NUR 529 Exam 1 Blueprint Completed.docx

**The University of Alabama** **Capstone College of Nursing** **NUR 529 Exam 1 Blueprint** Pages below are from Porth's Pathophysiology: Concepts of Altered States, 11^th^ ed., and the current e-book on Coursepoint. Older versions are not included, this course does not utilize older textbook vers...

**The University of Alabama** **Capstone College of Nursing** **NUR 529 Exam 1 Blueprint** Pages below are from Porth's Pathophysiology: Concepts of Altered States, 11^th^ ed., and the current e-book on Coursepoint. Older versions are not included, this course does not utilize older textbook versions. Format for page numbers below is Porth 10^th^ ed. "hard copy" book/ Course Point Porth E-Book. Example: p. 967/975. If the pages correlate between editions then only one will be listed. **Unit 1. Chapter 1. There are 2 questions from this unit. Starts on p. 2** 1\. Concepts of Health and Disease. Vocabulary: - Etiology- The cause of a disease - Pathogenesis- Explains how the disease process evolves. - Morphology- Reers to the fundamental structure or form of cells or tissues - Histology: Deals with the study of cells and the extracellular matrix of body tissues. (Microscopic anatomy) - clinical manifestations: - Conditions produced by a disease that make it evident the person is sick. - Symptoms are subjective complaints noted by the person with the disorder - Sign: is an objective manifestation noted by an observer. - Syndrome: Compilation of signs and symptoms - Complication: adverse extension of a disease or outcome of treatment. - Sequalae: Lesion or impairment that follow or are caused by a disease - Diagnosis: The designation as to the nature or cause of a health problem. - clinical course: Describes the evolution of a disease - Acute -- severe but self-limiting - Chronic- taking place over a long period of time - Sub-acute- Not as severe as acute, and not as prolonged as chronic 2\. Concepts of Health and Disease: - Disease: The nature and cause of a health problem. - The second question comes from the same content section. **Unit 2. Chapters 2- 6. There are 16 questions from this unit. Starts on p. 49** 3\. Chapter 3. Cellular Adaptation: Cells adapt to changes in the internal environment. - Adaptive cellular responses also include intracellular accumulations and storage in abnormal amounts. - Cells can adapt to increase work demands or threats to survival by changing: - SIZE -- ATROPHY AND HYPERTROPHY - NUMBER- HYPERPLASIA - FORM -- METAPLASIA - Cellular adaptation occurs in response to a normal stimulus and ceases once the need for adaptation ceases - Atrophy: - 5 categories of atrophy 1. Disuse: a reduction in skeletal muscle use 2. Denervation 3. Loss of endocrine stimulation 4. Inadequate nutrition 5. Ischemia or decreased blood flow. - Hypertrophy: Increase in cell size with an increase in functioning tissue mass - Can occur from 6. normal physiologic conditions 7. Abnormal pathological conditions - - Hyperplasia: Hyperplasia refers to an increase in the number of cells in an organ or tissue. An increase in the number of cells in an organ or tissues -physiologic vs pathologic, examples. Exercise induced "Athletes heart" vs. Hypertrophy from dilated cardiomyopathy 4\. Chapter 3. Cellular Adaptation: - Metaplasia: Represents a reversible change where one adult cell type is replaced by another adult cell type. Usually occurs in the case of chronic irritation or inflammation, - Examples: Barret Esophagus- the presence of a metaplastic columnar-lined esophagus induced by GERD. - People with BE are at higher risk of developing adenocarcinoma of the esophagus but most do not develop esophageal cancer. 5\. Chapter 3. Cellular Adaptation: Adaptive cellular responses also include intracellular accumulations and storage of products in abnormal amounts Cells are able to adapt to increased work demands or threats to survival by changing their size (atrophy and hypertrophy), number (hyperplasia), and form (metaplasia). Normal cellular adaptation occurs in response to an appropriate stimulus and ceases once the need for adaptation has ceased. - Dysplasia: Characterized by deranged cell growth of specific tissue that results in cells that vary in size, shape and organization. - Strongly implicated as a precursor to cancer. - Adaptive and potentially reversible if irritating cause is removed. - Mostly occurs in respiratory tract and uterine cervix - examples :Through use of Pap smears it\'s been documented that cervical cancer develops in a series of incremental epithelial changes from severe dysplasia to invasive cancer. - Read about Pap smear. 6\. & 7. Chapter 3. Cell Injury and Death: Mechanisms of Cell Injury: There seem to be at least three major mechanisms whereby most injurious agents exert their effects: 1. Free radical formation a. Free radicals are highly reactive chemical species with an unpaired electron in the outer orbit (valence shell) of the molecule b. In the literature, the unpaired electron is denoted by a dot, for example, NO. c. The unpaired electron causes free radicals to be unstable and highly reactive, so they react nonspecifically with molecules in the vicinity. d. Oxidative damage has been implicated in many diseases e. Oxidative stress is thought to play an important role in the development of cancer f. Reestablishment of blood flow after loss of perfusion, as occurs during heart attack and stroke, is associated with oxidative injury to vital organs g. Antioxidants are natural and synthetic molecules that inhibit the reactions of ROS with biologic structures or prevent the uncontrolled formation of ROS. h. Nonenzymatic antioxidants include carotenes (e.g., vitamin A), tocopherols (e.g., vitamin E), ascorbate (vitamin C), glutathione, flavonoids, selenium, and zinc ( Antioxidants include enzymatic and nonenzymatic compounds 2. Hypoxia and ATP depletion i. Hypoxia deprives the cell of oxygen and interrupts oxidative metabolism and the generation of ATP. j. Ischemia is characterized by impaired oxygen delivery and impaired removal of metabolic end products such as lactic acid. k. pure hypoxia, which depends on the oxygen content of the blood and affects all cells in the body, l. ischemia commonly affects blood flow through limited numbers of blood vessels and produces local tissue injury m. In hypermetabolic states, cells may require more oxygen than that can be supplied by normal respiratory function and oxygen transport n. Hypoxia causes a power failure in the cell, with widespread effects on the cell's structural and functional components. o. Infarction (i.e., tissue death) occurs when an artery supplying an organ or part of the body becomes occluded and no other source of blood supply exists. As a rule, the shape of the infarction is conical and corresponds to the distribution of the artery and its branches. An artery may be occluded by an embolus, a thrombus, disease of the arterial wall, or pressure from outside the vessel. 3. Disruption of intracellular calcium homeostasis Causes of Cell Injury Cell damage can occur in many ways. For purposes of discussion, the ways by which cells are injured have been grouped into five categories: 1. Injury from physical agents a. Mechanical Forces. Injury or trauma due to mechanical forces occurs as the result of body impact with another object. The body or the mass can be in motion, or, as sometimes happens, both can be in motion at the time of impact. These types of injuries split and tear tissue, fracture bones, injure blood vessels, and disrupt blood flow. b. Extremes of Temperature. Extremes of heat and cold cause damage to the cell, its organelles, and its enzyme systems. i. Exposure to cold increases blood viscosity and induces vasoconstriction by direct action on blood vessels and through reflex activity of the sympathetic nervous system. ii. The resultant decrease in blood flow may lead to hypoxic tissue injury, depending on the degree and duration of cold exposure. Injury from freezing probably results from a combination of ice crystal formation and vasoconstriction. iii. The decreased blood flow leads to capillary stasis and arteriolar and capillary thrombosis. Edema results from increased capillary permeability. c. Electrical Injuries. Electrical injuries can affect the body through extensive tissue injury and disruption of neural and cardiac impulses. iv. Alternating current is usually more dangerous than direct current because it causes violent muscle contractions, preventing the person from releasing the electrical source and sometimes resulting in fractures and dislocations. v. In electrical injuries, the body acts as a conductor of the electrical current vi. The current enters the body from an electrical source, such as an exposed wire, and passes through the body and exits to another conductor, such as the moisture on the ground or a piece of metal the person is holding. vii. The pathway that a current takes is critical because the electrical energy disrupts impulses in excitable tissues. viii. Current flow through the brain may interrupt impulses from respiratory centers in the brain stem, and current flow through the chest may cause fatal cardiac arrhythmias. 