FM2004 and PM2004 Course Details
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Questions and Answers

Where can students find the most up-to-date timetable information for FM2004 and PM2004?

Canvas and the UCC Online Timetable.

What types of sessions are FM2004 Med2 students divided into for weeks 27-35?

Groups A&B and Groups C&D.

If a student fails CA1 or CA2, are they required to repeat it?

No, not if they pass the module overall in the Summer exam.

What does MMID stand for in the context of the module topics?

<p>Medical Microbiology and Infectious Disease.</p> Signup and view all the answers

What are the components of the aggregate result considered for the UCC Pathology Undergraduate Medal for medical students?

<p>FM2004 and FM3005.</p> Signup and view all the answers

What is the passing grade percentage required for PM2004?

<p>40%.</p> Signup and view all the answers

Besides information found on Canvas, where else can students find information regarding the UCC Pathology Undergraduate Medal?

<p>UCC Scholarships and Prizes website.</p> Signup and view all the answers

Explain how the assessment for FM2004 and PM2004 comprised.

<p>Both FM2004 and PM2004 are assessed through CA1, CA2 and a Summer examination. CA1 and CA2 are worth 25 marks each and the Summer exam is worth 150 marks. FM2004 includes an oral examination in the Summer.</p> Signup and view all the answers

What are the three patterns of nuclear change observed in necrosis, and what cellular process causes them?

<p>Pyknosis (nuclear shrinkage and darkening), karyolysis (nuclear dissolution), and karyorrhexis (nuclear fragmentation). These are caused by the breakdown of DNA and chromatin.</p> Signup and view all the answers

Differentiate between autolysis that occurs during necrosis and the state of cells in a fixative.

<p>In necrosis, autolysis involves the progressive degradation of a cell by its own enzymes or those from inflammatory cells, leading to cell death and tissue damage. Cells in a fixative are dead, but the fixative prevents the enzymatic degradation of the cell.</p> Signup and view all the answers

Explain why coagulative necrosis is more likely to occur in the kidney than in the brain following a hypoxic event.

<p>Coagulative necrosis typically occurs in most tissues (like the kidney) after hypoxia due to the preservation of tissue architecture. In the brain, hypoxic events usually result in liquefactive necrosis because of the high lipid content and enzymatic activity.</p> Signup and view all the answers

How does liquefactive necrosis assist in the formation of a renal abscess during a fungal infection?

<p>Liquefactive necrosis digests dead cells, which leads to a liquid, viscous mass composed of liquefied cells, cellular debris, and white blood cells. This creates an environment conducive to abscess formation, obliterating the normal tissue architecture.</p> Signup and view all the answers

Describe the key macroscopic difference between coagulative and caseous necrosis.

<p>Coagulative necrosis typically preserves the general tissue architecture, while caseous necrosis results in a friable, cheese-like appearance with complete obliteration of tissue structure.</p> Signup and view all the answers

In tuberculosis, what is the significance of caseous necrosis in the lungs?

<p>In tuberculosis, caseous necrosis is a characteristic type of cell death that forms a large area of 'cheesy' debris in the lungs, which is indicative of the infection and the body's response to it.</p> Signup and view all the answers

A pathologist observes a tissue sample with cells that are larger and pinker than normal. If necrosis is suspected, what nuclear changes should they look for to confirm?

<p>The pathologist should look for pyknosis (shrunken, dark nucleus), karyolysis (nuclear dissolution), or karyorrhexis (nuclear fragmentation).</p> Signup and view all the answers

How would you differentiate between liquefactive necrosis caused by a bacterial infection and that caused by hypoxia in the central nervous system (CNS)?

<p>While both result in tissue liquefaction, bacterial infections typically involve an influx of inflammatory cells and pus formation. Hypoxia in the CNS leads to liquefaction without significant inflammation, due to the unique composition and response of brain tissue.</p> Signup and view all the answers

Briefly describe the key differences in the initiation and progression of apoptosis versus necrosis.

<p>Apoptosis is often triggered by programmed signals (physiological or pathological) leading to controlled self-destruction. Necrosis, however, typically results from overwhelming external injury, leading to uncontrolled cell death.</p> Signup and view all the answers

How do the features listed in Table 4.1 relate to the differing roles of apoptosis and necrosis in the body? Explain with reference to inflammation and outcome.

