What is wet gangrene?

A condition resulting from bacterial infection superimposed on coagulative necrosis.

p.25
Mechanisms of Cell Death: Necrosis and Apoptosis

What local reaction does necrosis elicit?

Inflammation.

p.63
Causes of Cell Injury

What is ischemia-reperfusion injury?

It occurs when blood supply returns to tissue after a period of ischemia, causing further damage.

p.82
Endoplasmic Reticulum Stress and Protein Misfolding

What role do chaperones in the ER play during protein synthesis?

They control the proper folding of newly synthesized proteins.

p.80
Oxidative Stress and Free Radicals in Cell Damage

How do ROS contribute to aging?

By causing cumulative damage to cellular structures over time.

p.67
Reversible vs. Irreversible Cell Injury

What is the initial result of ATP depletion due to hypoxia and ischemia?

Reversible injury.

p.51
Mechanisms of Cell Death: Necrosis and Apoptosis

How does necrosis differ from apoptosis?

Necrosis is uncontrolled and often results from injury, while apoptosis is a regulated and orderly process.

p.67
Mechanisms of Cell Death: Necrosis and Apoptosis

What can happen if hypoxia and ischemia are not corrected?

Necrosis.

p.78
Oxidative Stress and Free Radicals in Cell Damage

How do antioxidants help in relation to free radicals?

They may block the formation of free radicals or scavenge them after they have formed.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What is eliminated during physiologic apoptosis?

Cells that have served their useful purpose.

p.34
Mechanisms of Cell Death: Necrosis and Apoptosis

What is fibrinoid necrosis?

A type of necrosis characterized by the deposition of fibrin-like protein in the tissue, often seen in immune-mediated vascular damage.

p.22
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the morphological changes associated with apoptosis?

Cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

p.66
Oxidative Stress and Free Radicals in Cell Damage

What is oxidative stress?

An imbalance between free radicals and antioxidants in the body, leading to cell damage.

p.1
Impact of Toxins and Infectious Agents on Cells

What role do toxins play in cell injury?

They can disrupt cellular functions and lead to cell damage or death.

p.55
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the final outcome of the caspase cascade activated by cytochrome c?

Nuclear fragmentation and formation of apoptotic bodies.

p.29
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the cytoplasmic changes observed in necrotic cells?

Discontinuities in plasma and organelle membranes.

p.90
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Are cellular adaptations to stress permanent?

No, they are reversible changes.

p.76
Oxidative Stress and Free Radicals in Cell Damage

What role do exogenous chemicals play in free radical generation?

Their enzymatic metabolism can increase free radical production, such as with carbon tetrachloride.

p.67
Causes of Cell Injury

What is one of the most frequent causes of cell injury and necrotic cell death?

Oxygen deprivation.

p.98
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is endometrial hyperplasia?

Hyperplasia due to disturbed balance between estrogen and progesterone, often causing abnormal menstrual bleeding.

p.12
Causes of Cell Injury

What can specific vitamin deficiencies lead to?

Cell injury.

p.76
Oxidative Stress and Free Radicals in Cell Damage

How does inflammation contribute to free radical generation?

Free radicals are produced by leukocytes during the inflammatory response.

p.29
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to lysosomes in necrotic cells?

Disruption of lysosomes occurs.

p.36
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the role of leukocytes in necrosis?

They are recruited to the site and digest dead cells using lysosomal enzymes.

p.64
Reversible vs. Irreversible Cell Injury

What may larger doses of toxins or prolonged ischemia result in?

Irreversible injury and necrosis.

p.73
Mechanisms of Cell Death: Necrosis and Apoptosis

Why is ischemia-reperfusion injury clinically important?

It may significantly contribute to tissue damage, especially after myocardial and cerebral ischemia.

p.34
Mechanisms of Cell Death: Necrosis and Apoptosis

What is coagulative necrosis?

A type of tissue necrosis where the architecture of the tissue remains intact but the cells are dead.

p.69
Role of Hypoxia and Ischemia in Cell Injury

Where can glucose be derived from for anaerobic glycolysis?

From circulation or hydrolysis of intracellular glycogen.

p.25
Reversible vs. Irreversible Cell Injury

What often leads to necrosis?

It is often the culmination of reversible cell injury that cannot be corrected.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the function of the 'death domain' in death receptors?

It mediates interaction with other proteins involved in cell death.

p.50
Mechanisms of Cell Death: Necrosis and Apoptosis

What triggers necrosis?