2. Radiation injury d. Ionizing Radiation. Ionizing radiation impacts cells by causing ionization of molecules and atoms in the cell. e. This is accomplished by releasing free radicals that destroy cells and by directly hitting the target molecules in the cell. f. It can immediately kill cells, interrupt cell replication, or cause a variety of genetic mutations, which may or may not be lethal. g. Most radiation injury is caused by localized irradiation that is used in the treatment of cancer. h. Except for unusual circumstances such as the use of high-dose irradiation that precedes bone marrow transplantation, exposure to whole-body irradiation is rare. i. The injurious effects of ionizing radiation vary with the dose, dose rate (a single dose can cause greater injury than divided or fractionated doses), and the differential sensitivity of the exposed tissue to radiation injury. 3. Chemical injury j. Chemicals capable of damaging cells are everywhere around us. k. Air and water pollution contains chemicals capable of tissue injury, as does tobacco smoke and some processed or preserved foods. l. Some of the most damaging chemicals exist in our environment, including gases such as carbon monoxide, insecticides, and trace metals such as lead. m. Chemical agents can injure the cell membrane and other cell structures, block enzymatic pathways, coagulate cell proteins, and disrupt the osmotic and ionic balance of the cell. n. Corrosive substances such as strong acids and bases destroy cells as the substances come into contact with the body. o. Other chemicals may injure cells in the process of metabolism or elimination. ix. Carbon tetrachloride (CCl4), for example, causes little damage until it is metabolized by liver enzymes to a highly reactive free radical (CCl3 ). x. Carbon tetrachloride is extremely toxic to liver cells p. Many drugs---alcohol, prescription drugs, over-the-counter drugs, and street drugs---are capable of directly or indirectly damaging tissues. xi. Ethyl alcohol can harm the gastric mucosa, liver, developing fetus, and other organs. xii. Antineoplastic and immunosuppressant drugs can directly injure cells. q. Lead Toxicity xiii. Anemia is a cardinal sign of lead toxicity. xiv. Lead competes with the enzymes required for hemoglobin synthesis and with the membrane-associated enzymes that prevent hemolysis of red blood cells. xv. The gastrointestinal tract is the main source of symptoms in the adult. xvi. This is characterized by "lead colic," a severe and poorly localized form of acute abdominal pain. xvii. A lead line formed by precipitated lead sulfide may appear along the gingival margins. r. Mercury Toxicity. xviii. Mercury has been used for industrial and medical purposes for hundreds of years. xix. Mercury is toxic, and the hazards of mercury-associated occupational and accidental exposures are well known. xx. Currently, mercury and lead are the most toxic metals. xxi. Mercury is toxic in four primary forms: 1. mercury vapor 2. inorganic divalent mercury 3. methyl mercury 4. ethyl mercury xxii. Depending on the form of mercury exposure, toxicity involving the central nervous system and kidney can occur 4. Injury from biologic agents s. Biologic agents differ from other injurious agents in that they are able to replicate and can continue to produce their injurious effects. t. These agents range from submicroscopic viruses to larger parasites. 5. Injury from nutritional imbalances u. Nutritional excesses and nutritional deficiencies predispose cells to injury. v. Obesity and diets high in saturated fats are thought to predispose people to atherosclerosis. w. The body requires more than 60 organic and inorganic substances in amounts ranging from micrograms to grams. xxiii. These nutrients include 5. minerals, vitamins, 6. certain fatty acids 7. specific amino acids. xxiv. Dietary deficiencies can occur in the form of starvation, in which there is a deficiency of all nutrients and vitamins, or because of a selective deficiency of a single nutrient or vitamin. 8. Iron-deficiency anemia, scurvy, beriberi, and pellagra are examples of injury caused by the lack of specific vitamins or minerals. 9. The protein and calorie deficiencies that occur with starvation cause widespread tissue damage. x. Calcium functions as an important second messenger and cytosolic signal for many cell responses. y. Reversible cell injury, although impairing cell function, does not result in cell death. Two patterns of reversible cell injury can be observed under the microscope: cellular swelling and fatty change. 1. Apoptosis (programmed cell death) a. is a highly selective process that eliminates injured and aged cells, thereby controlling tissue regeneration. b. Cells undergoing apoptosis have characteristic morphologic features as well as biochemical changes. c. Two basic pathways for apoptosis have been described (Fig. 3.10). i. the extrinsic pathway, which is death receptor dependent ii. the intrinsic pathway, which is death receptor-independent. apoptosis, which functions in removing cells so that new cells can replace them, necrosis often interferes with cell replacement and tissue regeneration. Types of necrosis and Ischemia vs Infarction (2 questions from this content). 1. Liquefaction necrosis- a. occurs when some of the cells die but their catalytic enzymes are not destroyed b. An example of liquefaction necrosis is the softening of the center of an abscess with discharge of its contents 2. coagulation necrosis c. acidosis develops and denatures the enzymatic and structural proteins of the cell. d. This type of necrosis is characteristic of hypoxic injury and is seen in infarcted areas 3. Infarction (i.e., tissue death) e. occurs when an artery supplying an organ or part of the body becomes occluded and no other source of blood supply exists. f. As a rule, the shape of the infarction is conical and corresponds to the distribution of the artery and its branches. g. An artery may be occluded by an embolus, a thrombus, disease of the arterial wall, or pressure from outside the vessel. 4. Caseous necrosis h. is a distinctive form of coagulation necrosis in which the dead cells persist indefinitely i. It is most commonly found in the center of tuberculous granulomas or tubercles 1. 8\. Chapter 3. Cell Injury and Death-Intracellular Accumulations: Intracellular accumulations represent the buildup of substances that cells cannot immediately use or eliminate. 2. Fatty necrosis -In Tay-Sachs disease, another genetic disorder, abnormal lipids accumulate in the brain and other tissues, causing motor and mental deterioration beginning at approximately 6 months of age, followed by death at 2 to 5 years of age. In a similar manner, other enzyme defects lead to the accumulation of other substances. 9\. Chapter 3. Cell Injury and Death- Intracellular waste buildup. intracellular accumulations depends on the cause and severity of the condition. Many accumulations, such as lipofuscin and mild fatty change, have no effect on cell function. Some conditions, such as the hyperbilirubinemia that causes jaundice, are reversible. Other disorders, such as glycogen storage diseases, produce accumulations that result in organ dysfunction and other alterations in physiologic function. 