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Keypoints-Mc C H-2014 - study guide for exam 2
Pathophysiology (NSG 211)
Marian University
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Huether and McCance: Understanding Pathophysiology, 5th Edition Chapter 01: Cellular Biology Key Points Did You Understand? Cellular Functions 1. Cells become specialized through the process of differentiation or maturation. 2. The eight specialized cellular functions are movement, conductivity, metabolic absorption, secretion, excretion, respiration, reproduction, and communication. Structure and Function of Cellular Components 1. The eukaryotic cell consists of three general components: the plasma membrane, the cytoplasm, and the intracellular organelles. 2. The nucleus is the largest organelle and is found usually in the center. The chief functions of the nucleus are cell division and control of genetic information. 3. Cytoplasm, or the cytoplasmic matrix, is an aqueous solution, called cytosol, that fills the space between the nucleus and the plasma membrane. 4. The organelles are suspended in the cytoplasm and are enclosed in biologic membranes. 5. The endoplasmic reticulum is a network of tubular channels, called cisternae, that extend throughout the outer nuclear membrane. It specializes in the synthesis and transport of protein and lipid components of most of the organelles. 6. The Golgi complex is a network of smooth membranes and vesicles located near the nucleus. The Golgi complex is responsible for processing and packaging proteins into secretory vesicles that break away from the Golgi complex and migrate to a variety of intracellular and extracellular destinations, including the plasma membrane. 7. Lysosomes are saclike structures that originate from the Golgi complex and contain digestive enzymes. These enzymes are responsible for digesting most cellular substances down to their basic form, such as amino acids, fatty acids, and sugars. 8. Cellular injury leads to a release of the lysosomal enzymes, causing cellular digestion. 9. Peroxisomes are similar to lysosomes but contain several enzymes that either produce or use hydrogen peroxide. 10. Mitochondria contain the metabolic machinery necessary for cellular energy metabolism. The enzymes of the respiratory chain, found in the inner membrane of the mitochondria, generate most of the adenosine triphosphate. 11. The cytoskeleton is the and of the cell. The internal skeleton is composed of a network of protein filaments, including microtubules and actin filaments. 12. The plasma membrane encloses the cell and, controlling the movement of substances across it, exerts a powerful influence on metabolic pathways. 13. Protein receptors on the plasma membrane enable the cell to interact with other cells and with extracellular substances. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Huether and McCance: Understanding Pathophysiology, 5th Edition Chapter 01: Cellular Biology Key Points Did You Understand? Cellular Functions 1. Cells become specialized through the process of differentiation or maturation. 2. The eight specialized cellular functions are movement, conductivity, metabolic absorption, secretion, excretion, respiration, reproduction, and communication. Structure and Function of Cellular Components 1. The eukaryotic cell consists of three general components: the plasma membrane, the cytoplasm, and the intracellular organelles. 2. The nucleus is the largest organelle and is found usually in the center. The chief functions of the nucleus are cell division and control of genetic information. 3. Cytoplasm, or the cytoplasmic matrix, is an aqueous solution, called cytosol, that fills the space between the nucleus and the plasma membrane. 4. The organelles are suspended in the cytoplasm and are enclosed in biologic membranes. 5. The endoplasmic reticulum is a network of tubular channels, called cisternae, that extend throughout the outer nuclear membrane. It specializes in the synthesis and transport of protein and lipid components of most of the organelles. 6. The Golgi complex is a network of smooth membranes and vesicles located near the nucleus. The Golgi complex is responsible for processing and packaging proteins into secretory vesicles that break away from the Golgi complex and migrate to a variety of intracellular and extracellular destinations, including the plasma membrane. 7. Lysosomes are saclike structures that originate from the Golgi complex and contain digestive enzymes. These enzymes are responsible for digesting most cellular substances down to their basic form, such as amino acids, fatty acids, and sugars. 8. Cellular injury leads to a release of the lysosomal enzymes, causing cellular digestion. 9. Peroxisomes are similar to lysosomes but contain several enzymes that either produce or use hydrogen peroxide. 10. Mitochondria contain the metabolic machinery necessary for cellular energy metabolism. The enzymes of the respiratory chain, found in the inner membrane of the mitochondria, generate most of the adenosine triphosphate. 11. The cytoskeleton is the and of the cell. The internal skeleton is composed of a network of protein filaments, including microtubules and actin filaments. 12. The plasma membrane encloses the cell and, controlling the movement of substances across it, exerts a powerful influence on metabolic pathways. 13. Protein receptors on the plasma membrane enable the cell to interact with other cells and with extracellular substances. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 14. The plasma membrane is a bilayer of lipids including phospholipids and glycolipids and cholesterol, which gives the membrane its structural integrity. 15. Membrane functions are determined largely proteins. These functions include recognition protein receptors and transport of substances into and out of the cell. 16. The fluid mosaic model accounts for the fluidity of the lipid bilayer and the flexibility, properties, and selective impermeability of the plasma membrane. The model has been updated. 17. Cellular receptors are protein molecules on the plasma membrane, in the cytoplasm, or in the nucleus that are capable of recognizing and binding smaller molecules, called ligands. 18. The dynamic nature of the fluid plasma membrane enables it to vary the number of receptors on its surface. Altering receptor number and pattern is related to disease states. 19. The complex initiates a series of protein interactions, causing adenylate cyclase to catalyze the transformation of cellular adenosine triphosphate to messenger molecules that stimulate specific responses within the cell. Adhesions 1. adhesions are formed on plasma membranes, there allowing the formation of tissues and organs. Cells are held together three different means: (a) the extracellular membrane, (b) cell adhesion molecules in the plasma membrane, and (c) specialized cell junctions. 2. The extracellular matrix includes three groups of macromolecules: (1) fibrous structural proteins, (2) adhesive glycoproteins, and (3) proteoglycans and hyaluronic acid. The matrix helps regulate cell growth, movement, and differentiation. 3. The three major types of cell junctions are desmosomes, tight junctions, and gap junctions. Cellular Communication and Signal Transduction 1. Cells communicate in three main ways: (a) they form protein channels called gap (b) they display receptors that affect intracellular processes or other cells in direct physical and (c) receptor proteins inside the target cell. 2. Primary modes of intercellular signaling include paracrine, hormonal, neurohormonal, and neurotransmitter. 3. Signal transduction involves signals or instructions from extracellular chemical messengers that are conveyed to the interior for execution. Cellular Metabolism 1. The chemical tasks of maintaining essential cellular functions are referred to as cellular metabolism. Anabolism is the process of metabolism, whereas catabolism is the process. 2. Adenosine triphosphate functions as an molecule. Energy is stored molecules of carbohydrate, lipid, and protein, which, when catabolized, transfer energy to adenosine triphosphate. 