These cells are neurosecretory cells that develop from the neural crest along with the sympathetic ganglia buy levitra 10mg without a prescription, reinforcing the idea that the gland is cheap levitra 10mg without a prescription, functionally purchase genuine levitra on line, a sympathetic ganglion buy generic levitra 20 mg. The projections of the sympathetic division of the autonomic nervous system diverge widely, resulting in a broad influence of the system throughout the body. As a response to a threat, the sympathetic system would increase heart rate and breathing rate and cause blood flow to the skeletal muscle to increase and blood flow to the digestive system to decrease. All of those physiological changes are going to be required to occur together to run away from the hunting lioness, or the modern equivalent. This divergence is seen in the branching patterns of preganglionic sympathetic neurons—a single preganglionic sympathetic neuron may have 10–20 targets. An axon that leaves a central neuron of the lateral horn in the thoracolumbar spinal cord will pass through the white ramus communicans and enter the sympathetic chain, where it will branch toward a variety of targets. At the level of the spinal cord at which the preganglionic sympathetic fiber exits the spinal cord, a branch will synapse on a neuron in the adjacent chain ganglion. Other branches will pass through the chain ganglia and project through one of the splanchnic nerves to a collateral ganglion. All of these branches mean that one preganglionic neuron can influence different regions of the sympathetic system very broadly, by acting on widely distributed organs. Parasympathetic Division of the Autonomic Nervous System The parasympathetic division of the autonomic nervous system is named because its central neurons are located on either side of the thoracolumbar region of the spinal cord (para- = “beside” or “near”). The parasympathetic system can also be referred to as the craniosacral system (or outflow) because the preganglionic neurons are located in nuclei of the brain stem and the lateral horn of the sacral spinal cord. The connections, or “circuits,” of the parasympathetic division are similar to the general layout of the sympathetic division with a few specific differences (Figure 15. The preganglionic fibers from the cranial region travel in cranial nerves, whereas preganglionic fibers from the sacral region travel in spinal nerves. The targets of these fibers are terminal ganglia, which are located near—or even within—the target effector. These ganglia are often referred to as intramural ganglia when they are found within the walls of the target organ. The postganglionic fiber projects from the terminal ganglia a short distance to the target effector, or to the specific target tissue within the organ. Comparing the relative lengths of axons in the parasympathetic system, the preganglionic fibers are long and the postganglionic fibers are short because the ganglia are close to—and sometimes within—the target effectors. The postganglionic parasympathetic fibers then project to the smooth muscle of the iris to control pupillary size. In the upper medulla, the salivatory nuclei contain neurons with axons that project through the facial and glossopharyngeal nerves to ganglia that control salivary glands. Tear production is influenced by parasympathetic fibers in the facial nerve, which activate a ganglion, and ultimately the lacrimal (tear) gland. Neurons in the dorsal nucleus of the vagus nerve and the nucleus ambiguus project through the vagus nerve (cranial nerve X) to the terminal ganglia of the thoracic and abdominal cavities. Parasympathetic preganglionic fibers primarily influence the heart, bronchi, and esophagus in the thoracic cavity and the stomach, liver, pancreas, gall bladder, and small intestine of the abdominal cavity. The postganglionic fibers from the ganglia activated by the vagus nerve are often incorporated into the structure of the organ, such as the mesenteric plexus of the digestive tract organs and the intramural ganglia. The electrical signal of the action potential causes the release of a signaling molecule, which will bind to receptor proteins on the target cell. The terms cholinergic and adrenergic refer not only to the signaling molecule that is released but also to the class of receptors that each binds. The cholinergic system includes two classes of receptor: the nicotinic receptor and the muscarinic receptor. The nicotinic receptor is a ligand-gated cation channel and the muscarinic receptor is a G protein–coupled receptor. Whereas nicotine will bind to the nicotinic receptor, and muscarine will bind to the muscarinic receptor, there is no cross-reactivity between the receptors. Imagine