Michael G. Ison, M.D., M.S.

• Assistant Professor
• Divisions of Infectious Diseases & Organ Transplantation
• Northwestern University Feinberg School of Medicine
• Medical Director
• Transplant & Immunocompromised Host
• Infectious Diseases Service
• Northwestern Memorial Hospital
• Chicago, Illinois

With low mean arterial pressure as indicated by the dotted line medicine vs medication 20 mg vastarel mastercard, vasodilation occurs gas treatment 20mg vastarel amex, allowing more blood flow to the cerebral tissues symptoms 10dpo cheap 20 mg vastarel mastercard. This autoregulatory response helps to maintain a constant cerebral perfusion pressure as seen by the solid line medicine q10 discount 20mg vastarel otc. When blood pressure rises medicine dispenser buy vastarel 20mg amex, the cerebral capillaries constrict in treatment online discount vastarel uk, preventing a significant rise in blood flow, whereas the capillaries dilate to allow more blood flow to circulate when mean arterial blood pressure falls or brain metabolism increases. In the presence of severe hypotension or malignant hypertension, autoregulation is no longer effective. This autoregulatory response can cause detrimental increases in cerebral blood flow when respiratory compromise leads to hypercapnia. The cerebral vessels dilate in response to hypercapnia and can allow excessive cerebral blood volume that exacerbates cerebral edema. Increased neuronal activity with excessive release of catecholamines and excitatory amino acids drives up oxygen demand. Effort to reduce the release of excitatory neurotransmitters through sedation, pain management, and rest may be beneficial. Hypothermia is also used to reduce the metabolic demands of brain tissue after injury and to prevent further impairment of blood flow or ischemia. Other methods to maintain functional autoregulation include treating increased intracranial pressure, reducing cerebral edema, removing mass lesions or spaceoccupying tumors, or hemorrhage from the brain or spinal cord. The Monro-Kellie hypothesis describes the compensatory relationship in response to changes in volume of any of the three components. This is known as cerebral compliance, the ability to accommodate changes in volume without a significant rise in intracranial pressure. However, because the skull creates a closed compartment, compliance is limited to accommodation of only small volumes, whereas moderate to severe changes in volume result in significant increases in intracranial pressure. In addition to mass lesions, cytotoxic and vasogenic edema as well as hydrocephalus are common causes of increased intracranial pressure. In infants and young children, increased intracranial pressure can manifest as an increase in head circumference because the bones of the skull have not yet fused. At these ages, the skull can expand to accommodate the increased volume within the cranium. Injured brain tissue is susceptible to cytotoxic edema, which occurs in the intracellular compartment when ischemic tissue swells because of cellular energy failure. This type of edema, known as vasogenic edema, results from increased capillary pressure, damage to the capillary endothelium, or sudden increases in the vascular pressure beyond the limits of autoregulation. Therefore, unless the person has a comorbid cardiac condition or other process that requires a reduction in blood pressure, maintaining a higher blood pressure is safer than drastically reducing it. Pathologic changes in remote areas of the brain can contribute to chronic deficits after ischemic stroke. Diaschisis can lead to microvascular damage in areas outside of the ischemic region, adding to the long-term deficits experienced by patients with ischemic stroke. When cerebral blood pressure rises, what is the compensatory response of the cerebral capillaries What is an important risk to consider in using hyperventilation to decrease intracranial pressure Brain ischemia occurs when the supply of blood or extraction of oxygen and nutrients is insufficient to meet the metabolic demands of the brain tissue. Hypoxia is a deficiency of oxygen at the cellular level resulting from ischemia or hypoxemia, a state of decreased blood oxygenation. Ischemia and hypoxia often occur simultaneously when brain tissue is damaged, whether the damage is due to stroke, trauma, or infection. Mitochondrial dysfunction caused by a deficiency of cellular oxygen is a critical event leading to infarction and tissue death. Without enough oxygen, the transport proteins and cytochromes that normally accept electrons from the mitochondrial electron transport chain are reduced and cannot accept electrons from the Krebs (tricarboxylic acid) cycle. To compensate for the lack of oxygen and energy deficiency, anaerobic glycolytic pathways are initiated. Glycolysis produces pyruvate, a by-product that is converted to lactate with the release of hydrogen ions (H +). A buildup of hydrogen ions leads to cellular acidosis and loss of neuronal integrity. Energy deprivation and loss of ion homeostasis caused by ischemia cause inability of the cells to maintain a negative membrane potential. Anoxic depolarization causes potassium to leave the cell and sodium, chloride, and calcium to enter. Thus, the cells depolarize and open the voltage-gated calcium channels, thereby releasing excitatory amino acids into the extracellular space. The release and accumulation of excitatory amino acids, most specifically glutamate, in the extracellular space lead to cell death (apoptosis). Glutamine released by glia is then taken up by neurons and repackaged into synaptic vesicles for subsequent release. However, ischemia deprives the brain tissue of the oxygen and glucose required to maintain normal transmembrane ion gradients and conversion of glutamate to glutamine in glia. This leads to accumulation of intracellular Na+ and collapse of the transmembrane Na+ gradient, which in turn inhibits glutamate uptake and promotes accumulation of extracellular glutamate. The high level of extracellular glutamate stimulates glutamate receptors on surrounding neurons, causing entry of Ca2+ and Na+, which depolarizes these neurons and stimulates additional Ca2+ influx through voltage-gated channels. These events lead to a massive entry of calcium into the cell, which is transmitted to the matrix of mitochondria by calcium channels on the inner mitochondrial membrane. Exposure to toxic levels of excitatory neurotransmitters and release of calcium from the endoplasmic reticulum leads to mitochondrial calcium overload and activation of apoptosis. In particular, the neurons that are directly affected by the ischemic event die from energy deprivation while neurons at the edge of the ischemic region die from excessive stimulation of glutamate receptors. Neutrophils, vascular endothelium, and activated microglia increase the release of reactive oxygen species and stimulate activation of the nitric oxide/nitric oxide synthetase pathway, resulting in mitochondrial