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Questions and Answers
Which of the following is NOT involved in the process of protein degradation within a cell?
Which of the following is NOT involved in the process of protein degradation within a cell?
What is the primary function of mitochondria in a cell?
What is the primary function of mitochondria in a cell?
Which cellular component is responsible for modifying proteins for transportation?
Which cellular component is responsible for modifying proteins for transportation?
What is the key difference between rough endoplasmic reticulum (RER) and smooth endoplasmic reticulum (SER)?
What is the key difference between rough endoplasmic reticulum (RER) and smooth endoplasmic reticulum (SER)?
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Which of the following is NOT a function of the cytoskeleton?
Which of the following is NOT a function of the cytoskeleton?
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What is the role of lysosomes in cellular function?
What is the role of lysosomes in cellular function?
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Which of these cellular components is directly involved in apoptosis?
Which of these cellular components is directly involved in apoptosis?
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What is the main function of the plasma membrane in a cell?
What is the main function of the plasma membrane in a cell?
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Which of the following statements accurately describes the difference between neutrophils and macrophages in terms of their response to inflammation?
Which of the following statements accurately describes the difference between neutrophils and macrophages in terms of their response to inflammation?
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How does the prolonged inflammatory response mediated by macrophages contribute to chronic inflammation?
How does the prolonged inflammatory response mediated by macrophages contribute to chronic inflammation?
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What is a potential negative consequence of the potent activity of leukocytes, particularly neutrophils, during an acute inflammatory response?
What is a potential negative consequence of the potent activity of leukocytes, particularly neutrophils, during an acute inflammatory response?
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In the context of tuberculosis (TB) and hepatitis, how can prolonged host response lead to more damage than the causative microbe?
In the context of tuberculosis (TB) and hepatitis, how can prolonged host response lead to more damage than the causative microbe?
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What is one mechanism by which the physiological role of leukocytes in eliminating microbes can have pathological consequences for normal tissues?
What is one mechanism by which the physiological role of leukocytes in eliminating microbes can have pathological consequences for normal tissues?
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What is the role of selectins and integrins in the inflammatory process?
What is the role of selectins and integrins in the inflammatory process?
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What distinguishes the migration process of leukocytes in inflammation from their typical movement in the bloodstream?
What distinguishes the migration process of leukocytes in inflammation from their typical movement in the bloodstream?
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Which molecule is responsible for recruiting leukocytes to the site of inflammation through chemotaxis?
Which molecule is responsible for recruiting leukocytes to the site of inflammation through chemotaxis?
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What is the main function of leukocytes recruited to the site of inflammation?
What is the main function of leukocytes recruited to the site of inflammation?
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Which of the following is NOT a mechanism involved in the recruitment of leukocytes during inflammation?
Which of the following is NOT a mechanism involved in the recruitment of leukocytes during inflammation?
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The stage of inflammation that involves the recruitment of leukocytes and plasma proteins is known as:
The stage of inflammation that involves the recruitment of leukocytes and plasma proteins is known as:
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What are the two main types of molecules that contribute to the adherence and margination of leukocytes during inflammation?
What are the two main types of molecules that contribute to the adherence and margination of leukocytes during inflammation?
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What is the role of chemoattractants in the inflammatory process?
What is the role of chemoattractants in the inflammatory process?
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What are the two main categories of mediators involved in inflammation?
What are the two main categories of mediators involved in inflammation?
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What is a key characteristic of chronic inflammation?
What is a key characteristic of chronic inflammation?
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Which of the following is NOT a characteristic of acute inflammation?
Which of the following is NOT a characteristic of acute inflammation?
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Which specific chemical mediator is released by mast cells in response to physical injury, causing vasodilation and increased vascular permeability?
Which specific chemical mediator is released by mast cells in response to physical injury, causing vasodilation and increased vascular permeability?
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What is the main function of histamine in the inflammatory response?
What is the main function of histamine in the inflammatory response?
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Which group of mediators is involved in vascular and smooth muscle reactions, as well as leukocyte recruitment, during inflammation?