10\. Chapter 3. Cell Injury and Death-Pathologic Calcifications- 1. Pathologic calcification involves the abnormal tissue deposition of calcium salts, together with smaller amounts of iron, magnesium, and other minerals. a. Dystrophic Calcification- dystrophic calcification is when it occurs in dead or dying tissues i. represents the macroscopic deposition of calcium salts in injured tissues. ii. It is often visible to the naked eye as deposits that range from gritty, sandlike grains to firm, hard rock material. 11\. Chapter 3. Cell Injury and Death-Pathologic Calcifications-metastatic. Metastatic Calcification In contrast to dystrophic calcification, which occurs in injured tissues, metastatic calcification occurs in normal tissues as the result of increased serum calcium levels (hypercalcemia ). Almost any condition that increases the serum calcium level can lead to calcification in inappropriate sites such as the lung, renal tubules, and blood vessels. The major causes of hypercalcemia are hyperparathyroidism, chronic renal failure, and primary bone disease such as mobilization of calcium from the bone in Paget disease. Malignant causes include multiple myeloma, small cell lung carcinoma, and leukemia 12\. Chapter 3. Cell Injury and Death-Injury from physical agents: lead poisoning, clinical manifestations, vulnerable population. The formation of a blue lead line along the margins of the gum is one of the diagnostic features of lead poisoning. 13\. Chapter 4. Genetic Control of Cell Function: From Genes to Proteins Although DNA directs the synthesis of needed biochemical products in the cell, it is the RNA that is responsible for the actual assembly of the products. The RNA assembles the amino acids into functional protein in the ribosome by the process of translation. Messenger RNA is formed from DNA by a process called transcription. In this process, the weak hydrogen bonds of the DNA nucleotides are temporarily broken so that free RNA nucleotides can pair with their exposed DNA counterparts of the DNA molecule (see Fig. 4.4). As with the base pairing of the DNA strands, complementary RNA bases pair with the DNA bases. As with DNA, guanine pairs with cytosine. But in RNA, uracil (U) replaces thymine to pair with adenine. 14\. & 15. Chapter 6. Screening, Diagnosis, and Treatment: Diagnostic Methods (2 questions from this content) 1. The birth of a child with a congenital defect is a traumatic event. Usually, two issues must be resolved. a. The first deals with the immediate and future care of the affected child and b. the second with the possibility of future children in the family having a similar defect. 2. Genetic assessment and counseling can help to determine whether the defect was inherited and the risk of recurrence. 3. Prenatal diagnosis provides a means of determining whether an unborn child has certain types of abnormalities. 4. It is important that the biological parents are aware of the potential complications of acquiring more information from these genetic tests. 5. Effective genetic counseling requires accurate diagnosis and communication of the findings and of the risks of recurrence to the biological parents and other family members who need such information. Prenatal Screening and Diagnosis - The purpose of prenatal screening and diagnosis is not just to detect fetal abnormalities but also to allay anxiety and provide assistance to prepare for a child with a specific disability. - Prenatal screening cannot be used to rule out all possible fetal abnormalities. It is limited to determining whether the fetus has (or probably has) predesignated conditions as indicated by late maternal age, family history, or well-defined risk factors. - Diagnosis - Ultrasonography - Ultrasonography is a noninvasive diagnostic method that uses reflections of high-frequency sound waves to visualize soft-tissue structures - Maternal Serum Markers - Maternal blood testing began in the early 1980s. Since that time, a number of serum factors have been studied as screening tests for fetal anomalies. - AFP is a major fetal plasma protein and has a structure similar to the albumin found in postnatal life. - AFP is made initially by the yolk sac, gastrointestinal tract, and liver. - Fetal plasma levels of AFP peak at approximately 10 to 13 weeks' gestation and decrease until the third trimester when the level peaks again. - A complex glycoprotein, hCG, is produced exclusively by the outer layer of the trophoblast shortly after implantation in the uterine wall. - It increases rapidly in the first 8 weeks of gestation, declines steadily until 20 weeks, and then plateaus. - The single maternal serum marker that yields the highest detection rate for Down syndrome is an elevated level of hCG. Inhibin A, which is secreted by the corpus luteum and fetoplacental unit, is also a maternal serum marker for fetal Down syndrome. - Maternal and amniotic fluid levels of AFP are elevated in pregnancies where the fetus has an NTD (i.e., anencephaly and open spina bifida) or certain other malformations such as an anterior abdominal wall defect in which the fetal integument is not intact - Unconjugated estriol - produced by the placenta from precursors provided by the fetal adrenal glands and liver. - Amniocentesis - Amniocentesis is an invasive diagnostic procedure that involves the withdrawal of a sample of amniotic fluid from the pregnant uterus usually using a transabdominal approach - Chorionic villus sampling - is an invasive diagnostic procedure that obtains tissue that can be used for fetal chromosome studies, - Percutaneous Umbilical Cord Blood Sampling - PUBS is an invasive diagnostic procedure that involves the transcutaneous insertion of a needle through the uterine wall and into the umbilical artery. - Cytogenetic and DNA Analyses - Amniocentesis and chorionic villus sampling yield cells that can be used for cytogenetic and DNA analyses. - Cytogenetic studies are used for fetal karyotyping to detect abnormalities of chromosome number and structure in the fetus. - Karyotyping also reveals the sex of the fetus. - This may be useful when an inherited defect is known to affect only one sex. 16\. Chapter 1. Page 10. What is evidence-based practice? (definition) Evidence-based practice refers to making decisions in healthcare based on scientific data that have shown a specific way of managing a disease, patient symptoms, and complaints. Using evidence-based practice mandates that healthcare providers cannot practice according to only "their" way or according to "how it has always been done before." Evidence-based practice is based on the integration of the individual clinical expertise of the practitioner with the best external clinical evidence from systematic research 17\. Chapter 1. Prenatal care. Page 9. Describe dietary recommendations to prevent neural tube defects. Primary prevention is directed at keeping disease from occurring by removing all risk factors. Examples of primary prevention include the administration of folic acid to pregnant people and people who may become pregnant to prevent fetal neural tube defects, **Genetic and Congenital Disorders. Starts on p. 94** a. Structural Chromosomal Abnormalities i. The deletion of a portion of a chromosome leads to the loss of genetic material and a shortened chromosome. ii. A special form of translocation called a centric fusion or Robertsonian translocation involves two acrocentric chromosomes in which the centromere is near the end, most commonly chromosomes 13 and 14, or 14 and 21. iii. Having an abnormal number of chromosomes is referred to as aneuploidy. b. Down Syndrome iv. Approximately 95% of cases of Down syndrome are caused by nondisjunction or an error in cell division during meiosis, resulting in a trisomy of chromosome 21. v. A rare form of Down syndrome can occur in the offspring of people in whom there has been a Robertsonian translocation vi. the definitive diagnosis of Down syndrome in the fetus is through chromosome analysis using chorionic villus sampling, amniocentesis, or percutaneous umbilical blood sampling, c. Turner Syndrome vii. Turner syndrome describes an absence of all (45, X/0) or part