dysfunction and eventually apoptosis. James is to preserve tissue in the ischemic penumbra, the area of tissue surrounding the infarction where perfusion is decreased. Clinical Impact: these findings suggest that cognitive deterioration is due to hypoperfusion of the brain caused by atherosclerosis of the internal carotids. The authors suggest that earlier and more aggressive treatment of internal carotid atherosclerosis may be indicated even in asymptomatic individuals to prevent cognitive deterioration caused by hypoperfusion. Recanalization strategies aim to establish revascularization so that cells of the penumbra can be rescued before irreversible damage occurs. The accumulation of which excitatory neurotransmitter can damage neurons that are at the edge of the ischemic region Following subarachnoid hemorrhage, cerebral vasospasm can occur, resulting in ischemic regions of the brain. This typically occurs several days after the initial event, so continuous observation for signs and symptoms of cerebral vasospasm is important. What does a rise in the cerebral vascular resistance do to the cerebral blood flow However, because it is transient, it does not cause permanent tissue damage or infarction. The signs and symptoms depend on the area of the brain affected but can include facial drooping, arm or leg weakness especially on one side of the body, speech difficulty or sudden trouble seeing in one or both eyes, difficulty walking with dizziness, lack of balance or coordination, or severe headache without a known cause. To compensate for the lack of oxygen and energy deficiency during ischemia, which pathways are initiated that produce the by-product pyruvate Neurons that are directly affected by ischemia die as a result of which mechanism Atherosclerotic blood vessels from the heart to the brain can cause blockage or result in emboli. A body mass index of 25 or higher or a waist circumference greater than 35 inches in women and 40 inches in men. Elevated levels of this amino acid causes arteries to thicken and scar, thereby increasing the risk of clots. Increases the risk of excess weight, high blood pressure, high cholesterol, diabetes, and atherosclerosis. A 12-lead electrocardiography is performed to evaluate for arrhythmias or evidence of ischemia. Carotid Doppler ultrasonography of the neck can be used to identify occlusions of the internal carotids that may require surgical or endovascular therapy. Patients with ischemic stroke often present with focal neurologic deficits that are caused by damage to the area of brain supplied by the affected vessel. Hemorrhagic stroke often causes symptoms associated with elevated intracranial pressure. What percentage of people who have a transient ischemic attack have a stroke within 1 year A person with a past history of transient ischemic attack is how much more likely to have a stroke compared with a person without a history of transient ischemic attack Several vascular disorders can lead to cerebral ischemia, the most common being atherosclerosis. Decreased or blocked blood flow can occur from thrombus formation or an embolus, leading to ischemia and necrosis of brain tissue. As an atherosclerotic plaque forms and enlarges on the vessel wall, it begins to reduce the amount of blood that can travel through the vessel. Over time, the plaque can fully occlude blood from reaching the brain tissue, leading to an ischemic stroke, or the plaque may rupture, releasing emboli. Cardiac disorders including mural thrombus, rheumatic heart disease, arrhythmias, endocarditis, mitral valve prolapse, atrial myxoma, and the presence of prosthetic heart valves can increase the risk of stroke. In addition, hematologic disorders such as thrombocytosis, polycythemia, sickle cell disease, leukocytosis, and hypercoagulable states can increase the risk of ischemia. Thrombotic strokes caused by occlusion of a vessel as a result of the buildup of plaque along the vessel wall are more common and usually involve the internal carotid, middle cerebral, or basilar artery. Most cerebral embolisms are of cardiac origin, usually caused by atrial fibrillation or breakage of an atherosclerotic plaque from a carotid artery, which lodges in a cerebral vessel. Emboli that pass through the carotid arteries commonly occlude the middle cerebral artery, which carries more than 80% of blood flow to the cerebral hemisphere. Emboli that travel to the vertebral or basilar arteries can lodge at the apex of the basilar artery or in the posterior cerebral arteries. An intracerebral hemorrhage (also called an intraparenchymal hemorrhage) occurs in the brain tissue or parenchyma, most often in the basal ganglia or thalamus, and is commonly associated with long-standing hypertension. Cerebral aneurysms and arteriovenous malformations are two structural abnormalities that can cause a hemorrhagic stroke. The aneurysm can cause symptoms when it puts pressure on the brain tissue or surrounding nerves or when it leaks or ruptures, causing a hemorrhage. Aneurysms can occur anywhere in the brain or spinal cord but are most likely to form along regions of bifurcation, where vessels branch off, and along the circle of Willis. They can be congenital, from an abnormality when the vessel is formed, or may be associated with genetic diseases, including connective tissue disorders or polycystic kidney disease. Aneurysms can also form as a result of trauma, high blood pressure, atherosclerosis, tumors, or infection. Bleeding into the brain from a burst blood vessel, often caused by an aneurysm, can lead to necrosis of brain tissue. In the acute period of stroke, supplemental oxygen is used to improve oxygenation, glycemic control is maintained within a normal range, and blood pressure is managed to provide adequate cerebral perfusion. For patients who are not candidates to receive fibrinolytic therapy, permitting moderate hypertension is recommended. Antihypertensive therapy may be used in these patients when the blood pressure is higher than 220/120 mmHg, but care must be taken not to lower the blood pressure too quickly. A reasonable goal is to lower the blood pressure by 15% over the first 24 hours after the onset of stroke. Hypothermia has become a standard of care for patients who survive cardiac arrest from ventricular tachycardia or ventricular fibrillation; however, its role in the early treatment of ischemic stroke has not been demonstrated. During her hospital stay, she becomes depressed, which complicates her course of treatment. After a course of rehabilitation, she is discharged home with her son and visiting healthcare providers to coordinate care in the home. Clinical Manifestations Stroke is characterized by the sudden onset of a focal neurologic deficit that persists for at least 24 hours and is due to a reduction or occlusion of cerebral circulation or rupture of blood vessels. The focal signs and symptoms of stroke depend on the area of brain or spinal cord affected by the hemorrhage or lack of blood supply (Table 27.