Which group of mediators is involved in vascular and smooth muscle reactions, as well as leukocyte recruitment, during inflammation?
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Which two cytokines are particularly key in the systemic response to inflammation?
Which two cytokines are particularly key in the systemic response to inflammation?
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What is the role of macrophages in inflammation?
What is the role of macrophages in inflammation?
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What is the primary outcome of acute inflammation when the offending agent is successfully destroyed?
What is the primary outcome of acute inflammation when the offending agent is successfully destroyed?
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Which of the following is NOT a step of inflammation as described by the 'R's' mnemonic?
Which of the following is NOT a step of inflammation as described by the 'R's' mnemonic?
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What is the primary role of complement proteins in inflammation?
What is the primary role of complement proteins in inflammation?
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Which of the following is a possible outcome of chronic inflammation?
Which of the following is a possible outcome of chronic inflammation?
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How do prostaglandins contribute to the inflammatory response?
How do prostaglandins contribute to the inflammatory response?
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What is the main distinction between COX-1 and COX-2 in relation to inflammation?
What is the main distinction between COX-1 and COX-2 in relation to inflammation?
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What are the two major side effects associated with the use of prostaglandins in clinical settings?
What are the two major side effects associated with the use of prostaglandins in clinical settings?
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What is the primary mechanism by which Tylenol affects fever?
What is the primary mechanism by which Tylenol affects fever?
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Which of the following cellular processes is NOT directly involved in tissue repair by scar formation?
Which of the following cellular processes is NOT directly involved in tissue repair by scar formation?
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Which of the following contributes to the development of chills during inflammation?
Which of the following contributes to the development of chills during inflammation?
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Which of the following is NOT a characteristic of leukopenia?
Which of the following is NOT a characteristic of leukopenia?
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Which of the following conditions is characterized by an increase in the number of eosinophils?
Which of the following conditions is characterized by an increase in the number of eosinophils?
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Which of the following is a key difference between regeneration and scar formation in tissue repair?
Which of the following is a key difference between regeneration and scar formation in tissue repair?
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What is the primary function of NSAIDs in fever management?
What is the primary function of NSAIDs in fever management?
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Which of the following is a characteristic of the 'left shift' in a blood test?
Which of the following is a characteristic of the 'left shift' in a blood test?
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What is the primary way that a cell presenting a 'death receptor' initiates the process of apoptosis?
What is the primary way that a cell presenting a 'death receptor' initiates the process of apoptosis?
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Which of the following scenarios is an example of the intrinsic pathway of apoptosis?
Which of the following scenarios is an example of the intrinsic pathway of apoptosis?
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What is the role of BCL2 in the intrinsic apoptosis pathway?
What is the role of BCL2 in the intrinsic apoptosis pathway?
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Which of the following describes the role of caspases in apoptosis?
Which of the following describes the role of caspases in apoptosis?
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Which of the following is a characteristic of the inflammatory response?
Which of the following is a characteristic of the inflammatory response?
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Which of the following are considered cardinal signs of inflammation?
Which of the following are considered cardinal signs of inflammation?
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What is the main role of antigen-presenting cells in the immune system?
What is the main role of antigen-presenting cells in the immune system?
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Flashcards
Cell Components
Cell Components
Essential parts of a cell, each with distinct functions like energy production and protein synthesis.
Mitochondria
Mitochondria
Organelles responsible for energy production and initiating apoptosis through oxidative phosphorylation.
Ribosomes
Ribosomes
Cellular structures that synthesize proteins by translating mRNA.
