Study Guide - Cellular Injury/Adaptation/Death PDF

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CelebratedDogwood

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Tufts University

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tissue types cellular injury biochemistry biology

Summary

This study guide covers the hierarchy of tissue organization, including chemical, cellular, tissue, and system levels. It details the extracellular matrix and its components, such as collagen, elastin, and proteoglycans. The guide also explores the four main tissue types: epithelial, connective, muscle, and nervous tissue, along with their functions and roles. It then delves into cellular injury, adaptation, and oxidative stress, and the role of antioxidants.

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Study Guide Tissue Types and Cell Injury / Adaptation / Death A. Tissue Types 1. Briefly describe the hierarchy of tissue organization i. Chemical level (a) Atoms combine to form molecules ii....

Study Guide Tissue Types and Cell Injury / Adaptation / Death A. Tissue Types 1. Briefly describe the hierarchy of tissue organization i. Chemical level (a) Atoms combine to form molecules ii. Cellular level (a) Cells (a) Composed of lots of different molecules iii. Tissue level (a) Composed of cells AND the extracellular matrix they produce iv. System level (a) Composed of lots of different tissue types (b) For example, our skin includes all of the following tissue types (a) Epithelial tissue (i) The “skin cells” (i.e., the epidermis) and their extracellular matrix (ii) Blood vessels (b) Connective tissue (i) Loose connective tissue which fills space (i.e., the dermis) and its extracellular matrix, such as areolar tissue 1. Extracellular matrix includes collagen, elastin, proteoglycans to “glue” all of the cells together (ii) Blood, which supplies nutrients to the skin cells (c) Nervous tissue (i) Receptors and nerves, which give us sensation 2. Briefly describe the concept of the extracellular matrix i. Fluids and molecules secreted by cells ii. Influences the structure and function of that tissue type (a) For example: (a) The extracellular matrix secreted by bone cells makes bone tissue is hard and rigid (b) The extracellular matrix secreted by tendon cells makes tendon tissue stretchy (like a rubber band) 3. Briefly describe the most common molecules in the extracellular matrix (a) Collagen (a) Provides structure and strength (b) Triple helix structure (b) Elastin (a) Provides elasticity (stretchiness) (c) Proteoglycans (a) Fill space (b) Attract water – this determines how “soft” a tissue will be (i) Example – Cartilage has lots of proteoglycans, so it can provide some “cushioning” to joints (d) Integrins – The “glue” which connects cells to other cells, and also to the other various proteins mentioned above 4. Describe the four general categories of tissue, including function i. Epithelial Tissue (a) Serves the following functions, depending on location (a) Provides protection (e.g., skin, cornea) (b) Lines organs (e.g., inside of blood vessels, inside of intestines) (c) Produces glandular secretion (e.g., mucus, sweat) ii. Connective Tissue (a) Functions include: (a) Filling spaces (i) “Connective Tissue Proper” (ii) Blood (b) Structural support (i) Cartilage (ii) Bone (iii) Ligament (iv) Tendon (c) Energy storage (e.g., adipose tissue) (b) Fibroblasts are an important cell for connective tissue (a) Produce collagen, elastin, etc. (b) Involved in tissue healing / repair iii. Muscle (a) Able to contract to produce movement (b) Three types (a) Skeletal (under voluntary control) (b) Smooth (i) Lines organs (e.g., blood vessels, intestines) (ii) Not under voluntary control (c) Cardiac iv. Nervous (a) Transmits electrical impulses to carry information B. General Cellular Injury / Adaptation 1. Name factors which influence the reversal of injury / return to homeostasis i. Mechanism of injury ii. Duration of injury without intervention iii. Severity of injury 2. Discuss the free radial theory of cellular injury i. Reactive oxygen species (ROS) (a) Oxygen with unpaired electron (a) Reacts with various molecules (b) Can form toxic chemicals (i) Toxic to normal cells (ii) Toxic to pathogens (b) Normal part of metabolism (c) Formed continuously ii. Excess ROS production is “oxidative stress” (a) Cause cell injury and potentially cellular death (b) Implicated in MOST lifestyle disease processes (c) Caused by MANY stimuli (a) Excessive exercise (b) Radiation (c) Tobacco smoke (d) Heat 3. Describe the role of antioxidants in relation to ROS i. Neutralize ROS (a) Prevent DNA and cell damage ii. Endogenous antioxidants [specific names not mentioned in book] (a) Glutathione (b) Peroxidase (c) Catalase iii. Exogenous antioxidants (a) Vitamin C, E, beta-carotene 4. Describe the relationship between exercise, free radicals, and antioxidants i. Exercise itself acutely causes increased ROS formation [beyond that described in book] (a) Impairs muscle force production (b) ROS cause cell to adapt to develop more endogenous anti-oxidants and repair mechanisms (a) “Exercise is the best antioxidant” ii. Excessive exercise causes significant oxidative stress (a) “Excessive” is relative (a) Depends on person’s baseline fitness 5. Briefly describe three ways by which genetic alterations cause cellular injury/death, and some examples of these diseases i. Alterations in structure/number of chromosomes that cause abnormalities (a) Down’s syndrome ii. Single mutations in genes which change protein expression (a) Sickle cell anemia iii. Interaction of multiple genetic mutations, which may interact with various environmental factors (a) Type II diabetes (b) Obesity 6. Name the possible responses to physical stress (or lack thereof) i. Decreased stress tolerance (atrophy) ii. Maintenance iii. Increased stress tolerance (a) Hypertrophy – Increase in the size of cells (b) Hyperplasia – Increase in the number of cells iv. Injury v. Death 7. Name the types of mechanical stressors which can initiate a cellular response i. Overstretch ii. Compression iii. Friction iv. [Anoxia is listed with this, but it is not a mechanical stressor, rather it is metabolic] C. Cellular Injury 1. Describe the process of reversible cell injury i. Increased sodium and calcium into cell ii. Increased cellular swelling iii. Impaired organelle function (a) Impaired mitochondrial function decreases ATP production (a) This causes impairments in other cellular function (b) Cellular acidosis causes further impairments iv. Reversal happens as long as (a) Nucleus remains undamaged (b) Energy source is restored (c) Toxic injury is neutralized v. When reversal happens, the cell returns to its normal state of function 2. Describe the key responses to chronic cellular stress, and provide examples of each i. Atrophy (a) Reduction in size of cell / organ (b) Examples (a) Bone loss (b) Muscle wasting (c) Brain cell loss ii. Hypertrophy (a) Increase in size of cell (a) In response to increased (i) functional demands (ii) Hormonal input (b) True hypertrophy only occurs in cardiac and skeletal muscle (i) Cannot increase number of cells (c) Example (i) Left ventricular hypertrophy due to 1. Exercise training 2. Hypertension iii. Hyperplasia (a) Increase in number of cells (a) In response to increased functional demands (i) Increased hormonal stimulation (ii) Physical stimulation (iii) Often occurs simultaneously with hypertrophy (b) Examples (a) Callus formation on skin (b) Thickened uterine wall lining due to estrogen exposure (c) Smooth muscle proliferation in various diseases (i) Tubular obstruction 1. Bronchi in obstructive airway diseases 2. Urethra in prostate enlargement 3. Blood vessels in hypertension iv. Metaplasia (a) Change in cell morphology an function, converting one cell type into another (b) Examples (a) Ciliated pseudostratified epithelium becomes squamous epithelium in smokers v. Dysplasia (a) Increase in cell numbers AND loss of morphology AND loss of tissue organization (a) Occurs in chronically injured areas undergoing hyperplasia/metaplasia 3. Describe the processes / consequences of irreversible cell injury i. Ultimately results in cell death (a) Apoptosis (a) Genetically mediated (b) Programmed (c) No inflammatory response (b) Necrosis (a) Active process of degrading dead cells (b) Nuclear and mitochondrial damage occurs (c) Lysosomes release digestive enzymes in cytoplasm (i) Self-digesting of dead tissue (ii) Facilitates phagocytes breaking down dead tissue (d) Contents from dead cells released into ECF and ultimately circulation (i) Example: CK elevations in myocardial infarction (e) Requires removal for repair/regeneration (f) Can cause gangrene formation (i) Bacterial infection

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