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This fact is evident from Bernoullis equation cheap lamictal 100mg on-line treatment hypercalcemia, which shows that if the height and velocity of the uid remain constant lamictal 25 mg otc treatment zygomycetes, there is no pressure drop along the ow path lamictal 100mg low cost 20 medications that cause memory loss. The product of the pressure drop and the area of the pipe is the force required to overcome the frictional forces that tend to retard the ow in the pipe segment. Note that for a given ow rate the pressure drop required to overcome frictional losses decreases as the fourth power of the pipe radius. Thus, even though all uids are subject to friction, if the area of the ow is large, frictional losses and the accompanying pressure drop are small and can be neglected. The ow becomes turbulent with eddies and whirls disrupting the laminar ow (see Fig. In a cylindrical pipe the critical ow velocity vc above which the ow is turbulent, is given by vc (8. The symbol is the Reynolds number, which for most uids has a value between 2000 and 3000. Therefore, as the ow turns turbulent, it becomes more dicult to force a uid through a pipe. Blood is not a simple uid; it contains cells that complicate the ow, especially when the passages become narrow. Furthermore, the veins and arteries are not rigid pipes but are elastic and alter their shape in response to the forces applied by the uid. Still, it is possible to analyze the circulatory system with reasonable accuracy using the concepts developed for simple uids owing in rigid pipes. The blood in the circulatory system brings oxygen, nutrients, and various other vital substances to the cells and removes the metabolic waste products from the cells. The blood is pumped through the circulatory system by the heart, and it leaves the heart through vessels called arteries and returns to it through veins. The mammalian heart consists of two independent pumps, each made of two chambers called the atrium and the ventricle. The entrances to and exits from these chambers are controlled by valves that are arranged to maintain the ow of blood in the proper direction. Blood from all parts of the body except the lungs enters the right atrium, which contracts and forces the blood into the right ventricle. The ventricle then contracts and drives the blood through the pulmonary artery into the lungs. In its passage through the lungs, the blood releases carbon dioxide and absorbs oxygen. The contraction of the left atrium forces the blood into the left ventricle, which on contraction drives the oxygen-rich blood through the aorta into the arteries that lead to all parts of the body except the lungs. Thus, the right side of the heart pumps the blood through the lungs, and the left side pumps it through the rest of the body. These in turn branch into still smaller arteries, the smallest of which are called arterioles. As we will explain later, the arte- rioles play an important role in regulating the blood ow to specic regions in Section 8. The arterioles branch further into narrow capillaries that are often barely wide enough to allow the passage of single blood cells. The capillaries are so profusely spread through the tissue that nearly all the cells in the body are close to a capillary. The capillaries join into tiny veins called venules, which in turn merge into larger and larger veins that lead the oxygen-depleted blood back to the right atrium of the heart. First the atria contract, forcing the blood into the ventricles; then the ventricles contract, forcing the blood out of the heart. Because of the pumping action of the heart, blood enters the arteries in spurts or pulses. The maximum pressure driving the blood at the peak of the pulse is called the systolic pressure. Ina young healthy individual the systolic pressure is about 120 torr (mm Hg) and the diastolic pressure is about 80 torr. As the blood ows through the circulatory system, its initial energy, pro- vided by the pumping action of the heart, is dissipated by two loss mecha- nisms: losses associated with the expansion and contraction of the arterial walls and viscous friction associated with the blood ow. Due to these energy losses, the initial pressure uctuations are smoothed out as the blood ows away from the heart, and the average pressure drops. By the time the blood reaches the capillaries, the ow is smooth and the blood pressure is only about 30 torr. The pressure drops still lower in the veins and is close to zero just before returning to the heart. In this nal stage of the ow, the movement of blood through the veins is aided by the contraction of muscles that squeeze the blood toward the heart. The rate of blood ow Q through the body depends on the level of physical activity. Of course, as the aorta branches, the size of the arteries decreases, result- ing in an increased resistance to ow. Although the blood ow in the nar- rower arteries is also reduced, the pressure drop is no longer negligible (see Exercise 8-2). The ow through the arterioles is accompanied by a much larger pressure drop, about 60 torr. Since the pressure drop in the main arteries is small, when the body is horizontal, the average arterial pressure is approximately constant throughout the body. The arterial blood pressure, which is on the average 100 torr, can support a column of blood 129 cm high (see Eq. This means that if a small tube were introduced into the artery, the blood in it would rise to a height of 129 cm (see Fig.