It is usually triggered by external factors such as toxins, infections, or trauma.

p.34
Mechanisms of Cell Death: Necrosis and Apoptosis

What is fat necrosis?

Necrosis that occurs in adipose tissue, often due to trauma or pancreatitis.

p.51
Mechanisms of Cell Death: Necrosis and Apoptosis

What triggers apoptosis?

Cellular stress, DNA damage, or signals from other cells.

p.20
Reversible vs. Irreversible Cell Injury

What nuclear alterations are observed in reversible cell injury?

Clumping of chromatin.

p.55
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the effect of BH3 proteins on Bak and Bax?

They shift the balance in favor of pro-apoptotic Bak and Bax.

p.81
Causes of Cell Injury

What occurs to the smooth ER and ribosomes in hepatocytes due to CCl4?

Swelling of the smooth ER and dissociation of ribosomes from the RER.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What is pathologic atrophy in parenchymal organs often associated with?

Duct obstruction.

p.67
Mechanisms of Cell Death: Necrosis and Apoptosis

Why is oxygen important for cells?

It is required for oxidative phosphorylation and the generation of ATP.

p.112
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What diseases are associated with glycogen accumulation?

Glycogen storage diseases.

p.11
Causes of Cell Injury

What role does radiation play in cell injury?

It can cause DNA damage and disrupt cellular processes.

p.97
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What types of hyperplasia exist?

Hyperplasia can be physiologic or pathologic.

p.12
Causes of Cell Injury

What type of diet is implicated in the development of atherosclerosis and cancer?

Diets rich in animal fat.

p.44
Mechanisms of Cell Death: Necrosis and Apoptosis

In which type of diseases is fibrinoid necrosis commonly seen?

Immunologically mediated diseases, such as polyarteritis nodosa.

p.106
Causes of Cell Injury

What is one disease related to lipid accumulation in cells?

Atherosclerosis.

p.30
Mechanisms of Cell Death: Necrosis and Apoptosis

How long can it take for the nucleus in a dead cell to completely disappear?

1 to 2 days.

p.81
Causes of Cell Injury

How do direct-acting toxins cause cell injury?

By combining with a critical molecular component.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What is an example of physiologic involution of cells?

Regression of the lactating breast after weaning.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What are the types of adaptation mechanisms of the cell?

Hypertrophy, hyperplasia, atrophy, and metaplasia.

p.15
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necrosis?

A form of irreversible cell injury leading to cell death characterized by cell swelling and inflammation.

p.22
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the morphological changes associated with necrosis?

Cell swelling, rupture of cell membranes, and inflammation.

p.50
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the morphological changes associated with necrosis?

Cell swelling, rupture of the cell membrane, and inflammation.

p.63
Endoplasmic Reticulum Stress and Protein Misfolding

What is Endoplasmic Reticulum Stress?

It is a condition where the ER cannot properly fold proteins, leading to cellular dysfunction.

p.55
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens when Bak and Bax form channels in the mitochondria?

Cytochrome c and other mitochondrial proteins escape into the cytosol.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Can you give an example of hypertrophy?

Cardiac hypertrophy due to high blood pressure.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Can you give an example of metaplasia?

Squamous metaplasia in the respiratory tract due to smoking.

p.98
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Which viral infections are associated with hyperplasia?

Certain viral infections, such as papillomaviruses, which cause skin warts.

p.12
Causes of Cell Injury

How does obesity affect the risk of diabetes?

It markedly increases the risk for type 2 diabetes mellitus.

p.50
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necrosis?

An uncontrolled form of cell death that results from injury or disease, leading to inflammation.

p.29
Mechanisms of Cell Death: Necrosis and Apoptosis

What are intracytoplasmic myelin figures?

Collections of phospholipids derived from damaged cellular membranes.

p.82
Endoplasmic Reticulum Stress and Protein Misfolding

What can the accumulation of misfolded proteins in a cell lead to?

Cell death by apoptosis.

p.80
Oxidative Stress and Free Radicals in Cell Damage

What are the pathologic effects of ROS on cells?

They can cause oxidative stress, leading to cell injury and death.

p.86
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens if DNA damage is too great to repair?

p53 triggers apoptosis, primarily through the mitochondrial pathway.

p.77
Oxidative Stress and Free Radicals in Cell Damage

What can excessive ROS lead to in cells?