3. Oxidative phosphorylation occurs in the mitochondria and is the mechanism which the energy produced from carbohydrates, fats, and proteins is transferred to adenosine triphosphate. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 14. The plasma membrane is a bilayer of lipids including phospholipids and glycolipids and cholesterol, which gives the membrane its structural integrity. 15. Membrane functions are determined largely proteins. These functions include recognition protein receptors and transport of substances into and out of the cell. 16. The fluid mosaic model accounts for the fluidity of the lipid bilayer and the flexibility, properties, and selective impermeability of the plasma membrane. The model has been updated. 17. Cellular receptors are protein molecules on the plasma membrane, in the cytoplasm, or in the nucleus that are capable of recognizing and binding smaller molecules, called ligands. 18. The dynamic nature of the fluid plasma membrane enables it to vary the number of receptors on its surface. Altering receptor number and pattern is related to disease states. 19. The complex initiates a series of protein interactions, causing adenylate cyclase to catalyze the transformation of cellular adenosine triphosphate to messenger molecules that stimulate specific responses within the cell. Adhesions 1. adhesions are formed on plasma membranes, there allowing the formation of tissues and organs. Cells are held together three different means: (a) the extracellular membrane, (b) cell adhesion molecules in the plasma membrane, and (c) specialized cell junctions. 2. The extracellular matrix includes three groups of macromolecules: (1) fibrous structural proteins, (2) adhesive glycoproteins, and (3) proteoglycans and hyaluronic acid. The matrix helps regulate cell growth, movement, and differentiation. 3. The three major types of cell junctions are desmosomes, tight junctions, and gap junctions. Cellular Communication and Signal Transduction 1. Cells communicate in three main ways: (a) they form protein channels called gap (b) they display receptors that affect intracellular processes or other cells in direct physical and (c) receptor proteins inside the target cell. 2. Primary modes of intercellular signaling include paracrine, hormonal, neurohormonal, and neurotransmitter. 3. Signal transduction involves signals or instructions from extracellular chemical messengers that are conveyed to the interior for execution. Cellular Metabolism 1. The chemical tasks of maintaining essential cellular functions are referred to as cellular metabolism. Anabolism is the process of metabolism, whereas catabolism is the process. 2. Adenosine triphosphate functions as an molecule. Energy is stored molecules of carbohydrate, lipid, and protein, which, when catabolized, transfer energy to adenosine triphosphate. 3. Oxidative phosphorylation occurs in the mitochondria and is the mechanism which the energy produced from carbohydrates, fats, and proteins is transferred to adenosine triphosphate. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 21. Caveolae are cavelike pits, and are involved in transport and cell communication. 22. All body cells are electrically polarized, with the inside of the cell more negatively charged than the outside. The difference in voltage across the plasma membrane is the resting membrane potential. 23. When an excitable cell receives an electrochemical stimulus, cations enter the cell, causing a rapid change in the resting membrane potential known as the action potential. The action potential along the plasma membrane and is transmitted to an adjacent cell. This is how electrochemical signals convey information from cell to cell. Cellular Reproduction: The Cell Cycle 1. Cellular reproduction in body tissues involves mitosis and cytokinesis. 2. Only mature cells are capable of division. Maturation occurs during a stage of cellular life called interphase. 3. The cell cycle is the reproductive process that begins after interphase in all tissues with cellular turnover. There are four phases of the cell cycle: (1) the S phase, during which DNA synthesis takes place in the cell (2) the G2 phase, the period between the completion of DNA synthesis and the next phase (3) the M phase, which involves both nuclear and cytoplasmic and (4) the G1 phase, after which the cycle begins again. 4. The M phase involves four stages: prophase, metaphase, anaphase, and telophase. 5. The mechanisms that control cell division depend on control and protein growth factors. Tissues 1. Cells of one or more types are organized into tissues, and different types of tissues compose organs. Organs are organized to function as tracts or systems. 2. Three key factors that maintain the cellular organization of tissues are (a) recognition and cell communication, (b) selective adhesion, and (c) memory. 3. Tissue cells are linked at cell junctions, which are specialized regions on their plasma membranes called desmosomes, tight junctions, and gap junctions. Cell junctions attach adjacent cells and allow small molecules to pass between them. 4. The four basic types of tissues are epithelial, muscle, nerve, and connective tissues. 5. Neural tissue is composed of highly specialized cells called neurons that receive and transmit electrical impulses rapidly across junctions called synapses. 6. Epithelial tissue covers most internal and external surfaces of the body. The functions of epithelial tissue include protection, absorption, secretion, and excretion. 7. Connective tissue binds various tissues and organs together, supporting them in their locations and serving as storage sites for excess nutrients. 8. Muscle tissue is composed of long, thin, highly contractile cells or fibers called myocytes. Muscle tissue that is attached to bones enables voluntary movement. Muscle tissue in internal organs enables involuntary movement, such as the heartbeat. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 21. Caveolae are cavelike pits, and are involved in transport and cell communication. 22. All body cells are electrically polarized, with the inside of the cell more negatively charged than the outside. The difference in voltage across the plasma membrane is the resting membrane potential. 23. When an excitable cell receives an electrochemical stimulus, cations enter the cell, causing a rapid change in the resting membrane potential known as the action potential. The action potential along the plasma membrane and is transmitted to an adjacent cell. This is how electrochemical signals convey information from cell to cell. Cellular Reproduction: The Cell Cycle 1. Cellular reproduction in body tissues involves mitosis and cytokinesis. 2. Only mature cells are capable of division. Maturation occurs during a stage of cellular life called interphase. 3. The cell cycle is the reproductive process that begins after interphase in all tissues with cellular turnover. There are four phases of the cell cycle: (1) the S phase, during which DNA synthesis takes place in the cell (2) the G2 phase, the period between the completion of DNA synthesis and the next phase (3) the M phase, which involves both nuclear and cytoplasmic and (4) the G1 phase, after which the cycle begins again. 4. The M phase involves four stages: prophase, metaphase, anaphase, and telophase. 5. The mechanisms that control cell division depend on control and protein growth factors. Tissues 1. Cells of one or more types are organized into tissues, and different types of tissues compose organs. Organs are organized to function as tracts or systems. 2. Three key factors that maintain the cellular organization of tissues are (a) recognition and cell communication, (b) selective adhesion, and (c) memory. 3. Tissue cells are linked at cell junctions, which are specialized regions on their plasma membranes called desmosomes, tight junctions, and gap junctions. Cell junctions attach adjacent cells and allow small molecules to pass between them. 4. The four basic types of tissues are epithelial, muscle, nerve, and connective tissues. 