Leptin symptoms bacterial vaginosis order vastarel 20 mg, a hormone produced in adipose tissue symptoms multiple sclerosis 20 mg vastarel with visa, decreases the appetite and increases the amount of energy used; ghrelin treatment 24 seven buy vastarel canada, a hormone 150 Chapter 7 Risks Related to Sleep Alterations produced by the digestive system symptoms quit smoking purchase vastarel with amex, has the opposite effect treatment venous stasis purchase vastarel 20mg amex, increasing appetite and saving energy medicine 75 yellow buy discount vastarel 20 mg on-line. Thus, chronic short sleep, because of the associated imbalance of leptin and ghrelin levels, is a risk factor for weight gain and obesity. During sleep, secretion of prolactin and growth hormone increases, and secretion of thyroid-stimulating hormone decreases. Lack of sleep, or sleep deprivation, leads to psychologic and physiologic problems. Psychologic problems include memory loss, irritability, inattention, delusions, labile emotions, slurred speech, slowed reaction time, and decreased coordination. Physiologic problems include blurred vision, dysfunctional hormone secretion, increased energy expenditure, weight gain, impaired blood cell function, and impaired immune system function. During our waking hours, which neurotransmitter builds up in the brain and causes sleepiness However, it may be the opposite: Poor sleep can lead to memory problems and falling grades and can also be responsible for weight gain. What normal process that occurs during sleep is impaired by sleeping less than 6 hours per night Describe the normal hormonal fluctuations during the circadian cycle for prolactin, growth hormone, melatonin, cortisol, and thyroid hormone. Although sleep diaries are known to be inexact, they provide baseline information on routine bedtimes and wake time and help to determine how much (or little) a person is sleeping. Examples of such surveys include the Pittsburgh Sleep Quality Index,6,7 which asks about sleep itself, and the Epworth Sleepiness Scale8 and the Functional Outcomes of Sleep Questionnaire,9 which ask about the consequences of sleep. It is used to study normal sleep and to Sleep Diary Morning Questions What time did you go to bed last night Home (ambulatory) sleep studies, which measure two to four of the parameters, are often used to screen for sleep disorders or in research. Its data can be used as estimates of sleep characteristics, such as consecutive hours of sleep, number and length of awakenings during sleep period and total sleep time. If the Pittsburgh Sleep Quality Index, the Epworth Sleepiness Scale, or the Functional Outcomes of Sleep Questionnaire is administered to a patient, what information will be obtained There is also increasing evidence that insufficient sleep and poor sleep quality are related to development of cognitive decline, dementia, and Alzheimer disease. Circadian Rhythm Disorders the lack of synchrony between circadian rhythm and time of day can cause circadian rhythm mismatch, leading to sleep difficulties and sleep deprivation. If exposure to a strong zeitgeber, such as sunlight, occurs at the wrong time in relation to body rhythm, the lack of synchrony causes disruptions in sleep and alertness. One such circadian rhythm problem is shift work disorder, which occurs when an individual who works outside the usual work hours (7:00 a. Shift workers are often exposed to sunlight on their way to or from work, which resets their circadian rhythm. It is most often related to social causes, such as shift work, jet lag, or simply staying up late, and is not pathologic. Pathologic sleep disorders, such as obstructive sleep apnea and narcolepsy, also lead to insufficient sleep, causing sleep deprivation. The resulting sleep deprivation predisposes the individual to accidents and errors at work and at home. Adolescents often experience a shift in circadian rhythm called sleep phase delay. This phase delay is secondary to two factors that occur during puberty: (1) Melatonin secretion starts later in the day, and (2) the need to sleep (homeostatic sleep drive) builds up more slowly. The American Academy of Pediatrics recommends that middle schools and high schools start after 8:30 a. Because exposure to sunlight is the strongest zeitgeber, it is advisable to spend time outside during daylight at the destination. Stimulants such as caffeine, modafinil (Provigil), or armodafinil (Nuvigil) may help during the day. What strong zeitgeber may reset the circadian rhythm of individuals with shift work disorder Traveling across several time zones rapidly can cause what circadian rhythm disorder Precipitating factors, such as loss of a job, a death in the family, or other stressful event, trigger a period of poor sleep. However, in individuals who have perpetuating factors, such as inadequate coping skills or poor sleep habits, which contribute to prolongation of the episode, the insomnia may last over a month, becoming chronic. When a precipitating factor occurs, such as an unusual stress, the person will experience insomnia that will continue at varying levels for a few weeks and then disappear. However, if the individual experiences any perpetuating factors, such as anxiety related to poor sleep, after about 4 weeks the insomnia may become chronic, and it may last for years. Kelly Chambliss: Application the ongoing stresses of school are acting as perpetuating factors for Ms. She decides to seek help from a healthcare professional who specializes in sleep problems. Chambliss asks you whether she will be able to stop falling asleep or suffering loss of attention during the day. Chambliss tells you that she is not sure she will be able to maintain her sleep hygiene, since she is so busy with school. Linking Pathophysiology to Diagnosis and Treatment Diagnosis of insomnia is based on patient report. When someone complains of insomnia, it is necessary to perform a complete assessment to ascertain whether or not the insomnia is the presenting symptom of another sleep or medical disorder. Use of a subjective tool to measure sleep quality, such as the Pittsburgh Sleep Quality Index6 or the Insomnia Severity Index16,17 will aid in the diagnosis. Actigraphy can be used as an objective measure and to validate the information on the sleep diary. Acute insomnia may be treated with a short course of a hypnotic, such as a benzodiazepine receptor agonist. If the individual has a pronounced shift in circadian rhythm, phototherapy will be used to reset the internal clock in the suprachiasmatic nucleus. Insomnia in older adults is frequently related