<p>Apoptosis does not induce inflammation and leads to cell elimination for homeostasis. Whereas necrosis triggers inflammation and can lead to defense mechanisms and tissue repair.</p> Signup and view all the answers

Why is the maintenance or loss of cell membrane integrity a critical distinguishing factor between apoptosis and necrosis?

<p>Maintenance of membrane integrity in apoptosis prevents release of intracellular contents, avoiding inflammation. Loss of integrity in necrosis releases these contents, triggering an inflammatory response.</p> Signup and view all the answers

Describe three adaptive responses a cell can undergo when faced with stress or injury, and provide a brief example of each.

<p>Hypertrophy (increase in cell size, e.g., muscle growth due to exercise), atrophy (decrease in cell size, e.g., muscle wasting due to immobilization), and metaplasia (change in cell type, e.g., respiratory epithelium change in smokers).</p> Signup and view all the answers

Explain how the fate of dead cells differs in apoptosis versus necrosis, and why this difference is significant for the surrounding tissue.

<p>In apoptosis, dead cells are phagocytosed by neighboring cells without inflammation. In necrosis, cells lyse and are ingested by immune cells, causing inflammation which can affect surrounding tissue.</p> Signup and view all the answers

If a scientist is studying a tissue sample and observes cell shrinkage, chromatin condensation, and formation of apoptotic bodies, would they conclude the cells died by necrosis or apoptosis? Why?

<p>Apoptosis, because cell shrinkage, chromatin condensation, and formation of apoptotic bodies are morphological hallmarks of apoptosis, not necrosis, which presents with cell swelling and lysis.</p> Signup and view all the answers

Why is apoptosis considered a crucial process in development and cancer therapy, as highlighted in the 'Cell Death: summary'?

<p>In development, apoptosis eliminates unwanted cells, like the webbing between fingers. In cancer therapy, it's induced to kill cancerous cells, preventing their uncontrolled proliferation.</p> Signup and view all the answers

Considering the information on cardiac cell injury, describe the potential sequence of events from a normal cardiac cell to irreversible injury, including the terms 'adapted' and 'reversibly injured'.

<p>A normal cardiac cell, when stressed, may first undergo adaptation such as hypertrophy. If the stress continues, it may become reversibly injured. If the injury is too severe or prolonged, it will progress to irreversible injury and cell death (necrosis or apoptosis).</p> Signup and view all the answers

Differentiate between hyperplasia and hypertrophy in terms of cellular mechanisms and the resulting change in tissue size.

<p>Hyperplasia involves an increase in the number of cells, leading to tissue enlargement, while hypertrophy involves an increase in the size of individual cells, also resulting in tissue enlargement.</p> Signup and view all the answers

Provide an example of a physiological condition where both hyperplasia and hypertrophy occur simultaneously. Explain why both processes are necessary in this scenario.

<p>The uterus during pregnancy exhibits both hyperplasia and hypertrophy. Hyperplasia increases the number of cells to accommodate the growing fetus, while hypertrophy enlarges individual cells to enhance their functional capacity.</p> Signup and view all the answers

Explain why atrophy can be considered both a physiological and pathological process, providing a specific example for each case.

<p>Physiological atrophy occurs during normal development, such as the shrinkage of the thymus gland with age. Pathological atrophy results from adverse conditions like lack of use (e.g., muscle atrophy during prolonged bed rest) or reduced blood supply to the brain.</p> Signup and view all the answers

Describe the key differences between physiological and pathological hypertrophy, focusing on the underlying causes and potential outcomes.

<p>Physiological hypertrophy occurs due to normal stimuli, such as exercise leading to muscle growth, and is generally beneficial. Pathological hypertrophy results from abnormal conditions like hypertension causing heart enlargement, which can impair organ function.</p> Signup and view all the answers

Explain how a reduction in growth factors or nutrient supply can lead to cellular atrophy. What cellular processes are affected by this reduction?

<p>Reduced growth factors or nutrient supply causes a decrease in protein synthesis and an increase in protein degradation within the cell, leading to a reduction in cell size and organelle number, ultimately causing atrophy.</p> Signup and view all the answers

In the context of tissue repair, explain the potential roles of both hyperplasia and hypertrophy. Provide an example of a tissue where hyperplasia is more critical and another where hypertrophy is more important.