two locks—one for a classroom and the other for an office—that are opened by two separate keys. However, a master key can open multiple locks, such as a master key for the Biology Department that opens both the classroom and the office doors. The molecules that define these receptors are not crucial—they are simply tools for researchers to use in the laboratory. These molecules are exogenous, meaning that they are made outside of the human body, so a researcher can use them without any confounding endogenous results (results caused by the molecules produced in the body). The adrenergic system also has two types of receptors, named the alpha (α)-adrenergic receptor and beta (β)-adrenergic receptor. Unlike cholinergic receptors, these receptor types are not classified by which drugs can bind to them. There are three types of α-adrenergic receptors, termed α , α , and α , and there are two1 2 3 types of β-adrenergic receptors, termed β1 and β. An additional aspect of the adrenergic system is that there is a second2 signaling molecule called epinephrine. The term adrenergic should remind you of the word adrenaline, which is associated with the fight-or-flight response described at the beginning of the chapter. A similar construction from Greek instead of Latin results in the word epinephrine (epi- = “above”; nephr- = “kidney”). In scientific usage, epinephrine is preferred in the United States, whereas adrenaline is preferred in Great Britain, because “adrenalin” was once a registered, proprietary drug name in the United States. Though the drug is no longer sold, the convention of referring to this molecule by the two different names persists. Having understood the cholinergic and adrenergic systems, their role in the autonomic system is relatively simple to understand. All ganglionic neurons—the targets of these preganglionic fibers—have nicotinic receptors in their cell membranes. The nicotinic receptor is a ligand- gated cation channel that results in depolarization of the postsynaptic membrane. Autonomic System Signaling Molecules Sympathetic Parasympathetic Acetylcholine → Preganglionic Acetylcholine → nicotinic receptor nicotinic receptor Norepinephrine → α- or β-adrenergic receptors Acetylcholine → Postganglionic Acetylcholine → muscarinic receptor (associated with sweat glands muscarinic receptor and the blood vessels associated with skeletal muscles only Table 15. Neurotransmitters are released at synapses, whereas hormones are 664 Chapter 15 | The Autonomic Nervous System released into the bloodstream. But the adrenal medulla releases epinephrine and norepinephrine into circulation, so they should be considered hormones. Some sources will refer to the connection between a postganglionic fiber and a target effector as neuroeffector junctions; neurotransmitters, as defined above, would be called neuromodulators. The structure of postganglionic connections are not the typical synaptic end bulb that is found at the neuromuscular junction, but rather are chains of swellings along the length of a postganglionic fiber called a varicosity (Figure 15. Instead of a synaptic end bulb, a neurotransmitter is released from swellings along the length of a fiber that makes an extended network of connections in the target effector. The original usage of the epithet “fight or flight” comes from a scientist named Walter Cannon who worked at Harvard in 1915. The concept of homeostasis and the functioning of the sympathetic system had been introduced in France in the previous century. Cannon expanded the idea, and introduced the idea that an animal responds to a threat by preparing to stand and fight or run away. The nature of this response was thoroughly explained in a book on the physiology of pain, hunger, fear, and rage. When students learn about the sympathetic system and the fight-or-flight response, they often stop and wonder about other responses. If you were faced with a lioness running toward you as pictured at the beginning of this chapter, would you run or would you stand your ground? The common epithet of “fight or flight” is being enlarged to be “fight, flight, or fright” or even “fight, flight, fright, or freeze. The name “sympathetic” can be said to mean that (sym- = “together”; -pathos = “pain,” “suffering,” or “emotion”). As described in this video, the nervous system has a way to deal with threats and stress that is separate from the conscious control of the somatic nervous system. The system comes from a time when threats were about survival, but in the modern age, these responses become part of stress and anxiety. What other organ system gets involved, and what part of the brain coordinates the two systems for the entire response, including epinephrine (adrenaline) and cortisol?