Oxidative stress, which can cause cell injury and death.

p.22
Mechanisms of Cell Death: Necrosis and Apoptosis

What is apoptosis?

A programmed and controlled process of cell death that occurs as a normal part of growth and development.

p.34
Mechanisms of Cell Death: Necrosis and Apoptosis

What is gangrenous necrosis?

A type of necrosis that involves the death of tissue due to loss of blood supply, often associated with bacterial infection.

p.22
Mechanisms of Cell Death: Necrosis and Apoptosis

How does necrosis differ from apoptosis?

Necrosis is uncontrolled and often harmful, while apoptosis is a regulated and beneficial process.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the prototypic death receptors mentioned?

Type I TNF receptor and Fas (CD95).

p.81
Causes of Cell Injury

What happens to CCl4 in the liver?

It is converted to a toxic free radical.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What type of lymphocytes are eliminated to prevent harm?

Potentially harmful self-reactive lymphocytes.

p.82
Endoplasmic Reticulum Stress and Protein Misfolding

Through which pathway does apoptosis occur when there is significant ER stress?

The mitochondrial (intrinsic) pathway.

p.6
Causes of Cell Injury

How do nutritional imbalances lead to cell injury?

Lack of essential nutrients can impair cellular function and repair.

p.15
Causes of Cell Injury

What are light microscopic changes in cell damage?

Cell swelling, nuclear changes, and cytoplasmic granularity.

p.66
Mechanisms of Cell Death: Necrosis and Apoptosis

What is apoptosis?

A programmed cell death process that eliminates damaged or unnecessary cells.

p.35
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to the tissue architecture in coagulative necrosis?

It is preserved for several days despite the loss of details.

p.25
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necrosis?

A form of cell death where cellular membranes fall apart, and enzymes leak out to digest the cell.

p.46
Mechanisms of Cell Death: Necrosis and Apoptosis

How does necrosis differ from apoptosis?

Necrosis is uncontrolled and often results from acute injury, while apoptosis is a controlled process that is part of normal cellular regulation.

p.50
Mechanisms of Cell Death: Necrosis and Apoptosis

How does apoptosis affect surrounding cells?

It typically does not cause inflammation and is generally beneficial to surrounding tissues.

p.20
Reversible vs. Irreversible Cell Injury

What is a key characteristic of reversible cell injury?

Cellular swelling.

p.1
Causes of Cell Injury

What is cell injury?

A condition where cells are damaged due to various stressors or harmful agents.

p.24
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necroptosis?

A form of regulated cell death that shows features of both necrosis and apoptosis.

p.101
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What role does blood supply play in atrophy?

Diminished blood supply can lead to reduced oxygen and nutrients, causing atrophy.

p.20
Reversible vs. Irreversible Cell Injury

What changes occur to the plasma membrane in reversible cell injury?

Blebbing, blunting, or distortion of microvilli.

p.1
Reversible vs. Irreversible Cell Injury

What is the difference between reversible and irreversible cell injury?

Reversible injury allows cells to recover, while irreversible injury leads to cell death.

p.66
Role of Hypoxia and Ischemia in Cell Injury

What is hypoxia?

A condition where there is a deficiency of oxygen in the tissues.

p.55
Mechanisms of Cell Death: Necrosis and Apoptosis

What do Bcl-2 and Bcl-XL do in healthy cells?

They maintain the integrity of mitochondrial membranes by holding pro-apoptotic members Bax and Bak.

p.101
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is senile atrophy?

Atrophy that occurs as a result of aging.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens when T cells recognize Fas-expressing targets?

Fas molecules are crosslinked by FasL and bind adaptor proteins via the death domain.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

What is recruited and activated by the binding of adaptor proteins to death receptors?

Caspase-8.

p.66
Endoplasmic Reticulum Stress and Protein Misfolding

What is endoplasmic reticulum stress?

A condition where the endoplasmic reticulum cannot properly fold proteins, leading to cell dysfunction.

p.15
Clinical Significance of Cell Death and Aging

What is the clinical significance of apoptosis?

It plays a crucial role in tissue homeostasis and the elimination of damaged cells.

p.35
Mechanisms of Cell Death: Necrosis and Apoptosis

What is coagulative necrosis?

A form of necrosis where the underlying tissue architecture is preserved for at least several days, although details are lost.

p.84
Endoplasmic Reticulum Stress and Protein Misfolding

How does deprivation of glucose and oxygen affect protein folding?

