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All diagnostic and therapeutic procedures in the field of science and medicine are continuously evolving: Therefore the herein presented medical evidence is state of the technical and scientific art at the time of the editorial deadline for the respective edition of the book. All details provided herein related to a particular therapeutic mode of administration and dosing of drugs are screened employing utmost measures of accuracy and precision. Unless explicitly specified otherwise, all drug administration and dosing regimens presented herein are for healthy adults with normal renal and hepatic function. Liability cannot be assumed for any type of dosing and administration regimen presented herein. Each reader is advised to carefully consult the respective market authorization holders directions for use of the recommended drugs, medical devices and other means of therapy and diagnosis. This applies in particular also to market authorization holders summaries of product characteristics for pharmaceutical products. Despite all care, there may be translation errors. The reader is advised to carefully check information related to the indication for use, contraindications, dosing recommendations, side effects and interactions with other medications! All modes of medication use and administration are at the consumers risk. The author and his team cannot be held responsible for any damage caused by wrong therapy or diagnosis. Please refer to, i.e: www.leitlinien.de or www.guideline.gov The trade name of a trade name registered product does not provide the legal privilege to employ the trade name as a free trade mark even if it is not specifically marked as such. Drugs which are sold as generics are referred to throughout the book by their generic name and not necessarily by a particular brand name. Remark: ICD 10 code version 1.3 has been employed for the index. Since in the current edition ICD 10 code version 2.0 was used, different code numbers may have been assigned to indexed items! No part of the book neither in part or in toto may be reproduced in any format (print, copy, microfilm, electronic storage, use and/or distribution by any electronic format including the internet) in the absence of an explicit written permission by the editor. Be careful about reading health books. You may die of a misprint. (Mark Twain)

Abbreviations
AAA AB ACE ADB ADH AET AF AG AIDS AIHA AN ANA ANCA ANP A.O. APC APS APPROX ARDS ARF ASAP ASD ASL AT AT ATP AXR BMI BMT BNP BP BU BW C CA CA. CDC CH CHD CI CK CL CMV CNP CNS CO CON COPD COX CRP CSE CSF CT CU CVI CVP CXR DD DEF DHD DHS DI DIC DNA DSA DVT EBV ECF ECG EEG EF EHEC ELISA EN ENT EP ESP ESR ET EU F FFP Abdo minal aortic aneurism Antibodies Angiotensin converting enzyme Anti-Desoxyribonucleotidase B Antidiuretic hormone Aetiology Atrial fibrillation Antigen Acquired Immunodeficiency Syndrome Autoimmune hae molytic anaemia Autonomic neuropathy Anti nuclear antibodies Anti neutrophile cytoplasmatic antibodies Atrial natriuretic peptide And others Activated Protein C Antiphospholipid syndrome Approximately Adult respiratory distress syndro me Acute renal failure As soon as possible Atrial septum defect Antistreptolysin Antithrombin Antithrombin Adenosine Triphosphate Abdo minal X-ray Body Mass Index Bone marrow transplant brain natriuretic peptide Blood pressure Bread unit Body weight Celsius Carcinoma Circa Centres for disease control Carbohydrate Coronary heart disease Contraindications Creatine Kinase Clinical picture Cytomegaly Virus Type C natriuretic peptide Central Nervous System Complications Contagiousness Chronic obstructive pulmonary disease Cyclooxygenase C-reactive protein Cholesterol Synthesis Enzyme Cerebrospinal Fluid Computer tomography Carbohydrate unit Chronic venous insufficiency Central venous pressure Chest X-ray Differential diagnosis Definition Dengue haemorrhagic fever Dengue haemorrhagic shock Diagnosis Disseminated intravascular coagulation Deoxyribonucleic acid Digital subtraction angiography Deep vein thrombosis Epstein Barr Virus Extracellular fluid Electrocardiogram Electroencephalogram Effects Enterohaemorrhagic E. coli Enzyme linked immunosorbent assay Enteral nutrition Ear Nose & Throat Epidemiology Especially Erythrocyte Sedimentation Rate Etiology European Union Female Fresh Frozen Plasma FUO GBM GFR GI GN HBV HCT HI HIT HIV HLT HPV HSV HUS HX IA IBS ICA ICD ICF ICP ICU IFAT IG IHA I.M. INC IND INR ISF ITP IU I.V. IVF LAB LAS LDH LDL LDV LMWH LOC M MDS MI MI MIO MM MOA MRI MW NK (cells) NSAID OAC OAD OCC OCC PA PAT PAT PCR PE PEP PET PFO PG PI PID PMC PN PNH POSS PPC PPH PPSB PRG PRO PTCA PTH PTS PTT RA Fever of unknown origin Glo merular basement membrane Glo merular filtration rate Gastrointestinal Glo merulonephritis Hepatitis B Virus Haematocrit Histology Heparin induced thrombocytopenia Human Immunodeficiency Virus Half life time Human Papillo ma Virus Herpes Simplex Virus Haemolytic uraemic syndro me History Interaction Irritable bowel syndrome Internal carotid artery Implantable Cardioverter - Defibrillator Intracellular fluid Intracranial pressure Intensive care unit Indirect immunofluorescence antigen test Immunoglobulin Indirect Haemagglutinin test Intramuscular Incidence Indication International normalised ratio Interstitial fluid Idiopathic thrombocytopenia International units Intravenous Intravascular fluid Laboratory tests Lymphadenopathy syndrome Lactate Dehydrogenase Low density lipoprotein Lymphocyte doubling ti me Low molecular weight Heparin Localisation Male Myelodysplastic syndrome Mentzer index Myocardial infarction Million Multiple myeloma Mode of action Magnet resonance imaging Molecular weight Natural killer (cells) Non steroidal anti-inflammatory drug Oral anticoagulation Occlusive atherosclerotic disease Occasionally Occurrence Pulmonary artery Pathogen Pathology Polymerase chain reaction Pulmonary embolism Post exposure prophylaxis Positron emission tomography Persistent foramen ovale Pathogenesis Protease inhibitor Pelvic infla mmatory disease Pseudome mbranous Enterocolitis Parenteral nutrition Paroxysmal nocturnal haemoglobinuria Possibly Phenprocoumon Pathophysiology Prothrombin proconvertin Stuart-Prower factor antihaemophilic factor B Prognosis Prophylaxis Percutaneous transluminal coronary angioplasty Parathyroid hormone Post Thrombotic Syndrome Prothrombin time Rheumatoid arthritis

