Cell Biology Quiz: Organelles and Injuries
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Questions and Answers

Which organelle plays a crucial role in the production of lipids?

  • Golgi Apparatus
  • Rough Endoplasmic Reticulum
  • Mitochondria
  • Smooth Endoplasmic Reticulum (correct)

    • What is the primary function of lysosomes?

  • Degradation of macromolecules (correct)
  • Modification of proteins for transport
  • Protein synthesis
  • Energy production

    • Which of the following is a type of cell injury caused by toxins?

  • Direct-acting toxins
  • Latent toxins
  • Reactive Oxygen Species (ROS)
  • All of the above (correct)

    • Which of the following is NOT a function of the cytoskeleton?

    <p>DNA replication (B)</p> Signup and view all the answers

    What is a key characteristic of reversible cell injury?

    <p>Intracellular swelling (A)</p> Signup and view all the answers

    Which of the following is NOT an irreversible sign of cell injury?

    <p>Intracellular swelling (D)</p> Signup and view all the answers

    What is the role of the plasma membrane in cell function?

    <p>Regulated movement of solutes (A)</p> Signup and view all the answers

    Which cellular component is directly involved in the process of oxidative phosphorylation?

    <p>Mitochondria (A)</p> Signup and view all the answers

    What is the main difference between apoptosis and necrosis?

    <p>Apoptosis is programmed and controlled, while necrosis is unprogrammed and violent (B)</p> Signup and view all the answers

    Which cellular adaptation involves an increase in cell size?

    <p>Hypertrophy (B)</p> Signup and view all the answers

    Which of these organelles is NOT involved in the process of protein synthesis?

    <p>Mitochondria (A)</p> Signup and view all the answers

    Besides lysosomes, which other organelle is involved in protein degradation?

    <p>Proteasomes (B)</p> Signup and view all the answers

    Which of the following is an example of physiologic hyperplasia?

    <p>Growth of the uterus during pregnancy (D)</p> Signup and view all the answers

    Which cellular adaptation is characterized by a change in cell type?

    <p>Metaplasia (D)</p> Signup and view all the answers

    In which scenario would atrophy be most likely to occur?

    <p>A muscle that is not used for a long period of time (A)</p> Signup and view all the answers

    What does the term 'Left Shift' refer to in the context of blood cell analysis?

    <p>An increase in the number of immature neutrophils. (B)</p> Signup and view all the answers

    What is the primary cause of leukopenia?

    <p>Certain infections like typhoid fever, some viral infections, rickettsia, and certain protozoa. (C)</p> Signup and view all the answers

    Which of the following is NOT a characteristic of the inflammatory response?

    <p>Decreased body temperature. (B)</p> Signup and view all the answers

    What is the primary mechanism of action for NSAIDs in fever reduction?

    <p>Blocking the production of prostaglandins. (C)</p> Signup and view all the answers

    Which of the following is a key characteristic of the scar formation repair mechanism?

    <p>Deposition of connective tissue. (B)</p> Signup and view all the answers

    What is the role of macrophages in tissue repair?

    <p>They orchestrate the repair process by clearing debris and stimulating other cells. (C)</p> Signup and view all the answers

    What is the primary factor determining whether a tissue will regenerate or scar?

    <p>The proliferative potential of the tissue's cells. (C)</p> Signup and view all the answers

    Which of the following is NOT a factor that stimulates cell proliferation during tissue regeneration?

    <p>Decreased levels of oxygen. (C)</p> Signup and view all the answers

    Which of the following factors can directly impair tissue repair by interfering with the formation of granulation tissue?

    <p>Poor perfusion (D)</p> Signup and view all the answers

    Which of these is an example of an intrinsic factor that can impair tissue repair?

    <p>The type and extent of tissue injury (C)</p> Signup and view all the answers

    Which of these is a condition that can lead to excessive production of extracellular matrix (ECM), potentially resulting in the formation of keloids?

    <p>Chronic inflammatory diseases (C)</p> Signup and view all the answers

    Which of the following statements accurately describes the relationship between cellular aging and tissue repair?

    <p>Cellular aging impairs tissue repair due to decreased cellular replication. (D)</p> Signup and view all the answers

    Which of these pigments is an endogenous accumulation that can occur within cells?

    <p>Lipofuscin (B), Hemosiderin (C)</p> Signup and view all the answers

    Which of the following conditions is NOT directly linked to fatty liver changes?

    <p>Atherosclerosis (D)</p> Signup and view all the answers

    What is the primary mechanism responsible for the accumulation of lipofuscin within cells?