<p>In tissue repair, hyperplasia can replace damaged cells with new ones (e.g., epithelial cells in wound healing), while hypertrophy can enhance the function of existing cells (e.g., remaining liver cells after partial hepatectomy).</p> Signup and view all the answers

Describe a scenario where prolonged hormonal stimulation can initially cause hyperplasia, but if the stimulation becomes excessive or uncontrolled, it leads to neoplasia.

<p>Endometrial hyperplasia, caused by prolonged estrogen exposure, can progress to endometrial carcinoma (a neoplasm) if the hormonal imbalance persists and leads to uncontrolled cell proliferation.</p> Signup and view all the answers

How does the presence of an infection differentiate wet gangrene from dry gangrene, and what macroscopic change is associated with wet gangrene due to this infection?

<p>Wet gangrene involves an infection that leads to the liquefactive action of bacteria and inflammatory cells, whereas dry gangrene does not. This infection causes a more putrefactive appearance.</p> Signup and view all the answers

In acute pancreatitis, what is the role of released pancreatic enzymes in fat necrosis and what is the end result of this process regarding visible tissue changes?

<p>Released pancreatic enzymes cause necrosis of adipose tissue, which releases fatty acids that combine with calcium, leading to the formation of visible chalky white areas (fat saponification).</p> Signup and view all the answers

Compare and contrast the cellular changes observed in muscle atrophy due to denervation versus atrophy due to malnutrition. How do the underlying mechanisms differ?

<p>Denervation atrophy primarily involves a loss of neurotrophic factors, leading to decreased protein synthesis and increased protein degradation. Malnutrition leads to a general lack of nutrients, resulting in reduced metabolic activity and cellular shrinkage.</p> Signup and view all the answers

Briefly describe the role of energy in apoptosis, and contrast this with the energy requirements in necrosis.

<p>Apoptosis is an active, energy-dependent process regulated by intracellular programs, whereas necrosis does not require energy.</p> Signup and view all the answers

Describe the morphological changes that occur in a cell undergoing apoptosis, focusing on both the cytoplasm and the nucleus.

<p>In apoptosis, the cell shrinks and the cytoplasm becomes dense. The chromatin in the nucleus condenses, and the nucleus may break into fragments.</p> Signup and view all the answers

What is the significance of the membrane remaining intact during apoptosis, and how does this contrast with necrosis?

<p>The intact membrane in apoptosis prevents the release of cellular contents, avoiding inflammation. In necrosis, the cell membrane ruptures, leading to inflammation.</p> Signup and view all the answers

How are apoptotic bodies cleared from the tissue, and what role do neighboring cells play in this process?

<p>Apoptotic bodies are phagocytosed by neighboring cells, which then rapidly degrade them within lysosomes. Healthy adjacent cells may then migrate or proliferate to fill the space.</p> Signup and view all the answers

Differentiate between apoptosis and necrosis based on their effects on surrounding tissues, particularly concerning inflammation.

<p>Apoptosis does not induce inflammation in surrounding tissues because it is a controlled process where the cell breaks down into apoptotic bodies that are phagocytosed. Necrosis causes inflammation due to the release of cellular contents upon cell lysis.</p> Signup and view all the answers

Consider a tissue sample showing individual cell death without signs of inflammation. Would you suspect apoptosis or necrosis, and why?

<p>Apoptosis, because it is characterized by individual cell death without an inflammatory reaction.</p> Signup and view all the answers

What cellular changes define dysplasia, and why is it considered potentially pre-neoplastic?

<p>Dysplasia is characterized by abnormal cell growth and differentiation, leading to a loss of uniformity in cell size and shape (pleomorphism), increased mitotic activity, and disordered tissue architecture. It's considered pre-neoplastic because, while reversible in early stages, it can progress to cancer if the underlying causes persist.</p> Signup and view all the answers

How does metaplasia in the respiratory tract, specifically from columnar to squamous epithelium due to smoking, affect the function of the tissue?

<p>The change from columnar to squamous epithelium in the respiratory tract, due to smoking, results in the loss of specific functions such as mucous secretion. While the squamous epithelium is more rugged, it does not perform the specialized functions of the original columnar epithelium, impairing the lung's ability to clear debris and pathogens.</p> Signup and view all the answers

Differentiate between metaplasia and dysplasia in terms of cellular changes and potential reversibility.