More than 50% of cases are associated with an anomalous pancreaticobiliary junction lamictal 25mg for sale medications for fibromyalgia, due to an arrest of the normal descent of this junction from outside the duodenum to within the duodenal wall in the last eight weeks of gestation discount lamictal 25 mg symptoms your period is coming. A long common pancreaticobiliary channel (> 15 mm) may allow pancreatic juice reflux in the bile duct buy discount lamictal 25mg on line medications related to the female reproductive system, causing distal stricturing and thinning of the bile duct proximally, at least in some cases. Choledochal cysts have been classified into subtypes dependent upon site, most commonly as a fusiform dilatation of the extrahepatic bile duct, but also as a sidewall diverticulum or even bulging as a sac into the duodenum. Presentation may be as cholestasis in infants (if the cyst and/or stricture is complicated by sludge), as an abdominal mass, or rarely, as an acute abdomen if the cyst bursts and causes bile peritonitis. The cysts can be quite large: 2-8 cm in size and having up to 8 L of dark brown fluid. Later in life, they present as intermittent jaundice, biliary pain and cholangitis. Chronic obstruction rarely can lead to biliary cirrhosis and First Principles of Gastroenterology and Hepatology A. Because of the risk of malignancy, either related to the cyst itself or to the abnormal pancreaticobiliary junction, a radical excision with hepaticojejunostomy is preferred. This also helps reduce the postoperative risk of stricturing and stone formation when the bile duct is surgically attached to the intestine. Alagilles syndrome is a marked reduction in intrahepatic (actually interlobular) bile ducts. Although it is believed to be congenital, being inherited in an autosomal dominant pattern, presentation may be as a neonatal jaundice or as cholestasis in older children. Outcome is variable, depending upon the attendant anomalies and the severity of the liver disease. Complete absence of the extrahepatic bile ducts reflects either an arrest in remodeling of the ductal plate in utero or, more probably, an inflammatory destruction of the formed bile ducts during the postpartum period. An initial viral injury may initiate the epithelial injury that then progresses by an immune-mediated sclerosing process, abetted by bile salt leakage that adds detergent damage. The resultant sclerosing inflammation obliterates both the intra- and extrahepatic bile ducts, resulting in profound cholestasis and then secondary biliary cirrhosis. Chronic cholestasis then leads to steatorrhea, skin xanthomas, bone disease and failure to thrive. Surgery is usually necessary to confirm the diagnosis and attempt some form of biliary drainage. In some, existence of a patent hepatic duct or dilated hilar ducts allows correction of the obstruction by anastomosis to the small intestine (e. More common is an absence of patent ducts; dense fibrous tissue encases the perihilar area and precludes conventional surgery. Such obliteration of the proximal extrahepatic biliary system requires the Kasai procedure. A conduit for biliary drainage is fashioned by resecting the fibrous remnant of the biliary tree and anastomosing the porta hepatis to a roux-en-Y loop of jejunum. With either surgery, most children eventually develop chronic cholangitis, hepatic fibrosis/cirrhosis and portal hypertension. When the child is larger, hepatic transplantation dramatically improves the prognosis. Liver transplantation becomes necessary in 50% by 2 years of age, 80% by 20 years. Other causes of neonatal cholestasis can be attributed to hepatocellular transport defects, best exemplified by familial intrahepatic cholestatic syndromes. These small, multiple cysts are usually asymptomatic though potentially complicated by cholangiocarcinoma. Cholangitis Cholangitis is any inflammatory process involving the bile ducts, but common usage implies a bacterial infection, usually above an obstructive site (usually a bile duct stone). The presence of bacteria in the biliary tree plus increased pressure within the system results in severe First Principles of Gastroenterology and Hepatology A. Any condition producing bile duct obstruction is likely to cause bacterial infection of bile. A