Test Yourself: Cell Injury Pathology MCQs

1. What would be an example of hypertrophy?

Breast development at puberty

Enlargement of the uterus during pregnancy

Enlargement of the uterus during menstruation

A papillomavirus induced skin wart

Liver regeneration after partial hepatectomy

Hypertrophy is the increase in the volume of an organ or tissue due to the enlargement of its component cells. The number of cells remains the same but the cells become larger. This happens to the uterus during pregnancy when the uterus grows to accommodate the size of the fetus. This enlargement is a normal physiological response to accommodate the developing baby and provide a suitable environment for its growth.

Explanation

Hypertrophy is the increase in the volume of an organ or tissue due to the enlargement of its component cells. The number of cells remains the same but the cells become larger. This happens to the uterus during pregnancy when the uterus grows to accommodate the size of the fetus. This enlargement is a normal physiological response to accommodate the developing baby and provide a suitable environment for its growth.

2. Which tissue is the most susceptible to liquefactive necrosis following ischemic injury?

Pancreas

Liver

Spleen

Brain

Intestine

Brain tissue is the most susceptible to liquefactive necrosis following ischemic injury. Ischemic injury refers to a lack of blood supply to a tissue, leading to oxygen and nutrient deprivation. The brain is highly dependent on a constant supply of blood and oxygen, and any interruption in this supply can quickly lead to tissue damage. Liquefactive necrosis is a type of cell death characterized by the formation of liquid-filled spaces within the affected tissue. Liquefactive necrosis can also occur when lysosomes turn tissues into pus as a result of the lysosomal release of digestive enzymes. Neurons have a higher lysosomal content, leading to a higher tendency toward liquefactive necrosis.

Explanation

Brain tissue is the most susceptible to liquefactive necrosis following ischemic injury. Ischemic injury refers to a lack of blood supply to a tissue, leading to oxygen and nutrient deprivation. The brain is highly dependent on a constant supply of blood and oxygen, and any interruption in this supply can quickly lead to tissue damage. Liquefactive necrosis is a type of cell death characterized by the formation of liquid-filled spaces within the affected tissue. Liquefactive necrosis can also occur when lysosomes turn tissues into pus as a result of the lysosomal release of digestive enzymes. Neurons have a higher lysosomal content, leading to a higher tendency toward liquefactive necrosis.

3. What usually causes coagulative necrosis?

Abscess formation

Ischemia

Trauma

Tuberculosis

Syphilis

Coagulative necrosis usually results from ischemia, which is a lack of blood supply to tissues. Ischemia leads to oxygen deprivation and subsequent cell death. In coagulative necrosis, the architecture of dead tissues is preserved for a few days due to the denaturation of structural proteins and enzymes, which prevents the immediate breakdown of cells. This type of necrosis is typically seen in solid organs like the heart, kidney, and spleen following an infarction. The affected tissue appears firm and pale. Understanding the cause and characteristics of coagulative necrosis is crucial for diagnosing ischemic conditions and their effects on organs.

Explanation

Coagulative necrosis usually results from ischemia, which is a lack of blood supply to tissues. Ischemia leads to oxygen deprivation and subsequent cell death. In coagulative necrosis, the architecture of dead tissues is preserved for a few days due to the denaturation of structural proteins and enzymes, which prevents the immediate breakdown of cells. This type of necrosis is typically seen in solid organs like the heart, kidney, and spleen following an infarction. The affected tissue appears firm and pale. Understanding the cause and characteristics of coagulative necrosis is crucial for diagnosing ischemic conditions and their effects on organs.

4. What type of necrosis is associated with a well-developed infarct of the brain in a patient with left-sided weakness and paralysis in the upper extremity after a stroke?

Coagulative

Enzymatic fat

Liquefactive

Gangrenous

Liquefactive necrosis is the type of necrosis associated with a well-developed infarct of the brain. When a stroke occurs, the lack of blood supply leads to tissue death. In the brain, this results in liquefactive necrosis due to the high lipid content and the action of hydrolytic enzymes. The affected tissue becomes soft and liquid-like, forming a cystic space filled with necrotic debris. This contrasts with coagulative necrosis, typically seen in other organs like the heart or kidneys, where the tissue structure is preserved. Understanding the distinct features of liquefactive necrosis helps in diagnosing brain infarcts accurately.