<p>Metaplasia involves a reversible change from one mature cell type to another, while dysplasia involves disordered growth and differentiation within a tissue. Both are potentially reversible. However, dysplasia is more closely associated with a risk of progressing to neoplasia, while metaplasia is an adaptation to a stressor that can sometimes predispose to malignancy if the stimulus persists.</p> Signup and view all the answers

Describe the cellular characteristics observed in dysplastic cervical epithelium, and how do these differ from normal cervical epithelium?

<p>Dysplastic cervical epithelium shows a disruption of the normal maturation sequence, with proliferation restricted to the basal layer. Cells exhibit larger than normal nuclei, are small and darkly stained, and show mitotic figures above the basal layer. This contrasts with normal cervical epithelium, where cells mature towards the surface, nuclei are smaller, and mitotic activity is confined to the basal layer.</p> Signup and view all the answers

Why is the nuclear-to-cytoplasmic (N:C) ratio significant in identifying dysplasia, and how does it change in dysplastic cells?

<p>The N:C ratio is significant because it reflects the proportion of the cell occupied by the nucleus, which contains the genetic material. In dysplastic cells, the N:C ratio is typically increased compared to normal cells, indicating a larger nucleus relative to the cytoplasm. This reflects increased DNA content and abnormal cellular activity.</p> Signup and view all the answers

What is the relationship between metaplasia, dysplasia and cancer development?

<p>Metaplasia is an adaptive response to chronic irritation where one cell type is replaced by another. While metaplasia is reversible if the irritant is removed, persistent metaplasia can sometimes progress to dysplasia, characterized by abnormal cell growth and disordered differentiation. Dysplasia is considered pre-neoplastic, as it has the potential to develop into cancer if the underlying causes are not addressed.</p> Signup and view all the answers

In the context of dysplasia, what does 'loss of architectural orientation' mean, and how is it observed microscopically?

<p>Loss of architectural orientation in dysplasia refers to the disruption of the normal arrangement and organization of cells within a tissue. Microscopically, this is observed as a lack of the usual orderly layering or alignment of cells, with cells appearing haphazardly arranged and lacking the typical structural relationships seen in healthy tissue.</p> Signup and view all the answers

If a pathologist observes 'increased mitotic figures' in a tissue sample, what does this indicate about the cells, and why is it concerning?

<p>Increased mitotic figures indicate that there is a higher than normal rate of cell division occurring within the tissue. This is concerning because it suggests uncontrolled cellular proliferation, which is a hallmark of dysplasia and neoplasia, implying a potential for rapid growth and tumor formation.</p> Signup and view all the answers

Flashcards

FM2004 Module

A Pathology module for second-year medical students at UCC.

Passing Marks for FM2004

Students must achieve at least 100 out of 200 marks to pass FM2004.

PM2004 Pass Requirement

A minimum of 80 out of 200 marks is required to pass PM2004.

Assessment Structure

Module assessments include continuous assessments (CAs) and a summer exam.

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Oral Examination in FM2004

An oral examination is part of the assessment for FM2004 in the summer.

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UCC Pathology Medal

Award for the top-performing student in Pathology modules at UCC.

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Module Timetable

Available on Canvas, details lecture and practical sessions for FM2004 and PM2004.

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Course Topics

FM2004 covers Cellular Pathology, Genetics, MMID, and Immunology.

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Hyperplasia

Enlargement of an organ or tissue due to an increase in the number of cells.

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Causes of Hyperplasia

Growth factors and receptors stimulate hyperplasia and can be physiologic or pathologic.

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Physiologic Hyperplasia

Normal increase in cell numbers due to hormonal changes, such as breast development in puberty.

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Compensatory Hyperplasia

Increase in cell numbers in response to damage or loss, such as liver regeneration after damage.

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Hypertrophy

Enlargement of an organ or tissue due to an increase in the size of existing cells.

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Physiologic Hypertrophy

Normal increase in cell size due to functional demands, e.g., muscle growth in athletes.

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Atrophy

Shrinkage of an organ or tissue due to loss of cell substance or decreased activity.

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Causes of Atrophy

Reduced nutrient supply, lack of use, hormonal loss, or denervation can cause atrophy.