Lysosomes
Lysosomes
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Apoptosis
Apoptosis
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Stem Cells
Stem Cells
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Necrosis
Necrosis
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Inflammation
Inflammation
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Phagocytosis
Phagocytosis
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Neutrophils
Neutrophils
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Macrophages
Macrophages
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Collateral damage in inflammation
Collateral damage in inflammation
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Impact of leukocytes on chronic diseases
Impact of leukocytes on chronic diseases
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Extrinsic Pathway
Extrinsic Pathway
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Intrinsic Pathway
Intrinsic Pathway
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Caspase Cascade
Caspase Cascade
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Inflammation Causes
Inflammation Causes
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Fluid Accumulation in Inflammation
Fluid Accumulation in Inflammation
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Cell and Protein Mediated Damage
Cell and Protein Mediated Damage
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Signs of Inflammation
Signs of Inflammation
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Cell Necrosis
Cell Necrosis
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Lymphangitis
Lymphangitis
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Inflammation Stages
Inflammation Stages
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Vascular Response
Vascular Response
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Leukocyte Adhesion
Leukocyte Adhesion
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Diapedesis
Diapedesis
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Chemotaxis
Chemotaxis
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Leukocyte Functions
Leukocyte Functions
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Acute Inflammation
Acute Inflammation
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Chronic Inflammation
Chronic Inflammation
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Resolution of Inflammation
Resolution of Inflammation
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Fibrosis
Fibrosis
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Mediators of Inflammation
Mediators of Inflammation
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Cytokines
Cytokines
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Prostaglandins
Prostaglandins
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Leukotrienes
Leukotrienes
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Histamine
Histamine
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Tumor Necrosis Factor
Tumor Necrosis Factor
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Complement Proteins
Complement Proteins
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Leukemia Indicators
Leukemia Indicators
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Lymphocytosis
Lymphocytosis
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Eosinophilia
Eosinophilia
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Leukopenia Causes
Leukopenia Causes
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Effects of Inflammation
Effects of Inflammation
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Tissue Repair Mechanisms
Tissue Repair Mechanisms
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Cytokines in Liver Repair
Cytokines in Liver Repair
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Study Notes
Pathogen 3.1: Cells and Inflammation
- Objectives:
- Analyze the fundamental components of a typical cell and their functions.
- Analyze how the functions of cells are coordinated and integrated.
- Interpret the roles of growth factors in cellular activity.
- Illustrate the characteristics of stem cells and their involvement in regenerative medicine.
- Demonstrate reversible and irreversible cellular injury, encompassing cytoplasmic and nuclear changes.
- Analyze the key causes of cellular injury.
- Differentiate between various types of cellular adaptations.
- Distinguish between metaplasia and dysplasia.
- Examine the process of cellular aging.
- Compare and contrast necrosis and apoptosis, two forms of cell death.
- Compare different forms of necrosis, providing examples for each.
- Analyze the cellular and events of inflammation.
- Distinguish the distinct vascular changes in acute inflammation.
- Debate the terms associated with leukocytes' participation in inflammation (margination, diapedesis, emigration, exudation, chemotaxis, phagocytosis, and microbicidal substances).
- Analyze the functions of complement system proteins, cytokines, and the clotting system in inflammation.
- Compare and contrast the potential outcomes of acute and chronic inflammation.
- Describe granuloma formation and its characteristics.
- Analyze various pathological terms related to inflammation (serous, fibrinous, purulent, abscess, ulcer, wound, scar, and keloid).
- Debate the typical localized and systemic symptoms of inflammation.
- Analyze the pathogenesis of fever.
The Cell as a Unit of Health and Disease
- Key concepts:
- Cells are the fundamental units of health and disease.
- Understanding cell structure and function is crucial for comprehending health and disease processes.
Essential Components of Animal Cells
- Nucleus: DNA storage, transcription, and mRNA processing
- Ribosomes: protein synthesis
- Mitochondria: energy production; apoptosis
- Endoplasmic reticulum (ER):
- Rough ER: protein folding and processing
- Smooth ER: lipid synthesis and calcium storage
- Golgi apparatus: protein modification and sorting
- Lysosomes: intracellular digestion
- Peroxisomes: oxidation and detoxification
- Cytoskeleton: cell shape and structure
- Plasma membrane: regulated transport of molecules
Lysosomes/Proteasomes
- Lysosomes: contain enzymes that break down various macromolecules.