5. Neural tissue is composed of highly specialized cells called neurons that receive and transmit electrical impulses rapidly across junctions called synapses. 6. Epithelial tissue covers most internal and external surfaces of the body. The functions of epithelial tissue include protection, absorption, secretion, and excretion. 7. Connective tissue binds various tissues and organs together, supporting them in their locations and serving as storage sites for excess nutrients. 8. Muscle tissue is composed of long, thin, highly contractile cells or fibers called myocytes. Muscle tissue that is attached to bones enables voluntary movement. Muscle tissue in internal organs enables involuntary movement, such as the heartbeat. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Huether and McCance: Understanding Pathophysiology, 5th Edition Chapter 03: Altered Cellular and Tissue Biology Key Points Cellular Adaptation 1. Cellular adaptation is a reversible, structural, or functional response to both normal or physiologic conditions and adverse or pathologic conditions. Cells can adapt to physiologic demands or stress to maintain a steady state called homeostasis. 2. The most significant adaptive changes include atrophy, hypertrophy, hyperplasia, and metaplasia. 3. Atrophy is a decrease in cellular size caused aging, disuse or lack of blood supply, hormonal stimulation, or neural stimulation. The amounts of endoplasmic reticulum, mitochondria, and microfilaments decrease. The mechanisms of atrophy probably include decreased protein synthesis, increased protein catabolism, or both. 4. Hypertrophy is an increase in the size of cells caused increased work demands or hormonal stimulation. The amounts of protein in the plasma membrane, endoplasmic reticulum, microfilaments, and mitochondria increase. 5. Hyperplasia is an increase in the number of cells caused an increased rate of cellular division. Normal hyperplasia is stimulated hormones or the need to replace lost tissues. 6. Metaplasia is the reversible replacement of one mature cell type another less mature cell type. 7. Dysplasia, or atypical hyperplasia, is an abnormal change in the size, shape, and organization of mature tissue cells. It is not considered a true adaptational change but rather atypical. Cellular Injury 1. Cellular injury occurs if the cell is unable to maintain homeostasis. Injured cells may recover or die. Injury is caused lack of oxygen, free radicals, caustic or toxic chemicals, infectious agents, inflammatory and immune responses, genetic factors, insufficient nutrients, or physical trauma from many causes. 2. Six biochemical themes are important to cell injury: (a) adenosine triphosphate depletion, (b) mitochondrial damage, (c) oxygen and free radicals, (d) membrane damage, (e) protein folding defects, and (f) increased intracellular calcium and loss of calcium steady state. 3. The sequence of events leading to cell death is commonly decreased adenosine triphosphate production, failure of mechanisms, cellular swelling, detachment of ribosomes from the endoplasmic reticulum, cessation of protein synthesis, mitochondrial swelling as a result of calcium accumulation, vacuolation, leakage of digestive enzymes from lysosomes, autodigestion of intracellular structures, lysis of the plasma membrane, and death. 4. The initial insult in hypoxic injury is usually ischemia. Ischemia is the cessation of blood flow into vessels that supply the cell with oxygen and nutrients. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Huether and McCance: Understanding Pathophysiology, 5th Edition Chapter 03: Altered Cellular and Tissue Biology Key Points Cellular Adaptation 1. Cellular adaptation is a reversible, structural, or functional response to both normal or physiologic conditions and adverse or pathologic conditions. Cells can adapt to physiologic demands or stress to maintain a steady state called homeostasis. 2. The most significant adaptive changes include atrophy, hypertrophy, hyperplasia, and metaplasia. 3. Atrophy is a decrease in cellular size caused aging, disuse or lack of blood supply, hormonal stimulation, or neural stimulation. The amounts of endoplasmic reticulum, mitochondria, and microfilaments decrease. The mechanisms of atrophy probably include decreased protein synthesis, increased protein catabolism, or both. 4. Hypertrophy is an increase in the size of cells caused increased work demands or hormonal stimulation. The amounts of protein in the plasma membrane, endoplasmic reticulum, microfilaments, and mitochondria increase. 5. Hyperplasia is an increase in the number of cells caused an increased rate of cellular division. Normal hyperplasia is stimulated hormones or the need to replace lost tissues. 6. Metaplasia is the reversible replacement of one mature cell type another less mature cell type. 7. Dysplasia, or atypical hyperplasia, is an abnormal change in the size, shape, and organization of mature tissue cells. It is not considered a true adaptational change but rather atypical. Cellular Injury 1. Cellular injury occurs if the cell is unable to maintain homeostasis. Injured cells may recover or die. Injury is caused lack of oxygen, free radicals, caustic or toxic chemicals, infectious agents, inflammatory and immune responses, genetic factors, insufficient nutrients, or physical trauma from many causes. 2. Six biochemical themes are important to cell injury: (a) adenosine triphosphate depletion, (b) mitochondrial damage, (c) oxygen and free radicals, (d) membrane damage, (e) protein folding defects, and (f) increased intracellular calcium and loss of calcium steady state. 3. The sequence of events leading to cell death is commonly decreased adenosine triphosphate production, failure of mechanisms, cellular swelling, detachment of ribosomes from the endoplasmic reticulum, cessation of protein synthesis, mitochondrial swelling as a result of calcium accumulation, vacuolation, leakage of digestive enzymes from lysosomes, autodigestion of intracellular structures, lysis of the plasma membrane, and death. 4. The initial insult in hypoxic injury is usually ischemia. Ischemia is the cessation of blood flow into vessels that supply the cell with oxygen and nutrients. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 21. Errors in health care are a leading cause of injury or death in the United States. Such errors may involve medicines, surgery, diagnosis, equipment, and laboratory reports. They can occur anywhere in the health care system including hospitals, clinics, outpatient surgery centers, offices, pharmacies, and the home. Manifestations of Cellular Injury 1. An important manifestation of cell injury is the resultant metabolic disturbances of intracellular accumulation of abnormal amounts of various substances. Two categories of accumulations are (a) a normal cellular substances, such as water, proteins, lipids, and carbohydrate and (b) abnormal substances, either endogenous, such as from abnormal metabolism, or exogenous, like a virus. 2. Most accumulations are attributed to four types of mechanisms, all abnormal: (a) endogenous substance is produced in excess or at an increased (b) an abnormal substance, often the result of a mutated gene, (c) an endogenous substance is not effectively and (d) a harmful exogenous substance accumulates because of inhalation, ingestion, or infection. 3. Accumulations harm cells the organelles and causing excessive metabolites to be produced during their catabolism. The metabolites are released into the cytoplasm or expelled into the extracellular matrix. 4. Cellular swelling, the accumulation of excessive water in the cell, is caused the failure of transport mechanisms and is a sign of many types of cellular injury. Oncosis is a type of cellular death resulting from cellular swelling. 5. Accumulations of organic carbohydrates, glycogen, proteins, caused disorders in which (a) cellular uptake of the substance exceeds the capacity to catabolize (digest) or use it or (b) cellular anabolism (synthesis) of the substance exceeds the capacity to use or secrete it. 6. Dystrophic calcification is always a sign of pathologic change because it occurs only in injured or dead cells. Metastatic calcification, however, can occur in uninjured cells in individuals with hypercalcemia. 