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Necrosis

Cell death due to irreversible injury, leading to tissue breakdown.

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Autolysis

Breakdown of a cell by its own enzymes after death.

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Pyknosis

Shrinkage and darkening of the nucleus during necrosis.

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Karyolysis

Dissolution of the nucleus during necrosis.

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Karyorrhexis

Fragmentation of the nucleus in necrotic cells.

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Coagulative Necrosis

Most common necrosis type, preserving tissue architecture after hypoxia.

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Liquefactive Necrosis

Necrosis where tissue becomes a liquid mass due to enzymatic digestion.

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Caseous Necrosis

Cheesy-like necrosis often seen in tuberculosis, with a friable appearance.

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Metaplasia

Reversible change of one mature cell type to another adult cell type.

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Columnar to Squamous Metaplasia

Specific metaplasia where normal columnar epithelium transforms to stratified squamous epithelium.

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Dysplasia

Abnormal growth with disordered architecture and cell uniformity.

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Pleomorphism

Variation in shape and size of cells, often seen in dysplasia.

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Mitosis

Process of cell division that increases mitotic figures in dysplastic tissue.

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Hyperchromatic Nuclei

Nuclei that are larger and darker than normal, characteristic of dysplastic cells.

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Reversibility in Dysplasia

Dysplasia can be reversible in its early stages, but may lead to cancer.

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Malignant Transformation

Potential for metaplastic changes to lead to cancer if influencing factors persist.

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Gangrene

Tissue death due to lost blood supply; can be dry or wet.

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Dry Gangrene

Coagulative necrosis without infection; tissue appears dry and shriveled.

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Wet Gangrene

Coagulative necrosis combined with bacterial infection, leading to liquefactive necrosis.

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Fat Necrosis

Destruction of fat due to pancreatic enzymes, leading to chalky white areas (saponification).

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Apoptosis

Programmed cell death that is energy-dependent and does not cause inflammation.

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Apoptosis Morphology

Involves cell shrinkage, chromatin condensation, and formation of apoptotic bodies.

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Cell Shrinkage

A stage in apoptosis where the cytoplasm becomes dense and organelles are tightly packed.

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Phagocytosis in Apoptosis

Process where neighboring cells engulf and degrade apoptotic bodies, promoting tissue repair.

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Induction of Apoptosis

Can be triggered by physiological or pathological stimuli.

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Induction of Necrosis

Always caused by pathological conditions or injuries.

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Cell Membrane Integrity in Apoptosis

Remains intact during apoptosis.

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Cell Membrane Integrity in Necrosis

Lost; cell contents leak out causing damage.

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Inflammatory Response in Necrosis

Typically results in an inflammatory response; leads to repair processes.

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Outcome of Apoptosis

Dead cells are ingested by neighboring cells, aiding in tissue homeostasis.

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Study Notes

FM2004 & PM2004 Cell Injury and Death

  • Course is taught by Dr Collette Hand in UCC's Department of Pathology
  • The course dates are January 2025
  • Access course materials online via Canvas

Canvas Information

  • Course information, welcome details and module overview available
  • Modules' descriptions
  • Recommended textbooks
  • Reading lists
  • Module timetables for FM2004 (Dental and Medical) and PM2004
  • Module assessments

Weekly Content Module

  • Cellular Pathology lectures begin in Week 24, Monday, January 13, 2025
  • Self-Assessment Multiple Choice Questions (MCQs) will be available
  • Discussion board for questions/queries on Cellular Pathology

Module Timetables

  • Lectures are consolidated for all programs
  • Practical and Clinicopathological case sessions (CPCs) are scheduled for weeks 27-35
  • FM2004 for medical students: Monday afternoons and Friday mornings
  • FM2004 for dental students: Tuesday afternoons
  • PM2004 for medical students: Wednesday afternoons
  • Other program schedules vary; check relevant timetable for details

Module Assessment

  • CA1: 25 marks
  • CA2: 25 marks
  • Summer exam: 150 marks
  • Total: 200 marks
  • Assessment dates for the EMQ/MCQs.
  • FM2004 pass mark: 100/200 (50%) oral exam in summer
  • PM2004 pass mark: 80/200 (40%)
  • No oral exam for PM2004
  • Students do not need to pass each assessment independently