    <p>Free-radical peroxidation of membrane lipids (D)</p> Signup and view all the answers

    Which of the following is an example of a condition associated with exogenous carbon accumulation in the lungs?

    <p>Anthracosis (B)</p> Signup and view all the answers

    What primarily induces vasodilation in acute inflammation?

    <p>Histamine released by mast cells (C)</p> Signup and view all the answers

    What is one of the early manifestations of vasodilation during acute inflammation?

    <p>Erythema (D)</p> Signup and view all the answers

    What is the effect of endothelial cell retraction during an inflammatory response?

    <p>Opening of inter-endothelial spaces (D)</p> Signup and view all the answers

    What can result from endothelial injury during inflammation?

    <p>Cell necrosis and detachment (A)</p> Signup and view all the answers

    Which of the following best describes the term 'vascular leakage' in the context of inflammation?

    <p>Increased fluid and protein movement from vessels (D)</p> Signup and view all the answers

    What is the primary component involved in fat necrosis that results in saponification?

    <p>Triglycerides (A)</p> Signup and view all the answers

    Which type of necrosis is characterized by a 'moth eaten' appearance on microscopy?

    <p>Caseous necrosis (D)</p> Signup and view all the answers

    In which type of necrosis do dead cells leave behind a creamy yellow liquid?

    <p>Liquefactive necrosis (D)</p> Signup and view all the answers

    What key cellular changes are associated with necrosis?

    <p>Nuclear deformation (B)</p> Signup and view all the answers

    What is the main characteristic of fibroid necrosis observable under microscopy?

    <p>Bright pink amorphous appearance (D)</p> Signup and view all the answers

    Which type of necrosis is associated with the formation of granulomas?

    <p>Caseous necrosis (A)</p> Signup and view all the answers

    What distinguishes apoptosis from necrosis?

    <p>Apoptosis involves fragmentation without spilling cellular contents (C)</p> Signup and view all the answers

    Which biomarkers can indicate damage to cardiac muscle cells during necrosis?

    <p>Creatine kinase and troponin (A)</p> Signup and view all the answers

    Study Notes

    Pathogen 3.1: Cells and Inflammation

    • This unit examines cells and the inflammatory process.

    Objectives

    • Analyze the components of a typical cell and their function.
    • Analyze how cells coordinate and integrate their functions.
    • Interpret the role of growth factors in cellular activity.
    • Understand stem cells, and their roles in regenerative medicine.
    • Illustrate how cells are injured (reversible and irreversible), including changes in cytoplasm and nucleus.
    • Analyze common causes of cell injury.
    • Contrast four types of cellular adaptations.
    • Differentiate between metaplasia and dysplasia.
    • Discuss cellular aging.
    • Compare necrosis and apoptosis as cell death forms.
    • Compare different forms of necrosis and provide examples.
    • Analyze cellular and events of inflammation.
    • Define vascular changes in acute inflammation.
    • Debate the role of leukocytes in an inflammatory response, including margination, diapedesis, emigration, exudation, chemotaxis, phagocytosis, and microbicidal substances.
    • Analyze the complement system, cytokines, and clotting system in inflammation.
    • Compare and contrast acute and chronic inflammation.
    • Describe the formation of granulomas and analyze pathologic terms related to inflammation (serous, fibrinous, purulent, abscess, ulcer, wound, scar, keloid).
    • Investigate the typical local and systemic symptoms of inflammation.
    • Analyze the pathogenesis of fever.

    The Cell as a Unit of Health and Disease

    • Cells are the basic units of health and disease.

    Essential Components of Animal Cells

    • Nucleus: DNA storage, transcription, mRNA processing
    • Ribosomes: Translation
    • Mitochondria: Energy production, apoptosis
    • Endoplasmic Reticulum (ER): Rough - protein synthesis, Smooth - lipid synthesis, calcium storage
    • Golgi Apparatus: Modifies proteins for transport
    • Lysosomes: Digestive enzymes for macromolecules
    • Proteasomes: Degrade proteins
    • Cytoskeleton: Cell shape, polarity, organization
    • Plasma membrane: Regulated movement of solutes, cell-to-cell interaction

    Lysosomes/Proteasomes

    • Lysosomes contain hydrolases to break down substances.
    • Proteasomes dismantle denatured or misfolded proteins.
    • Lysosomes form in three ways - pinocytosis, receptor-mediated endocytosis, and autophagy.