of the X chromosome. viii. Characteristically, a female with Turner syndrome is short in stature but has normal body proportions. ix. They lose the majority of their oocytes by the age of 2 years. Therefore, they do not menstruate and show no signs of secondary sex characteristics. x. There are variations in the syndrome, with abnormalities ranging from essentially a normal phenotype to cardiac abnormalities such as bicuspid aortic valve and coarctation of the aorta, and a small webbed neck d. Klinefelter syndrome xi. is a condition of testicular dysgenesis accompanied by the presence of one or more extra X chromosomes in excess of the usual male XY complement. xii. Most males with Klinefelter syndrome have one extra X chromosome (47, XXY). xiii. In rare cases, there may be more than one extra X chromosome (48, XXXY) xiv. Males with Klinefelter syndrome have congenital hypogonadism, which results in an inability to produce normal amounts of testosterone accompanied by an increase in hypothalamic gonadotrophic hormones e. Mitochondrial Gene Disorders xv. The mitochondria contain their own DNA, which is distinct from the DNA contained in the cell nucleus. xvi. Although the majority of inherited disorders come from nuclear DNA abnormalities, there are multiple disease-causing rearrangements and mutations that can occur in mitochondrial DNA (mtDNA). xvii. This DNA is packaged in a double-stranded circular chromosome and contains 37 genes: 2 ribosomal RNA genes, 22 transfer RNA genes, and 13 structural genes encoding subunits of the mitochondrial respiratory chain enzymes, which participate in oxidative phosphorylation and generation of adenosine triphosphate. f. Period of Vulnerability xviii. Period of Vulnerability xix. The embryo's development is most easily disturbed during the period when differentiation and development of the organs are taking place. This time interval, which is often referred to as the period of organogenesis, extends from day 15 to day 60 after conception. Environmental influences during the first 2 weeks after fertilization may interfere with implantation and result in abortion or early resorption of the products of conception. Each organ has a critical period during which it is highly susceptible to environmental derangements a. Infectious Agents: i. Many microorganisms cross the placenta and enter the fetal circulation, often producing multiple malformations. ii. The acronym TORCH stands for toxoplasmosis, other, rubella (i.e., German measles), cytomegalovirus, and herpes, which are the agents most frequently implicated in fetal anomalies. b. TERATOGENIC AGENTS iii. A teratogenic agent is one that produces abnormalities during embryonic or fetal life iv. Teratogenic agents such as radiation, chemicals and drugs, and infectious organisms are agents that produce abnormalities in the developing embryo. PEDIATRIC Considerations a. 1 in 150 live births has a chromosomal anomaly causing cognitive impairment and birth defects. Chromosomal abnormalities are even more prevalent among stillbirths and spontaneous abortions. b. Inborn errors of metabolism, caused by gene mutations, may be lethal if not treated, thus prompting many states to require mandatory newborn screening. c. Creation of a family pedigree can help to identify genetic disorders and is useful when going for genetic counseling. a. Genetic influences on aging are evident by a substantially longer life (up to 65%) when single-gene mutations occur in specific signaling pathways (Singh et al., 2019). b. The shortening or erosion of telomeres contributes to organismal aging Single autosomal Dominant disorders: - Autosomal dominant disorders also may manifest as a new mutation. Whether the mutation is passed on to the next generation depends on the affected person's reproductive capacity. Many autosomal dominant mutations are accompanied by reduced reproductive capacity; therefore, the defect is not perpetuated in future generations. - Although there is a 50% chance of inheriting a dominant genetic disorder from an affected biological parent, there can be wide variation in gene penetrance and expression. When a person inherits a dominant mutant allele but fails to exhibit the associated phenotype, the trait is described as having reduced penetrance 1. 23\. Chapter 5, page 84. Marfan's disorder. Also, in lecture in module. - Two relatively common disorders of autosomal inheritance, Marfan syndrome and neurofibromatosis (NF), are described here. - Neurofibromatosis. NF is a condition that causes tumors to develop from the Schwann cells of the neurologic system. - Marfan Syndrome: Connective tissue disorder with abnormalities in the skeletal, ocular, cardiovascular systems **Unit 3. Chapters 7- 8. There are 3 questions from this unit.** 24\. Chapter 7. Stress and Adaptation- 1. Treatment and Research of Stress Disorders a. The traumatic stress response is the change that occurs in the biochemical stress response system of people who have experienced some type of mistreatment as a child so that they are not able to respond effectively to stressors in the future Evidence supports that early intervention can assist such people in developing new and effective coping mechanisms to better manage stress in the future (Cabrera et al., 2020). b. For caregivers, stress can contribute to burnout. Multiple studies have shown that burnout leads to decreased patient satisfaction and increased safety risks c. A study conducted with caregivers of a spouse or family member during the COVID-19 pandemic demonstrated that they reported higher levels of caregiver stress and had poorer self-perceived global health ratings due to the reduction in home and community resources and limited contact with friends and family during the pandemic The following are examples of research that has been done on stress: 1. Geriatric Considerations a. An interpreter may be helpful when bilingual people use their home language when stressed (Eliopoulos, 2022). b. Caregiver stress contributes to abuse of older adults, highlighting the importance of educating about available resources and support systems (Eliopoulos, 2022). c. Role fulfillment is key to stress management in the aging adult. Sharing the need to allow the person to perform roles within limitations is encouraged (Eliopoulos, 2022). d. Stress is twice as common in people aged 50 to 65 than those aged 65 to 80 years (American Institute of Stress, 2023). 2. PEDIATRIC Considerations e. Stress in children can be due to normal developmental issues or atypical events including sickness, violence, or trauma. Resilience (coping skills to effectively deal with stress) will help the child to achieve balance (Kyle & Carman, 2022). f. Infants deal with stress by sucking. Regression back to a pacifier or bottle may occur during times of stress. Praise for age-appropriate behavior is recommended (Kyle & Carman, 2022). g. Comfort measures such as rocking, stroking, cuddling, and holding the child can reduce stress (Kyle & Carman, 2022). h. Children who are left home alone after school may experience a high degree of stress. This may be age-dependent, with children under the age of 11 or 12 experiencing self-care stress and those over the age of 12 feeling safe and confident in staying home alone. Some states have laws to help parents/caregivers make these decisions The Stress Response: Acute vs Chronic Stress & hormonal 1. Acute a. The stress response is a normal, coordinated physiologic system meant to increase the probability of survival, but also designed to be an **acute** response---turned on when necessary to bring the body back to a stable state and turned off when the challenge to homeostasis abates. b. Under normal circumstances, the neural responses and the hormones that are released during the response do not persist long enough to cause damage to vital tissues. 