RES RF RNA RS RV SC SE SIADH SK SLE ST STD SU SYM SYN TAA TEA TEE

Reticular Endothelial Syncythium Rheumatoid factor Ribonucleic acid Raynauds Syndrome right ventricular Subcutaneous Side effects Syndrome of inadequate ADH secretion Streptokinase Systemic lupus erythematosus Stage Sexually transmitted disease Sulfonyl urea Symptoms Synonym Thoracic aortic aneurism Thrombendarteriectomy Transoesophageal echocardiography

TH THR TIA TOA TPHA TPN TSH TURP UFH URTI US UTI UV VUR VV VZV WHO Y

Therapy Total hip replacement Transitory ischaemic attack Thrombangiitis obliterans Treponema Pallidum Hae magglutinin Total parenteral nutrition Thyroid stimulation hormone Transurethral resection of the prostate Unfractioned Heparin Upper Respiratory Tract Infection Ultrasound Urinary tract infection Ultraviolet Vesico-ureteric-renal reflux Varicose veins Varicella Zoster Virus World health organisation Year

Find more medical abbreviations at Find more general abbreviations at

www.medizinische-abkuerzungen.de www.acronymdb.com www.chemie.fu-berlin.de/cgi-bin/acronym

Di.:

1. History and clinic : Discomfort for years carcinoma, rel. short history 2. Oesophagus x-ray (oesophagus-barium swallow): Beaklike narrowing stenosis in the terminal oesophagus; pre-narrowed wide atonic megaoesophagus (champagne glass form). According to the extension of the oesophagus (absent, higher, extreme) 3 severity degrees can be distinguished. 3. Oesophagoscopy with biopsies (obligatory!): exclusion of carcinoma 4. Manometry: Missing atonia of the LES while swallowing Mostly elevated resting pressure of the LES Peristaltic contractions are missing in the tubular oesophagus According to the manometrically registrable oesophageal motility, a hyper-, hypo and amotile form can be distinguished.