Explanation

Liquefactive necrosis is the type of necrosis associated with a well-developed infarct of the brain. When a stroke occurs, the lack of blood supply leads to tissue death. In the brain, this results in liquefactive necrosis due to the high lipid content and the action of hydrolytic enzymes. The affected tissue becomes soft and liquid-like, forming a cystic space filled with necrotic debris. This contrasts with coagulative necrosis, typically seen in other organs like the heart or kidneys, where the tissue structure is preserved. Understanding the distinct features of liquefactive necrosis helps in diagnosing brain infarcts accurately.

5. In hypoxic cell injury, what causes cell swelling?

Lipid

Protein

Lipofuscin

Water

Glycogen

In hypoxic cell injury, cell swelling occurs because of increased intracellular water. Hypoxia, or lack of oxygen, impairs the cell's ability to produce ATP through aerobic respiration. Without sufficient ATP, the sodium-potassium pumps in the cell membrane fail, leading to an influx of sodium ions into the cell. Water follows sodium into the cell due to osmotic forces, causing the cell to swell. This swelling is one of the earliest signs of reversible cell injury. Understanding this mechanism is crucial for recognizing and managing conditions that lead to hypoxic injury in tissues.

Explanation

In hypoxic cell injury, cell swelling occurs because of increased intracellular water. Hypoxia, or lack of oxygen, impairs the cell's ability to produce ATP through aerobic respiration. Without sufficient ATP, the sodium-potassium pumps in the cell membrane fail, leading to an influx of sodium ions into the cell. Water follows sodium into the cell due to osmotic forces, causing the cell to swell. This swelling is one of the earliest signs of reversible cell injury. Understanding this mechanism is crucial for recognizing and managing conditions that lead to hypoxic injury in tissues.

6. What is the term for the pattern of cell death characterized by the conversion of a single cell to an acidophilic body, usually with loss of the nucleus but with preservation of its shape to permit recognition of cell boundaries?

Apoptosis

Caseous necrosis

Fibrinoid necrosis

Liquefactive necrosis

Apoptosis is the term used for the pattern of cell death characterized by the conversion of a single cell to an acidophilic body. In apoptosis, there is controlled cellular self-destruction regulated by specific pathways. The cell shrinks and forms apoptotic bodies that retain cellular boundaries and often have condensed, fragmented nuclei. This process is essential for normal development and tissue homeostasis, allowing the removal of damaged or unwanted cells without causing inflammation or damage to surrounding tissues. Understanding apoptosis is crucial in various physiological and pathological processes, including embryogenesis, immune response, and cancer.

Explanation

Apoptosis is the term used for the pattern of cell death characterized by the conversion of a single cell to an acidophilic body. In apoptosis, there is controlled cellular self-destruction regulated by specific pathways. The cell shrinks and forms apoptotic bodies that retain cellular boundaries and often have condensed, fragmented nuclei. This process is essential for normal development and tissue homeostasis, allowing the removal of damaged or unwanted cells without causing inflammation or damage to surrounding tissues. Understanding apoptosis is crucial in various physiological and pathological processes, including embryogenesis, immune response, and cancer.

7. What do cloudy swelling, hydropic change, and fatty change in the liver of a patient with a history of alcohol abuse represent morphologically?

Early neoplastic change

Hyaline change

Patterns of cell death

Postmortem artifact

Reversible cell injury

Cloudy swelling, hydropic change, and fatty change observed in the liver of a patient with a history of alcohol abuse are examples of reversible cell injury. These morphological changes indicate cellular responses to stress, such as alcohol toxicity. Cloudy swelling (also known as hydropic change) involves the swelling and enlargement of cells due to the influx of water and sodium ions. Hydropic change is an early manifestation of cellular injury. Fatty change (or steatosis) refers to the accumulation of fat within liver cells, a response to metabolic disturbances caused by alcohol abuse. Recognizing these reversible changes is crucial in assessing and managing liver pathology associated with alcohol-related conditions.

Explanation

Cloudy swelling, hydropic change, and fatty change observed in the liver of a patient with a history of alcohol abuse are examples of reversible cell injury. These morphological changes indicate cellular responses to stress, such as alcohol toxicity. Cloudy swelling (also known as hydropic change) involves the swelling and enlargement of cells due to the influx of water and sodium ions. Hydropic change is an early manifestation of cellular injury. Fatty change (or steatosis) refers to the accumulation of fat within liver cells, a response to metabolic disturbances caused by alcohol abuse. Recognizing these reversible changes is crucial in assessing and managing liver pathology associated with alcohol-related conditions.