less likely cause of infection is a stricture (such as a neoplasm) that has not been contaminated by a stent; only 10-15% of malignant biliary obstructions are associated with infection at presentation. The difference relates to the slowly progressive obstruction of non- contaminated strictures versus the intermittent blockage with a stone or acute blockage of as stent within a duct that has been colonized by bacteria via the stent. Such intermittent blockage allows retrograde ascent of bacteria: the stone or stent acting as a nidus for infection. The bacteria ascend the biliary tree (hence the term ascending cholangitis), but may also enter from above via the portal vein or from periductular lymphatics. In acute bacterial cholangitis, particularly if severe, the classical Charcots triad of intermittent fever and chills, jaundice and abdominal pain may be followed by septic shock. The duration of antibiotics needed after successful biliary drainage can be as short as three to five days, unless bacteremia coexists. The entity may appear either alone (20%) or in association with inflammatory bowel disease (80%), particularly ulcerative colitis and less commonly, Crohns colitis. The basis for the patchy scarring (sclerosis) that leads to fibrotic narrowing and eventually obliteration of the bile ducts is unknown. In a genetically predisposed individual, biliary epithelial damage likely begins with exposure to an infectious agent and/or enterohepatic toxin. In inflammatory bowel disease with defective intestinal permeability, this might originate from transmigration of bacteria and toxins.
After the Chief for Infection Prevention and Antimicrobial Stewardship residency she became the Pediatric Infectious Diseases Clinical at Jackson Health System cheap 200 mg lamictal with mastercard treatment 02 binh. Abbo has direct responsibility Pharmacist at Holtz Childrens Hospital lamictal 200 mg visa treatment, associated with Jackson and authority for the strategic assessment and implementation Health System lamictal 50 mg on line symptoms pulmonary embolism, where she resided until 2017. She now lives in of programs to prevent healthcare associated infections and Portland, Maine where she serves as the Pediatric Infectious monitor the appropriate use of antimicrobials in an extremely Diseases Clinical Pharmacist for Barbara Bush Childrens large, complex system that deals with an incredible range of Hospital and the Health-System Antimicrobial Stewardship patient populations and clinical conditions. Abbo obtained her medical degree from the Universidad Central de Venezuela, Luis Razetti Medical School followed by a fellowship in Infectious Diseases at Jackson Memorial Hospital/ University of Miami. She has co-authored over 70 peer-reviewed publications, 3 book chapters and more than 80 abstracts in the felds of antimicrobial stewardship, transplant associated infections and infection prevention. She been an invited speaker in more than 35 international and over 100 regional/ local oral conferences. She has received several awards from the University of Miami for her leadership in diversity and for her work in the advancement of women in academia and healthcare. Together, they partner awarded a PhD in Microbiology by the same institution in 2002. She is also Senior Associate Editor for the Control and an Associate Medical Director, as well as a international peer reviewed journal Public Health. She enjoys training in all aspects of bacteriology and senior honorary lecturer at Imperial College London, together in particular orthopaedic and soft tissue infections. Interests with being a spokesman on antimicrobials and fellow of the outside of work include cycling, surfng and kayaking. William is a frm believer in the ability of informatics as a driver for optimization of antibiotic use to improve patient outcomes and minimize harm in patients with and at risk from infection. Jacqueline holds a Pharmacy degree Health Protection Research Unit for Healthcare Associated from Heriot-Watt University, a PhD in Medicinal Chemistry and Infections and Antimicrobial Resistance. The focus of her research has been behaviour change interventions and the role of mobile health technologies to infuence decision making. Population Health Sciences the Antimicrobial Resistance Programme at Public Health Division, Medical School, University of Dundee England. An antimicrobial pharmacist by background; she started working in public health in 2010 as part of the Health Peter is the Medical School Lead for Healthcare Improvement at Protection Agency. He studied Medicine at St Marys Hospital, London and of Melbourne and Royal Melbourne Hospital in Melbourne, specialized in Infectious Diseases at Addenbrookes Hospital, Australia. He is a qualitative researcher whose interests include Cambridge, where he attained his PhD. Marc is Chair of the South African Ministerial Advisory Committee