By S. Mitch. Reinhardt College.
In persons with steatorrhea cheap prevacid 15 mg fast delivery gastritis diet symptoms, fatty acids in the intestinal lumen preferentially bind to calcium purchase prevacid 15 mg on-line gastritis diet øàðëîòêà, leaving the oxalate soluble and available for absorption in the colon buy generic prevacid 30mg gastritis reflux. The short bowel syndrome may also give rise to cholelithiasis; with extensive bile acid malabsorption lithogenic bile will be produced, predisposing to gallstone formation. The small size of the gastric remnant causes inadequate mixing of food with digestive juices, particularly after a gastroenterostomy. Incoordinated secretion and poor mixing of bile and pancreatic juice leads to fat maldigestion. Small bowel intestinal overgrowth (in a blind loop or following vagotomy) results in maldigestion of fat, carbohydrate, protein, vitamins and minerals. Gastric surgery that allows food to enter into the upper small intestine without dilution and with minimal digestion may unmask clinically occult celiac disease, lactase deficiency or pancreatic insufficiency. Definition Celiac disease, also known as celiac sprue or gluten-sensitive enteropathy, is a life-long disorder characterized by malabsorption of macronutrients and micronutrients along with mucosal inflammatory changes in the proximal small intestine (duodenum), sometimes extending more distally into the jejunoileum. These appear to be precipitated by ingestion of gluten peptides found in wheat rye and barley. As a result, many celiac patients have intestinal or extra-intestinal symptoms, while others may be entirely asymptomatic. By definition, however, clinical and histological improvement results from a strict gluten-free diet, and relapse occurs with re-introduction of dietary gluten. Learn to suspect and test for it in persons with typical gastrointestinal symptoms, as well as knowing when to screen for celiac disease in persons with associated disorders, such as autoimmune conditions. Although early autopsy descriptions for celiac disease are available, an evolution in technology for procurement of small intestinal biopsies led to earlier clinical diagnosis, and an explosion of information on many disorders of the small intestine, besides celiac disease. In recent years, the extended recognition of clinical features and protean presentations of celiac disease has resulted in markedly improved awareness. Finally, development of improved screening methods in the laboratory has resulted in appreciation that celiac disease is common, particularly in Europe and North America, with rates of about 1 in every 100 persons. Definition of celiac disease in adults depends on two sequential criteria: first, demonstration of the typical biopsy changes of untreated celiac disease; and second, improvement with absolute dietary gluten restriction. Most often, resolution of diarrhea and evidence of weight gain is sufficient to establish improvement. In others, especially in children, a second set of intestinal biopsies after a prolonged period of dietary gluten restriction may be needed to document this improvement. High Risk Populations The true prevalence of celiac disease has not been defined, in part, because many are now recognized for the first time with atypical, few or no symptoms. Some have suggested that screening measures have especially increased recognition of celiac disease, at least in comparison to those known to have already established disease. In North Americans, the reported general population prevalence is approximately 1:100 (1%) with a range of 1:80 to 1:140 (1. A study in Swedish youth (<20 years old) diagnosed with Type 1Diabetes confirmed the low prevalence (0. High-risk groups that exceed this general population prevalence are listed in Table 1. However, for unknown reasons this female sex preponderance disappears with increased aging. These may include perinatal infections, or viral infections such as Adenovirus 12 and Hepatitis C virus (Plot and Amital, 2009). The timing was possibly owing to the time of introduction of cereal grains into their diet. Now, however, it is appreciated that most clinically evident celiac disease is usually first detected between ages 25 and 40 years, not during childhood. Furthermore, in recent years the initial definition of celiac disease in the elderly has become increasingly appreciated, with some studies recording that about 20% of celiacs are older than age 60 years. Clinical Gem While the peak age of diagnosis