Th.:

1. Pharmaceutical: Nifedipine, taken 30 min. before eating, lowers the pressure in the LES. Long-term effects are disappointing. 2. Method of 1st choice: balloon dilatation, long-term success rate: about 60 %; relapses can be dilated anew Compl.: Perforation (1 - 5 %) x-ray with hydrosoluble contrast medium after dilatation 3. Endoscopic injection of botulismotoxin into the LES: Initial therapy effect are as good as with balloon dilatation. In younger patients smaller success rate. Long term effects are disappointing. Very high costs. 4. Alternative: Surgical or laparoscopical extramucoid myotomy of the LES. In case of hypermotile achalasia additional semifundoplication for the prophylaxis of a postoperative following reflux disease. Ind: alternative therapy to the balloon dilatation or after several dilatations and only brief success Mortality < 0,3 %. Success rate: up to 90 %. Remark.: After both methods (dilatation, surgical procedure) an occlusive insufficiency of the LES with reflux oesophagitis (about 10 % of cases) can be developed.

Aftercare: Regular control endoscopies due to elevated danger of oesophageal cancer.

GASTROOESOPHAGEAL REFLUX DISEASE

Syn: Def.: GERD (gastro-oesophageal reflux disease); Reflux disease Gastrooesophageal reflux: backflow of stomach contents into the oesophagus due to failure of the occlusion mechanism of the lower oesophageal sphincter (LES ) Physiologic reflux: Rare reflux in healthy persons, e. g. after rich meals and wine consumption Endoscopically negative reflux disease ( NERD = Non-erosive reflux disease) : Frequent reflux problems without endoscopic or histologic evidence of reflux oesophagitis Endoscopically positive reflux disease = Reflux oesophagitis (ERD = erosive reflux disease) : reflux disease with macroscopically detectable epithelial defects or histologically traceable inflammatory mucosa infiltration

Oc.:

About 20% of the population of western industry nations are affected by GERD. 60 % of GERD patients have no endoscopically perceptible lesions (NERD) 40 % of GERD patients have endoscopically perceptible lesions (ERD) = reflux oesophagitis Up to 5% of GERD-patients develop Barretts oesophagus, m:f = 10 : 1 10 % of the patients with Barretts oesophagus develop adenocarcinoma The risk of developing cancer in Long-Segment-Barrett (length of the intraepithelial neoplasia = IEN (former name: Dysplasia) > 3 cm) is estimated to be 0.5% per year. With Short-Segment-Barrett (length of the IEN <3 cm; in case of Ultra-Short Barrett ( only microscopically visible small IEN in the cardia region), the cancer risk is smallest. The incidence of both GERD and adenocarcinoma of the distal oesophagus have been steadily increasing in the western industry nations during the last few decades. 1. Primary: Faulty occlusion mechanism of the LES of unknown cause (most frequently) 2. Secondary with known causes: e. g. pregnancy (50 % of all pregnant women, esp. frequently in the last trimester), condition after surgical procedure of achalasia, gastric outlet stenosis, scleroderma, among other things 1. Insufficient antireflux barrier of the LES: The LES forms a pressure barrier between the stomach and the oesophagus. The resting pressure in the LES is usually 10 - 25 mm Hg higher than the intragastric pressure. It is only while swallowing that a short reflex relaxation of the LES occurs. Manometry in reflux disease: Inadequate atonia of the LES out of swallowing (most frequent) Too low pressure in the LES and missing pressure barrier of the LES Abnormal contraction sequence in the lower oesophagus delayed acid-clearence and prolonged time of contact of sour fluid in the oesophagus.
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Aet.:

Pg.:

Most patients have a simultaneous axial hiatus hernia that represents a predisposing factor. However, just 10 % of the individuals with axial hiatus hernia suffer from reflux disease. Insufficiency of the crus of diaphragm is a further predisposing factor. Overweight also can have a favouring impact, for example due to an increased abdominal pressure. Larger meals late in the evening, alcohol, coffee are factors as well. 2. Aggressive reflux fluids: The damage of the oesophagus mucosa arises most frequently from sour reflux (hydrochloric acid), rarely from alkaline reflux (bile) after gastrectomy. 3. Faulty self-cleaning (clearance) of the oesophagus 4. Faulty gastric emptying Note: Main causes are incompetence of the LES and aggressive reflux fluids! Cl.: Brash (75 %)= burning substernal pain ("heart-burn"), esp. while lying down and after meals Feeling of pressure behind the sternum and the xiphoid (DD: CHD!) Air belch (60 %), aerophagia, meteorism, flatulence (odorless) Difficulty in swallowing (50 %) Regurgitation of food residue (40 %) Epigastric pain and burning (30 %) Salty or soapy taste in the mouth after belch; enamel damage Nausea, vomiting Extraoesophageal manifestation of reflux disease: - Pot. stenocardial pain (cardia-cardial reflex pathway) DD: CHD (disappearance of the discomfort under therapy with proton pump inhibitory drugs !) - Irritant cough ( reflux bronchitis) and release/intensification of bronchial asthma, chronic bronchitis - Possibly hoarseness ( posterior laryngitis) due to laryngo-pharyngial reflux = LPR, globus feeling - Sleep-apnoea syndrome - sleep disorders Consider: The pain will be increased by bending down, pressing, in supine position, effort, stress, certain foods and some drugs (see below). Co.: Ulcerations, rarely haemorrhage Nightly aspiration of stomach contents Barrett-syndrome, Barretts oesophagus : Substitute of the squamous epithelium of the terminal oesophagus by specialized columnar epithelium (SCE). The transition (Z-line) of the epithels is unsharp, with extensions or islands of metaplastic columnar epithel into the oesophagus. Barretts oesophagus is an precancerosis. The risk of adenocarcinoma is highest in LongSegment-Barrett with high inflammatory activity, i. e. persistent reflux (see above) Hi: 1. Low grade IEN = LGIN 2. High grade EIN = HGIN Stenosis of the oesophagus with dysphagy and pot. odynophagia ( = pain during the swallowing) 1. Secondary forms of reflux oesophagitis (see above) 2. Motility disorders of the oesophagus [K22.4] - Diffuse oesophageal spasm: Neuromuscular dysfunction of unknown etiology. Cl.: Intermittently occurring cramping pains retrosternally (DD: Coronary heart disease!). X-ray.: Uncoordinated contractions in the distal oesophagus. Manometry: Simultaneous , increased and long-lasting oesophagus contractions - Hypercontractible oesophagus (nutcrackers oesophagus) [K22.4]: Manometry: in quality normal (= peristaltically running) oesophagus contractions that show excessive amplitudes > 120 mm Hg and single amplitudes > 200 mm Hg and/or prolonged (> 5 s) duration Th.: Attempt with Nifedipine or nitroglycerine .Oesophageal ulcers due to sticking tablets (e.g. Doxycycline- or potassium capsules tablets should not be taken in the supine position and always with copious amounts of fluids!) Other oesophageal diseases (e. g. diverticulum, carcinoma, achalasia Upper abdomen diseases (ulcer disease, gastric carcinoma, irritable stomach , among other things) Coronary heart disease (ergometry) Functional oesophagus problems (irritable oesophagus): Exclusion diagnose! Remark.: Since both diseases are frequent, coincidence of reflux disease and CHD is possible. History/clinical/probatory therapy with proton pump inhibitors (PPI) can lead to the diagnose reflux problems.

DD:

Di.:

Reflux oesophagitis is an endoscopic diagnose, Diagnosing of the Barrett-Oesophagus is possible only endoscopically: Bioptic detection of columnar epithel of the intestine type; main characteristic: occurrence of goblet cells: 1. Low grade IEN (LGIN) 2. High grade IEN (HGIN). Still no routine procedure: High-resolution-endoscopy, magnification-endoscopy (up to 150fold magnification), chromoendoscopy with utilisation of acetic acid (contrast imaging by means of denaturation/ change of the tertiary structure of mucosal surface proteins) or methylene blue (selective absorption by the Barrett epithel), endomicroscopy ( In-vivo-histology, makes the identification of individual goblet cells possible)