8. Which type of myocardial cell death would best account for elevated serum levels of CK-MB and cardiac muscle troponin I (cTnI) in a 75-year-old woman with shortness of breath and chest pain radiating to the left shoulder?

Apoptosis

Caseous necrosis

Coagulative necrosis

Fat necrosis

Liquefactive necrosis

Coagulative necrosis is the type of myocardial cell death that best accounts for elevated serum levels of CK-MB and cardiac muscle troponin I (cTnI). These markers are released when heart muscle cells are damaged, such as during a myocardial infarction (heart attack). In myocardial infarction, the blood supply to a part of the heart is blocked, leading to cell death. Coagulative necrosis is characterized by the preservation of the cell's structural outline for a few days while the cell's proteins and enzymes coagulate. This type of necrosis is typical of ischemic conditions affecting solid organs like the heart.

Explanation

Coagulative necrosis is the type of myocardial cell death that best accounts for elevated serum levels of CK-MB and cardiac muscle troponin I (cTnI). These markers are released when heart muscle cells are damaged, such as during a myocardial infarction (heart attack). In myocardial infarction, the blood supply to a part of the heart is blocked, leading to cell death. Coagulative necrosis is characterized by the preservation of the cell's structural outline for a few days while the cell's proteins and enzymes coagulate. This type of necrosis is typical of ischemic conditions affecting solid organs like the heart.

9. What characteristic describes a circumscribed mass of light yellow crumbly to pasty material associated microscopically with a macrophage response?

Caseous necrosis

Coagulative necrosis

Fibrinoid necrosis

Gangrenous necrosis

Caseous necrosis is characterized by a circumscribed mass of light yellow crumbly to pasty material, often resembling cottage cheese grossly. Microscopically, it shows an amorphous appearance with loss of cellular detail and is associated with a surrounding macrophage response. This type of necrosis is commonly observed in tuberculosis infections, where the immune system attempts to contain and degrade the necrotic material. Understanding the characteristic features of caseous necrosis helps pathologists diagnose and differentiate it from other forms of tissue necrosis based on its distinct gross and microscopic appearance.

Explanation

Caseous necrosis is characterized by a circumscribed mass of light yellow crumbly to pasty material, often resembling cottage cheese grossly. Microscopically, it shows an amorphous appearance with loss of cellular detail and is associated with a surrounding macrophage response. This type of necrosis is commonly observed in tuberculosis infections, where the immune system attempts to contain and degrade the necrotic material. Understanding the characteristic features of caseous necrosis helps pathologists diagnose and differentiate it from other forms of tissue necrosis based on its distinct gross and microscopic appearance.

10. What results from the action of putrefactive bacteria on necrotic tissue?

Coagulation

Infarction

Gangrene

Embolism

Caseation

The action of putrefactive bacteria on necrotic tissue results in gangrene. Gangrene is a condition where body tissues die due to a lack of blood flow or a bacterial infection. When putrefactive bacteria act on necrotic tissue, they break down proteins, leading to the production of foul-smelling gases and fluids. This bacterial activity worsens tissue damage and can lead to further complications if not treated promptly. Gangrene can be dry (without infection) or wet (with bacterial infection), and it requires medical intervention to prevent the spreading and potential loss of affected tissues. Understanding the role of bacterial action in gangrene is crucial for effective management and treatment strategies.

Explanation

The action of putrefactive bacteria on necrotic tissue results in gangrene. Gangrene is a condition where body tissues die due to a lack of blood flow or a bacterial infection. When putrefactive bacteria act on necrotic tissue, they break down proteins, leading to the production of foul-smelling gases and fluids. This bacterial activity worsens tissue damage and can lead to further complications if not treated promptly. Gangrene can be dry (without infection) or wet (with bacterial infection), and it requires medical intervention to prevent the spreading and potential loss of affected tissues. Understanding the role of bacterial action in gangrene is crucial for effective management and treatment strategies.