on Antimicrobial Resistance, the South African lead for Antimicrobial Resistance on the Global Health Security Agenda, co-chair of the South African Antibiotic Stewardship Programme, and co-author the South African Antimicrobial Strategic Framework. He is Past-President of the Federation of Infectious Diseases Societies of Southern Africa, and President-Elect of the International Society for Infectious Diseases. She is the international advisor to journal Clinical Microbiology and Infection, Professor Pulcini has the Federation of Infectious Diseases Society of South Africa also authored or co-authored over 160 international publications. She serves as a faculty mentor to young African leaders as part of the Mandela Washington Fellowship Program. She lectures nationally and internationally as an antimicrobial stewardship advocate and tweets regularly on topics relevant to antibiotic stewardship. He graduated with Centre for Antimicrobial Stewardship and chief investigator a PharmD degree from King Abdulaziz University. Kirsty serves on advisory disease/antibiotic stewardship pharmacy fellowship and Master groups at state, national and international levels in the areas of Science in clinical translational sciences at University of of antimicrobial stewardship, guideline development and Arizona. His Twitter She has served as part of the authorship group for Therapeutic account is called Antibiotic Tweets and his handle is Guidelines: Antibiotic, working on national prescribing @khalideljaaly. As an advisor to the Australian Commission for Safety and Quality in Healthcare, she has had a role in infuencing policy. The National Centre for Antimicrobial Stewardship team have conducted national surveys to gather data on antibiotic use in Australia. The Guidance team have developed electronic tools for antimicrobial stewardship that have been implemented in over 60 Australian hospitals and run national workshops to build capacity amongst doctors, nurses and pharmacists to improve the way we use antibiotics to optimise patient outcomes, and help to tackle antibiotic resistance. Kirsty has taught at international workshops and advised on regional initiatives to improve antimicrobial use. She joined Internal of Pretoria in South Africa in 1984, before completing further Medicine residency training program in Riyadh, King Khalid medical training including his M Med (Clinical Microbiology) university hospital/ King Saud university where she obtained degree, in 1994. He currently works in Johannesburg, South the regional Arab Board in Internal Medicine & was selected as Africa, as Head of Clinical Microbiology at the Ampath National the best resident in performance as R2. Infectious Diseases in Clinical Practice, Frontiers in Microbiology and the Southern African Journal of Infectious Diseases. Dr Brink is senior author of the Massive Open Online Course on Antimicrobial Stewardship and interactive e-Book of Antimicrobial Stewardship (British Society of Antimicrobial Chemotherapy and University of Dundee, Scotland). Her doctoral investigation analyses the antimicrobial Use and Resistance in Resource Constrained process of developing antibiotic policies in Mexico. Areas of her special interests include bacteriology, mycobacteriology, antimicrobial stewardship, quality control and controlling spread of tuberculosis. She has presented many papers & posters and delivered lectures in various national and regional conferences. She is an integral part of the organization team conducting various National conferences and workshops by Sir Ganga Ram Hospital. He is an expert to the technical advisory laurels to his institution through such awards.
The fundamental feature of colonic electrolyte transport that enables this efficient water absorption is the ability of the colonic mucosa to generate a large osmotic gradient between the lumen and the intercellular space generic 200mg lamictal with amex treatment abbreviation. In contrast to the small intestine generic 200 mg lamictal visa rust treatment, where sodium in the intercellular space can diffuse back into the lumen and become iso-osmotic order lamictal 25mg without a prescription symptoms hypothyroidism, hypertonic solutions are maintained in the intercellular space of the colon because the tight junctions are much less permeable to sodium diffusion. The net result is that the hypertonic fluid within the intercellular space draws water passively into the mucosa from the colonic lumen. In the colon there is also a highly efficient + + absorption of sodium (Na ): of the 150 mEq of Na that enters the colon each day, less than 5 + mEq is lost in the stool. In contrast to Na, the tight junctions of the colon are highly permeable + + + to potassium (K ), allowing K to move from the plasma to the lumen. K is normally secreted into the lumen unless intraluminal potassium rises above 15 mEq/L. This handling of potassium may