- Formed via pinocytosis, receptor-mediated endocytosis, and autophagy.
- Proteasomes: degrade misfolded or denatured proteins.
Plasma Membrane
- Permeable to very small particles (water, oxygen, carbon dioxide, etc) and non-polar molecules.
- Impermeable to polar molecules and ions.
- Methods for transport across the membrane:
- Passive transport: diffusion through channels or carriers
- Active transport: pumps using ATP
- Endocytosis: engulfing large molecules or particles
- Exocytosis: releasing molecules from the cell
- Receptor-mediated endocytosis: targeted uptake of specific molecules
ER/Golgi
- Rough ER modifies and folds proteins.
- Smooth ER synthesizes lipids, metabolizes certain molecules, and stores calcium.
- Golgi apparatus processes and packages proteins for transport.
Mitochondria
- Role in cellular respiration and energy production (oxidative phosphorylation).
- Critical role in apoptosis (programmed cell death).
Receptors
- Extracellular and intracellular receptors.
- Ligands bind to receptors, initiating intracellular responses.
- Receptors can influence DNA transcription directly.
Kinase Activity
- Kinases are molecules which phosphorylate other molecules to initiate cellular activity.
- Receptor tyrosine kinases (RTKs) involved in signalling pathways (insulin, epidermal growth factor).
A few Receptor Types
- G-Protein coupled receptors (GPCRs): bind to signaling molecules
- Steroid receptors: enter into the cell to initiate changes and regulate genes
Transcription Factors
- Transcription factors bind to specific DNA sequences.
- They control gene expression and regulate cellular processes.
- Can bind to promoter region or enhancers.
Growth Factors
- Promote cell entry into cell cycle, replication, and biosynthesis of cellular components (nucleic acids, proteins, lipids, carbohydrates).
- Necessary to create daughter cells, and to prevent apoptosis.
Stem Cells
- Totipotent stem cells give rise to all types of cells in the body.
- Adult stem cells have a limited capacity; able to replace damaged cells of the same type.
- The use of stem cells in regenerative medicine is still evolving.
Cell Injury
- Causes of cellular injury:
- Hypoxia/ischemia
- Infectious agents (bacteria, virus, fungi)
- Toxins
- Autoimmune diseases
- Genetic abnormalities
- Immunologic reactions
- Physical agents
- Nutritional imbalances
Toxic Cell Injury
- Direct-acting toxins bind to essential cellular components, disrupting normal function.
- Some toxins are latent, becoming reactive metabolites.
- Reactive oxygen species (ROS) are highly reactive chemicals that cause damage.
Reversible Cell Injury
- Signs of reversible cell injury:
- Increased intracellular swelling Mitochondrial and ER swelling Plasma membrane blebbing Clumping of chromatin in the nucleus
Irreversible Cell Injury
- Symptoms of irreversible injury include:
- Inability to restore mitochondrial function Loss of structure and function of the plasma membrane. Loss of DNA and chromatin integrity
Apoptosis vs. Necrosis
- Necrosis: uncontrolled cell death causing inflammation, and is generally caused by extracellular stimuli
- Apoptosis: regulated process of cell death without inflammations; is intracellularly mediated; often from intracellular stimuli
Adapting to Cellular Injury
- Types of adaptation: hypertrophy, hyperplasia, atrophy, and metaplasia
Hypertrophy
- Increased cell size; usually in response to increased workload; it is available in many cell types.
- Can be pathologic, as in heart muscle
Hyperplasia
- Increased cell number; usually in physiologic situations.
- Can be pathologic, leading to various diseases including cancer.
Atrophy
- Decreased cell size; often due to decreased workload, blood supply, or loss of stimulation.
- Can be caused by changes in nutrition.
Metaplasia
- Change in cell type; a reversible adaptation to stress, possibly in response to ongoing injury
- Can be a precursor to cancerous changes.
Metaplasia vs. Dysplasia
- Dysplasia refers to abnormal cell proliferation, development and maturation.
- Dysplasia isn't always an indicator of cancer; however it is a risk factor for developing cancer.