11. What would microscopic examination of the spleen most likely reveal in a 10-year-old black male with sickle cell disease presenting with left upper quadrant pain suggestive of a splenic infarct?

Caseous necrosis

Coagulative necrosis

Fibrinoid necrosis

Gangrenous necrosis

Liquefactive necrosis

In sickle cell disease, particularly during a splenic infarction, the microscopic examination of the spleen would most likely reveal coagulative necrosis. This type of necrosis occurs when blood supply is interrupted, leading to cell death while maintaining the basic tissue architecture. In sickle cell disease, the abnormal sickle-shaped red blood cells can block blood vessels, reducing blood flow to the spleen and causing infarction. Coagulative necrosis is typical of ischemic injuries in most organs, except the brain. The other forms of necrosis mentioned (caseous, fibrinoid, gangrenous, and liquefactive) are more commonly associated with different pathological conditions, such as infections or specific tissue types.

Explanation

In sickle cell disease, particularly during a splenic infarction, the microscopic examination of the spleen would most likely reveal coagulative necrosis. This type of necrosis occurs when blood supply is interrupted, leading to cell death while maintaining the basic tissue architecture. In sickle cell disease, the abnormal sickle-shaped red blood cells can block blood vessels, reducing blood flow to the spleen and causing infarction. Coagulative necrosis is typical of ischemic injuries in most organs, except the brain. The other forms of necrosis mentioned (caseous, fibrinoid, gangrenous, and liquefactive) are more commonly associated with different pathological conditions, such as infections or specific tissue types.

12. You are asked to write a microscopic description of the coagulative necrosis that was noted in the heart of a patient who died of a heart attack because of cocaine abuse. Which of the following best described coagulative necrosis?

Eosinophilic cytoplasm with cell outlines preserved

Granular, friable mass of material devoid of cell outlines

A localized, solid, basophilic lesion with calcification

Necrosis in which tissue is converted into a fluid

Coagulative necrosis is a type of cell death characterized by the preservation of cell outlines and the presence of eosinophilic cytoplasm. This means that the cells maintain their shape and structure, but the cytoplasm takes on a pink color when stained with eosin dye. This type of necrosis is commonly seen in ischemic injury, such as in a heart attack, where there is a lack of blood supply to the affected tissue. In this case, the heart tissue of a patient who died of a heart attack due to cocaine abuse would show eosinophilic cytoplasm with preserved cell outlines, indicating coagulative necrosis.

Explanation

Coagulative necrosis is a type of cell death characterized by the preservation of cell outlines and the presence of eosinophilic cytoplasm. This means that the cells maintain their shape and structure, but the cytoplasm takes on a pink color when stained with eosin dye. This type of necrosis is commonly seen in ischemic injury, such as in a heart attack, where there is a lack of blood supply to the affected tissue. In this case, the heart tissue of a patient who died of a heart attack due to cocaine abuse would show eosinophilic cytoplasm with preserved cell outlines, indicating coagulative necrosis.

13. What causes cell death due to autolysis?

Antibodies

Endogenous enzymes

Phagocytic leukocytes

Bacterial enzymes

Anoxia

Cell death caused by autolysis is produced by endogenous enzymes. These endogenous enzymes are naturally present within the cells. They break down the cellular components and structures, leading to cell death. This process can occur due to various reasons, such as injury, disease, or natural cell turnover. Antibodies, phagocytic leukocytes, bacterial enzymes, and anoxia (lack of oxygen) are not directly involved in the process of autolysis.

Explanation

Cell death caused by autolysis is produced by endogenous enzymes. These endogenous enzymes are naturally present within the cells. They break down the cellular components and structures, leading to cell death. This process can occur due to various reasons, such as injury, disease, or natural cell turnover. Antibodies, phagocytic leukocytes, bacterial enzymes, and anoxia (lack of oxygen) are not directly involved in the process of autolysis.

14. What is characteristic of a well-demarcated lesion with increased cytoplasmic eosinophilia, karyolysis, and intact tissue architecture?

