NURSING 5140 All SG Questions Combined (Module 1-12) Study Questions And 100% Verified Answers 2023.

NURSING 5140 All SG Questions Combined (Module 1-12) Study Questions And 100% Verified Answers 2023. Module 1 Study Questions Altered Cellular & Tissue Biology Ch. 2 1. Compare and contrast cellular injury and adaptation. 1. Compare and Contrast cellular injury and adaptation. Cellular Adaptation  Cellular adaptation is an alteration that enables the cell to maintain a steady state called homeostasis despite adverse conditions. It is the cells response to protect itself from injury  Example- uterus adapts in pregnancy, with high blood pressure myocardial cells enlarge by increased work of pumping.  An adapted cell is neither normal nor injured  Most common are atrophy, hypertrophy, hyperplasia, and metaplasia, dysplasia (atypical hyperplasia)  Atrophy: Decrease in cell size  Hypertrophy: Increase in cell size  Hyperplasia: Increase in cell number  Metaplasia: Reversible replacement of one mature cell type by another less mature cell type  Dysplasia: Deranged cellular growth; is not a true cellular adaptation but rather an atypical hyperplasia Cellular Injury  Cellular injury ensues when severe or long term stressors overwhelm adaptive processes and cellular injury or death happens.  Caused by any factor that disrupts cellular structures or deprives the cell of oxygen and nutrients for survival  Reversible or irreversible  Chemical, hypoxic, free radical, unintentional, intentional, immunologic, inflammatory Cellular Injury ● Injury to cells and ECM (Extracellular matrix) ● Leads to injury of tissues and organs, determining structural patterns of disease ● Can be reversible (cells recover) or Irreversible (cells die) ● Caused by hypoxia, free radicals, caustic or toxic chemicals, infectious agents, intentional and unintentional injury, inflammatory and immune responses, genetic factors, insufficient nutrients or physical trauma. Injurious stimuli can cause cell stress ● Can be acute or chronic ● Can involve necrosis, apoptosis, autophagy, accumulation, or pathologic calcification 4 Biochemical Themes 1. ATP depletion 2. Oxygen and oxygen-derived free radicals 3. Intracellular calcium and loss of calcium steady state 4. Defects in membrane permeability (found in all forms of cell injury) Adaptation ● Reversible, structural or functional response to both normal or physiologic conditions and adverse or pathologic conditions ● Enables cells to maintain steady state, despite adverse conditions 2. Describe the following cellular adaptations: atrophy, hypertrophy, hyperplasia, dysplasia (atypical hyperplasia), and metaplasia and identify under which conditions these adaptations occur. ● Atrophy - Decrease or shrinkage in cell size. Most common in skeletal muscles, heart, secondary sex organs, and the brain. Physiologic atrophy - occurs with early development (Ex. Thymus during childhood). Pathologic- occurs as a result of decrease in workloads, use, pressure, blood supply, nutrition, hormonal stimulation, and nervous stimulation. (Ex. Brain atrophy with age). With muscle atrophy there is decreased protein synthesis, increased protein catabolism or both. The ubiuitin-proteasome pathway is the primary pathway of protein catabolism. (This paragraph was very confusing to me because it was very specific to muscle atrophy - not necessarily atrophy in cells in general) ● Hypertrophy - increase in cell size and consequently the affected organ. Caused by increased work demands or hormones. Triggers are mechanical (stretch) and trophic signals (growth factors and vasoactive agents). (Ex- cardiac hypertrophy or removal of one kidney- the other kidney compensates and becomes hypertrophic). ● Hyperplasia - Increase in the number of cells caused by an increased rate of cellular division. Two types, consempatory - allows organs to regenerate (Ex. removal part of the liverhyperplasia of remaining cells- regeneration) hormonal - replaces los tissue or supports new growth (pregnancy- uterus enlargement). Pathologic hyperplasia- abnormal proliferation of normal cells and can occurs from excessive hormonal stimulation (Ex. pathologic hyperplasia of the endometrium) ● Dysplasia (AKA Atypical Hyperplasia) (Not a true adaptive change) - refers to abnormal changes in the size, shape and organization of mature cells. (Ex. Dysplastic changes found in the cervix or respiratory tract). Doesn’t indicate cancer but are strongly associated with neoplastic growths. ● Metaplasia - Reversible replacement of one mature cell by another less mature cell type. (Ex. replacement of normal bronchial columnar ciliated epithelial cells by stratified squamous epithelial cells - new cells do not secrete mucus or have cilia. To reverse - quit smoking). Thought to develop from a reprogramming of stem cells Atrophy  Atrophy is a decrease in cellular size. The mechanisms probably include decreased protein synthesis, increased protein catabolism, or both.  