UCC Pathology Undergraduate Medal

  • Awarded annually to the student with the highest aggregate result in the first sitting of Pathology examinations (FM2004 and FM3005/ PM3009)
  • Two medals are presented annually; one for medical students and one for dental students

Textbooks

  • Recommended textbooks include: Robbins & Cotran Pathologic Basis of Disease, Underwood's General & Systemic Pathology, Kumar, Abbas, Aster's Robbins Basic Pathology, Robbins & Cotran Atlas of Pathology, Young, Stewart, O'Dowd's Wheater's Basic Pathology

A Word About Information

  • Half of the population seeks health information online
  • The challenge is deciding between reliable and unregulated health information

Introduction to Pathology

  • Pathology is the study of suffering.
  • It involves investigating the causes of diseases and the changes it makes at the level of cells, tissues, and organs, along with patient signs/symptoms.
  • Pathology's areas of investigation include: aetiology, pathogenesis, morphology, evolution and diagnosis, complication prognosis, management

Cell Responses to Stress/Injury 1

  • Cells undergo adaptation, and injury.
  • Cells can adapt to stimuli; if the cell is unable to adapt injury occurs
  • Reversible injury leads to possible cell death

Cell Injury Causes

  • Causes of cell injury include: oxygen deprivation (hypoxia, ischaemia), physical factors (trauma, temperature, radiation), toxins, infectious agents, immune reactions, genetic abnormalities, nutritional imbalances, and aging

Factors Affecting Cell Damage

  • Factors affecting cell damage include duration of the injury, nature of the harmful agent, proportion and type of cells involved, and the tissue's ability to regenerate

Regeneration

  • Adult cells are categorized into three groups by proliferative potential.
  • Labile cells divide continuously (ex. surface epithelium, lining mucosa, blood-forming tissues)
  • Stable cells can divide when needed (ex. liver, kidney),
  • Permanent cells do not divide past a critical period of development (ex. neuron, cardiac muscle)

Adaptive Responses

  • Hyperplasia is an increase in the number of cells
  • Hypertrophy is an increase in cell size
  • Atrophy is a decrease in cell size
  • Metaplasia is a transformation of one cell type to another
  • Dysplasia is an abnormal growth and maturation of cells.

Hyperplasia & Hypertrophy

  • Hyperplasia increases cell number, while hypertrophy increases cell size
  • Combined hyperplasia and hypertrophy cause enlargement in organs and tissues.
  • Understand that different cells exhibit varying responsiveness in the context of hyperplasia and hypertrophy

Hyperplasia

  • Causes enlargement of organs/tissues by increasing the number of cells.
  • Can be due to hormonal stimuli (e.g., breast development during puberty) or compensatory growth after tissue damage (e.g., liver regeneration).
  • Physiologic hyperplasia involves adaptive responses or growth factors, and pathologic hyperplasia is uncontrolled growth.

Hypertrophy

  • Organ/tissue enlargement because of increased cell size
  • It is not an increase in cell numbers but rather cell growth in size.
  • Common examples are skeletal muscle hypertrophy in athletes and myocardial hypertrophy.
  • Differentiate between physiological and pathological situations that induce size alterations

Physiological Hypertrophy

  • An example is the increased size of the uterus during pregnancy. (R9, Fig 2.3; R10, Fig 2.25; RBP9, Fig 1.3; RBP10, Fig 2.20)

Atrophy

  • Shrinkage or reduction in size of cells/tissue
  • Can be pathological (impaired blood supply in the brain, tissue damage) or physiological (skeletal muscle atrophy after bed rest)
  • Understand loss of cell substance (e.g., skeletal muscle after bed rest).

Metaplasia

  • Reversible change in the type of cells in a tissue
  • The change in cell type is usually a response to environmental stimuli or damage (e.g., smoking affecting the respiratory tract)

Dysplasia

  • Abnormal cellular growth and maturation.
  • Cellular characteristics include disordered growth, abnormal cell shape, and increase in mitotic figures.
  • Often a pre-cancerous condition in tissues like the cervix and skin

Dysplasia in Cervix and Skin

  • The cervix's epithelium transforms from normal stratified squamous to a dysplastic stratified squamous configuration (showing increased mitotic figures above the basal layer, with large nuclei and cells). (W5, Fig 7-1)
  • Normal skin's stratified squamous epithelium may show dysplasia (exhibiting cells that look abnormal, multinucleate cells that extend up strata, more mitotic figures above the basal layer, the presence of a layer of keratin clinically apparent as a scaling effect