2. Chronic Stress c. The stress response is designed to be an acute self-limited response in which activation of the ANS and the HPA axis (The hypothalamic-pituitary-adrenal (HPA) axis is a neuroendocrine system that connects stress to physiological responses in the body) is controlled in a negative feedback manner. d. Chronicity and excessive activation of the stress response can result from chronic illnesses and can contribute to the development of long-term health problems. e. Chronic activation of the stress response is an important public health issue from both a health and a cost perspective. f. Stress is linked to a myriad of health disorders, such as diseases of the cardiovascular, gastrointestinal, immune, and neurologic systems, as well as depression, substance use disorder, eating disorders, accidents, and suicide. g. Allostatic load describes the cumulative effects of chronic stress on one's health. Stress hormones such as cortisol lead to negative effects on the immune, cardiovascular, and metabolic processes leading to inflammation, hypertension, hyperglycemia, and other health problems causing health risks (Cherry, 2022). Increased allostatic load contributes to health disparities in marginalized communities 3. Hormonal Stress: h. Neuroendocrine Responses i. effects on the body. 25\. Chapter 8. Compartmental Distribution of Body Fluids: Edema can be defined as palpable swelling produced by expansion of the interstitial fluid volume. Assessment: daily weight, visual assessment, measurement of the affected part, application of finger pressure to assess for pitting edema. Treatment: directed toward maintaining life when the swelling involves vital structures, correcting or controlling the cause, and preventing tissue injury. Edema of the lower extremities may respond to simple measures such as elevating the feet. Diuretic therapy is commonly used for an increase in ECF volume. Albumin may be administered to raise the plasma colloidal osmotic pressure when the cause of the edema is hypoalbuminemia. Elastic support stockings and sleeves increase interstitial fluid pressure and resistance to outward movement of fluid from the capillary into the tissue spaces. Edema assessment and treatment. 26\. Chapter 8. Mechanisms of Acid-Base: Function of the lungs and kidneys in acid-base Regulation. Respiratory: Control of extracellular co2 by the lungs. Only comes into play when the chemical buffers do not minimize H+ changes. Only about 50 to 75% effective as a buffer system, occurring within minutes and is maximal within 12 to 24 hours. In acting rapidly, it prevents large changes in pH from occurring while waiting for the much more slowly reacting kidneys to respond. Kidneys: Third line of defense in acid-base disturbances and play three major roles. First is through excretion of H+ from fixed acids that result from protein and lipid metabolism. Second is accomplished through the reabsorption of HCO3 that is filtered through the glomerulus, so it's not lost in the urine. The third is the production of new HCO3 that is released back into the blood **Unit 4. Chapters 10- 12. There are 10 questions from this unit. Begins on p. 263.** 27\. Chapter 10. Infectious Diseases. Diagnosis and Treatment of Infectious Diseases: Detection and Diagnosis of infectious diseases. The diagnosis of an infectious disease requires 2 criteria: the recovery of a probable pathogen or some evidence of its presence from the infected sites of a diseased host and accurate documentation of clinical signs and symptoms compatible with an infectious process. Culture: refers to the growth of a microorganism outside of the body, usually on or in artificial growth media such as agar plates or broth. In the case of bacterial pathogen, identification is based on microscopic appearance and gram stain reaction, shape, texture, and color (morphology) of the colonies and by a panel of biochemical reactions that fingerprint salient biochemical characteristics of the organism. Fungi and mycoplasmas are cultured in much the same way as bacteria but with more reliance on microscopic and colonial morphology for identification. Some fungi can take weeks to grow and identify through culture. In the setting of acute infection, it is important that cultures are obtained prior to antibiotic administration. The causative organism cannot be identified by culture in up to 33% of people presenting with sepsis. Serology: indirect means of identifying infectious agents by measuring serum antibodies in the diseased host. A tentative diagnosis can be made if the antibody level, also called the antibody titer, against a specific pathogen rises during the acute phase of the disease and falls during convalescence. Serologic identification of an infectious agent is not as accurate as a culture, but may be a useful adjunct. IgM specific antibodies generally rise and fall during the acute phase of the disease, whereas the synthesis of IgG increases during the acute phase and remains elevated until or beyond resolution. IgM antibodies do not cross the placenta, so if IgM is elevated in a neonate it did not come from mother, it originated in child. Antigen detection incorporates features of culture and serology but reduces to a fraction the time required for diagnosis. This method relies on purified antibodies to detect antigens of infectious agents in specimens obtained from the diseased host. DNA and RNA sequencing: DNA probe hybridization -- small fragements of DNA are cut from the genome of a specific pathogen and labeled with compounds that allow detection. Polymerase chain reaction (PCR) -- this method incorporates two unique reagents: a specific pair of oligonucleotides called primers and heat-stable DNA polymerase. 28\. Chapter 10. Infectious Diseases. Diagnosis and Treatment of Infectious Diseases: General intervention methods used in treatment of infectious diseases. Antimicrobial Agents: can be categorized roughly according to mechanism of anti-infective activity, chemical structure, and target pathogen. Antibacterial agents: antibiotics. Most antibiotics are actually produced by other microorganisms, primarily bacteria and fungi, as by-products of metabolism. Effective only against other prokaryotic organisms. Bactericidal if it causes irreversible and lethal damage Antiviral agents: Viral replication requires the use of eukaryotic host cell enzymes, and the drugs the effectively interrupt viral replication are likely to interfere with host cell production as well. Protease inhibitors are solely for the treatment of HIV, they inhibit an HIV-specific enzyme that is necessary for late maturation events in the virus life cycle. Antifungal agents: The target site of the two most important families of antifungal agents is the cytoplasmic membranes of yeasts or molds. Antiparasitic agents: Treatment of parastitic illness is based on exploiting essential components of the parasites metabolism or cellular anatomy that are not shared by the host. Any relatedness between the target site and the cells of the host increases the likelihood for toxic reactions in the host. 29\. Chapter 11. Innate and Adaptive Immunity: Epithelial Barriers. The intact skin is by far the most formidable physical barrier available to infection because of its design. It is comprised of closely packed cells that are organized in multiple layers that are continuously shed. In addition, a protective layer of protein, known as keratin, covers the skin. Sheets of tightly packed epithelial cells line and protect the gastrointestinal, respiratory, and urogenital tracts and physically prevent microorganisms from entering the body. These cells destroy the invading organisms by secreting antimicrobial enzymes, proteins, and peptides. When pathogens are able to breach the epithelial defenses, the innate immune response is initiated by the bodys leukocytes, which recognize common surface receptors present on the invading microorganisms. 