7. Disturbances in urate metabolism can result in hyperuricemia and deposition of sodium urate crystals in to a painful disorder called gout. 8. Systemic manifestations of cellular injury include fever, leukocytosis, increased heart rate, pain, and serum elevations of enzymes in the plasma. Cellular Death 1. Cellular death has historically been classified as necrosis or apoptosis. Necrosis is characterized rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction, and the lack of features of apoptosis. Apoptosis is known as regulated or programmed cell death, characterized of cellular fragments called apoptotic bodies. It is now understood that under certain conditions necrosis is regulated or programmed, hence the new term or necroptosis. 2. There are four major types of necroses: coagulative, liquefactive, caseous, and fat necroses. Different types of necroses occur in different tissues. 3. Structural signs that indicate irreversible injury and progression to necrosis are the dense clumping and disruption of genetic material and the disruption of the plasma and organelle membranes. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 21. Errors in health care are a leading cause of injury or death in the United States. Such errors may involve medicines, surgery, diagnosis, equipment, and laboratory reports. They can occur anywhere in the health care system including hospitals, clinics, outpatient surgery centers, offices, pharmacies, and the home. Manifestations of Cellular Injury 1. An important manifestation of cell injury is the resultant metabolic disturbances of intracellular accumulation of abnormal amounts of various substances. Two categories of accumulations are (a) a normal cellular substances, such as water, proteins, lipids, and carbohydrate and (b) abnormal substances, either endogenous, such as from abnormal metabolism, or exogenous, like a virus. 2. Most accumulations are attributed to four types of mechanisms, all abnormal: (a) endogenous substance is produced in excess or at an increased (b) an abnormal substance, often the result of a mutated gene, (c) an endogenous substance is not effectively and (d) a harmful exogenous substance accumulates because of inhalation, ingestion, or infection. 3. Accumulations harm cells the organelles and causing excessive metabolites to be produced during their catabolism. The metabolites are released into the cytoplasm or expelled into the extracellular matrix. 4. Cellular swelling, the accumulation of excessive water in the cell, is caused the failure of transport mechanisms and is a sign of many types of cellular injury. Oncosis is a type of cellular death resulting from cellular swelling. 5. Accumulations of organic carbohydrates, glycogen, proteins, caused disorders in which (a) cellular uptake of the substance exceeds the capacity to catabolize (digest) or use it or (b) cellular anabolism (synthesis) of the substance exceeds the capacity to use or secrete it. 6. Dystrophic calcification is always a sign of pathologic change because it occurs only in injured or dead cells. Metastatic calcification, however, can occur in uninjured cells in individuals with hypercalcemia. 7. Disturbances in urate metabolism can result in hyperuricemia and deposition of sodium urate crystals in to a painful disorder called gout. 8. Systemic manifestations of cellular injury include fever, leukocytosis, increased heart rate, pain, and serum elevations of enzymes in the plasma. Cellular Death 1. Cellular death has historically been classified as necrosis or apoptosis. Necrosis is characterized rapid loss of the plasma membrane structure, organelle swelling, mitochondrial dysfunction, and the lack of features of apoptosis. Apoptosis is known as regulated or programmed cell death, characterized of cellular fragments called apoptotic bodies. It is now understood that under certain conditions necrosis is regulated or programmed, hence the new term or necroptosis. 2. There are four major types of necroses: coagulative, liquefactive, caseous, and fat necroses. Different types of necroses occur in different tissues. 3. Structural signs that indicate irreversible injury and progression to necrosis are the dense clumping and disruption of genetic material and the disruption of the plasma and organelle membranes. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 4. Apoptosis, a distinct type of sublethal injury, is a process of selective cellular destruction that occurs in both normal and pathologic tissue changes. 5. Death apoptosis causes loss of cells in many pathologic states, including (a) severe cell injury, (b) accumulation of misfolded proteins, (c) infections, and (d) obstruction in tissue ducts. 6. Excessive accumulation of misfolded proteins in the endoplasmic reticulum leads to a condition known as endoplasmic reticulum stress. Endoplasmic reticulum stress results in apoptotic cell death and this mechanism has been linked to several degenerative diseases of the central nervous system and other organs. 7. Excessive or not enough apoptosis is known as dysregulated apoptosis. 8. Autophagy means of and as a recycling factor it is a process and a survival mechanism. When cells are starved or the autophagic process institutes cannibalization and recycles the digested contents. Autophagy can maintain cellular metabolism under starvation conditions and remove damaged organelles under stress conditions, improving the survival of cells. Autophagy may slow down as a critical garbage collector and recycling process, thus contributing to aging. 9. Gangrenous necrosis, or gangrene, is tissue necrosis caused hypoxia and the subsequent bacterial invasion. Aging and Altered Cellular and Tissue Biology 1. It is difficult to determine the physiologic from the pathologic changes of aging. Cellular aging is the result of increasing molecular disorder or entropy. 2. Humans have an inherent maximal life span, which is 80 to 100 years, that is dictated currently unknown intrinsic mechanisms. 3. Although the maximal life span has not changed significantly over time, the average life span, or life expectancy, has increased but not for all Americans. Life expectancy is the average number of years of life remaining at a given age. 4. The physiologic mechanisms of aging apparently are associated with (a) cellular changes produced genetic and factors, (b) changes in cellular regulatory or control mechanisms, and (c) degenerative extracellular and vascular alterations. 5. Frailty is imprecisely defined as a wasting syndrome of aging leaving a person vulnerable to falls, functional decline, disease, and death. Somatic Death 1. Somatic death is death of the entire organism. Postmortem change is diffuse and does not involve the inflammatory response. 2. Manifestations of somatic death include cessation of respiration and circulation, gradual lowering of body temperature, pupil dilation, loss of elasticity and transparency in the skin, muscle stiffening, and skin discoloration Signs of putrefaction are obvious about 24 to 48 hours after death. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 4. Apoptosis, a distinct type of sublethal injury, is a process of selective cellular destruction that occurs in both normal and pathologic tissue changes. 5. Death apoptosis causes loss of cells in many pathologic states, including (a) severe cell injury, (b) accumulation of misfolded proteins, (c) infections, and (d) obstruction in tissue ducts. 6. Excessive accumulation of misfolded proteins in the endoplasmic reticulum leads to a condition known as endoplasmic reticulum stress. Endoplasmic reticulum stress results in apoptotic cell death and this mechanism has been linked to several degenerative diseases of the central nervous system and other organs. 7. Excessive or not enough apoptosis is known as dysregulated apoptosis. 