of persons with celiac disease is 25-40 years of age, initial diagnosis of celiac disease may be established at any age, including the elderly. The highest reported prevalence of celiac disease is from western European countries, North America, particularly Canada and the United States, and Australia. Celiac disease also occurs in the Indian subcontinent, particularly in the Punjab region of northwest India as well as in Indian emigrants to the United Kingdom and Canada. Celiac disease has also been described in First Nations persons living on the west coast of Canada; these persons sometimes also have other concomitant immune-mediated disorders. Pathogenesis Celiac disease results from the interaction between dietary gluten and specific immune, genetic and environmental factors. The current pathogenesis can be summarized as follows: in genetically-primed individuals, an inappropriate T-cell mediated immune response occurs against ingested dietary gluten, the major storage protein of wheat and related grains. This response leads to inflammation mostly in the proximal small intestine, loss or shortening of intestinal villi, and both intestinal as well as extra-intestinal symptoms. When gluten is withdrawn from the diet, these abnormalities improve, or disappear. Immune Factors Gluten generally refers to the entire protein content of wheat, rich in glutamine and proline. Most proteins or peptides that arrive in the proximal small intestine can be digested by luminal and brush border hydrolytic enzymes into amino acids and peptides. Gluten and other proline-rich proteins are poorly digested in the normal human small intestine, because of an apparent deficiency of prolyl-endopeptidases.
The development of atrophic gastritis and intesti- nal metaplasia is considered to be premalignant although the incidence of gastric cancer in gastric intestinal metaplasia is unknown and surveillance is not widely practised discount 30mg prevacid otc gastritis diet journals. In the Western world purchase prevacid 15mg with amex gastritis diet and recipes, histologic changes of chronic gas- tritis occur in up to 50% of the population in later life although the incidence of gastric cancer is falling discount 15 mg prevacid fast delivery gastritis y probioticos, almost certainly due to the decreasing prevalence of H. Chronic gastritis rarely causes symptoms although it can be associated with nausea, vomiting and upper abdominal discomfort. Shaffer 143 In addition to elements of chronicity, gastritis can also be categorized on the basis of identifiable etiology (e. There are numerous causes of histologically diagnosed gastritis, and the importance of knowing the cause of the gastritis is to treat the underlying condition. It must be stressed that even when the cause of the gastritis is treated, such as in the person withy dyspepsia and a chronic H. The characteristic histo- logical finding is owl-eye, intranuclear inclusions in cells of the mucosal epithelium, vascular endothelium and connective tissue. At endoscopy, the gastric mucosa has a cobblestone appearance due to multiple superficial linear ulcers and small raised ulcerated plaques, while histology shows numerous cells with ground-glass nuclei and eosinophilic, intranuclear inclusion bodies surrounded by halos. Over time, the initial antral-predominant gastritis progresses to a pangastri- tis and then to atrophic gastritis and intestinal metaplasia precursors to the development of gastric cancer (the Correa hypothesis). Phlegmonous (suppurative) gastritis is a rare bacterial infection of the submucosa and muscularis propria and is associated with massive alcohol ingestion, upper respiratory tract infection, and immune compromise; it has a mortality rate in excess of 50%. Emphysematous gastritis, due to Clostridium welchii, may lead to the formation of gas bubbles, along the gastric contour on x-ray. Treatment requires gastric resection or drainage and high-dose systemic antibiotics. Mycobacterium tuberculosis gastritis is rare; ulcers, masses, or gastric outlet obstruction may be seen at endoscopy and biopsies show necrotizing granulomas with acid-fast bacilli. Mycobacterium avium complex gastritis is very rare, even in immunocompromised individuals; gastric mucosal biopsies show foamy histiocytes containing acid-fast bacilli. In actinomycosis, endoscopy may reveal appearances suggestive of a gastric malignancy; biopsies show multiple abscesses containing Actinomyces israelii, a gram-positive filamentous anaerobic bacterium. Parasitic