Physiologic atrophy occurs with early development; for example, the thymus gland involutes and atrophies. Pathologic atrophy occurs as a result of decreases in workload, use, pressure, blood supply, nutrition, hormonal stimulation, and nervous stimulation.  Aging causes brain cells and endocrine-dependent organs, such as the gonads, to become atrophic.  Most commonly skeletal muscle, heart, sex organs, and brain  Pathologic atrophy- Results from decreases in workload, use, pressure, blood supply, nutrition, hormonal stimulation, and nervous stimulation. It is not normal.  Disuse- Don’t use it you lose it  Decreased protein synthesis, increased protein catabolism, or both  Ubiquitin-proteasome pathway- the primary pathway of protein catabolism.  Primarily accompanied by self-eating “ autophagic vacuoles.” Hypertrophy  Caused by increased work demand or hormones  Trigger signals: Mechanical and trophic  Mechanical signals- stretch  Trophic signals- growth factors and vasoactive agents  Physiologic- uterus enlarges in pregnancy  Pathologic- cardiomegaly (increased heart size, HTN, CHF)  Hypertrophy is an increase in the size of cells caused by increased work demands or hormonal stimulation.. Amounts of protein in the plasma membrane, endoplasmic reticulum, microfilaments, and mitochondria are increased. Hyperplasia  Caused by increased rate of cellular division causes increased number of cells  Physiologic  Compensatory: Allows organs to regenerate ( liver, epidermal & intestinal epithelia, hepatocytes, bone marrow, fibroblasts, bone, cartilage, and smooth muscle cells. Further example is callus formation and wound healing.  Hormonal: Replaces lost tissue or supports new growth (estrogen dependent organs, uterus & breasts)  Pathologic hyperplasia is the abnormal proliferation of normal cells in response to excessive hormonal stimulation of growth factors on target cells. Most common example is pathologic endometrial hyperplasia caused by an imbalance of estrogen and progesterone with over secretion of estrogen. Causes excessive menstrual bleeding. Dysplasia (Atypical Hyperplasia)  Dysplasia, or atypical hyperplasia, is an abnormal change in the size, shape, and organization of mature tissue cells.  Does not indicate cancer.  Most commonly in cervix and respiratory tracts  Strong predictor of breast cancer development Metaplasia  Is the reversible replacement of one mature cell by another less mature cell type  Replacement of normal bronchial columnar ciliated epithelial cells by stratified squamous epithelial cells  The newly formed squamous epithelial cells do not secrete mucus or have cilia, causing loss of a vital protective mechanism.  Is a reprogramming of stem cells  Most commonly occurs in lungs- bronchial metaplasia can be reversed typically if smoking is removed.  Case study question— Mr. Young normal columnar epithelial cells of bronchial airway. Metaplasia adaption causes new cells to be exchanged not to secrete mucus and have the bronchial protective mechanism. Makes more susceptible to respiratory infection. ● 3. Discuss physiologic versus pathogenic cellular adaptations. ● Physiologic: normal cellular adaptations ● Pathogenic: Disease-causing cellular adaptations ● Physiologic- occurs with early adaptation (Ex. Thymus Gland) Pathologic atrophy occurs as a result of decreases in workload, use, pressure, blood supply, nutrition, hormonal stimulation, and nervous stimulation. 4. Describe the sequence of cellular events preceding cell death. Two types of cell death - necrosis and apoptosis Necrosis - Sum of cellular changes after local cell death and autolysis Involves inflammatory response, swelling of endoplasmic reticulum and mitochondria, breakdown of plasma membrane, organelles and nucleus leading to a leakage of contents. In later stages of necrosis, most organelles are disrupted and karyolysis (nucelar dissolution and lysis of chromatin) is under way. In some cells, the nucleus shrinks and becomes a small, dense mass of genetic material (pyknosis)  Apoptosis - Regulated or programmed cell death. Characterized by the “dropping off” of cellular fragments called apoptic bodies. Is the active process of cellular destruction, can occur normally or pathologically. Main outcome in ischemia, toxin exposure, certain infections, and trauma. Can lead to cancer, autoimmune disorders, neurodegenerative diseases, and ischemic injury. Hypoxic injury causes mitochondrial phosphorylation which causes lack of ATP  Decreased ATP production leads to anaerobic metabolism which generates ATP from glycogen when there is lack of oxygen. Depleted glycogen stores causes anaerobic metabolism to cease  Failure of active transport mechanisms (sodium-potassium [Na+/K+] pump) happens when there is lack of ATP. The sodium- calcium exchange also fails causing intracellular accumulation of sodium and calcium, which equals cell swelling.  