8. Autophagy means of and as a recycling factor it is a process and a survival mechanism. When cells are starved or the autophagic process institutes cannibalization and recycles the digested contents. Autophagy can maintain cellular metabolism under starvation conditions and remove damaged organelles under stress conditions, improving the survival of cells. Autophagy may slow down as a critical garbage collector and recycling process, thus contributing to aging. 9. Gangrenous necrosis, or gangrene, is tissue necrosis caused hypoxia and the subsequent bacterial invasion. Aging and Altered Cellular and Tissue Biology 1. It is difficult to determine the physiologic from the pathologic changes of aging. Cellular aging is the result of increasing molecular disorder or entropy. 2. Humans have an inherent maximal life span, which is 80 to 100 years, that is dictated currently unknown intrinsic mechanisms. 3. Although the maximal life span has not changed significantly over time, the average life span, or life expectancy, has increased but not for all Americans. Life expectancy is the average number of years of life remaining at a given age. 4. The physiologic mechanisms of aging apparently are associated with (a) cellular changes produced genetic and factors, (b) changes in cellular regulatory or control mechanisms, and (c) degenerative extracellular and vascular alterations. 5. Frailty is imprecisely defined as a wasting syndrome of aging leaving a person vulnerable to falls, functional decline, disease, and death. Somatic Death 1. Somatic death is death of the entire organism. Postmortem change is diffuse and does not involve the inflammatory response. 2. Manifestations of somatic death include cessation of respiration and circulation, gradual lowering of body temperature, pupil dilation, loss of elasticity and transparency in the skin, muscle stiffening, and skin discoloration Signs of putrefaction are obvious about 24 to 48 hours after death. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 2. Most cells express plasma membrane pattern recognition receptors that recognize molecules produced infectious microorganisms called molecular patterns, or products of cellular damage called molecular patterns. Cellular Products 1. The cells of the innate immune system secrete many biochemical mediators that are responsible for activating other these cytokines include interleukins, chemokines, interferons, and other molecules. 2. The most important proinflammatory cytokines are and tumor necrosis 3. Interferons are produced cells that are infected viruses. Once released from infected cells, interferons can stimulate neighboring healthy cells to produce substances that prevent viral infection. 4. Chemokines are synthesized a number of different cells and induce leukocytes through chemotaxis. Mast Cell 1. The most important activator of the inflammatory response is the mast cell, which initiates inflammation releasing biochemical mediators from preformed cytoplasmic granules and synthesizing other mediators in response to a stimulus. 2. Histamine is the major vasoactive amine released from mast cells. It causes dilation of capillaries and retraction of endothelial cells lining the capillaries, which increases vascular permeability. Endothelium and Platelets 1. The endothelial cells lining the circulatory system normally regulate circulating components of the inflammatory system and maintain normal blood flow preventing spontaneous activation of platelets and members of the clotting system. 2. During inflammation the endothelium expresses receptors that help leukocytes leave the vessel and retract to allow fluid to pass into the tissues. 3. Platelets interact with the coagulation cascade to stop bleeding and release a number of mediators that promote and control inflammation. Phagocytes 1. The polymorphonuclear neutrophil, the predominant phagocytic cell in the early inflammatory response, exits the circulation diapedesis through the retracted endothelial cell junctions and moves to the inflammatory site chemotaxis. 2. Eosinophils release products that control the inflammatory response and are the principal cell that kills parasitic organisms. 3. The macrophage, the predominant phagocytic cell in the late inflammatory response, is highly phagocytic, responsive to cytokines, and promotes wound healing. 4. Dendritic cells connect the innate and acquired immune systems collecting antigens at the site of inflammation and transporting them to sites, such as the lymph nodes, where immunocompetent B and T cells reside. 5. Phagocytosis is a multistep cellular process for the elimination of pathogens and Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 2. Most cells express plasma membrane pattern recognition receptors that recognize molecules produced infectious microorganisms called molecular patterns, or products of cellular damage called molecular patterns. Cellular Products 1. The cells of the innate immune system secrete many biochemical mediators that are responsible for activating other these cytokines include interleukins, chemokines, interferons, and other molecules. 2. The most important proinflammatory cytokines are and tumor necrosis 3. Interferons are produced cells that are infected viruses. Once released from infected cells, interferons can stimulate neighboring healthy cells to produce substances that prevent viral infection. 4. Chemokines are synthesized a number of different cells and induce leukocytes through chemotaxis. Mast Cell 1. The most important activator of the inflammatory response is the mast cell, which initiates inflammation releasing biochemical mediators from preformed cytoplasmic granules and synthesizing other mediators in response to a stimulus. 2. Histamine is the major vasoactive amine released from mast cells. It causes dilation of capillaries and retraction of endothelial cells lining the capillaries, which increases vascular permeability. Endothelium and Platelets 1. The endothelial cells lining the circulatory system normally regulate circulating components of the inflammatory system and maintain normal blood flow preventing spontaneous activation of platelets and members of the clotting system. 2. During inflammation the endothelium expresses receptors that help leukocytes leave the vessel and retract to allow fluid to pass into the tissues. 3. Platelets interact with the coagulation cascade to stop bleeding and release a number of mediators that promote and control inflammation. Phagocytes 1. The polymorphonuclear neutrophil, the predominant phagocytic cell in the early inflammatory response, exits the circulation diapedesis through the retracted endothelial cell junctions and moves to the inflammatory site chemotaxis. 2. Eosinophils release products that control the inflammatory response and are the principal cell that kills parasitic organisms. 3. The macrophage, the predominant phagocytic cell in the late inflammatory response, is highly phagocytic, responsive to cytokines, and promotes wound healing. 4. Dendritic cells connect the innate and acquired immune systems collecting antigens at the site of inflammation and transporting them to sites, such as the lymph nodes, where immunocompetent B and T cells reside. 5. Phagocytosis is a multistep cellular process for the elimination of pathogens and Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points foreign debris. The steps include recognition and attachment, engulfment, formation of a phagosome and phagolysosome, and destruction of pathogens or foreign debris. Phagocytic cells engulf microorganisms and enclose them in phagocytic vacuoles, within which toxic products and degradative lysosomal enzymes kill and digest the microorganisms. 6. Opsonins, such as antibody and complement component C3b, coat microorganisms and make them more susceptible to phagocytosis binding them more tightly to the phagocyte. Local Manifestations of Acute Inflammation 1. Local manifestations of inflammation are the result of the vascular changes associated with the inflammatory process, including vasodilation and increased capillary permeability. The symptoms include redness, heat, swelling, and pain. Systemic Manifestations of Acute Inflammation 1. The principal systemic effects of inflammation are fever and increases in levels of circulating leukocytes and plasma proteins. Chronic Inflammation 1. Chronic inflammation can be a continuation of acute inflammation that lasts 2 weeks or longer. It also can occur as a distinct process without much preceding acute inflammation. 