30\. Chapter 11. Innate and Adaptive Immunity. See p. 261: Infectious disease terminology. Toxins produced by bacteria. Host -- any organism capable of supporting the nutritional and physical growth requirements of another Infection -- presence and multiplication within a host of another living organism, with subsequent injury to the host Microflora -- Internal and external exposed surfaces of the human body are normally and harmlessly inhabited by a multitude of bacteria Mutualism -- interaction in which both the microorganism and the host derive benefits from the interaction Parasitic relationship -- only the infecting organism benefits from the relationship and the host either gains nothing or sustains injury from the interaction. Plasmids -- smaller extrachromosomal pieces of circular DNA that bacteria often harbor (sometimes contain genetic material that increased the virulence or antibiotic resistance) 31\. Chapter 11. Adaptive Immunity. Passive Immunity. Adaptive immunity: acquired when the host mounts an immune response to an antigen either through the process of vaccination or from environmental exposure. It is called active immunity because it requires the host's own immune system to develop an immunologic response including the development of memory. Usually long lasting but requires a few days to weeks after a first exposure to sufficiently develop an appropriate immunologic response that culminates in the destruction of the presenting antigen. Passive immunity: Immunity transferred from another source. Most common form of passive immunity is that conferred from mother to fetus. IgG antibodies are transferred to the fetus via the placenta and also after birth in breast milk and colostrum so infants have some degree of protection from infection for 3 to 6 months. Produces only short-term protection that lasts weeks to months. 32\. Chapter 11. Pg. 292. Innate and Adaptive Immunity: Immunoglobulins. Primary & secondary immune response. Antibodies are protein molecules are also known as immunoglobulins. Igs are classified into 5 different categories based upon their role in the humoral defense mechanism. The Ig is compromised of four-polypeptide chains with at least 2 identical antigen-binding sites.  33\. Chapter 9: Page 317. Describe the emergency care of a client with anaphylaxis. Anaphylaxis is a castastropic, systemic, life-threatening IgE-mediated hypersensitivity reaction associated with the widespread release of histamine into the systemic circulation that produces massive vasodilation, hypotension, arterial hypoxia, and airway edema. Clinical manifestations occur along a continuum in severity and can be graded on a scale of I to IV. Grade I reactions are usually confined to the cutaneous and mucosal tissues manifesting as erythema and urticaria, with or without angioedema. Grade II reactions progress to include moderate multisystem signs such as hypotension, tachycardia, dyspnea, and GI disturbances. Grade III reactions become life threatening because of the development of bronchospasm, cardiac dysrhythmias, and cardiac collapse. Once a hypersensitivity reaction reaches grade IV, cardiac arrest has occurred and management is purely resuscitative in nature. Preventing exposure to potential triggers that cause anaphylaxis is essential. The initial management should focus on withdrawal of the offending allergen, maintenance of a patent airway, establishment of appropriate intravenous access, volume resuscitation, and administration of epinephrine. **Unit 5: Disorders of Neural Function. Chapters 13-16, 18. There are 12 questions from this** **unit.** 35\. Chapter 13. Metabolic Requirements of Nervous Tissue. Consequences of unmet Demand. Nervous tissue has a high rate of metabolism. The brain receives 15% to 20% of the total resting cardiac output and consumes 20% of its oxygen. Despite its substantial energy requirements, the brain cannot store oxygen or effectively engage in anaerobic metabolism. An interruption in the blood or oxygen supply to the brain rapidly leads to clinically observable signs and symptoms. Inte 36\. Chapter 14. Somatosensory Function, Pain, Headache, and Temperature Regulation: Acute pain: elicited by injury to body tissues and activation of nociceptive stimuli at the site of local tissue damage. Generally short duration and tends to resolve when the underlying pathologic process has resolved. Chronic pain: Pain that persists longer than might be reasonably expected after an inciting event. Continues for years. Sustained by factors that are both pathologically and physically remote from the originating cause. Cutaneous and Deep Somatic Pain: cutaneous pain arises from superficial structures. Deep somatic pain originates in deep body structures (muscles, tendons, joints, blood vessels). It is more diffuse than cutaneous pain. Visceral Pain: Origin in the visceral organs and is one of the most common pains produced by disease. The important difference between surface pain and visceral pain is the type of damage that causes pain. Strong contractions, distention, or ischemia affecting the walls of the viscera can cause severe pain. Referred Pain: pain that is perceived at a site different from its point of origin but innervated by the same spinal segment. Example: STEMI pain is referred to left arm, neck, and chest. Types of pain- compare definitions, begins on p. 402-403. 37\. Chapter 15. Disorders of the motor unit/Disorders of the Neuromuscular Junction: Myasthenia gravis, neuromuscular junction pathophysiology.p. 443. Myasthenia Gravis is a disorder of transmission at the neuromuscular junction because of antibody-mediated attack on the nicotinic AChR or muscle-specific tyrosine kinase that affects communication between the motor neuron and the innervated muscle. Can occur at any age but peak incidence is young adulthood. The exact mechanism is unclear but it is thought to be caused by sensitized helper T cells and an antibody-directed attack on the acetylcholine receptor in the neuromuscular junction. The antibody attack leads to a shedding of the acetylcholine receptor-rich terminal portions of the folds in the end plate of the muscle fiber, fewer receptors, and a widened synaptic space that impairs signal transmission. The antibodies do not directly block the binding. The neuromuscular junction serves as a synapse between a motor neuron and a skeletal muscle fiber. The transmission of impulses at the neuromuscular junction is mediated by the release of the neurotransmitter acetylcholine from the axon terminals. Acetylcholine binds to the specific receptors in the end-plate region of the muscle fiber surface to cause muscle contraction. 38\. Chapter 15. Disorders of Motor Function: Multiple Sclerosis. Clinical manifestations and Course. Multiple sclerosis is characterized by inflammation and destruction of mostly the white matter of the CNS myelin of the brain, spinal cord, and optic nerve. The peripheral nervous system is spared, and there is usually no evidence of an associated systemic disease. The lesions of MS consist of hard, sharp-edged, demyelinated patches that are visible throughout the white matter as well as sometimes the gray matter of the CNS. Areas commonly affected by MS are the optic nerve, corticobulbar tracts (speech and swallowing), corticospinal tracts (muscle strength), cerebellar tracts (gait and coordination), spinocerebellar tracts (balance), medial longitudinal fasciculus (conjugate gaze function of the extraocular eye muscles), and posterior cell columns of the spinal cord (position and vibratory sensation). Usually presents with an acute or subacute episode of parathesias, optic neuritis, diplopia, or specific types of gaze paralysis. Other common symptoms are abnormal gait, bladder and sexual dysfunction, vertigo, nystagmus, fatigue, and speech disturbance. These symptoms usually last for days to weeks and then completely or partially resolve. Four categories of the disease: Relapsing-remitting, secondary progressive, primary progressive, or progressive relapsing. 39\. Chapter 15. Disorders of the cerebellum and basal ganglia: Parkinson's Disease Degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity, akinesia/bradykinesia, and postural changes. Characterized by progressive destruction of the nigrostriatal pathway with subsequent reduction in striatal concentrations of dopamine. Mean onset is 57 years old. Because the basal ganglia also influence the autonomic nervous system, people with Parkinson disease often have excessive sweating, sebaceous gland secretion, and salivation. Cognitive dysfunction may also be present. Treatment must be highly individualized. No treatment will prevent the disease progression, only symptom management. Botulinum toxin injections may be used in the treatment of dystonias such as eyelid spasm and limb dystonias. Antiparkinson drugs act by increasing the functional ability of the underactive dopaminergic system or by reducing the excessive influence of excitatory cholinergic neurons. 