Caseous necrosis

Enzymatic fat necrosis

Coagulative necrosis

Cloudy swelling

Liquefactive necrosis

Coagulative necrosis is characterized by a well-demarcated lesion with increased cytoplasmic eosinophilia, karyolysis (nucleus dissolution), and intact tissue architecture. This type of necrosis occurs typically in organs like the heart, kidney, and spleen following ischemic injury. The tissue retains its structural outline due to the denaturation of structural proteins, maintaining the architectural integrity for a period after cell death. This characteristic appearance under microscopy helps pathologists identify coagulative necrosis and differentiate it from other forms, such as liquefactive necrosis, which involves tissue liquefaction and loss of tissue architecture. Understanding these features aids in diagnosing and managing conditions leading to tissue necrosis.

Explanation

Coagulative necrosis is characterized by a well-demarcated lesion with increased cytoplasmic eosinophilia, karyolysis (nucleus dissolution), and intact tissue architecture. This type of necrosis occurs typically in organs like the heart, kidney, and spleen following ischemic injury. The tissue retains its structural outline due to the denaturation of structural proteins, maintaining the architectural integrity for a period after cell death. This characteristic appearance under microscopy helps pathologists identify coagulative necrosis and differentiate it from other forms, such as liquefactive necrosis, which involves tissue liquefaction and loss of tissue architecture. Understanding these features aids in diagnosing and managing conditions leading to tissue necrosis.

15. A patient is admitted with severe substernal chest pain for 4 hours. Lab tests reveal an increased level of serum creatine kinase. This is most likely due to:

Mitochondrial swelling

Nuclear lysis

Damage of plasma membranes

Increased endoplasmic reticulum

Increased Golgi activity

The increased level of serum creatine kinase in a patient with severe substernal chest pain suggests damage of plasma membranes. Creatine kinase is an enzyme found in various tissues, including the heart muscle. When the plasma membrane of the heart muscle cells are damaged, creatine kinase leaks into the bloodstream, resulting in an increased level of serum creatine kinase. This can occur during a heart attack or myocardial infarction, where the lack of blood flow to the heart muscle causes cell death and membrane damage.

Explanation

The increased level of serum creatine kinase in a patient with severe substernal chest pain suggests damage of plasma membranes. Creatine kinase is an enzyme found in various tissues, including the heart muscle. When the plasma membrane of the heart muscle cells are damaged, creatine kinase leaks into the bloodstream, resulting in an increased level of serum creatine kinase. This can occur during a heart attack or myocardial infarction, where the lack of blood flow to the heart muscle causes cell death and membrane damage.

16. What characterizes caseous necrosis morphologically?

Preservation of tissue outlines

Basophilia

Semi-liquid consistency

Wedge-shaped periphery

Amorphous appearance

Caseous necrosis is characterized by an amorphous appearance morphologically. This type of necrosis is named for its cheese-like appearance, with a soft, friable texture. The affected tissue appears amorphous and granular under the microscope, lacking any distinct cellular outlines. This is in contrast to other types of necrosis where the tissue structure may be preserved. Caseous necrosis is commonly associated with tuberculosis infections, where the body's immune response leads to the destruction of tissue, resulting in this characteristic appearance. Understanding these morphological features is crucial for accurately diagnosing and differentiating caseous necrosis from other forms.

Explanation

Caseous necrosis is characterized by an amorphous appearance morphologically. This type of necrosis is named for its cheese-like appearance, with a soft, friable texture. The affected tissue appears amorphous and granular under the microscope, lacking any distinct cellular outlines. This is in contrast to other types of necrosis where the tissue structure may be preserved. Caseous necrosis is commonly associated with tuberculosis infections, where the body's immune response leads to the destruction of tissue, resulting in this characteristic appearance. Understanding these morphological features is crucial for accurately diagnosing and differentiating caseous necrosis from other forms.

17. Which of the following is an example of an agent capable of producing a toxic metabolite and indirect chemical injury?

Alcohol

Aspirin

Carbon monoxide

Mercury poisoning

Cyanide

Alcohol is an example of an agent capable of producing a toxic metabolite and indirect chemical injury. When alcohol is metabolized in the liver, it produces acetaldehyde, which is a toxic substance. Accumulation of acetaldehyde can lead to liver damage and other health problems. Additionally, alcohol can indirectly cause chemical injury by impairing judgment and coordination, leading to accidents or risky behaviors that can result in injury or poisoning.

Explanation

Alcohol is an example of an agent capable of producing a toxic metabolite and indirect chemical injury. When alcohol is metabolized in the liver, it produces acetaldehyde, which is a toxic substance. Accumulation of acetaldehyde can lead to liver damage and other health problems. Additionally, alcohol can indirectly cause chemical injury by impairing judgment and coordination, leading to accidents or risky behaviors that can result in injury or poisoning.