Cell Response to Stress/Injury 2

  • Cells unable to adapt to stress/injury leads to injury
  • Injury can be reversible or irreversible, depending on the nature of the injury and the cell's characteristics

Reversible Cell Injury

  • Characterized by cell swelling due to disruption of energy-dependent pumps in the plasma membrane, resulting in loss of ionic and fluid homeostasis
  • Fatty changes occur due to hypoxic or toxic injury, visible as lipid vacuoles within the cytoplasm

Intracellular Deposits & Calcifications

  • Abnormal deposits of substances in cells/tissues occur due to issues in catabolism, excessive intake/production, or defective transport
  • Examples include lipids (fatty changes, cholesterol deposition), pigments (carbon, iron), and pathological calcifications (dystrophic, metastatic)

Cell Injury

  • The cellular response to injury depends on the type, duration, and severity of the injury.
  • The consequences of cell injury differ depending on the injured cell's characteristics, state, and ability to adapt.
  • Cell injury arises from functional and biochemical abnormalities in cellular components

Mechanisms of Cell Injury

  • Injury mechanisms include mitochondrial damage, entry of calcium ions, reactive oxygen species (ROS), membrane damage, and protein misfolding/DNA damage
  • These cause multiple downstream effects

Cell Death

  • Cell death can be either necrosis or apoptosis.
  • Necrosis is the result of irreversible cell injury caused by damage, and involves damage to the structure of the cell (ex. loss of membrane integrity), leakage, and inflammation.
  • Apoptosis is a programmed, energy-dependent process of cellular self-destruction vital for development and homeostasis. (R9, Fig 1.1;R10, Fig 2.2; R9/R10, Fig 2.1)

Necrosis

  • Is a natural process of cellular death in response to injury.
  • Characterized by the following:
    • Cellular degradation,
    • enzymatic action from cells,
    • or inflammation processes,
    • loss of membrane integrity,
    • inflammation,
    • and the influence on neighboring cells.

Necrosis Morphology

  • Necrotic cells typically appear pink and larger than normal cells
  • Nuclear changes (pyknosis, karyolysis, karyorrhexis) occur due to DNA breakdown.

Types of Necrosis

  • Five main types of necrosis:
    • Coagulative: most common, preserving tissue architecture
    • Liquefactive: digestion by enzymes, often seen in bacterial/fungal infections or CNS hypoxic injury
    • Caseous: characteristic of tuberculosis, with a cheese-like appearance
    • Gangrene: necrosis with putrefaction; can be dry (coagulative) or wet (liquefactive with infection)
    • Fat necrosis: lipid breakdown from damage, often found in acute pancreatitis

Apoptosis

  • Is a programmed cell death mechanism.
  • Characterized by: energy dependence, maintained membrane integrity, regulated processes of degradation, and the absence of an inflammatory response.
  • Also characterized by cell shrinkage and the formation of apoptotic bodies. (R9, Fig 2.5; RBP9, Fig 1.6; RBP10, Fig 2.3, Fig 2.11)

Apoptosis Figures

  • In the early stages, cells show condensation of their chromatin, while later stages show cell shrinkage and membrane blebbing

Apoptosis vs Necrosis

  • Critical differences distinguish the two processes (U6/U7 Table 4.1)

Injury to Cardiac Cells

  • The relation between normal cells to adaptable cells to reversibly/irreversibly injured myocytes to dead myocytes (RBP9, Fig 1.2; RBP10, Fig 2.21; R9, Fig 2.2)

Review

  • Covers: adaptive responses (hyperplasia, hypertrophy, atrophy, metaplasia, dysplasia), apoptosis (characteristics), necrosis (characteristics, types

Learning Outcomes

  • Students will be able to identify cells and molecules involved in pathological processes, outline cellular responses to injuries, define cellular adaptations, compare/contrast apoptosis and necrosis, and differentiate the various types of necrosis.

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FM2004 Cell Injury & Death Past Paper PDF

Description

Key information about FM2004 and PM2004 courses. It covers topics like timetables, session types, assessment criteria, and the MMID acronym. Furthermore, it details requirements for the UCC Pathology Undergraduate Medal.

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