Necrosis
- Coagulative, liquefactive, caseous, and fat necrosis each have distinct characteristics, cellular appearances, and origins.
- Coagulative is frequently seen in organs like the heart.
- Liquefactive necrosis is characteristic of the brain, as it is highly metabolic and actively functioning.
- Caseous necrosis is commonly observed in TB, and occurs when walled off by macrophages.
- Fat necrosis involves the breakdown of triglycerides in the pancreas.
- Fibrinoid necrosis results from immune complex deposits in blood vessels
Key signs of Necrosis
- Increased eosinophilia
- Nuclear changes (pyknosis, karyorrhexis, karyolysis)
Fate of Cells in Coagulative Necrosis
- Cells don't completely autodigest.
- Leukocytes are recruited and digest debris.
- Can result in dry gangrene.
Fate of Liquefactive Necrosis
- Cells are completely digested, leading to a liquid solution.
- Inflammation frequently ensues.
- "Wet gangrene" is a possibility.
Fate of Caseous Necrosis
- Tissue architecture is disrupted.
- Macrophages and other inflammatory cells are commonly observed
- Lesions are commonly seen in clusters, or nodules.
Fate of Fat Necrosis
- Enzymes and fatty acids are involved.
- Calcium may bind resulting in soap formation.
Fate of Fibrinoid Necrosis
- Hypersensitivity reactions are involved
- Complex deposits are seen in blood vessels
- RBCs are often affected.
Biomarkers in Necrosis
- Intracellular proteins released due to cell lysis are found in specific bodily fluid tests, used to locate the source of damage.
Apoptosis
- Programmed cell death; a regulated and controlled cell dismantling process.
- Intracellular contents aren't released; so inflammation doesn't occur.
- It is used in development and in purging self-reactive cells of the immune system.
Apoptosis: 2 Categories
- Physiological apoptosis is necessary for embryonic development and immune system regulation.
- Pathological apoptosis occurs in response to severe or irreversible damage.
Apoptosis: 2 Pathways
- Intrinsic pathway - activated by the intracellular, internal cellular conditions, and results from damaged mitochondria
- Extrinsic pathway - activated by extracellular signals and triggers the activation of death-receptor pathway.
Intrinsic Pathway
- The intrinsic pathway is triggered mainly from intracellular damage or stress.
- The cell must activate its pathway to trigger programmed cell death.
- It is a crucial process that enables proper maturation.
- P53 protein (a tumor suppressor) plays a vital role, regulating DNA damage and cellular responses.
Extrinsic Pathway
- The extrinsic pathway is triggered by stimuli from outside the damaged cell and results in the activation of death-receptor pathways.
- The cell is induced to self-destruct.
- Primarily, self-reactive cells are killed in the thymus.
Inflammation: Recognition
- Microbes and necrotic cells activate immune responses.
- Internal cellular sensors (DAMPs) signal cellular distress.
- Circulating proteins (e.g., complement) can trigger inflammation.
Inflammation: Stages
- Recognition of threat
- Response of vascular tissues to insult.
- Recruitment of leukocytes and plasma proteins.
- Destruction of offending substance.
- Termination of sequence.
- Tissue repair.
Phagocytes, dendritic cells
- These specialized cells are capable of capturing foreign invaders and sensing the presence of an invading microorganism.
- Trigger protein secretions like inflammation cytokines, anti-viral cytokines (interferons), and other cytokines and membrane proteins that activate lymphocytes to initiate inflammation
Internal Cellular Sensors
- Intracellular damage triggers a signal cascade.
- Excessive uric acid, deficient ATP, and reduced K+ levels within a cell indicate intracellular damage.
- These substances (DAMPs) are released to activate the inflammatory response.
- The inflammasome, a protein cascade, is activated to regulate the inflammatory response to the damage.
Complement System
- Complement proteins operate with the immune system and contribute to the inflammatory process.
- These proteins are produced in the liver, and circulate freely in the bloodstream.