18. You are asked to review a liver biopsy from a patient with a history of alcohol abuse. Which of the following pathologic changes will most likely lead to the death of hepatocytes and liver cirrhosis?

Fatty change in liver cells

Hydropic change of hepatocytes

Karyolysis in myocardial cells

Glycogen deposition in hepatocyte nuclei

Fatty change in liver cells, also known as hepatic steatosis, refers to the abnormal accumulation of fat within liver cells. This condition is commonly associated with alcohol abuse and can lead to the death of hepatocytes and the development of liver cirrhosis. The excessive accumulation of fat within the liver cells disrupts their normal function and can cause inflammation and cell death. Over time, this can progress to liver cirrhosis, a condition characterized by the irreversible scarring of the liver tissue.

Explanation

Fatty change in liver cells, also known as hepatic steatosis, refers to the abnormal accumulation of fat within liver cells. This condition is commonly associated with alcohol abuse and can lead to the death of hepatocytes and the development of liver cirrhosis. The excessive accumulation of fat within the liver cells disrupts their normal function and can cause inflammation and cell death. Over time, this can progress to liver cirrhosis, a condition characterized by the irreversible scarring of the liver tissue.

19. What is the likely age of the myocardial infarct described as a well-demarcated area of the myocardium appearing paler than surrounding tissue, consisting microscopically of eosinophilic muscle fibers with few karyorrhectic and pyknotic nuclei, and many polys seen especially at the margin?

2 minutes

2 hours

2 days

2 weeks

2 months

The described characteristics of a well-demarcated area of the myocardium with eosinophilic muscle fibers, few karyorrhectic and pyknotic nuclei, and polymorphonuclear leukocytes (polys) at the margin indicate a myocardial infarct approximately 2 days old. During this time frame after a myocardial infarction (heart attack), the affected tissue shows early signs of coagulative necrosis. Eosinophilic muscle fibers with intact cell boundaries and few fragmented nuclei are typical findings microscopically. Polys, or neutrophils, are recruited to the area as part of the inflammatory response to clear cellular debris and initiate tissue repair. Understanding the histological changes over time helps in dating myocardial infarcts accurately for diagnostic and prognostic purposes.

Explanation

The described characteristics of a well-demarcated area of the myocardium with eosinophilic muscle fibers, few karyorrhectic and pyknotic nuclei, and polymorphonuclear leukocytes (polys) at the margin indicate a myocardial infarct approximately 2 days old. During this time frame after a myocardial infarction (heart attack), the affected tissue shows early signs of coagulative necrosis. Eosinophilic muscle fibers with intact cell boundaries and few fragmented nuclei are typical findings microscopically. Polys, or neutrophils, are recruited to the area as part of the inflammatory response to clear cellular debris and initiate tissue repair. Understanding the histological changes over time helps in dating myocardial infarcts accurately for diagnostic and prognostic purposes.

20. Which type of cell death is catalyzed by its own enzymes in a biopsy from the lungs showing morphologic changes indicative of irreversible injury and cell death with no external cause?

Cytolysis

Necrosis

Putrefaction

Autolysis

Somatic death

Autolysis is a type of cell death catalyzed by the cell's own enzymes. In autolysis, cells self-digest due to the action of their lysosomal enzymes. This process occurs when the cell's internal environment becomes disrupted, leading to the breakdown of cellular components. Autolysis is typically seen in cells that have undergone irreversible injury, where the damage is so severe that recovery is not possible. Understanding autolysis helps pathologists identify cell death mechanisms in tissues, particularly when there is no external cause, as in the case of certain pathological conditions affecting the lungs.

Explanation

Autolysis is a type of cell death catalyzed by the cell's own enzymes. In autolysis, cells self-digest due to the action of their lysosomal enzymes. This process occurs when the cell's internal environment becomes disrupted, leading to the breakdown of cellular components. Autolysis is typically seen in cells that have undergone irreversible injury, where the damage is so severe that recovery is not possible. Understanding autolysis helps pathologists identify cell death mechanisms in tissues, particularly when there is no external cause, as in the case of certain pathological conditions affecting the lungs.