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An outbreak of multi-drug resistant tuberculosis among hospitalized patients with the acquired immunodeficiency syndrome cheap 20mg levitra with mastercard. Transmission of multi-drug resistant Mycobacterium tuberculosis among persons with human immunodeficiency virus infection in an urban hospital: epidemiologic and restriction fragment length polymorphism analysis cheap levitra 10 mg with mastercard. Transmission of drug-resistant Mycobacterium tuberculosis among persons with human immunodeficiency virus infection in urban hospital: epidemiologic and restriction fragment length polymorphism analysis levitra 10 mg lowest price. Private pharmacies in tuberculosis control- a neglected link International Journal of Tuberculosis and Lung Disease buy 20mg levitra visa, 2002, 6(2):171-173. Survey of knowledge, attitudes and practices for tuberculosis among general practitioners in Delhi, India. Use of thiacetazone, thiophen-2-carboxylic acid hydrazide and triphenyltetrazolium chloride. Advances in techniques of testing mycobacterial drug sensitivity, and the use of sensitivity tests in tuberculosis control programmes. Human Development Report 2003: Millennium Development Goals: A compact among nations to end human poverty. A comparison of three molecular assays for rapid detection of rifampin resistance in Mycobacterium tuberculosis. Evaluation of a commercial probe assay for detection of rifampin resistance in Mycobacterium tuberculosis directly from respiratory and non respiratory clinical specimens. European Journal of Clinical Microbiology and Infectious Diseases, 1998, 17:189-192. Detection of rifampicin resistance in Mycobacterium tuberculosis isolates from diverse countries by a commercial line probe assay as an initial indicator of multidrug resistance. Rifampin- and multidrug-resistant tuberculosis in Russian civilians and prison inmates: dominance of the beijing strain family. Low levels of drug resistance amidst rapidly increasing tuberculosis and human immunodeficiency virus: co-epidemics in Botswana. Epidemiological analysis of tuberculosis treatment outcome as a tool for changing tuberculosis control policy in Israel. Drug- resistant pulmnonary tuberculosis in Israel, a society of immigrants: 1985-1994. Screening and management of tuberculosis in immigrants: the challenge beyond professional competence. The new National Tuberculosis Control Programme in Israel, a country of high immigration. Drug-resistant tuberculosis in Poland in 2000: second national survey and comparison with the 1997 survey. Drug resistance among failure and relapse cases of tuberculosis: is the standard re-treatment regimen adequate? P was established 1948 early Notification all cases (rate) /100,000 Year of Rifampicin introduction 1970s early Estimated incidence (all cases) 5. P was established 1963 Notification all cases (rate) 10 /100,000 Year of Rifampicin introduction 1982 Estimated incidence (all cases) 10. P was established 1973 Notification all cases (rate) 47 /100,000 Year of Rifampicin introduction 1983 Estimated incidence (all cases) /100,000 Year of Isoniazid introduction 1973 Notification new sputum smear + 4439 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 34. P was established 1989 Notification all cases (rate) 16 /100,000 Year of Rifampicin introduction 1980 Estimated incidence (all cases) 29 /100,000 Year of Isoniazid introduction 1970s Notification new sputum smear + 4889 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 7. P was established 1950 Notification all cases (rate) 72 /100,000 Year of Rifampicin introduction 1985 Estimated incidence (all cases) >80 /100,000 Year of Isoniazid introduction 1970 Notification new sputum smear + 2802 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 45. P was established 1962 Notification all cases (rate) 120 /100,000 Year of Rifampicin introduction 1969 Estimated incidence (all cases) 190. P was established 1998 Notification all cases (rate) /100,000 Year of Rifampicin introduction 1972 Estimated incidence (all cases) 74. P was established 1989 Notification all cases (rate) 125 /100,000 Year of Rifampicin introduction 1990 Estimated incidence (all cases) 201 /100,000 Year of Isoniazid introduction 1965 Notification new sputum smear + 13683 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 58 /100,000 % Use of Short Course Chemotherapy Yes % Treatment Success 86 % Use of Directly Observed Therapy Yes 70. P was established 1963 Notification all cases (rate) 28 /100,000 Year of Rifampicin introduction 1970 Estimated incidence (all cases) 28. P was established 1931 Notification all cases (rate) 3 /100,000 Year of Rifampicin introduction 1971 Estimated incidence (all cases) 3. P was established 1920 Notification all cases (rate) 93 /100,000 Year of Rifampicin introduction 1972 Estimated incidence (all cases) /100,000 Year of Isoniazid introduction 1950s Notification new sputum smear + 380 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 40. P was established 1957 Notification all cases (rate) /100,000 Year of Rifampicin introduction 1970s Estimated incidence (all cases) 44. P was established (revised programme) Notification all cases (rate) 251 /100,000 Year of Rifampicin introduction 1979 Estimated incidence (all cases) 827 /100,000 Year of Isoniazid introduction 1968 Notification new sputum smear + 12393 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 135 /100,000 % Use of Short Course Chemotherapy Yes 100 % Treatment Success 58. P was established (revised programme) Notification all cases (rate) 400 /100,000 Year of Rifampicin introduction 1979 Estimated incidence (all cases) 875 /100,000 Year of Isoniazid introduction 1968 Notification new sputum smear + 15346 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 219 /100,000 % Use of Short Course Chemotherapy Yes 100 % Treatment Success 60. P was established (revised programme) Notification all cases (rate) 188 /100,000 Year of Rifampicin introduction 1979 Estimated incidence (all cases) 578 /100,000 Year of Isoniazid introduction 1968 Notification new sputum smear + 4296 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 138 /100,000 % Use of Short Course Chemotherapy Yes 100 % Treatment Success 67. P was established (revised programme) Notification all cases (rate) 423 /100,000 Year of Rifampicin introduction 1979 Estimated incidence (all cases) 530 /100,000 Year of Isoniazid introduction 1968 Notification new sputum smear + 6455 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 228 /100,000 % Use of Short Course Chemotherapy Yes 100 % Treatment Success 69. P was established (revised programme) Notification all cases (rate) 632 /100,000 Year of Rifampicin introduction 1979 Estimated incidence (all cases) 932 /100,000 Year of Isoniazid introduction 1968 Notification new sputum smear + 15264 Use of Standardized Regimens Yes Notification new sputum smear + (rate) 359 /100,000 % Use of Short Course Chemotherapy Yes 100 % Treatment Success 70. P was established 1953 Notification all cases (rate) 6 /100,000 Year of Rifampicin introduction 1971 Estimated incidence (all cases) 5. Surveillance of resistance to anti-tuberculosis drugs is an essential component of a monitoring system. The benefits of surveillance are multiple: strengthening of laboratory networks, evaluation of programme performance, and the collection of data that inform appropriate therapeutic strategies. Most importantly, global surveillance identifies areas of high resistance and draws the attention of national health authorities to the need to reduce the individual or collective shortcomings that have created them. Prevalence of resistance among previously untreated patients reflects programme performance over a long period of time (the previous 10 years), and indicates the level of transmission within the community. The prevalence of bacterial resistance among patients with a history of previous treatment has received less attention because surveillance of this population is a more complex process. Re-treatment patients are a heterogeneous group composed of chronic patients, those who have failed a course of treatment, those who have relapsed, and those who have returned after defaulting. In some settings, this population constitutes more than 40% of smear-positive cases. The association between drug resistance and re- treatment has been repeatedly demonstrated, both at the individual and the programme level; however, the prevalence of drug resistance varies greatly among subgroups of this population. This report therefore recommends that all subgroups of re-treatment cases be separately notified and their outcomes reported, and that surveillance of resistance be conducted on a representative sample of this population. This will make the comparison of resistance prevalence within and between countries more robust and will elucidate patterns of resistance among the subgroups, which will allow better definition of appropriate re- treatment strategies. It is now critical that we recognize the importance of the laboratory in the control of tuberculosis. The two previous reports were published in 1997 and 2001 and included data from 35 and 58 settings,a respectively. The goal of this third report is to expand knowledge of the prevalent patterns of resistance globally and explore trends in resistance over time. It includes 39 settings not previously included in the Global Project and reports trends for 46 settings. Data were reported on a standard reporting form, either annually or at the completion of the survey. The prevalence of resistance to at least one antituberculosis drug (any a Setting is defined as a country or a subnational setting (i. Trends in drug resistance in new cases were determined in 46 settings (20 with two data points and 26 with at least three). Significant increases in prevalence of any resistance were found in Botswana, New Zealand, Poland, and Tomsk Oblast (Russian Federation). Previously treated cases Data on previously treated cases were available for 66 settings. Among countries of the former Soviet Union the median prevalence of resistance to the four drugs was 30%, compared with a median of 1. Given the small number of subjects tested in some settings, prevalence of resistance among previously treated cases should be interpreted with caution. Drug resistance trends in previously treated cases were determined in 43 settings (19 with two data points and 24 with at least three data points). A significant increase in the prevalence of any resistance was observed in Botswana.