to chronic disease and medication use. It is a risk factor for several mental disorders, particularly major depression, anxiety disorders, and substance abuse. Chronic insomnia is also associated with decreased cognitive ability and impaired performance of monotonous tasks, particularly driving. Insomnia-related fatigue and irritability can lead to decreased exercise and social isolation. Insomnia has been implicated as a risk factor for type 2 diabetes, chronic pain, hypertension, and cardiovascular disease. The cost of insomnia in the United States is over $1 billion a year, consisting of the direct costs of healthcare visits and medications and the indirect costs of accidents, decreased work productivity, and absenteeism from work. Within 2 months, she begins sleeping better, her grades are starting to improve, and she is able to continue the sleep improvement program on her own. Will she have to remain under active clinical care, or can she maintain these methods on her own Chambliss had not sought treatment for her insomnia, would she be at risk of any physical complications of chronic sleep deprivation Her perpetuating factors that created a chronic condition included the stress of school. She has asked whether there is a possibility of having episodes of insomnia in the future. Etiology and Pathogenesis Excess body weight leads to enlargement of fat pads, which narrow the pharyngeal airway. Fat deposition in the chest or abdominal wall increases the work of breathing and leads to hypoventilation and increased secretion of leptin, which influences breathing. An impairment in the performance of monotonous tasks such as driving, with the resultant increase in automobile accidents, occurs in what common sleep disorder With which complementary/alternative therapies has insomnia been successfully treated Sleep-disordered breathing is the most common primary sleep disorder in the United States. It can range from simple, uncomplicated snoring to life-threatening obstructive sleep apnea. In people who sleep on their backs, the tongue may relax and fall backwards, leading to airway narrowing or blockage. To be classified as an apnea for an adult, the cessation of airflow must last at least 10 seconds. These movements of the abdomen and thorax are termed paradoxical because they are opposite to each other; as the chest rises, the abdomen sinks, and vice versa. Because sympathetic nervous system activity increases, the heart rate rises briefly, leading to an increase in venous return, which in turn causes a transient rapid rise in blood pressure. This process repeats itself several hundred times a night and is thought to lead over the course of years to permanent thickening of arteriolar walls, narrowed arteriolar lumens, increased peripheral resistance, and hypertension that is resistant to treatment. The reoxygenation that follows hypoxia leads to a surge in production of free radicals, particularly reactive oxygen species, which combine with nitric oxide, causing a decrease in circulating nitric oxide. The combination of increased reactive oxygen species and decreased nitric oxide causes oxidative stress, which leads to increased levels of inflammatory mediators (cytokines, adipokines, and adhesion molecules) and decreased circulating antioxidants. The resulting inflammation and endothelial dysfunction constitute another cause of treatment-resistant hypertension and atherosclerosis. The individual then takes a breath and falls back to sleep, and the cycle begins again. Although the individual may gasp for air or snort during the associated arousal, these arousals are too short for the individual to remember on wakening in the morning. However, they may be noticed by the sleep partner, who often reports having witnessed breathing pauses, gasping, or snorting. The upper airway is smaller and the soft palate is longer in the patient with sleep apnea, clearly blocking the airway. The amount of subcutaneous fat (shown in yellow at the back of the neck and under the chin) is greater in the apneic patient than in the normal subject. What possible postoperative anesthesia complication is increased for someone like Mr. Linking Pathophysiology to Diagnosis and Treatment People are sometimes screened for sleep apnea by using overnight pulse oximetry at home. Jackson told his healthcare provider that he has difficulty concentrating and falls asleep several times a day. Jackson were not middle-aged but were 65 years old or older, why would you ask about snoring as part of the health history Evidence-based recommendations for the assessment and management of sleep disorders in older persons. In the awake individual, muscle tone maintains an open airway against negative pressure during inspiration. When the individual is asleep, the tongue, soft palate, and oropharyngeal walls collapse, closing off the airway. For the few patients who have apneas only when they sleep on their backs, measures to prevent back sleeping (such as putting hard pillows behind them in bed or sewing a tennis ball in the neck of their pajamas) may prevent the apneas. Nasal reconstruction can be performed if the blockage is within the nose or nasopharynx. Uvulopalatopharyngoplasty (surgery to remove the uvula and parts of the soft palate and soft tissues of the pharynx), laser-assisted uvulopalatoplasty, and procedures to decrease the size or position of the base of the tongue have all been used to increase the size of the airway. Jackson would like to know why his blood pressure is finally responding to his hypertension medication. It is generally caused by a neurologic or cardiac problem, such as stroke, renal failure, or congestive heart failure or by sleeping at high altitude. After a month, he reports that he is feeling more energetic, that he can stay awake at work and at home in the evening, and that his wife has started sleeping as his bed partner again. Effects of positive airway pressure treatment on clinical measures of hypertension and type 2 diabetes. The short sleep latency that is seen in narcolepsy is secondary to nighttime sleep loss. Patients with narcolepsy experience a hypnagogic hallucination (a vivid dreamlike experience at the waketo-sleep transition) or a hypnopompic hallucination at the sleep-to-wake transition because there is no sense of transition between waking and sleep. Sleep paralysis, a transient inability to move, occurs during transitions to or from sleep. Although narcolepsy can occur in young children, it is both rare and difficult to diagnose. Excessive daytime sleepiness may be difficult to diagnose because napping is expected.