Deprivation of glucose and oxygen can contribute to the accumulation of misfolded proteins.

p.45
Clinical Significance of Cell Death and Aging

What isoform of enzyme is found in hepatic bile duct epithelium?

Alkaline phosphatase.

p.22
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necrosis?

A form of cell death characterized by the uncontrolled breakdown of cell structures, often due to injury or disease.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What is one cause of physiologic apoptosis during embryogenesis?

Embryogenesis itself is a cause of physiologic apoptosis.

p.78
Oxidative Stress and Free Radicals in Cell Damage

What does catalase do?

It catalyzes the decomposition of hydrogen peroxide (H2O2) into oxygen (O2) and water (H2O).

p.82
Endoplasmic Reticulum Stress and Protein Misfolding

What happens to misfolded polypeptides in the ER?

They are ubiquitinated and targeted for proteolysis.

p.64
Causes of Cell Injury

How long can cardiac muscle survive ischemia before dying?

20 to 30 minutes.

p.47
Mechanisms of Cell Death: Necrosis and Apoptosis

What is autophagy?

Autophagy is a cellular process that degrades and recycles cellular components, helping to maintain cellular homeostasis.

p.81
Causes of Cell Injury

What must many toxic chemicals be converted to in order to cause injury?

Reactive metabolites.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is hypertrophy?

An increase in the size of cells, leading to an increase in the size of the organ.

p.6
Causes of Cell Injury

What are immunologic agents?

Substances that can trigger an immune response, potentially leading to cell injury.

p.81
Causes of Cell Injury

What cellular structures are damaged by CCl4?

ER membranes of hepatocytes.

p.81
Causes of Cell Injury

What is a consequence of the damage caused by CCl4?

Decline in the synthesis of enzymes and plasma proteins.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What type of cells can undergo apoptosis due to viral infections?

Viral infected cells.

p.15
Causes of Cell Injury

What are electron microscopic changes in cell damage?

Mitochondrial swelling, endoplasmic reticulum dilation, and membrane blebbing.

p.78
Oxidative Stress and Free Radicals in Cell Damage

What is the function of glutathione (GSH) peroxidases?

They catalyze the breakdown of hydrogen peroxide (H2O2) into water (H2O).

p.47
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the causes of apoptosis?

Causes include developmental signals, DNA damage, oxidative stress, and cellular stress.

p.50
Mechanisms of Cell Death: Necrosis and Apoptosis

How does necrosis affect surrounding cells?

It often leads to inflammation and can damage surrounding tissues.

p.69
Role of Hypoxia and Ischemia in Cell Injury

Which tissues have a greater glycolytic capacity?

The liver and striated muscle.

p.80
Oxidative Stress and Free Radicals in Cell Damage

What cellular components can ROS damage?

DNA, proteins, and lipids.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What happens to endometrial cells during the menstrual cycle?

Endometrial cell breakdown occurs.

p.20
Reversible vs. Irreversible Cell Injury

What happens to mitochondria during reversible cell injury?

Mitochondrial swelling and presence of phospholipid-rich amorphous densities.

p.101
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is an example of endocrine-related atrophy?

Physiologic atrophy of the endometrium after menopause.

p.15
Mechanisms of Cell Death: Necrosis and Apoptosis

What is apoptosis?

A programmed form of cell death that occurs in a controlled manner without causing inflammation.

p.1
Mechanisms of Cell Death: Necrosis and Apoptosis

What is apoptosis?

Programmed cell death that occurs in a controlled manner.

p.15
Reversible vs. Irreversible Cell Injury

What are some examples of reversible changes related to cell injury?

Cell swelling, fatty change, and chromatin clumping.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

What does caspase-8 activate?

Downstream caspases.

p.66
Causes of Cell Injury

What is DNA damage?

Alterations to the DNA structure that can lead to mutations and cell death.

p.6
Causes of Cell Injury

What is hypoxia?

A condition where there is a deficiency of oxygen in the tissues.

p.64
Causes of Cell Injury

How long can skeletal muscle in the leg survive complete ischemia?

2 to 3 hours.

p.1
Causes of Cell Injury

What are common causes of cell injury?

Hypoxia, toxins, infections, and physical trauma.

p.78
Oxidative Stress and Free Radicals in Cell Damage

What are some examples of endogenous or exogenous antioxidants?

Vitamins E, A, C, and β-carotene.

p.6
Causes of Cell Injury

How do toxins contribute to cell injury?