    Plasma Membrane

    • Permeable: Very small particles, non-polar particles (water, O2, CO2, ethanol, steroids, vit D)
    • Impermeable: Polar particles, large particles (proteins, glucose, ions)
    • Ways to get through:
    • Passive transport (channels, carriers)
    • Receptor-mediated
    • Active transport (pumps - ATPase)
    • Endocytosis (caveolae, receptor-mediated, phagocytosis)
    • Exocytosis

    ER/Golgi

    • Rough ER synthesizes transmembrane proteins and lipids; chaperones ensure proper folding.
    • Smooth ER synthesizes steroids, catabolizes lipid-soluble molecules, and stores calcium.
    • Golgi apparatus packages proteins for organelles or plasma membrane; modifies N-linked oligosaccharides.

    Mitochondria

    • Oxidative phosphorylation
    • Cell death (apoptosis)

    Receptors

    • Extracellular and intracellular receptors
    • Ligands bind to receptors, initiating intracellular function or DNA interaction
    • Effects: transcription

    Kinase Activity

    • Kinase is a molecule that phosphorylates other molecules, initiating cellular activity
    • Receptor tyrosine kinases (RTKs)
    • G-protein coupled receptors
    • Steroids

    Transcription Factors

    • DNA-binding domains permit specific binding to short DNA sequences (promotor region or enhancers).
    • Some elements interact with genes.

    Growth Factors

    • Promote cell entry into the cell cycle and replication.
    • Enhance cellular component synthesis (nucleic acids, proteins, lipids, carbohydrates).
    • Prevent apoptosis.
    • Involved in regeneration and repair.

    Stem Cells

    • Totipotent stem cells give rise to all differentiated tissues.
    • Adult stem cells replace damaged cells of the same type.
    • Regenerative medicine uses stem cells to heal patients.

    Cell Injury

    • Underlying causes: Hypoxia/ischemia, infection, autoimmune diseases, toxins, immunologic reactions, physical agents, genetic abnormality, nutritional imbalance, aging
    • Reversible injury: Intracellular swelling, mitochondrial/ER disturbance, plasma membrane blebbing, chromatin clumping
    • Irreversible injury: mitochondrial failure, loss of membrane structure and function, DNA damage

    Toxic Cell Injury

    • Direct-acting toxins combine with cellular components, disrupting their function (mercury).
    • Latent toxins are converted into reactive metabolites that damage target cells.
    • Reactive Oxygen Species (ROS) are highly reactive and damage cellular components.

    Reversible Injury Signs

    • Intracellular swelling
    • Mitochondrial and ER disturbance
    • Plasma membrane blebbing
    • Clumping of chromatin in nucleus
    • Myelin figures (phospholipids of damaged membrane)

    Cell Injury: When Badness Happens

    • Normal cell (homeostasis) → Injurious stimulus → Reversible injury (if mild or transient) → Irreversible injury (severe, progressive) → Necrosis (or apoptosis)
    • Irreversible signs: Inability to restore mitochondrial function, Loss of plasma membrane structure or function, Loss of DNA structural integrity

    Apoptosis vs. Necrosis

    • Apoptosis: Controlled programmed cell death. Organized disassembly, membrane bound, no inflammation.
    • Necrosis: Unprogrammed violent, eventual lysis, swelling, inflammation, usually widespread.
    • Apoptosis vs. necrosis overview.

    Adapting to Cellular Injury

    • Types of Adaptation: Hypertrophy, hyperplasia, atrophy, metaplasia.

    Hypertrophy

    • Size of cells increases. (due to increased demands, in relation to muscle for example)
    • Pathological when concerning heart muscle

    Hyperplasia

    • Increased cell numbers. (physiological - puberty, pregnancy; pathological - if growth control is lost)
    • Hyperplasia alone does not cause cancer

    Atrophy

    • Decrease in cell size (due to loss of workload, loss of innervation, diminished blood supply, nutritional difficulties etc).
    • Aging is a factor.

    Metaplasia

    • Change in cell type. (smokers' bronchi, Barrett's esophagus)
    • Distinguish between metaplasia and dysplasia

    Metaplasia vs Dysplasia

    • Dysplasia is disorderly proliferation of cells
    • Polarity and uniformity are lost
    • Dysplasia does not indicate cancer, though it is on the pathway to becoming cancerous

    Types of Necrosis

    • Coagulative
    • Liquefactive
    • Caseous
    • Fat necrosi
    • Fibrinoid
    • Key features included: Increased eosinophilia.Nuclear changes (pyknosis, karyorrhexis, karyolysis)Fate of cells in types of necrosis: Coagulative, Liquefactive, Caseous, Fat, Fibrinoid.Biomarkers in necrosis: Identification of affected organs using biomarkers like creatine kinase, contractile protein troponin, alkaline phosphatase.