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Classification of reflux disease according to Savary and Miller: (St. I - IV: Reflux oesophagitis): St. 0: Gastrooesophageal reflux without mucous membrane changes St. I: Isolated mucous membrane erosion IA: Superficial erosion (red patches) IB: Deeper erosion with fibrinoid necrosis (red patches with whitish centre) St. II: Longitudinally confluent erosions along the mucosal folds IIA and IIB (see above) St. III: Circularly confluent erosions in the entire area of the terminal oesophagus St. IV: Complication stage: ulcerations, strictures/stenosis, columnar cell metaplasia (see above) IVA: With inflammatory changes IVB: Irreversible scar stage without inflammatory changes MUSE-classification according to Armstrong: Severity degree M (Metaplasia) U (Ulcer) 0 None 1 low 2 moderate 3 severe 0 1 stripe 2 stripes Circular 0 Border ulcer Barrett ulcer Both ulcer types S (Stricture) 0 > 9 mm 9 mm + oesophagus is getting shorter E (Erosion) 0 1 folding protuberance 2 folding protuberances circular

Los Angeles-classification: Stage A : One or more erosions < 5 mm which do not extend between the tops of mucosa folds Stage B: Like A, but erosions 5 mm Stage C: Erosions extend between two or more mucosa folds, but cover < 75% of the circumference Stage D: Like C, but 75% of the circumference affected Note: Often, there is no correlation between symptoms and endoscopic findings. Longtime-pH-measuring > 24 h of the lower oesophagus: Registration of the times of reflux of sour stomach contents (pH 4). Healthy persons show no reflux after midnight and postprandially just short (5 minutes) reflux episodes. In case of reflux disease reflux episodes also occur especially at night. The measurement result is considered pathological if the reflux times during the day are > 8 % or at night > 3 % of the total measuring time. Correlation of the reflux episodes with symptoms. Th.: A) Conservative: 1. General measures are helpful in case of slight reflux problems: Weight normalisation, small low-fat meals, no meals late in the evening, no clothing that constricts the abdomen. Avoid noxious causes: e. g. chocolate and sweets, nicotine, acidic fluids (wine, juice from citrus fruits, tomatoes), alcohol consumption (esp. strong drinks), coffee, tomato sauce, carbonated drinks, tomato sauce, garlic ; do not sleep immediately after eating , sleeping on elevated head of the bed (blocks under the feet of the bed) as well as in right side position. If possible, stopping of drugs which lower the pressure in the LES: e. g. anticholinergics, -adrenergics, calcium antagonists, Nitro-preparation, theophylline, peppermint, among other things. 2. Drugs are necessary in reflux oesophagitis or if there are frequent problems: Proton pump inhibitors (PPI): If the dosage is sufficient , there is a total acid suppression highest and fastest cure rates (ca. 90%) Means of choice for treating reflux oesophagitis Note: Reflux disease is an acid disease with an occlusion disturbance of the LES. The curing rate rises with the degree of acid suppression! Omeprazol, , Lansoprazol, Pantoprazol (Pantozol , Rifun ), Rabeprazol (Pariet ), Esomeprazo(Nexium )l + + Eff.: Depending on dose up to 100% acid suppression by inhibition of H /K -ATPase. The bond of the PPI + + to the H /K -ATPase is irreversible, secretion inhibition is only cancelled out by the natural regeneration of the parietal cells. E: Diarrhoea and other gastrointestinal SE, vertigo, headaches, change of mood. Very rarely sight defects (esp. in case of high i.v. dosage), hearing disorders, enzym modification, interstitial nephritis, blood count alterations, skin rash.Total acid suppression leads ( just like after gastrectomy) to hypergastrinemia and to hypertrophy of enterochromaffine cells Long-term therapy can cause chronic atrophic gastritis! The pharmacologically induced achlorhydria favours a colonisation of the stomach by bacteria, and the risk of pneumonia is slightly increased. IA: As with Cimetidin interference with the liver enzyme Cytochrome P450 , hence a delayed decomposition of some drugs (only in case of high dosage)