2. Chronic inflammation is characterized a dense infiltration of lymphocytes and macrophages. The body may wall off and isolate the infection to protect against tissue damage formation of a granuloma. Resolution and Repair 1. Resolution or regeneration is the return of tissue to nearly normal structure and function. Repair is healing scar tissue formation. 2. Damaged tissue proceeds to resolution if little tissue has been lost or injured tissue is capable of regeneration. This is called healing primary intention. 3. Tissues that sustained extensive damage or those incapable of regeneration heal the process of repair resulting in the formation of a scar. This is called healing secondary intention. 4. Resolution and repair occur in two separate phases, the reconstructive phase, in which the wound begins to heal, and the maturation phase, in which the healed wound is remodeled. 5. Dysfunctional wound healing can occur as a result of abnormalities in either the inflammatory response or the reconstructive phase of resolution and repair. PEDIATRICS Factors Affecting Innate Immunity in the Newborn Child 1. Neonates often have transiently depressed inflammatory function, particularly neutrophil chemotaxis and alternative complement pathway activity. 2. The T immune response is adequate in the fetus and neonate, but the T immune response develops slowly during the first 6 months of life. 3. Maternal immunoglobulin antibodies are transported across the placenta into the fetal Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points foreign debris. The steps include recognition and attachment, engulfment, formation of a phagosome and phagolysosome, and destruction of pathogens or foreign debris. Phagocytic cells engulf microorganisms and enclose them in phagocytic vacuoles, within which toxic products and degradative lysosomal enzymes kill and digest the microorganisms. 6. Opsonins, such as antibody and complement component C3b, coat microorganisms and make them more susceptible to phagocytosis binding them more tightly to the phagocyte. Local Manifestations of Acute Inflammation 1. Local manifestations of inflammation are the result of the vascular changes associated with the inflammatory process, including vasodilation and increased capillary permeability. The symptoms include redness, heat, swelling, and pain. Systemic Manifestations of Acute Inflammation 1. The principal systemic effects of inflammation are fever and increases in levels of circulating leukocytes and plasma proteins. Chronic Inflammation 1. Chronic inflammation can be a continuation of acute inflammation that lasts 2 weeks or longer. It also can occur as a distinct process without much preceding acute inflammation. 2. Chronic inflammation is characterized a dense infiltration of lymphocytes and macrophages. The body may wall off and isolate the infection to protect against tissue damage formation of a granuloma. Resolution and Repair 1. Resolution or regeneration is the return of tissue to nearly normal structure and function. Repair is healing scar tissue formation. 2. Damaged tissue proceeds to resolution if little tissue has been lost or injured tissue is capable of regeneration. This is called healing primary intention. 3. Tissues that sustained extensive damage or those incapable of regeneration heal the process of repair resulting in the formation of a scar. This is called healing secondary intention. 4. Resolution and repair occur in two separate phases, the reconstructive phase, in which the wound begins to heal, and the maturation phase, in which the healed wound is remodeled. 5. Dysfunctional wound healing can occur as a result of abnormalities in either the inflammatory response or the reconstructive phase of resolution and repair. PEDIATRICS Factors Affecting Innate Immunity in the Newborn Child 1. Neonates often have transiently depressed inflammatory function, particularly neutrophil chemotaxis and alternative complement pathway activity. 2. The T immune response is adequate in the fetus and neonate, but the T immune response develops slowly during the first 6 months of life. 3. Maternal immunoglobulin antibodies are transported across the placenta into the fetal Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Huether and McCance: Understanding Pathophysiology, 5th Edition Chapter 06: Adaptive Immunity Key Points Third Line of Defense: Adaptive Immunity 1. Adaptive immunity is a state of protection, primarily against infectious agents, that differs from inflammation being slower to develop, being more specific, and having memory, that makes it much 2. The adaptive immune response is most often initiated cells of the innate system. These cells process and present portions of invading pathogens to lymphocytes in peripheral lymphoid tissue. 3. The adaptive immune response is mediated two different types of lymphocytes and T lymphocytes. Each has distinct functions. B cells are responsible for humoral immunity that is mediated circulating antibodies, whereas T cells are responsible for immunity, in which they kill targets directly or stimulate the activity of other leukocytes. 4. Adaptive immunity can be either active or passive depending on whether immune response components originated in the host or came from a donor. Antigens and Immunogens 1. Antigens are molecules that bind and react with components of the immune response, such as antibodies and receptors on B and T cells. Most antigens can induce an immune response, and these antigens are called immunogens. 2. All immunogens are antigens but not all antigens are immunogens. 3. Some pathogens are successful because they mimic but avoid inducing an immune response. 4. Large molecules, such as proteins, polysaccharides, and nucleic acids, are most immunogenic. Thus molecular size is an important factor for antigen immunogenicity. 5. Haptens are antigens too small to be immunogens themselves but become immunogenic after combining with larger molecules. 6. The or epitope, is the precise chemical structure with which an antibody or B cell receptor reacts. 7. are antigens on an own cells. The immune system does not normally recognize as immunogenic, a condition known as tolerance. 8. The response to antigen can be divided into two phases: the primary and secondary responses. The primary response of humoral immunity is usually dominated IgM, with lesser amounts of IgG. The secondary immune response has a more rapid production of a larger amount of antibody, predominantly IgG. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Huether and McCance: Understanding Pathophysiology, 5th Edition Chapter 06: Adaptive Immunity Key Points Third Line of Defense: Adaptive Immunity 1. Adaptive immunity is a state of protection, primarily against infectious agents, that differs from inflammation being slower to develop, being more specific, and having memory, that makes it much 2. The adaptive immune response is most often initiated cells of the innate system. These cells process and present portions of invading pathogens to lymphocytes in peripheral lymphoid tissue. 3. The adaptive immune response is mediated two different types of lymphocytes and T lymphocytes. Each has distinct functions. B cells are responsible for humoral immunity that is mediated circulating antibodies, whereas T cells are responsible for immunity, in which they kill targets directly or stimulate the activity of other leukocytes. 4. Adaptive immunity can be either active or passive depending on whether immune response components originated in the host or came from a donor. Antigens and Immunogens 1. Antigens are molecules that bind and react with components of the immune response, such as antibodies and receptors on B and T cells. Most antigens can induce an immune response, and these antigens are called immunogens. 