- They recognize microbes and mark them for destruction by phagocytes.
- They directly kill microbes by forming membrane attack complexes (MACs), which cause cell lysis.
Mediators: Others
- Platelet-activating factor (PAF) participates in platelet aggregation and inflammation.
- Kinins (like bradykinin) increase vascular permeability and induce pain.
Mediators: Suppressing Inflammation
- Lipoxins: suppress inflammation by deterrents of protein release and leukocyte recruitment
- NSAIDs (non-steroidal anti-inflammatory drugs)
- COX-2 inhibitors (e.g. some NSAIDS): particularly important for pain and fever reduction.
Mediators: Recap
- Many mediators with distinctive characteristics act upon vascular systems and cellular systems
- Including histamine, prostaglandins, leukotrienes, cytokines, chemokines and complement proteins, each with individual contributions to the inflammatory process
Morphologic Patterns of Acute Inflammation
- Serous inflammation involves the exudation of fluid that is low in cell content.
- Fibrinous inflammation involves excessive fibrinogen.
- Purulent inflammation features a large number of neutrophils and a pus-like exudate.
Ulcers
- Ulcers are local defects in tissue surfaces resulting from inflamed and necrotic tissue sloughing.
Granulomatous Inflammation
- Characterized by the accumulation of macrophages, often with T lymphocytes.
- Granulomatous inflammation is a specific type of chronic inflammation often encountered when the initial stimuli causing inflammation cannot be resolved.
Systemic Inflammation
- Fever, elevated body temperatures.
- Elevated blood counts; with immature neutrophils.
- Other effects include: chills, anorexia, somnolence, and malaise
- Septic shock: a life-threatening systemic inflammatory response caused by massive bacterial infections, which can lead to cardiovascular collapse, multiple organ failures or death.
Fever Pathogenesis
- Cytokines (like TNF and IL-1) from inflammatory responses stimulate the hypothalamus to increase body set point and temperature.
- Non-steroidal anti-inflammatory medications inhibit prostaglandins to reduce fever reaction.
- Mechanisms regulating and maintaining temperature response is still not fully elucidated
Tissue Repair
- Regeneration (re-growth of new tissue) vs. Scar tissue regeneration (a less functional substitute of the original tissue).
- Factors that inhibit tissue repair: infection, diabetes, reduced nutrition, use of glucocorticoids, poor tissue blood supply, and the degree of tissue injury.
Cutaneous Wound Healing
- Inflammation, granulation tissue formation, and ECM remodeling are phases.
- Excessive ECM production can cause keloids.
Cellular Aging
- Accumulations of errors in DNA (ROS, mutations).
- Decreased cellular replication
- Limited capacity for replication.
Intracellular Accumulations
- Steatosis (fatty change) is the accumulation of triglycerides.
- Cholesterol accumulation can be observed in atherosclerosis.
- Excess glycogen storage is seen in some metabolic disorders.
- Other substances like pigments will accumulate in the affected tissue(s).
Fatty Liver Changes
- Steatosis: Accumulation of triglycerides in liver cells.
- Causes: Alcohol abuse, diabetes, obesity, and NASH (non-alcoholic steatohepatitis).
Atherosclerosis
- Cholesterol accumulation in arterial walls.
Exogenous Carbon
- Anthracosis (coal dust in the lungs, commonly seen in coal miners lungs).
Lipofuscin
- Wear and tear of cells; yellow-brown pigment.
- Accumulation of free-radicals peroxidation of lipids in damaged tissues, and the by-products of oxidation accumulate lipids inside cells.
Calcification
- Mineralization in tissues.
- Seen in aortic valve.
Conclusion:
- Comprehensive understanding of cells, inflammation, and related processes is crucial for comprehending health and disease.
- Various mechanisms and factors influence these processes.
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Test your knowledge of key concepts in cell biology with this quiz focused on cellular components and their functions. Explore the roles of mitochondria, lysosomes, and the cytoskeleton, along with the differences between various types of cells. Perfect for students studying cell biology.