account for hypokalemia seen with colonic diarrhea and may play a role in maintaining potassium balance in the late stages of renal failure. One important difference is the effect of the hormone aldosterone, which is absent in the small intestine. Aldosterone is secreted in response to total body Na+ depletion or K+ loading, and in the colon, aldosterone stimulates sodium absorption and potassium secretion. The movement of fecal material from cecum to rectum is a slow process, occurring normally over 3-4 days. Several contractile patterns exist within the circular and longitudinal muscle of the colon. Ring contractions are due to circular muscle contraction, and these are either tonic or rhythmic. Tonic contractions are sustained over hours, form the haustral markings evident on barium x-rays and play a role in mixing. Regular contractions are nonocclusive, occur over a few seconds, and migrate cephalad (right colon) and caudad (left colon). Intermittent ring contractions occur every few hours, occlude the lumen, and migrate caudad. They result in the mass movement of stool, particularly in the sigmoid colon and rectum. Contractions of the longitudinal muscle produce bulging of the colonic wall between the taeniae coli, but the physiological importance of this action remains poorly understood. The origin of the contractions of the longitudinal muscle is not completely understood, but it depends upon the slow wave frequency of smooth muscle. Action potentials occur on the peaks of these membrane oscillations and hence they control the frequency of contractions. The nature of the contractile patterns within the colon depends upon the fed state. This is best exemplified during eating when the gastrocolic reflex is activated. Food in the duodenum, particularly fatty foods, evokes reflex intermittment rhythmic contractions within the colon, and corresponding mass movement of stool. This action, which is mediated by neural and humoral mechanisms, accounts for the observation by many individuals that eating stimulates the urge to defecate. These bacteria digest a number of undigested food products normally found in the effluent delivered to the colon, such as the complex sugars contained in dietary fiber. They are passively and actively transported into the colonocytes where they become an First Principles of Gastroenterology and Hepatology A. Examination of this area devoid of luminal content typically reveals signs of inflammation, termed diversion colitis. Fermentation of sugars by colonic bacteria is also an important source of colonic gases such as hydrogen, methane and carbon dioxide. These gases, particularly methane, largely account for the tendency of some stools to float in the toilet. Nitrogen gas, which diffuses into the colon from the plasma, is the predominant gas. However, the ingestion of large quantities of undigested complex sugars such as found in beans of the maldigestion of simple sugars such as lactose can result in large increases in production of colonic gas. View of the normal submucosal vessels visible through the healthy transparent mucosa overlying the vessels. Normal ileocecal valve seen in the bottom left of the image, looking down at the cecal pole. When bile salts or long-chain fatty acids are malabsorbed in sufficient quantities, their digestion by colonic bacteria generates potent secretagogues. Shaffer 318 Bile salt malabsorption typically occurs following resection of less than 100cm of the terminal ileum, usually for management of Crohn disease. When the resection involves segments greater than 100 cm of ileum, the liver cannot sufficiently increase the synthesis of bile acids from cholesterol. A deficiency of bile acids enters the duodenum and if the concentration of bile acids is below the critical micellar concentration, bile salf micelles do not form, lipids are malabsorbed, and fatty" Diarrhea (known as steatorrhea) develops. The mechanisms by which multiple metabolites of bile salts and hydroxylated metabolites of long-chain fatty acids act as secretagogues provide an example of how multiple regulatory systems can interact to control colonic function. These mechanisms include disruption of mucosal permeability, stimulation of chloride and water secretion by activating enteric secretomotor neurons, enhancement of the paracrine actions of prostaglandins by increasing production, and direct effects on the enterocyte that increase intracelluar calcium. Non-pathogenic bacteria also signal to mucosal cells and can evoke cytokine signaling from colonocytes to effector cells (e. Some species of bacteria stimulate pro-inflammatory responses whereas others are anti-inflammatory. These signaling pathways are enhanced when the tight junctions between epithelial cells are altered. This increased leakiness or permeability of the colon allows bacteria greater access to the epithelium and immune cells in the lamina propria.