40\. Chapter 16. Mechanisms of Brain Injury. Primary and Secondary Brain Injuries. Primary brain injuries: Damage is caused by impact. Include focal (contusion, laceration, hemorrhage) or diffuse (concussion, diffuse axonal injury). Secondary brain injuries: damage results from the subsequent brain swelling, infection, or cerebral hypoxia. Most common cause is ischemia. Hematomas. Subdural, acute vs chronic subdural hematomas. Epidural Hematoma: usually caused by head injury in which the temporal area of the skull is fractured. Develops between the inner table of the bones of the skull and the dura. Usually results from a tear in an artery associated with a skull fracture. More common in younger people because the dura is less firmly attached to the skull surface than in an older person. Traumatic Intracerebral Hematomas: single or multiple. Occur in any lobe of the brain but are most common in the frontal or temporal lobes, related to the bony prominences on the inner skull surface. Subdural: Develops in the area between the dura and the arachnoid (subdural space) and usually is the result of a tear in the small bridging veins that connect veins on the surface of the cortex to dural sinuses. These veins are snapped in head injury when the brain moves suddenly in relation to the skull. Acute: Acute subdural hematomas progress rapidly and have a high mortality rate because of the severe secondary injuries related to edema and increased ICP. Chronic: Symptoms of chronic subdural hematoma develop weeks after a head injury, so much later that the person may not remember having a head injury. More common in alcoholics and older adults because brain atrophy causes the brain to shrink away from the dura and stretch fragile bridging veins. 41\. Chapter 16. Mechanisms of Brain Injury. Stroke. Ischemic vs hemorrhagic. Ischemic: Caused by cerebrovascular obstruction by thrombosis or emboli. Five main mechanisms of stroke subtypes and their frequency: 20% large artery thrombosis (atherosclerotic disease), 25% small penetrating artery thrombosis disease (lacunar stroke), 20% cardiogenic embolism, 30% cryptogenic stroke (undetermined cause), and 5% other. Hemorrhagic: Most frequently fatal stroke results from the spontaneous rupture of a cerebral blood vessel. Common predisposing factors are advancing age and hypertension. Vomiting commonly occurs at onset, and headache occurs after. 42\. Chapter 16. Disorders of Brain Function/Cerebrovascular Disease/Stroke. Clinical Manifestations. Specific manifestations are determined by the cerebral artery that is affected, by the area of brain tissue that is supplied by that vessel, and by the adequacy of the collateral circulation. Always sudden in onset and focal and usually are one sided. Most common symptoms are a facial droop, arm weakness, and slurred speech. Other frequent symptoms are unilateral numbness, vision loss in 1 eye or to 1 side, language disturbance, and sudden unexplained imbalance or ataxia. 43\. Chapter 18. Neurocognitive Disorders: Alzheimer's Disease. Diagnosis and treatment. See chap 18 ppt and page 534. A diagnosis of alzheimers can only be confirmed by microscopic examination of tissue obtained from a cerebral biopsy or at autopsy. The diagnosis is based on clinical findings. Neuroimaging and metabolic screening are important steps in excluding other conditions when diagnosing. There is no curative treatment for AD. Medications may slow the progression and improve depression, agitation, or sleep disorders. Cholinesterase inhibitors have been shown to be effective in slowing the progression of the disease by potentiating the action of available acetylcholine and inhibiting acetylcholinesterase. Antipsychotics are not approved for using in treating agitation. Two major goals of care are maintaining socialization and providing support for caregivers. 44\. Chapter 15. Disorders of the motor unit/Polyneuropathies: Guillain-Barre Syndrome. Cause, clinical manifestations, and treatment. Guillain-Barre syndrome is an acute immune-mediated polyneuropathy. The syndrome defines a clinical entity that is characterized by rapidly progressive ascending symmetrical limb weakness and loss of tendon reflexes. Most common cause of acute, flaccid nontraumatic paralysis. Manifested by infiltration of mononuclear cells around the capillaries of the peripheral neurons, edema of the endoneurial compartment, and demyelination of ventral spinal roots. Cause probably has an immune component. Most people report an acute, influenza-like illness before the onset of symptoms. Clinical manifestations include progressive ascending muscle weakness of the limbs, producing a flaccid paralysis. Parasthesia and numbness often accompany the loss of motor function. Paralysis will progress to involve the respiratory muscles. Treatment includes support of vital functions and prevention of complications such as skin breakdown and thrombophlebitis. Treatment is most effective if initiated early in the course of the disease. Plasmapheresis and high-dose intravenous immunoglobulin therapy and generally the mainstay of treatment. 45\. Chapter 18. Neurocognitive Disorders: Schizophrenia-neurophysiology of symptoms. Page 530. The complete set of pathogenic mechanisms underlying schizophrenia is not clear. Research suggest that changes in the dysregulation of the dopamine and serotonergic system and other neurotransmitter changes such as decreased glutamate activity through dysfunction of its N-methyl-Daspartate receptor play a role. Many of the symptoms of impaired cognition seen in schizophrenia are through to be tied to deficits in GABA. Neuroimaging suggests several functional abnormalities occur which include loss of cortical gray matter, abnormal cortical thinning, reduced numbers of synaptic structures on neurons, reduced dendritic spine density of pyramidal neurons in the prefrontal cortex, and arrested migration of hippocampal neurons. 46\. Chapter 18. Neurocognitive Disorders: Mood disorders-neurophysiology of symptoms. Page 531. Epidemiologic and neurobiologic studies suggest interactions between biologic and psychosocial factors over time explain the risk of developing MDD. Multiple possible biologic theories have been identified in the development of depressive disorder including inflammation, HPA axis hyperactivity, low levels of neurotrophic growth factor, and low levels of vitamin D. Growing evidence supports some forms of depression may be linked to ongoing inflammation in the body. Neuroimaging indicates smaller hippocampal volumes and hippocampal hypertrophy in people who have depression and have experienced early abuse. Neurologic disorders of the limbic system and basal ganglia are also involved in the development of mood disorders. Dopamine plays a role in depression. **Unit 6. Disorders of Special Sensory Function. Chapters 19, 20. There are 4 questions from** **this unit.** 47\. Disorders of Eye Movement. Begins on p. 577. Strabismus vs amblyopia: differences in presentation. Strabismus (squint) refers to any abnormality of eye coordination or alignment that results in loss of binocular vision. When images from the same spots in the visual space do not fall on corresponding points of the two retinas, diplopia (double vision) occurs. May be divided into two forms: nonparalytic forms (concomitant) where there is no primary muscle impairement, and paralytic (nonconcomitant) in which there is weakness or paralysis of one or more of the extraocular muscles. Called intermitted, or periodic, when there are periods in which the eyes are parallel. Amblyopia: Sometimes called lazy eye. Decrease in visual acuity resulting from abnormal visual development in infancy or early childhood. Vision loss ranges from mild (worse than 20/25) to severe (legal blindness, 20/200 or worse). 48\. Disorders of the Conjunctiva. Begins on p. 550. Compare the clinical manifestation of allergic, viral, and bacterial conjunctivitis. 