    Apoptosis

    • Controlled dismantling of the cell. "Edible" fragments break off.
    • This process occurs without inflammation because it's done in a controlled manner.
    • Types: Physiologic (embryonic development, immune system) and Pathologic (severe or irreversible damage, cancer emergence)
    • Pathways: Intrinsic (Mitochondrial) and Extrinsic (Death Receptor)

    Intrinsic Pathway

    • The intrinsic pathway is the most common cause of physiological and pathological apoptosis.
    • If the intrinsic pathway is not stopped, mitochondria release cytochrome C.
    • This initiates the formation of caspase cascades.
    • Key features like the role of BCL-2, BAD protein, and P53 are mentioned.

    Extrinsic Pathway

    • For apoptosis, the presence of antigens recognizes if a cell needs to be destroyed.
    • Two main types - TNF-alpha and Fas ligand.
    • These receptors initiate a caspase cascade.
    • This is mainly for self-reactive T cells (in the thymus)
    • Intrinsic/Extrinsic pathway

    Pathways leading to cell demise

    • Hypoxia, ischemia - Cellular injury -> Necrosis
    • Multiple injurious stimuli - cellular Damage to proteins, lipids, nucleic acids -> Apoptosis
    • Mutations, cell stress, infections - Accumulation of misfolded proteins - -> Apoptosis
    • Radiation, other insults - DNA damage -> Apoptosis
    • Infections, immunologic disorders, inflammation - Toxic molecules -> Necrosis/Apoptosis

    Causes of Inflammation

    • Infections, Bacteria, Viruses, Fungal, Parasitic, Microbial toxins, Tissue Necrosis, Foreign bodies, Immune reactions (hypersensitivity).

    Two Big Things Happen in inflammation

    • More fluid is sent to the area.
    • Cells in the body actively "go to war".

    External Manifestations of Inflammation

    • Rubor - redness, Calor - heat, Tumor - swelling, Dolor - Pain, loss of function

    Inflammation: Recognition

    • Microbes and necrotic cells are recognized by foreign invaders from outside of the cell
    • Internal stimuli within the cell, as cellular distress
    • Circulating proteins that indicate damage has occurred

    Inflammation: Stages

    • Recognition of threat
    • Vascular tissue response to insult
    • Leukocytes and plasma proteins recruitment
    • Destruction of offending substance
    • Termination of sequence.
    • Repair of injured tissue.

    Recognition: Foreign Invaders

    • Phagocytes (capture foreign invaders) & dendritic cells
    • Detection of infectious invaders, which then trigger secretion of specific proteins.
    • Cytokines for inflammation, anti-viral cytokines (interferons), cytokines & membrane proteins for lymphocyte activation.

    Recognition of Internal Cellular Damage

    • Signals inside the cytoplasm indicate issues like uric acid build-up, reduced ATP, reduced intracellular potassium and DNA in the cytoplasm.
    • DAMPs (Damage-associated molecular patterns) are activated.
    • Multiprotein cytosolic complex (inflammasome) recruits leukocytes, inducing inflammation

    Recognition of Circulating Proteins

    • Complement system reacts against microbes, produces inflammation mediators, destroys infectious organisms, activates further inflammatory cells, and opsonizes targeted agents.

    Inflammation: Vascular Changes

    • Two big steps: increased blood flow (vasodilation) and increased vessel permeability. Exudate (high protein, cellular debris) by contrast transudate (low content, less cells).

    Changes in Vessels: Vasodilation

    • Histamine is released from mast cells causing vasodilation and increased blood flow, one of the first signs of acute inflammation
    • Vasodilation leads to increased permeability and exudative fluid build-up.
    • Blood flow slows, and vessels become engorged.

    Changes in Vessels: Permeability

    • Histamine, Bradykinin, Leukotrienes cause endothelial cells to retract and open inter-endothelial spaces creating leakage.
    • endothelial injury occurs due to tissue damage - microbes, burns.
    • Continues until vessels are thrombosed or repaired.

    Lymph Involvement

    • Lymphatic vessels become involved, draining away extravascular fluid and its contents.
    • Lymphangitis and secondary inflammation can occur, which sometimes lead to lymph node enlargement (lymphadenopathy).

    Acute vs Chronic Inflammation

    • Acute: Minutes to days, exudation of fluid, plasma proteins, edema, neutrophils, and macrophages
    • Chronic: Longer duration, more tissue destruction, macrophages, blood vessel proliferation, fibrosis.