Aortic valve replacement for aortic stenosis is the primary treatment70 and accounts for approximately two thirds of heart valve operations medications known to cause weight gain buy vastarel 20 mg mastercard. Transcatheter aortic valve implant is less invasive alternative to surgical placement medicine hollywood undead buy cheapest vastarel and vastarel. Tricuspid regurgitation with pulmonary hypertension requires surgical intervention because it is associated with heart failure and mortality treatment efficacy order vastarel online. However 10 medications doctors wont take buy vastarel once a day, all patients with suspected or known valvular disorders should be managed by a heart valve clinic symptoms vaginitis discount vastarel online. Children may be born with a congenital heart defect symptoms quotes buy 20 mg vastarel amex, which is the most common type of birth defect and may be critical or may cause no symptoms and have 606 Chapter 24 Coronary Circulation Disorders a good prognosis. Some examples of congenital heart defects are septal defects of the ventricles or atria, narrowing of heart valves, and a combination of defects. Tetralogy of Fallot is a complex heart defect that involves pulmonary valve stenosis, a large ventricular septal defect, an overriding aorta causing deoxygenated blood from the right ventricle to flow directly into the aorta instead of the pulmonary artery, and right ventricular hypertrophy, in which the right ventricle is thicker and must work harder to contract. Infants and children with simple ventricular septal defects are usually asymptomatic and have an excellent long-term prognosis,67 whereas a ventricular septal defect as part of the complex disease process of tetralogy of Fallot requires open heart surgery, typically during the first year of life. What is commonly caused by right ventricle dilation as a complication of right ventricular failure and its causes, possibly related to right ventricular hypertension as a result of a mitral valve disorder, right ventricle infarction, congenital heart disease, or pulmonary hypertension If a patient has severe mitral regurgitation, what will the patient be placed on as a result of being hemodynamically unstable Coronary circulation is the blood flow to and from the heart muscle (myocardium) through the coronary arteries and cardiac veins. Diagnosis, and Treatment of Coronary Artery Disease Outline the pathophysiology, diagnosis, and treatment of coronary artery disease. Insufficient blood supply to the heart may trigger the development of coronary collateral circulation. Atherosclerosis is characterized by the deposition of lesions on the intima called atheromas, or atheromatous plaques, leading to narrowing and reduced blood flow. The general goal for most adults older than 20 years old is to attain less than 120 mmHg systolic and less than 80 mmHg diastolic blood pressure. The coronary arteries sufficiently supply the myocardium with blood to meet oxygen and nutrient demands under normal conditions. In the presence of atherosclerosis, complications arise as a result of narrowed coronary arteries and decreased blood flow. Most atherosclerotic plaque rupture involves a fracture in its fibrous cap, but a second mechanism has been described that involves superficial erosion of the intima. Injury may range from reversible to irreversible effects when blood flow is decreased or completely blocked, resulting in hypoxia of the myocardial cells. Myocardial cells that are ischemic have reduced contractility, leading to decreased cardiac output. The progression from ischemia to infarction can be thought of as an ischemic cascade in which coronary occlusion from problems such as atherosclerotic plaque disruption and thrombosis initiates the steps. Stable angina usually occurs with increased myocardial oxygen demand and reduced blood flow during exertion or emotional stress, commonly caused by atherosclerosis. Episodes of silent ischemia are possibly present in one third of patients treated for angina with a higher prevalence likely for patients with diabetes. A ventricular septal rupture is a type of ventricular septal defect in which there is an abnormal opening between the left and right ventricles, causing oxygenated blood (from the left ventricle) to mix with deoxygenated blood (from the right ventricle) as a result of left-to-right shunting. Pericarditis is swelling and inflammation of the pericardium, the thin double-layered sac surrounding the 24. Cardiac tamponade is a life-threatening condition of increased pericardial pressure as a result of blood or fluid buildup between the myocardium and the pericardium. Valvular disorders include problems that disrupt flow through atria and ventricles of the heart as a result of abnormal functioning of one or more of the four heart valves. Which of the following diagnoses would be appropriate for a client who is having leg pain while walking According to the American Heart Association, there are seven modifiable risk factors. You are a nurse educating a client about a procedure that may be used to identify whether the client is at risk for sudden cardiac death. Loneliness and social isolation as risk factors for coronary heart disease and stroke: Systematic review and metaanalysis of longitudinal observational studies. Association of Helicobacter pylori infection with coronary artery disease: Is Helicobacter pylori a risk factor Periodontal disease in patients with chronic coronary heart disease: Prevalence and association with cardiovascular risk factors. Multiplex sibling history of coronary heart disease is a strong risk factor for coronary heart disease. Large-scale association analysis identifies new risk loci for coronary artery disease. Future directions to establish lipoprotein(a) as a treatment for atherosclerotic cardiovascular disease. Ideal cardiovascular health predicts lower risks of myocardial infarction, stroke, and vascular death across whites, blacks, and Hispanics: the northern Manhattan study. Lifetime perspectives on primary prevention of atherosclerotic cardiovascular disease. Dietary patterns and the risk of major adverse cardiovascular events in a global study of high-risk patients with stable coronary heart disease. Influence of beta-blockers on endothelial function: A meta-analysis of randomized controlled trials. Lipoprotein apheresis in patients with maximally tolerated lipid-lowering therapy, lipoprotein(a)-hyperlipoproteinemia, and progressive cardiovascular disease: Prospective observational multicenter study. Consequences of brief ischemia: Stunning, preconditioning, and their clinical implications: Part 2. Comparison of approaches to revascularization in patients with multivessel coronary artery disease presenting with st-segment elevation myocardial infarction: Meta-analyses of randomized control trials. Simplified predictive instrument to rule out acute coronary syndromes in a high-risk population. Effect of losmapimod on cardiovascular outcomes in patients hospitalized with acute myocardial infarction: A randomized clinical trial. Cardiovascular disease in the developing world: Prevalences, patterns, and the potential of early disease detection. Serum magnesium and the risk of death from coronary heart disease and sudden cardiac