causes of gastri- tis include Cryptosporidia, Strongyloides stercoralis, Anisakis (from raw marine fish), Ascaris lumbricoides and Necator americanus (hookworm). Endoscopic findings are non-specific and histology shows cell necrosis (apoptotic bodies intraepithelial vacuoles containing karyorrhectic debris and fragments of cytoplasm) in the neck region of the gastric mucosa. It is associated with other autoimmune disorders such as Hashimotos thyroiditis and Addisons disease. Mucosal atrophy, with loss of parietal cells, leads to decreased production of acid and intrinsic factor; about 10% of these patients develop low serum vitamin B12 levels and pernicious anemia. Chemical Gastropathy (Reactive Gastropathy) A number of different agents can produce gastric mucosal injury, characterized at endoscopy by hemorrhagic lesions and erosions (necrosis to the level of the muscularis mucosa) or ulcers (necrosis extending deeper than the muscularis mucosa). Portal hyper- tension produces a congestive gastropathy, with vascular ectasia but, again, only a minimal inflammatory infiltrate. Crohn disease of the stomach is uncommon, particularly in the absence of disease elsewhere in the gastrointestinal tract. Endoscopy may show mucosal reddening and nodules with or without overlying erosions and ulcers that may be elongated or serpiginous. Histological features include non-caseating granu- lomata, ulceration, chronic inflammation and submucosal fibrosis. Sarcoidosis of the stomach can be difficult to distinguish endoscopically and histologically from Crohn disease and the diagnosis must be based on the presence of other systemic features. Gastritis with Specific Diagnostic Features Collagenous gastritis has been reported in association with collagenous colitis and lymphocytic colitis; it is very rare. At endoscopy, non-specific findings include mucosal hemorrhages, erosions and nodularity while histology shows a chronic gastritis (plasma cells and intra-epithelial lymphocytes), focal atrophy and focal collagen deposition (2075 m) in the lamina propria. Histology shows an infiltrate of the lamina propria in the antrum or body by plasma cells, lymphocytes and rare neutrophils, and a marked intraepithelial infiltrate with T lymphocytes. Eosinophilic gastritis is associated with peripheral eosinophilia and eosinophilic infiltration of the stomach, involving one or more layers of the gastrointestinal tract (mucosa, muscle or subserosa). Hypertrophic Gastropathies There are numerous causes of thickened gastric folds seen on endoscopy or diagnostic imaging (Table 2). Mntriers disease is associated with protein- losing gastropathy and hypochlorhydria whereas hyperplastic, hypersecretory gastropathy is associated with increased or normal acid secretion and hyper- plasia of the parietal and chief cells, with or without protein loss. Endoscopy, in both cases, typically shows irregular hypertrophic folds involving the body of the stomach, although there is a polypoid variant that resembles multiple hyperplastic gastric polyps. The characteristic histological features are foveolar hyperplasia with cystic dilation; inflammatory infiltrates may be present, as in hypertrophic lymphocytic gastritis, but this is variable. Gastric resection for refractory protein loss, hemorrhage or obstruction is a last resort. Miscellaneous Gastritides Gastritis cystica profunda is a rare sequela of partial gastrectomy with gastro- jejunostomy but it may also develop in the absence of prior gastric surgery. Endoscopy typically shows multiple exophytic gastric masses, which on sec- tion reveal multiple cysts. At histology, foveolar hyperplasia is accompanied by cystic glands that extend through the muscularis mucosae into the submucosa and muscularis propria. It may be associated with chronic atrophic gastritis, hyperplasia or primary gastric stump cancer after surgery. Gastric Polyps and Gastric Malignancy There are numerous types of gastric polyps (Table 4) which are usually incidental findings with little risk of developing into cancer.