Toxins can damage cellular structures and disrupt metabolic processes.

p.22
Causes of Cell Injury

What are common causes of irreversible cell injury?

Severe hypoxia, toxins, infections, and physical trauma.

p.50
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the morphological changes associated with apoptosis?

Cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

p.1
Mechanisms of Cell Death: Necrosis and Apoptosis

What is necrosis?

A form of cell death resulting from acute cellular injury.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is atrophy?

A decrease in the size of cells, leading to a reduction in the size of the organ.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is metaplasia?

The reversible replacement of one differentiated cell type with another.

p.55
Mechanisms of Cell Death: Necrosis and Apoptosis

What does cytochrome c activate once it enters the cytosol?

Caspase-9.

p.66
Causes of Cell Injury

How does inflammation contribute to cell injury?

By causing tissue damage through the release of inflammatory mediators.

p.11
Causes of Cell Injury

What effect do sudden changes in atmospheric pressure have on cells?

They can cause physical stress and damage to cellular structures.

p.63
Reversible vs. Irreversible Cell Injury

How does ATP reduction contribute to cell damage?

ATP reduction leads to impaired cellular functions and energy-dependent processes.

p.6
Causes of Cell Injury

What is ischemia?

A reduction in blood flow to tissues, leading to a lack of oxygen and nutrients.

p.69
Role of Hypoxia and Ischemia in Cell Injury

Which tissues are more likely to survive hypoxia?

Tissues with greater glycolytic capacity, like the liver and striated muscle.

p.55
Mechanisms of Cell Death: Necrosis and Apoptosis

Which family of proteins controls mitochondrial permeability?

Bcl-2 family proteins.

p.6
Causes of Cell Injury

What role do infectious agents play in cell injury?

Infectious agents can invade cells and cause damage or death.

p.66
Role of Hypoxia and Ischemia in Cell Injury

What is ischemia?

A reduction in blood flow to a tissue, leading to a shortage of oxygen and nutrients.

p.55
Mechanisms of Cell Death: Necrosis and Apoptosis

What activates BH3 proteins?

Deprivation of growth factors, exposure to DNA-damaging agents, or accumulation of misfolded proteins.

p.6
Causes of Cell Injury

What are physical agents that can cause cell injury?

Factors such as trauma, temperature extremes, and radiation.

p.66
Impact of Toxins and Infectious Agents on Cells

How do toxins cause cell injury?

By disrupting cellular functions and structures, leading to cell death.

p.1
Impact of Toxins and Infectious Agents on Cells

How do infectious agents cause cell injury?

By invading cells and disrupting normal cellular processes.

p.15
Clinical Significance of Cell Death and Aging

What is the clinical significance of autophagy?

It helps in cellular maintenance and response to stress, preventing cell death.

p.27
Mechanisms of Cell Death: Necrosis and Apoptosis

What types of cellular components can be irreversibly damaged in necrosis?

Cellular lipids, proteins, and nucleic acids.

p.55
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the primary role of the mitochondrial (intrinsic) pathway?

It is responsible for apoptosis in most physiologic and pathologic situations.

p.34
Mechanisms of Cell Death: Necrosis and Apoptosis

What is caseous necrosis?

A form of necrosis characterized by the cheese-like appearance of tissue, often associated with tuberculosis.

p.80
Oxidative Stress and Free Radicals in Cell Damage

What role do antioxidants play in relation to ROS?

They neutralize ROS and protect cells from oxidative damage.

p.1
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the mechanisms of cell death?

Necrosis and apoptosis.

p.63
Impact of Toxins and Infectious Agents on Cells

What are the mechanisms of chemical injury?

Chemical injury can occur through direct toxicity, reactive metabolites, or disruption of cellular processes.

p.51
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the morphological features of necrosis?

Cell swelling, rupture, and inflammation.

p.20
Reversible vs. Irreversible Cell Injury

What may be present in the cytoplasm during reversible cell injury?

Myelin figures.

p.15
Reversible vs. Irreversible Cell Injury

What are some examples of irreversible changes related to cell injury?

Necrosis, apoptosis, and loss of membrane integrity.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

What pathway is described in the text?

The death receptor (extrinsic) pathway.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

Which family do most death receptors belong to?

The tumor necrosis factor (TNF) receptor family.

p.50
Mechanisms of Cell Death: Necrosis and Apoptosis

What triggers apoptosis?