death. Comparison of 24-hour Holter monitoring with 14-day novel adhesive patch electrocardiographic monitoring. Wearable cardioverter-defibrillator therapy for the prevention of sudden cardiac death: A science advisory from the American Heart Association. Left ventricular aneurysm and pseudoaneurysm following acute myocardial infarction. Surgical and transcatheter mitral valve repair for severe chronic mitral regurgitation: A review of clinical indications and patient assessment. Cardiology patient page: Screening for critical congenital heart disease in newborns. Chapter 25 Cardiac Structural Disorders Laura Robbins-Frank and Dawna Martich Chapter Outline and Learning Outcomes 25. According to Hoffman and Kaplan, the probable reasons for this apparent increase are multifactorial. In the 21st century, it is important to investigate underlying genetic patterns, such as deletions, duplications, or mutations, as there may be other important organ involvement and increased reproductive risks that the family needs to consider, as well as prognostic information for clinical outcomes. As genetic research proceeds, more information will become available about the possible underlying genetic involvement as well as tests for diagnostic purposes. Case Studies the following cases will be addressed throughout the chapter to assist in application of chapter content to clinical situations that involve individuals with structural heart disorders. He had an Apgar score of 6 at 1 minute with points taken off for muscle tone and cry; his 5-minute Apgar score was 8 with points taken off for muscle tone. The mother might not even know that she is pregnant while this complex system is developing; this situation can contribute to the environmental exposures that can have a deleterious impact on the structural outcome of heart development. Once implantation of the embryo has occurred, around the 12th day of human development, the cells begin to undergo mitosis, resulting in differentiation of cell types. On day 26 of human development, the neural tube forms after neurulation is complete. The cephalocaudal and lateral folding on day 20 result in development of the bilateral endocardial tubes into the ventral midline of the embryo. The fusion of the heart Geraldine McNamara: Introduction Geraldine McNamara runs a personal home cleaning business. At the age of 65, she starts to notice increased difficulty with breathing when she is performing routine housecleaning chores. McNamara smoked for over 40 years, she attributes her shortness of breath to years of smoking. McNamara mentions the increasing shortness of breath with walking and performing light chores around the house. In addition, she notes that since retiring, her ankles have been swollen nearly every day, making wearing shoes uncomfortable. In addition, the proepicardial cells line the outer layer of the heart tube, which will eventually form into the epicardium and coronary vasculature. By the end of the sixth week of gestation, the cardiac neural crest has migrated through the aortic arches and has entered the outflow tract of the heart, which is completed by the ninth week, resulting in the completion of the ventricular septation. This blood then shunts through the foramen ovale from the right atrium to the left atrium as a result of the high right atrial pressures and the lower left atrial pressures. From the left atrium, the blood travels to the left ventricle for ejection through the aorta to the body. Some blood does travel from the right atrium to the right ventricle via the pulmonary trunk; however, this blood is shunted across the ductus arteriosus to the aorta as a result of the very high pulmonary pressures. At birth, the infant takes its first breath, which quickly reduces the pulmonary pressures as the pulmonary vasculature dilates in response to the change in the partial pressure of oxygen. Pulmonary blood flow increases as this pulmonary pressure decreases, as does the blood flow to the left atrium as the left atrial pressure increases. After the umbilical cord has been cut, systemic vascular resistance increases in response to the decrease in the right atrial pressures. As the pressure increases in the left atrium, the foramen ovale closes shortly after birth. The conditions in which the ductus arteriosus remains open include low saturations, decreased pulmonary blood flow, and pulmonary pressures that remain elevated after birth. After circulating through the fetus, the blood returns to the placenta through the umbilical arteries. The ductus venosus, the foramen ovale, and the ductus arteriosus allow the blood to bypass the fetal liver and lungs. Idaho was the only state that had yet to enact legislation and had no plans to implement it as part of the official newborn screening program. It consists of a preductal and a postductal pulse oximeter reading; both sites are monitored for 5 minutes, and then the reading is recorded. The right ventricle has a lower pressure during systole than the left ventricle because less pressure is needed to pump blood to the lungs than to the rest of the body. A confirmed positive result, that is, SpO2 of less than 90% in hand or foot or three repeated positive screens, results in referral of the infant for echocardiography and further medical evaluation. These changes affect blood flow, oxygenation, and fluid balance, creating immediate or longterm manifestations. The echocardiography is the most reliable diagnostic tool, and the chest x-ray can identify increased pulmonary blood flow as well as possible chamber hypertrophy. Pathophysiology of Altered Blood Flow In assessing a newborn in the first hours of life, it is not unusual to auscultate a murmur. A murmur indicates turbulent blood flow through a valve or congenital heart defect such as a ventricular septal defect or a ductus arteriosus. The intensity of the murmur directly correlates with the size of the defect through which the blood is flowing. A grade 1 murmur is barely audible, a grade 2 murmur is louder, and a grade 3 murmur is loud but not accompanied by a thrill. A grade 5 murmur is associated with a thrill, and the murmur can be heard with the stethoscope partially off the chest. All murmurs louder than grade 3 are considered pathologic and require further evaluation by a pediatric cardiologist. Previously, congenital heart defects were grouped according to whether or not they caused cyanosis. The left side of the heart has higher pressures in both the atria and the ventricles than the right side does. Because of this pressure gradient, when there is an opening between the right and left sides of the heart, as in an atrial septal defect, a ventricular septal defect, or a patent ductus arteriosus, blood naturally flows from an area of high pressure (the left side) to an area of lower pressure (the right side), resulting in an increased amount of blood moving through the pulmonary system. This movement of blood is called a shunt; when the blood moves from the left side (high pressure) to the right side (lower pressure), it is referred to as a left-to-right shunt. A murmur is heard on auscultation, and the intensity of the murmur is directly related to the turbulence of the blood flow through the defect and the size of the defect.