Also kitten faeces (eg cyst in garden pregnant gardeners should wear gloves) Presentation: Immunocompetent: Lymphadenopathy (eg unilateral) Maybe: fever purchase prevacid 15mg on line gastritis and celiac diet, myalgia discount 30mg prevacid otc gastritis diet àâàòàí, acute pharyngitis discount 15 mg prevacid free shipping gastritis symptoms for dogs, hepatosplenomegaly, atypical mononucleosis Usually self-limiting may take months to settle If persistent/recurrent lymphadenopathy ? If you dont, they will relapse Relapse common (20%) maybe several months later. Serum antibody test Treatment: Intestinal amoebiasis: metronidazole then diloxanide furoate Extra-intestinal: metronidazole (surgical drainage may be necessary) Asymptomatic: Diloxanide furoate Giardiasis Diagnosis: Stool examination for Giardia Lamblia cysts, 3 samples 48 hours apart Duodenal aspirate and direct examination for trophozoites Treatment: Tinidazole 2g stat or Metronidazole 400 mg 8 hourly for 7 days Test for cure with repeat stool sample. Dogs infected from eating raw sheep offal (ie liver) containing hydatid cysts Clinical: Often acquired in childhood, present in older age with solitary cysts (liver, lung, brain) Treatment: surgical drainage + aldendazole as adjunct Diagnosis: Serology: haemaglutination test + complement fixation test Cryptosporidium Common protozoan parasite Profuse watery diarrhoea for 48 hours. Relapse in 25% See also Other pneumonias, page 70 Travel Medicine Travel History: Where are you going How are you getting there How long there What will you be doing Where are you staying Have you been there before Examples: 3 week package to Hong Kong, Singapore, Bangkok: Hep A and Tetanus up to date. Risk in main resort areas of Asia is low Typhoid: Injectable: salmonella typhi antigen, 70% protection for 3 years Oral vaccine: attenuated live strain, doses at 0, 3 and 5 days gives protection for one year. Resistant (eg kids): Ceftriaxone Resistant and Meningitis: Cefotaxime + Vancomycin (act synergistically) Resistant and Endocarditis: Vancomycin Strep faecalis Trimethoprim Strep agalactiae Penicillin. Also sensitive to flucloxacillin Strep sanguis Penicillin [ haemolytic] Staph aureus Flucloxacillin. Elderly/immunocompromised: ciprofloxacin (quinolone not in kids) Clostridium difficile Metronidazole Enterococcus faecalis Amoxycillin G ive Bacilli E Coli Trimethoprim. Consider gentamycin or cotrimoxazole Campylobacter Jejuni Erythromycin Infectious Diseases 511 H Influenzae Cefaclor, Augmentin, Tetracycline 5% resistant to penicillin, not sensitive to erythromycin Legionella Erythromycin. Maybe Tobramycin or piperacillin Meningitis: Ceftazidine Gardnerella Vaginalis Metronidazole. Metronidazole is otherwise inactive against aerobes Bordetella Pertussis Erythromycin Branhamella Catarrhalis Augmentin, cefaclor, tetracycline, cefuroxime 70% penicillinase Anaerobes Bacteroides Fragilis Metronidazole. Not penicillin or cephalosporins Helicobacter Pylori Clarithromycin + metronidazole + omeprazole (7 days) Cocci Neisseria Meningitidis Penicillin. Prophylaxis: Rifampicin, ceftriaxone if pregnant Neisseria Gonorrhoea Stat: Amoxycillin + Probenecid Ciprofloxacin or tetracycline if penicillin allergy or resistant. Cellular wall similar to G-ive but not actually a G-ive bacteria Others nd Mycoplasma Erythromycin. Maybe Paromomycin (oral, non-absorbed aminoglycoside) Giardiasis Tinidazole stat or metronidazole 7 days Trichomonas Doxycycline, Metronidazole Pneumocystis Carinii Cotrimoxazole Pneumonia Malaria Prophylaxis Mefloquine weekly: good for chloroquine resistant falciparum. Not epilepsy, pregnant, babies Doxycycline daily: Esp Mefloquine resistant falciparum. Principle use is infectious exacerbations of chronic bronchitis Haemophilus influenzae Increasing E coli resistance Branhamella Catarrhalis Flucloxacillin Staph Aureus Penicillinase producers. If true anaphylaxis seek specialist advice Immune suppression: dont give live vaccine. If Heart failure vasoconstriction to maintain blood flow liver flow elimination (eg lignocaine, propranolol). Total body clearance cant exceed cardiac output (5 l/min) Clearance and Volume of Distribution are independent of each other, but T is dependent on both Maintenance Dose = clearance * desired concentration Compartments: One or multi compartment models Ka = absorption into compartment Ke = elimination from compartment th th 522 4 and 5 Year Notes Linear kinetics First order kinetics: rate of transport or elimination proportional to drug concentration in the compartment Zero order kinetics: elimination has maximum value rate is non-linear and its a capacity limited process. So if dose rate is greater than clearance rate, then a small increase in dose rate leads to a dramatic increase in plasma concentration (ie accumulation) Michaelis-Menten kinetics For a drug that undergoes zero-order elimination, when the concentration is low enough, elimination no longer occurs at its maximum rate (V max) but at a rate