    Three outcomes of acute inflammation

    1. Complete resolution
    2. Healing by connective tissue replacement or scarring/fibrosis
    3. Chronic inflammation

    Chronic Inflammation

    • Prolonged, lasting weeks to months.
    • Inflammation, tissue injury and repair occur simultaneously and in varying combinations.

    Inflammation: Destruction, Termination and Repair

    • The body's inflammatory response may destroy the source of inflammation.
    • If the offending agent isn't destroyed, the inflammation becomes chronic.
    • Mechanisms for repair and tissue healing may then occur.

    Inflammation Recap

    • Inflammation is a favorable host response to foreign invaders.
    • Vascular reactions and cellular responses are key parts of this process.
    • The major steps include recognition, recruitment of leukocytes, and removal of the offending agent.
    • The outcome can be acute or chronic inflammation, depending on the body's ability to destroy the source of damage.

    Mediators of Inflammation

    • Multifunctional mediators.
      • Effects: Vasodilation, vasoconstriction, altered permeability, activation of inflammatory cells, chemotaxis, cytotoxicity, tissue degradation, pain, and fever.
    • Two types: Cellular and plasma-derived.
    • Major cells are macrophages, dendritic cells, and mast cells.
    • Plasma-derived mediators are compliment proteins

    Mediators: (Cell-derived)

    • Histamine and serotonin
    • Prostaglandins and leukotrienes
    • Cytokines (TNF, IL-1, IL-6)
    • Chemokines
    • Platelet-activating factor

    Mediators: (Plasma-derived)

    • Complement system
    • Kinins

    Mediators: Suppression

    • Lipoxins (suppress inflammation, and inhibit leukocyte recruitment)
    • Pharmacologic interventions
      • Cyclooxygenase inhibitors (COX inhibitors) NSAIDS (COX-2 of particular interest)
      • Lipoxygenase Inhibitors
      • Corticosteroids (reduce transcription of genes)
      • Leukotriene receptor antagonists

    Morphological Patterns of Acute Inflammation

    • Serous inflammation (cell-poor fluid)
    • Fibrinous inflammation (fibrinogen passes through vessels)
    • Purulent inflammation (exudate, pus)
    • Ulcers (defect in an organ or tissue surface)
    • Granulomatous inflammation (collections of activated macrophages (epithelioid cells & giant cells))

    Effects of Inflammation

    • Systemic effects like fever (high temperature (>38°C), sometimes <36°C), Elevated temperature, pyrogens (chemicals that trigger fever), leukocytosis, left shift (immature neutrophils).
    • Additional effects: chills, anorexia, somnolence, malaise, septic shock.

    Fever Pathogenesis

    • Treatment with NSAIDs (turn down prostaglandins), Tylenol (unknown mechanism but possibly targets prostaglandin production).

    Tissue Repair Mechanisms

    • Tissue repair involves either regeneration or scarring.
    • Different tissue exhibit different capacities to regenerate or heal.

    Tissue Repair Factors that Inhibit Repair

    • Infection,
    • diabetes
    • Nutritional status
    • Glucocorticoids
    • Mechanical factors
    • Poor perfusion
    • Foreign bodies
    • Type and extent of injury
    • Site of injury; different tissues/organs heal differently

    Cutaneous Wound Healing

    • Main phases: inflammation, granulation tissue formation, and ECM remodeling.
    • Primary union (first intention): more rapid healing.
    • Secondary union (secondary intention): more extensive scarring.

    Cellular Aging Processes

    • Accumulations of errors in DNA (ROS, mutations)
    • Decreased cellular replication
    • Cells have a limited capacity for replication.
    • Build up of various substances
      • Steatosis (triglycerides)
      • Cholesterol
      • Proteins
      • Glycogen Pigments (exogenous & endogenous)

    Fatty Liver Changes

    • Related to alcohol abuse, diabetes with obesity NASH (non-alcoholic steatohepatitis)

    Atherosclerosis/Cholesterol

    • Accumulation of cholesterol in vessels impacting blood flow

    Exogenous Carbon

    • Anthracosis (coal miner's lung): accumulation of carbon.

    Lipofuscin

    • Yellow-brown pigment (wear and tear pigment)
    • Free-radical peroxidation of membrane lipids

    Calcification

    • Aortic valve.

    Summary of Presented Information

    • This detailed unit covers essential biological processes, including cells, inflammation, apoptosis, necrosis, and tissue repair.

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    Pathogen 3.1 Cells and Inflammation (Student) PDF

    Description

    This quiz tests your knowledge on various organelles in cell biology, their functions, and the types of cell injury. Explore concepts such as apoptosis, necrosis, and cell adaptations, along with specific roles of cellular components in physiological processes. Perfect for students studying cell biology.

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