2. All immunogens are antigens but not all antigens are immunogens. 3. Some pathogens are successful because they mimic but avoid inducing an immune response. 4. Large molecules, such as proteins, polysaccharides, and nucleic acids, are most immunogenic. Thus molecular size is an important factor for antigen immunogenicity. 5. Haptens are antigens too small to be immunogens themselves but become immunogenic after combining with larger molecules. 6. The or epitope, is the precise chemical structure with which an antibody or B cell receptor reacts. 7. are antigens on an own cells. The immune system does not normally recognize as immunogenic, a condition known as tolerance. 8. The response to antigen can be divided into two phases: the primary and secondary responses. The primary response of humoral immunity is usually dominated IgM, with lesser amounts of IgG. The secondary immune response has a more rapid production of a larger amount of antibody, predominantly IgG. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points Humoral Immune Response 1. The humoral immune response consists of molecules produced B cells. B cells are lymphocytes. 2. Antibodies are plasma glycoproteins that can be classified chemical structure and biologic activity as IgG, IgM, IgA, IgE, or IgD. 3. A typical antibody molecule is constructed of two identical heavy chains and two identical light chains and has portions that bind antigen and portion that interacts with complement or receptors on cells. 4. The protective effects of antibodies may be direct or indirect. 5. Direct effects result from the binding of antibody directly to a harmful antigen or infectious agent. These include inhibition of processes that are necessary for infection, such as the reaction of an infectious agent with a particular cell in the body or neutralization of harmful bacterial toxins. 6. Indirect effects result from activation of inflammation antibodies through the fragment, crystalline binding portion of the molecule. These include opsonization to increase phagocytosis, killing the infectious agent through activation of complement, and widespread activation of inflammation through the production of biologically active complement components, such as C5a. 7. IgE is a special class of antibody that helps defend against parasitic infections. 8. Antibodies of the systemic immune system function internally, in the bloodstream and tissues. Antibodies of the secretory, or mucosal, immune system function externally, in the secretions of mucous membranes. Immunity 1. T cells are responsible for the immune response. T cells are lymphocytes. 2. There are several types of mature T cells including the cells, cells, cells, and memory cells. Immune Response: and Together 1. The production of B and T lymphocytes with receptors against millions of antigens that possibly will be encountered in an lifetime occurs in the fetus in the primary lymphoid organs: the thymus for T cells and portions of the bone marrow for B cells. This diversity is called clonal diversity. 2. Immunocompetent T and B cells migrate from the primary lymphoid organs into the circulation and secondary lymphoid organs to await antigen. 3. Induction of an immune response, or clonal selection, begins when antigen enters the body. 4. Most antigens must first interact with cells. Dendritic cells are present in the skin, mucosa, and lymphoid tissues also present antigen. 5. Antigen is processed in the cells and presented on the cell surface molecules of the major histocompatibility complex. The particular major histocompatibility complex molecule that presents antigen determines which cell will respond to that antigen. cells require that the antigen be presented in a complex with MHC class II molecules. cells require that antigen be presented MHC class I molecules. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points Humoral Immune Response 1. The humoral immune response consists of molecules produced B cells. B cells are lymphocytes. 2. Antibodies are plasma glycoproteins that can be classified chemical structure and biologic activity as IgG, IgM, IgA, IgE, or IgD. 3. A typical antibody molecule is constructed of two identical heavy chains and two identical light chains and has portions that bind antigen and portion that interacts with complement or receptors on cells. 4. The protective effects of antibodies may be direct or indirect. 5. Direct effects result from the binding of antibody directly to a harmful antigen or infectious agent. These include inhibition of processes that are necessary for infection, such as the reaction of an infectious agent with a particular cell in the body or neutralization of harmful bacterial toxins. 6. Indirect effects result from activation of inflammation antibodies through the fragment, crystalline binding portion of the molecule. These include opsonization to increase phagocytosis, killing the infectious agent through activation of complement, and widespread activation of inflammation through the production of biologically active complement components, such as C5a. 7. IgE is a special class of antibody that helps defend against parasitic infections. 8. Antibodies of the systemic immune system function internally, in the bloodstream and tissues. Antibodies of the secretory, or mucosal, immune system function externally, in the secretions of mucous membranes. Immunity 1. T cells are responsible for the immune response. T cells are lymphocytes. 2. There are several types of mature T cells including the cells, cells, cells, and memory cells. Immune Response: and Together 1. The production of B and T lymphocytes with receptors against millions of antigens that possibly will be encountered in an lifetime occurs in the fetus in the primary lymphoid organs: the thymus for T cells and portions of the bone marrow for B cells. This diversity is called clonal diversity. 2. Immunocompetent T and B cells migrate from the primary lymphoid organs into the circulation and secondary lymphoid organs to await antigen. 3. Induction of an immune response, or clonal selection, begins when antigen enters the body. 4. Most antigens must first interact with cells. Dendritic cells are present in the skin, mucosa, and lymphoid tissues also present antigen. 5. Antigen is processed in the cells and presented on the cell surface molecules of the major histocompatibility complex. The particular major histocompatibility complex molecule that presents antigen determines which cell will respond to that antigen. cells require that the antigen be presented in a complex with MHC class II molecules. cells require that antigen be presented MHC class I molecules. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Huether and McCance: Understanding Pathophysiology, 5th Edition Chapter 07: Infection and Defects in Mechanisms of Defense Key Points Infection 1. Bacteria injure cells producing exotoxins or endotoxins. Exotoxins are enzymes that can damage the plasma membranes of host cells or can inactivate enzymes critical to protein synthesis, and endotoxins activate the inflammatory response and produce fever. 2. Septicemia is the proliferation of bacteria in the blood. Endotoxins released borne bacteria cause the release of vasoactive enzymes that increase the permeability of blood vessels. Leakage from vessels causes hypotension that can result in septic shock. 3. Viruses enter host cells and use the metabolic processes of host cells to proliferate. 4. Viruses that have invaded host cells may decrease protein synthesis, disrupt lysosomal membranes, form inclusion bodies where synthesis of viral nucleic acids is occurring, fuse with host cells to produce giant cells, alter antigenic properties of the host cell, and transform host cells into cancerous cells. 5. Diseases caused fungi are called mycoses, and they occur in two forms: yeasts and molds. 6. Dermatophytes are fungi that infect skin, hair, and nails with diseases such as ringworm and foot. 7. Fungi release toxins and enzymes that are damaging to tissue. 