Osmolarity ranges from 50 to 1200 milliosmoles buy levitra 20 mg without prescription, and is a reflection of the amount of water being recovered or lost by renal nephrons order cheapest levitra. Urination is controlled by an involuntary internal sphincter of smooth muscle and a voluntary external sphincter of skeletal muscle buy generic levitra. The male urethra receives secretions from the prostate gland purchase levitra 10 mg online, Cowper’s gland, and seminal vesicles as well as sperm. Loss of control of micturition is called incontinence and results in voiding when the bladder contains about 250 mL urine. The ureters are retroperitoneal and lead from the renal pelvis of the kidney to the trigone area at the base of the bladder. A thick muscular wall consisting of longitudinal and circular smooth muscle helps move urine toward the bladder by way of peristaltic contractions. The renal arteries arise directly from the aorta, and the renal veins drain directly into the inferior vena cava. A portal system is formed when the blood flows through a second capillary bed surrounding the proximal and distal convoluted tubules and the loop of Henle. This filtrate is processed and finally gathered by collecting ducts that drain into the minor calyces, which merge to form major calyces; the filtrate then proceeds to the renal pelvis and finally the ureters. Cortical nephrons have short loops of Henle, whereas juxtamedullary nephrons have long loops of Henle extending into the medulla. A filtration membrane is formed by the fused basement membranes of the podocytes and the capillary endothelial cells that they embrace. Contractile mesangial cells further perform a role in regulating the rate at which the blood is filtered. The hydrostatic pressure of the glomerulus depends on systemic blood pressure, autoregulatory mechanisms, sympathetic nervous activity, and paracrine hormones. The kidney can function normally under a wide range of blood pressures due to the autoregulatory nature of smooth muscle. Even so, it only influences the last 10 percent of water available for recovery after filtration at the glomerulus, because 90 percent of water is recovered before reaching the collecting ducts. Depending on the body’s fluid status at any given time, the collecting ducts can recover none or almost all of the water reaching them. Movement of water from the glomerulus is primarily due to pressure, whereas that of peritubular capillaries and vasa recta is due to osmolarity and concentration gradients. The descending loop of the juxtaglomerular nephrons reaches an osmolarity of up to 1200 mOsmol/kg, promoting the recovery of water. The ascending loop is impervious to water but + actively recovers Na , reducing filtrate osmolarity to 50–100 mOsmol/kg. The descending and ascending loop and vasa + recta form a countercurrent multiplier system to increase Na concentration in the kidney medulla. The collecting ducts actively pump urea into the medulla, further contributing to the high osmotic environment. Sympathetic nervous activity decreases blood flow to the kidney, making more blood available to other areas of the body during times of stress. The arteriolar myogenic mechanism maintains a steady blood flow by causing arteriolar smooth muscle to contract when blood pressure increases and causing it to relax when blood pressure decreases. Natriuretic hormones, released primarily from the atria of the heart in response to stretching of the atrial walls, stimulate + Na excretion and thereby decrease blood pressure. Progesterone is similar in structure to 1244 Chapter 25 | The Urinary System aldosterone and can bind to and weakly stimulate aldosterone receptors, providing a similar but diminished response. Blood pressure is a reflection of blood volume and is monitored by baroreceptors in the aortic arch and carotid sinuses. The kidneys catalyze the final reaction in the synthesis of active vitamin D that in turn helps regulate ++ Ca. The kidneys work with the adrenal cortex, lungs, and liver in the renin–angiotensin–aldosterone system to regulate blood pressure. The kidneys share pH regulation with the lungs and plasma buffers, so that proteins can preserve their three-dimensional conformation and thus their function. Give the approximate osmolarity of fluid in the large urine volumes, but how would other characteristics of proximal convoluted tubule, deepest part of the loop of the urine differ between the two diseases? In the human body, the substances that participate in chemical reactions must remain within narrows ranges of concentration. Because metabolism relies on reactions that are all interconnected, any disruption might affect multiple organs or even organ systems. The interactions of