The body senses this inflammation and sends white blood cells to the joint tissue treatment lupus generic 20 mg vastarel with visa, which release enzymes that cause further joint tissue degradation treatment resistant depression order 20 mg vastarel mastercard. In response symptoms rsv discount vastarel american express, these membranes become hyperactive and form new tissue called pannus treatment yellow tongue buy 20 mg vastarel amex. This tissue covers joint cartilage and produces enzymes that encourage additional tissue damage symptoms meaning purchase vastarel 20mg online. Added to the immune complexes xerogenic medications order vastarel no prescription, the body activates osteoclasts, which cause underlying bone to demineralize. This involves more than one joint and is bilateral, or affecting both sides and same body joints. The joints of the fingers, wrists, knees, ankles, and toes are most frequently affected. Stiffness is more acute in the morning although it can occur with inactivity during the day or after strenuous activity. Rheumatoid nodules may develop in subcutaneous tissue that is prone to pressure, such as the forearm, elbow, joints of the hands, and the toes. Spondyloarthropathies Spondyloarthropathies are a group of diseases that affect the joints and include ankylosing spondylitis, reactive arthritis, psoriatic arthritis and enteropathic arthritis or joint problems that occur with inflammatory bowel disease. They can occur in both children and adults and usually involve the sacroiliac joint and enthesitis, or inflammation of the areas around the sites where the ligaments and tendons attach to the bone in the knee, foot, or hip. Ankylosing spondylitis is more likely to run in families than other forms of rheumatic disease. Specific treatments are based on the therapy prescribed for inflammatory bowel or psoriasis that accompanies the spondyloarthropathy. The symptoms of a specific type of spondyloarthropathy are used to guide whether further diagnostic testing is required before diagnosis. Overall, spondyloarthropathies are considered mild nuisance disorders and might not be diagnosed. However, in some individuals, spinal stiffness and fusion can lead to significant issues with daily activities. Research has indicated that a genetic marker needs to be present before a trigger, such as a virus, starting the disease process. The manifestations of arthritis, including intra-articular swelling and synovitis, develop as part of the autoinflammatory or autoimmune process, causing the immune system to attack healthy tissue. The child may need additional interventions to support nutrition, psychosocial development, and school performance. Surgical procedures that may be considered for extreme cases include joint replacement, synovectomy, osteotomy, and arthrodesis. These diseases occur because of insufficient or poorly metabolized calcium, phosphorus, and vitamin D. Osteoporosis is a weakening of bone that has already been formed, whereas osteomalacia is a softening of the bones during the building process. Other common metabolic bone diseases that are of importance include osteopenia and Paget disease. Not all people with osteopenia need extensive treatment; however, actions should be taken to strengthen the bone. Although osteopenia can occur in men, women are more prone to developing osteopenia because of hormonal changes during menopause. Etiology and Pathogenesis As people age, bone resorption (breakdown) is greater than formation. This reduces the density of the bone and leads to bone weakness, which increases the risk of fractures. The most common reasons for the development of osteopenia are as follows: Check Your Progress: Section 36. The only time it may be detected is during a routine diagnostic test or at the time of a spontaneous fracture. However, pain does not always occur at the time of a fracture in a person with osteopenia. The lack of symptoms and limited pain with fractures contribute to the number of people who have the disorder that is undiagnosed. This scan is recommended for all women over the age of 65 to screen for osteoporosis. This scan may also be prescribed for any adult who sustains a fracture as a measure to diagnose osteopenia as a possible cause. The patient is encouraged to increase Psoriatic Enthesitis-related Undifferentiated 898 Chapter 36 Chronic Musculoskeletal Disorders weight-bearing exercises, since bone forms in response to stress. Smoking cessation and reduction of cola-based and alcoholic beverages are other actions to slow the loss of bone. Medications are not routinely prescribed for osteopenia but are considered as options should the disease process progress and additional bone loss occurs. The osteocalcin level test measures osteoclastic activity and helps to determine bone turnover. This is achieved through nutritional support, exercise, and measures to prevent falls. It is caused by low bone density that occurs because of low intake of nutrients for bone growth or an increase in bone resorption that naturally occurs with aging. Etiology and Pathogenesis More than 53 million people in the United States have osteoporosis or are at risk for developing it. Osteoporosis is more common in non-Hispanic white women, although it can affect older people of any race or either sex. Primary osteoporosis may be either type 1, which is associated with menopause, or type 2, which is associated with decreasing bone formation that accompanies the aging process. Renal hypercalciuria is one of the more common causes of secondary osteoporosis and is treated with thiazide diuretics. Many patients with primary osteoporosis also have one or more secondary factors, such as Cushing syndrome, adrenal insufficiency, calcium deficiency, or diabetes mellitus. Osteoporosis is believed to be caused by an imbalance between bone resorption and bone formation. Once peak bone mass has been reached, which occurs around the age of 30, the amount of bone resorption begins to increase. The amount of bone resorption will be heightened with a diet low in calcium and low vitamin D intake; this leads to weakening of the bone structure. Paget Disease Paget disease is a metabolic disorder that causes select bones to overgrow and become weak. It can occur in more than one bone in the