8. Parasitic microorganisms range from unicellular protozoa to large worms. Although less common in the United States, parasites and protozoa are common causes of infection worldwide. 9. Parasitic and protozoal infections are rarely transmitted from human to human. Infection mainly spreads through vectors or through contaminated water or food. Deficiencies in Immunity 1. Immunodeficiency is the failure of mechanisms of to function in their normal capacity. 2. Immunodeficiencies are either congenital or acquired. Congenital immunodeficiencies are caused genetic defects that disrupt lymphocyte development, whereas acquired immunodeficiencies are secondary to disease or other physiologic alterations. 3. The clinical hallmark of immunodeficiency is a propensity to unusual or recurrent severe infections. The type of infection usually reflects the immune system defect. 4. The most common infections in individuals with defects of immune response are fungal and viral, whereas infections in individuals with defects of the humoral immune response or complement function are primarily bacterial. 5. Severe combined immunodeficiency is a total lack of T cell function and a severe lack of B cell function. 6. DiGeorge syndrome is characterized complete or partial lack of the thymus, the parathyroid glands, and cardiac anomalies. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Huether and McCance: Understanding Pathophysiology, 5th Edition Chapter 07: Infection and Defects in Mechanisms of Defense Key Points Infection 1. Bacteria injure cells producing exotoxins or endotoxins. Exotoxins are enzymes that can damage the plasma membranes of host cells or can inactivate enzymes critical to protein synthesis, and endotoxins activate the inflammatory response and produce fever. 2. Septicemia is the proliferation of bacteria in the blood. Endotoxins released borne bacteria cause the release of vasoactive enzymes that increase the permeability of blood vessels. Leakage from vessels causes hypotension that can result in septic shock. 3. Viruses enter host cells and use the metabolic processes of host cells to proliferate. 4. Viruses that have invaded host cells may decrease protein synthesis, disrupt lysosomal membranes, form inclusion bodies where synthesis of viral nucleic acids is occurring, fuse with host cells to produce giant cells, alter antigenic properties of the host cell, and transform host cells into cancerous cells. 5. Diseases caused fungi are called mycoses, and they occur in two forms: yeasts and molds. 6. Dermatophytes are fungi that infect skin, hair, and nails with diseases such as ringworm and foot. 7. Fungi release toxins and enzymes that are damaging to tissue. 8. Parasitic microorganisms range from unicellular protozoa to large worms. Although less common in the United States, parasites and protozoa are common causes of infection worldwide. 9. Parasitic and protozoal infections are rarely transmitted from human to human. Infection mainly spreads through vectors or through contaminated water or food. Deficiencies in Immunity 1. Immunodeficiency is the failure of mechanisms of to function in their normal capacity. 2. Immunodeficiencies are either congenital or acquired. Congenital immunodeficiencies are caused genetic defects that disrupt lymphocyte development, whereas acquired immunodeficiencies are secondary to disease or other physiologic alterations. 3. The clinical hallmark of immunodeficiency is a propensity to unusual or recurrent severe infections. The type of infection usually reflects the immune system defect. 4. The most common infections in individuals with defects of immune response are fungal and viral, whereas infections in individuals with defects of the humoral immune response or complement function are primarily bacterial. 5. Severe combined immunodeficiency is a total lack of T cell function and a severe lack of B cell function. 6. DiGeorge syndrome is characterized complete or partial lack of the thymus, the parathyroid glands, and cardiac anomalies. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 7. Defects in B cell function are diverse, ranging from a complete lack of the human bursal equivalent, the lymphoid organs required for B cell maturation, to deficiencies in a single class of immunoglobulins. 8. Acquired immunodeficiencies are caused superimposed conditions, such as malnutrition, medical therapies, physical or psychologic trauma, or infections. 9. Immunodeficiency syndromes usually are treated replacement therapy. Deficient antibody production is treated replacement of missing immunoglobulins with commercial preparations. Lymphocyte deficiencies are treated with the replacement of host lymphocytes with transplants of bone marrow, fetal liver, or fetal thymus from a donor. 10. AIDS is an acquired dysfunction of the immune system caused a retrovirus that infects and destroys CD4 lymphocytes. Hypersensitivity: Allergy, Autoimmunity, and Alloimmunity 1. Hypersensitivity is an inappropriate immune response misdirected against the own tissues or directed against beneficial foreign tissues, such as transfusions or or it can be exaggerated responses against environmental antigens. 2. Mechanisms of hypersensitivity are classified as reactions, specific reactions, reactions, and reactions. 3. Hypersensitivity reactions can be immediate. 4. Anaphylaxis, the most rapid immediate hypersensitivity reaction, is an explosive reaction that occurs within minutes of reexposure to the antigen and can lead to cardiovascular shock. 5. Allergens are antigens that cause allergic responses. 6. Type I Hypersensitivity: reactions occur after antigen reacts with IgE on mast cells, leading to mast cell degranulation and the release of histamine and other inflammatory substances. 7. Type II Hypersensitivity: reactions are caused four possible mechanisms: lysis, opsonization and phagocytosis, dependent cytotoxicity, and modulation of cellular function. 8. Type Hypersensitivity: Immune reactions are caused the formation of immune complexes that are deposited in target tissues, where they activate the complement cascade, generating chemotactic fragments that attract neutrophils into the inflammatory site. 9. disease can be a systemic reaction, such as serum sickness, or localized, such as the Arthus reaction. 10. Type IV Hypersensitivity: reactions are caused specifically sensitized T cells, which either kill target cells directly or release lymphokines that activate other cells, such as macrophages. 11. Allergies can be mediated any of the four mechanisms of hypersensitivity. 12. Clinical manifestations of allergic reactions are usually confined to the areas of initial intake or contact with the allergen. Ingested allergens induce gastrointestinal symptoms, airborne allergens induce respiratory or skin manifestations, and contact allergens induce allergic responses at the site of contact. 13. Atopic individuals are genetically predisposed to the development of allergies. 14. Alloimmunity is the immune reaction against antigens on the tissues of other members of the same species. Mos items and derived items 2012 Mos, Inc., an imprint of Elsevier Inc. Key Points 7. Defects in B cell function are diverse, ranging from a complete lack of the human bursal equivalent, the lymphoid organs required for B cell maturation, to deficiencies in a single class of immunoglobulins. 8. Acquired immunodeficiencies are caused superimposed conditions, such as malnutrition, medical therapies, physical or psychologic trauma, or infections. 9. Immunodeficiency syndromes usually are treated replacement therapy. Deficient antibody production is treated replacement of missing immunoglobulins with commercial preparations. Lymphocyte deficiencies are treated with the replacement of host lymphocytes with transplants of bone marrow, fetal liver, or fetal thymus from a donor. 10. AIDS is an acquired dysfunction of the immune system caused
Keypoints-Mc C H-2014 - study guide for exam 2
Course: Pathophysiology (NSG 211)
University: Marian University
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