Cellular swelling causes diffusion of potassium out of the cell. Cell membrane damage causes rapid movement of calcium into the cell. Movement of water into the cell causes ribosomes to detach from endoplasmic reticulum.  Detachment of ribosomes from endoplasmic reticulum causes decreased protein synthesis.  Cessation of protein synthesis causes cell to become markedly swollen  Mitochondrial swelling from calcium accumulation causes vacuolation  Vacuolation is the formation of vacuoles or cytoplasmic small cavities  Continued injury causes leakage of digestive enzymes from lysosomes; autodigestion of intracellular structures  Lysis of the plasma membrane  Cell death 5. Identify and describe the mechanisms of cellular injury for the following causes: hypoxia, chemicals, free radicals, infectious agents, asphyxial injuries, immunologic and inflammatory responses, genetic factors, nutritional imbalances, and physical trauma. ● Hypoxia - lack of oxygen. Single most common cause of cellular injury. Most common cause of hypoxia is Ischemia (reduced blood supply). Ischemia - lack of blood flow into the vessels that supply the cell with oxygen and nutrients (arteriosclerosis or thrombosis). Cellular responsesdecrease in ATP, causing failure of sodium/potassium pump and sodiumcalcium exchange/ cellular swelling (pushes potassium out of the cell) ● Chemicals - Two general mechanisms 1. Direct toxicity to the cell that damages or destroys plasma membrane. 2. Reactive free radicals and lipid peroxidation. Examples - dry cleaning, lead, carbon monoxide, ethanol, mercury, social or street drugs. ● Free Radicals - Electrically uncharged atom or group of atoms having an unpaired electron. Results in membrane damage (lipid peroxidation [destruction of unsaturated fatty acids]), alteration of proteins, alteration of DNA. Free radicals may be initiated within cells by the absorption of extreme energy sources (x-ray, UV light), endogenous reactions (redox reactions) or the enzymatic metabolism of exogenous chemicals or drugs. Inactivation of free radicals using antioxidants such as vitamin E, vitamin C, cysteine, album (see Table 2-4) or Enzymes. Mitochondrial oxidative stress has been implicated in head disease, Alzheimer’s, Parkinson’s, ALS, and prion diseases. ● Infectious Agents - The pathogenicity (virulence) of microorganisms lies in their ability to survive and proliferate in the human body, where they injure cells and tissues. The disease-producing potential of a microorganism depends on its ability to (1) invade and destroy cells, (2) produce toxins, and (3) produce damaging hypersensitivity reactions ● Asphyxial Injuries - Cause- failure of cells to receive or use oxygen. Include suffocation, strangulation (hanging, ligature, manual), chemical asphyxiants (cyanide, sewer gas), drowning ● Immunologic and Inflammatory responses - Injury and alteration to cell membrane caused by exposure to direct contact with cellular and chemical components of the immune and inflammatory responses, such as phagocytic cells (lymphocytes, macrophages) and substances such as histamine, antibodies, lymphokines, complement, and proteases. They can combine to and occupy receptors on the plasma membrane. Antibodies also can block or destroy cellular junctions, interfering with intercellular communication and are capable of damaging normal (uninjured and uninfected) cells. This type of injury is found in certain forms of DM and Myasthenia gravis. ● Genetic Factors - Alterations to nucleus and in the plasma membrane structure, shape, receptors, or transport mechanisms. Example: sickle cell anemia ● Nutritional Imbalances - Essential nutrients (proteins, carbs, lipids, vitamins and minerals) are required for cells to function normally. Alter cellular structure and function, especially transport mechanisms, chromosomes, nucleus, and DNA. Examples - starvation, deficient intake or excessive intake.