body, but it does not affect every bone in the body. Etiology and Pathogenesis Paget disease affects approximately one million people in the United States. The body compensates by accelerating the creation of new bone; however, this new tissue is weak, brittle, and easily fractured. Paget disease is believed to be a genetic disorder initiated by an environmental factor, such a virus. Clinical Manifestations the vast majority of people with Paget disease are unaware of having the disorder. Others may have mild or more exaggerated symptoms that depend on the bone affected. General manifestations of Paget disease include pain, an enlarged or several enlarged bones, fractures, or damaged joint cartilage. If the disorder affects the bones of the skull then headaches, hearing loss, and a large head size may be the major clinical manifestations. In general, symptoms of the disorder progress slowly, and the disease does not metastasize to other body areas. Linking Pathophysiology to Diagnosis and Treatment A person may be unaware of having Paget disease until a fracture occurs. At this time, the disorder may be diagnosed with x-rays and blood tests such as bone-specific alkaline phosphatase level, which is elevated in people with the disorder, and a bone scan, which is used to identify the affected bones. Depending on the bone or bones that are affected, Paget disease can contribute to the development of arthritis, deafness, heart disease, kidney stones, neuropathic pain, bone cancer, poor dentition, and vision changes. The goals of treatment for Paget disease are to strengthen the bone, prevent fractures, and reduce the Clinical Manifestations the most common manifestations of osteoporosis are loss of height; progressive curvature of the spine; low back pain; and fractures of the forearm, spine, or hip. The patient may develop a progressive "buffalo hump" or "dowager hump" between the shoulder blades. Osteoporosis is often called a silent disease, because bone loss occurs without symptoms; the problem may not become apparent until the patient has a fracture or radiologic studies reveal the condition. Exercise is recommended to maintain healthy bones, maintain a healthy weight, and prevent fractures. Surgery may be indicated to repair fractures, correct bone malformations, or replace arthritic joints. Chronic musculoskeletal disorders persist despite treatment for an injury or develop as a part of a pathologic condition. These disorders can develop as a result of lifestyle choices, employment, or strenuous recreational activity. These health problems can affect the bones, muscles, and joints and may begin with an acute ailment. These disorders relate to the concepts of mobility, inflammation and oxidative stress, immunity, comfort/ pain, stress and coping, and sensory perception. This causes pressure on the spinal cord and creates symptoms similar to nerve compression. Manifestations include numbness, weakness, cramping, generalized pain, or pain that radiates down an arm or a leg. Besides involving an alteration in spinal structure, additional symptoms of scoliosis include uneven leg length, spinal fatigue, and back pain. Lordosis, where the spinal column is more concave; it is seen frequently in individuals who are pregnant or obese. Differentiate the causes, classification, underlying pathogenesis, and clinical manifestations of rheumatic and arthritic disorders and approaches to diagnosis and treatment of these conditions across the lifespan. Lower back pain can be caused by degenerative disc changes, a herniated disc, inflammation, or a spinal deformity. Intervertebral disc degeneration can occur through normal body wear and tear or as the result of an arthritic condition. A herniated or ruptured disc permits the fluid within vertebral disc to be released into the disc space and adjacent tissues. Arthritis and rheumatic disorders include osteoarthritis, rheumatoid arthritis, spondyloarthropathies, and juvenile rheumatoid arthritis. Osteoarthritis is the most common form of arthritis and causes the most disabilities in older adults. Manifestations of osteoarthritis include joint pain, stiffness, tenderness, effusion, and crepitus. Rheumatoid arthritis is a chronic systemic autoimmune disorder that causes inflammation of connective tissue in the joints. Clinical manifestations include joint swelling, stiffness, warmth, tenderness, and pain. Patients with this disorder are at risk for joint deformities, primarily of the fingers. Treatment includes pharmacologic approaches, rest, exercise, application of heat or cold, use of assistive devices, and other complementary approaches. Manifestations of these disorders include back pain, stiffness, and generalized fatigue. The cause is unknown; however, it leads to changes in mobility and joint swelling and pain. Osteopenia is a change in bone density that occurs when bone resorption occurs faster than bone generation. Treatment of osteopenia includes diet therapy, calcium and vitamin D supplementation, weight bearing exercises, smoking cessation, and reducing the intake of cola-based and alcoholic beverages. Osteoporosis is caused by a low intake of bonesupporting nutrients or an increase in bone resorption. Manifestations of this disorder include a loss of height, curvature of the spine, low back pain, and fractures. Treatment includes medication, nutritional supplements, exercise, and measures to prevent falls. Paget disease is a metabolic disorder that causes bone resorption faster than bone formation. Manifestations can range from no symptoms to pain, enlarged bones, fractures, or damaged cartilage. Treatment includes medication, nutritional supplements, exercise, and efforts to prevent fractures. Metabolic bone diseases alter bone strength and occur because of insufficient or poorly metabolized calcium, phosphorus, and vitamin D. Which of the following statements indicates to the nurse that a client with rheumatoid arthritis understands discharge instructions During the physical assessment of a child with oligoarticular juvenile idiopathic arthritis, the nurse is most likely to observe which of the following Which of the following statements should the nurse make to the pregnant woman experiencing back pain

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