1. Allergic: Usually characterized by itching. Bilateral tearing, itching, and redness of the eye. Treatment includes allergen avoidance, use of cold compresses, eye washes with tear substitute, and oral antihistamines. 2. Viral: Common cause is adenovirus. Symptoms include generalized conjunctival hyperemia, copious tearing, and minimal exudate. Usually associated with upper respiratory tract infection. Usually resolves over time with use of cool compresses and artificial tears. Topical antivirals are not recommended. 3. Bacterial: Burning, tearing, mucopurulent or purulent discharge. Normally begins in one eye and within 24 to 48 hours it speards to the unaffected eye. Drainage may be green, white, or yellow. Treatment includes antibiotic drops or ointments. N. gonorrhoeae is the most serious form of conjunctivitis than can lead to corneal ulceration/perforation and permanent blindness if not treated; symptoms include conjunctival redness, chemosis (swelling around the cornea), lid swelling, and tender/swollen periauricular lymph nodes. How can tell one from the other Diagnostically? 49\. Disorders of the Retina. Page 581. DISORDERS OF THE RETINAL BLOOD SUPPLY 1. The blood supply for the retina is derived from the central retinal artery, which supplies blood flow for the entire inside of the retina, and from vessels in the choroid, which supply the rods and cones. 2. The retinopathies, which are disorders of the retinal vessels, interrupt blood flow to the visual receptors, leading to visual impairment. 3. Retinal detachment separates the visual receptors from the choroid, which provides their major blood supply. 4. Functioning of the retina, like that of other cellular portions of the CNS, depends on an oxygen supply from the vascular system. One of the earliest signs of decreased perfusion pressure in the head region is a graying-out or blackout of vision, which usually precedes loss of consciousness. This can occur during large increases in intrathoracic pressure, which interfere with the return of venous blood to the heart, as occurs with the Valsalva maneuver, with systemic hypotension, and during sudden postural changes (e.g., postural hypotension) 5. Ischemia of the retina occurs during general circulatory collapse. If a person survives cardiopulmonary arrest, for instance, permanently decreased visual acuity can occur as a result of edema and the ischemic death of retinal neurons. This is followed by primary optic nerve atrophy proportional to the extent of ganglionic cell death. The ophthalmic artery, the source of the central artery of the retina, takes its origin from the internal carotid artery (Capriotti, 2020). Intermittent retinal ischemia can accompany internal carotid or common carotid stenosis. Amaurosis fugax is characterized by transient episodes of monocular visual loss lasting 5 to 10 minutes (Capriotti, 2020). People with the disorder often describe a curtain coming down from Diabetic Retinopathy. Diabetic retinopathy is the most common cause of blindness in the industrialized countries of the world. It ranks first as the cause of newly reported cases of blindness in people between the ages of 20 and 74 years (Wykoff et al., 2021). Advances in treatment have greatly reduced the risk of blindness from diabetes, but because diabetes is so common, retinopathy remains an important cause of visual impairment. 6. Diabetic retinopathy can be divided into two types: nonproliferative (i.e., background) and proliferative (Capriotti, 2020; Drinkwater et al., 2021; Wykoff et al., 2021). Background or nonproliferative retinopathy is confined to the retina. It involves engorgement of the retinal veins, thickening of the capillary endothelial basement membrane, and development of capillary microaneurysms (Fig. 19.18A). Small intraretinal hemorrhages may develop and microinfarcts may cause cotton-wool spots and leakage of exudates. A sensation of glare (because of the scattering of light) is a common complaint. The most common cause of decreased vision in people with background retinopathy is macular edema. The edema is caused primarily by the breakdown of the inner blood--retina barrier at the level of the capillary endothelium, allowing leakage of fluid and plasma constituents into the surrounding retina. 7. Hypertensive Retinopathy. a. As with other blood vessels in the body, the retinal vessels undergo changes in response to chronically elevated blood pressure. b. In the initial, vasoconstrictor stage, there is vasospasm and an increase in retinal arterial tone because of local autoregulatory mechanisms. i. On ophthalmoscopy, this stage is represented by a general narrowing of the retinal arterioles. ii. Persistently elevated blood pressure results in the compensatory thickening of arteriolar walls, which effectively reduces capillary perfusion pressure. c. These changes are manifested in the retina by iii. microaneurysms, iv. intraretinal hemorrhages, v. hard exudates, and 1. cotton-wool spots. d. Swelling of the optic disc may occur at this stage and usually indicates severely elevated blood pressure (malignant hypertension). e. Older adults often have more rigid vessels that are unable to respond to the same degree as those in younger people. 8. Retinal Detachment f. Retinal detachment involves the separation of the neurosensory retina from the pigment epithelium (Fig. 19.19). It occurs when traction on the inner sensory layer or a tear in this layer allows fluid, usually vitreous, to accumulate between the two layers (Capriotti, 2020). There are four types of retinal detachments: exudative, traction, rhegmatogenous, and combined traction/rhegmatogenous (Capriotti, 2020). 9. Assessing Papilledema and its significance. 1. Funduscopic examination of the eye with an ophthalmoscope provides an opportunity to examine the retinal blood vessels and other aspects of the retina (Fig. 19.16). 2. Because the retina is an embryonic outgrowth of the brain and the blood vessels are to a considerable extent representative of brain blood vessels, the ophthalmoscopic examination of the fundus of the eye permits the study and diagnosis of metabolic and vascular diseases of the brain as well as pathologic processes that are specific to the retina. 50\. Disorders of Hearing and Vestibular Function: Otitis Media-Clinical Manifestations 1. Acute onset of otalgia (pulling of the ears in an infant) that may interfere with sleep and/or activity, fever (\>39), irritability, otorrhea, hearing loss, evidence of middle ear inflammation, middle ear effusion (decreases mobility of the tympanic membrane). 2. Children older than 3 may have rhinorrhea, vomiting, and diarrhea. 3. Ear pain usually increases as the effusion accumulates behind the tympanic membrane. Perforation of the tympanic membrane may occur acutely, allowing purulent material from the eustachian tube to drain into the external auditory canal. 4. Otitis media with effusion symptoms: Complaint of intermittent ear pain, sensation of fullness in ear, complaint of hearing loss, dizziness, decreased tympanic membrane mobility, visible air-fluid level with or without bubble. 51\. Disorders of Hearing and Vestibular Function: Otitis Media-Risk Factors. Page 589. 1. May occur in any age group, but is more frequently diagnosed in children between the ages of 3 months and 3 years. Smoking in the house is a significant risk factor. Other risk factors include prematurity, daycare attendance, having an unimmunized status, bottle-feeding, feeding in the supine position, being overweight or obese, a family history of otitis media, being male, and sharing a bedroom. More frequent in children with craniofacial anomalies or congenital syndromes associated with craniofacial abnormalities. 2. Strucutural immaturity contributes to the increased risk because the eustachian tube is shorter and more horizontal, and it can spread more easily through the eustachian canal of infants who spend most of their day supine. To reduce the risk of contracting otitis media: routine childhood vaccinations against pneumococci and flu, elimination of household smoking, exclusive breast-feeding until 6 months of age, avoiding of feeding while lying down and propping bottles, use of xylitol, and selecting daycare facilities with small staff-to-child ratio.