various aqueous solutions—solutions in which water is the solvent—are continuously monitored and adjusted by a large suite of interconnected feedback systems in your body. Understanding the ways in which the body maintains these critical balances is key to understanding good health. In the human body, solutes vary in different parts of the body, but may include proteins—including those that transport lipids, carbohydrates, and, very importantly, electrolytes. Often in medicine, a mineral dissociated from a salt that carries an + - electrical charge (an ion) is called and electrolyte. In the body, water moves through semi-permeable membranes of cells and from one compartment of the body to another by a process called osmosis. Osmosis is basically the diffusion of water from regions of higher concentration to regions of lower concentration, along an osmotic gradient across a semi-permeable membrane. As a result, water will move into and out of cells and tissues, depending on the relative concentrations of the water and solutes found there. An appropriate balance of solutes inside and outside of cells must be maintained to ensure normal function. Body Water Content Human beings are mostly water, ranging from about 75 percent of body mass in infants to about 50–60 percent in adult men and women, to as low as 45 percent in old age. The percent of body water changes with development, because the proportions of the body given over to each organ and to muscles, fat, bone, and other tissues change from infancy to adulthood (Figure 26. Your brain and kidneys have the highest proportions of water, which composes 80–85 percent of their masses. Fluid Compartments Body fluids can be discussed in terms of their specific fluid compartment, a location that is largely separate from another compartment by some form of a physical barrier. This fluid volume tends to be very stable, because the amount of water in living cells is closely regulated. If the amount of water inside a cell falls to a value that is too low, the cytosol becomes too concentrated with solutes to carry on normal cellular activities; if too much water enters a cell, the cell may burst and be destroyed. Plasma travels through the body in blood vessels and transports a range of materials, including blood cells, proteins (including clotting factors and antibodies), electrolytes, nutrients, gases, and wastes. These include the cerebrospinal fluid that bathes the brain and spinal cord, lymph, the synovial fluid in joints, the pleural fluid in the pleural cavities, the pericardial fluid in the cardiac sac, the peritoneal fluid in the peritoneal cavity, and the aqueous humor of the eye. Thus, cations, or positively charged ions, and anions, or negatively charged ions, are + - balanced in fluids. The hydrostatic pressure of blood is the pressure exerted by blood against the walls of the blood vessels by the pumping action of the heart. In capillaries, hydrostatic pressure (also known as capillary blood pressure) is higher than the opposing “colloid osmotic pressure” in blood—a “constant” pressure primarily produced by circulating albumin—at the arteriolar end of the capillary (Figure 26. Fluid and the cellular wastes in the tissues enter the capillaries at the venule end, where the hydrostatic pressure is less than the osmotic pressure in the vessel. The surplus fluid in the interstitial space that is not returned directly back to the capillaries is drained from tissues by the lymphatic system, and then re-enters the vascular system at the subclavian veins. Hydrostatic pressure is especially important in governing the movement of water in the nephrons of the kidneys to ensure proper filtering of the blood to form urine. As hydrostatic pressure in the kidneys increases, the amount of water leaving the capillaries also increases, and more urine filtrate is formed. If hydrostatic pressure in the kidneys drops too low, as can happen in dehydration, the functions of the kidneys will be impaired, and less nitrogenous wastes will be removed from the bloodstream. Recall that an osmotic gradient is produced by the difference in concentration of all solutes on either side of a semi-permeable membrane. The magnitude of the osmotic gradient is proportional to the difference in the concentration of solutes on one side of the cell membrane to that on the other side. Water will move by osmosis from the side where its concentration is high (and the concentration of solute is low) to the side of the membrane where its concentration is low (and the concentration of solute is high). In the body, water moves constantly into and out of fluid compartments as conditions change in different parts of the body.

By J. Larson. University of Southern Maine. 2019.