It can be triggered by internal signals (like DNA damage) or external signals (like cytokines).

p.15
Reversible vs. Irreversible Cell Injury

What are the two main types of cell injury?

Reversible cell injury and irreversible cell injury.

p.51
Causes of Cell Injury

What are common causes of necrosis?

Infection, toxins, and lack of blood flow.

p.82
Endoplasmic Reticulum Stress and Protein Misfolding

What does the unfolded protein response do?

Increases the production of chaperones and decreases protein translation.

p.57
Mechanisms of Cell Death: Necrosis and Apoptosis

Where is Fas ligand (FasL) mainly expressed?

On activated T lymphocytes.

p.66
Reversible vs. Irreversible Cell Injury

How does ischemia-reperfusion injury occur?

It occurs when blood supply returns to the tissue after a period of ischemia, causing inflammation and oxidative damage.

p.51
Mechanisms of Cell Death: Necrosis and Apoptosis

What are the morphological features of apoptosis?

Cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is the clinical significance of cellular adaptations?

They can indicate underlying disease processes and help in diagnosis and treatment.

p.6
Causes of Cell Injury

How can genetic mutations cause cell injury?

Genetic mutations can disrupt normal cellular processes and lead to dysfunction.

p.47
Mechanisms of Cell Death: Necrosis and Apoptosis

What is the mechanism of apoptosis?

Apoptosis involves a series of biochemical events leading to cell shrinkage, chromatin condensation, and DNA fragmentation, often mediated by caspases.

p.81
Causes of Cell Injury

What is an example of a direct-acting toxin?

Mercuric chloride poisoning.

p.82
Endoplasmic Reticulum Stress and Protein Misfolding

What is the unfolded protein response?

A protective cellular response to the accumulation of unfolded or misfolded proteins.

p.63
Oxidative Stress and Free Radicals in Cell Damage

How are free radicals formed?

Free radicals are formed through various processes, including metabolic reactions and exposure to toxins.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

What is hyperplasia?

An increase in the number of cells in an organ or tissue.

p.15
Mechanisms of Cell Death: Necrosis and Apoptosis

What is autophagy?

A cellular process that degrades and recycles cellular components, often in response to stress.

p.1
Role of Hypoxia and Ischemia in Cell Injury

How does hypoxia contribute to cell injury?

It leads to a lack of oxygen, impairing cellular metabolism.

p.6
Causes of Cell Injury

What is the impact of aging on cells?

Aging can lead to decreased cellular function and increased susceptibility to injury.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Can you give an example of hyperplasia?

Benign prostatic hyperplasia.

p.35
Mechanisms of Cell Death: Necrosis and Apoptosis

In which type of tissue is coagulative necrosis typically observed?

Infarcts (areas of ischemic necrosis) in all solid organs except the brain.

p.77
Oxidative Stress and Free Radicals in Cell Damage

What is the relationship between ROS and aging?

Accumulation of ROS over time is linked to aging and age-related diseases.

p.63
Oxidative Stress and Free Radicals in Cell Damage

What role do free radicals play in cell damage?

Free radicals cause oxidative stress, leading to cellular injury and death.

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Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

How does inadequate nutrition contribute to atrophy?

It deprives cells of essential nutrients needed for maintenance and growth.

p.69
Role of Hypoxia and Ischemia in Cell Injury

Which tissue has limited glucose stores and is less likely to survive hypoxia?

The brain.

p.20
Reversible vs. Irreversible Cell Injury

What occurs to ribosomes in the context of reversible cell injury?

Detachment of ribosomes.

p.82
Endoplasmic Reticulum Stress and Protein Misfolding

What activates proapoptotic sensors of the BH3 in the context of ER stress?

A large amount of misfolded protein accumulation.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What can cause pathologic apoptosis related to DNA?

Severe DNA damage from radiation or cytotoxic anticancer drugs.

p.53
Mechanisms of Cell Death: Necrosis and Apoptosis

What can accumulate in the endoplasmic reticulum leading to apoptosis?

Misfolded proteins.

p.81
Causes of Cell Injury

What is the result of decreased synthesis of apoproteins in hepatocytes?

Accumulation of lipids in hepatocytes and other cells.

p.89
Cellular Adaptations: Hypertrophy, Hyperplasia, Atrophy, Metaplasia

Can you give an example of atrophy?

Muscle atrophy due to disuse.

Study Smarter, Not Harder
Study Smarter, Not Harder