dependent on but not proportional to the plasma concentration. As the concentration reaches the maximum rate (km), first order elimination occurs So, elimination will increase with increasing dose, but not proportional to the dose Zero-order kinetics will be approached risk of accumulation Issue for any drug having zero-order kinetics within its therapeutic range E. In one compartment model: Ke = Cl/Vd = Measure of how the whole body handles the drug how quickly it gets out But it doesnt work in practice For slowly excreted drugs, 5 * T and it will be eliminated for practical purposes But for anaesthetic drugs that you want to switch on and off quickly the therapeutic window is often in the redistribution phase not the elimination phase. Need a more complex model where the drug redistributes to (then from) slow and fast compartments, as well as being excreted from blood context sensitive half-life. If drug is over infused, it builds up in other compartments and then takes a long time to wash out. Fe, Ca) Gastric emptying: emptying absorption rate Food: may slow gastric emptying, alter ionisation, decrease first pass metabolism. Lipid soluble undergo tubular reabsorption Only unbound particles excreted if highly bound then slower excretion Some are secreted by active tubular secretion e. Divided into families and sub-families 3 polymorphisms have been well defined: Acetylation: enzyme: n-acetyl-transferase 2. But normally total plasma concentration measured (and this will be reduced) danger of overdose Cardiac disease altered distribution (eg due to reduced gut flow poor absorption, renal and hepatic perfusion clearance) Obesity increased Vd for lipophilic drugs Metabolism: Most biotransformation occurs in liver. For some drugs, extraction depends on blood flow (where extraction ratio tends to 1) Liver disease capacity of metabolising enzymes (eg warfarin, phenytoin) and possibly shunting of blood around liver (affects drugs with high first pass metabolism) Thyroid diseases or metabolism Diabetes mellitus fatty liver change in metabolism Low clearance with high (>90%) degree of protein binding generally clearance Low clearance, low binding (e. If elderly excretion plasma concentration Dose rate for a drug excreted 100% by the kidney (e. Eg smaller loading dose of drugs with low Vd (eg digoxin and cimetidine) Protein binding: Albumin declines with age significant change only in tightly bound drugs (ie small Vd, eg phenytoin) or zero order elimination (eg warfarin) Metabolism: Hepatic clearance: Liver has significant residual capacity so not much decline with age, especially given lean body weight But significant (50%) reduction in liver blood flow, so significant reduction in metabolism of st 1 pass metabolism (eg propranolol) or capacity limited metabolism (phenytoin or theophylline). Problems with digoxin, lithium and gentamycin Renal clearance (see creatinine clearance above). Eg Slower absorption + variations in 1 pass metabolism wider variation in clinical effect Effect of variation in gastric emptying reduced Adhesive patches cause skin reaction in 30% Fixed dose: harder to titrate Cost Pharmacodynamics =Study of drug/receptor interactions. Most common targets are transmembrane receptors linked to G proteins Receptor interactions: Agonists: Bind and produce a full effect Partial agonists: bind and produce sub-maximal effect (ie lower dose-response curve) Inverse agonists: bind and have opposite effect to that of agonists Non-competitive agonists cannot be displaced Competitive agonists reversibly interact, can be reversed by an antagonist. Eg adrenaline can over-ride -blockers Non-competitive: dont allow a maximal response regardless (ie lower-dose response curve). Progressively lowers maximal response of agonist Agonist antagonist: has an agonist effect at one subtype of receptor and an antagonist effect at another Specificity = effect produced by interaction with a single receptor Ka = concentration required to occupy 50% of receptor sites at equilibrium Up-regulation/down-regulation: a very common response to an antagonist/agonist. Watch for rebound when it stops Pharmacology 527 Dose response curves: Relationship between plasma concentration and drugs effect Efficacy: maximal ceiling of effect, regardless of dose. Effectiveness of drug once bound to a receptor Potency: quantity required for maximal effect Affinity: if a drug has lower affinity, it can still produce a maximal effect but will require a larger dose (ie pushes dose response curve to the right).