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CI.: For children, pregnant and breast-feeding women Dos.: Equipotent standard doses: Omeprazol, Rabeprazol, Esomeprazol: 20 mg/d Lansoprazol: 30 mg/d Pantoprazol: 40 mg/d Step-down-therapy = initially high PPI-dose ( fast cure of lesions), afterwards as maintenance dose half of the therapeutic dose. Taking of the PPI h before breakfast, if acid suppression is insufficient at night, splitting of the PPI into the morning and evening dose. As a relapse can occur in 50% of cases after the end of the therapy, long term relapse-prophylaxis is indicated in case of frequent relapses. If relapses occur only occasionally, a therapy on demand is sufficient. Causes of therapy resistance: - Stomach-emptying disturbance ( gastroscopy) , leads to gastral inactivation of the PPI - Zollinger- Ellison- syndrome ( basal gastrin level ; Warning: Stop taking PPI before!) - Taking of NSAIDs - Nightly acid breach; high volume reflux ( 24 h pH metry) - Other cause of disease (check diagnosis) 3. Other drugs are only indicated for the treatment of slight reflux discomfort without oesophagitis H2- Receptor antagonists (H2-blockers) Less effective than PPI and used only in case of reflux discomfort without oesophagitis (also as OTC preparations without prescription). Cimetidine, Ranitidine, Nizatidine, Famotidine, Roxatidine Eff.: With average dose only about 50% acid suppression (via inhibition of histamin effect in the parietal cells), for this reason by far not up to PPI SE: e.g. headache, skin rash, diarrhoea, gynecomastia, erectile dysfunction, confusion in case of liver- or renal insufficiency, rarely creatinine- or transaminase increase, rarely leukocytopenia, thrombocytopenia, allergic reactions IA: With cimetidine, inhibition of encymatic drug decomposition in the liver (Cytochrome P450 ) increased / prolonged effect of some drugs! Therefore, cimetidine is not recommendable. By inhibiting alcoholdehydrogenase, cimetidine and ranitidine can increase the alcohol concentration in the blood. CI: For children, pregnant and breast-feeding women Dos.: Equipotent doses: Cimetidine 800 mg/d; ranitidine and nizatidine 300 mg/d , resp.; Roxatidine 150 mg/d; famotidine 40 mg/d; dose reduction in case of renal insufficiency. Antacids: Eff.: Due to their low efficacy, application only for the therapy of mild reflux pain without oesophagitis, mostly within self-medication (OTC-preparations). Buffering (neutralisation) of the gastric acid + adsorption of bile acids SE: Aluminiumhydroxide: constipation, hypophosphatemia (formation of insoluble aluminium phosphate in the small intestine), in renal insufficiency deposit of aluminum in bones and brain. Aluminous antacids should not be taken for more than 6 weeks, if possible. Magnesium hydroxide: diarrhoea, hypermagnesemia (esp. in renal insufficiency, contraindicated!) I.a.: Adsorption of different drugs; do not take antacids simultaneously with other drugs. Dos: Antacids should be administered one and three hours after the meals and shortly before bedtime. B) Surgical or laparoscopic fundoplication (Nissen`s fundoplication): In order to increase the pressure on the LES, a fundus cuff is applied around the oesophagus. Ind: Stage IV, failure of the conservative therapy, incompatibility of acid suppressing drugs, recurrent aspiration. Operation mortality: in good centres < 0.5 %, good operation result in about 85 % of cases. Post fundoplication syndrome [K91.1] : pain following fundoplication: 1. Relapse problems of a reflux oesophagitis 2. Gas bloat syndrome: intolerance of CO2-containing drinks with feeling of pressure in the medial/left epigastrium caused by air in the stomach or meteorism with reflectory cardial pain (=Roemheld-syndrome). Causes: -Wrong operation indication - Operation technique - Newly occurred disease C) Transoral endoscopic procedures By means of endoscopic technique, folds or cushions of mucosal membrane are formed, for example in the cardia zone; different variations are in clinical testing. D) Surveillance strategy in Barretts oesophagus Video-endoscopy control with biopsy of all suspicious findings as well as quadrant biopsies every 2 cm and from suspect parts. Chromoendoscopy may facilitate the localisation of test excisions. LGIN: As a procedure to detect LGIN , controlling under PPI therapy is suggested after 3-6 months. If LGIN is identified anew, endoscopic mucosa resection (EMR) of the lesion or the ablation of the Barrett by EMR is recommended. HGIN: After verification of the histology by an additional pathologist, EMR (with ablation of the Barrett) or the surgical procedure is recommended after identification.
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Remark: So far, it has not been prooved whether acid-suppressing therapy or surgery reduces the risk of carcinoma.

HIATUS HERNIA
1. Normal findings 2. Cardiofundal malformation 3. Axial sliding hernia [K40.9] 4. Paraesophageal hernia [K44.9] 5. Mixed forms (no sketch)

Cardiofundal malformation (open oesophagogastric transition): Preliminary stage of the axial sliding hernia with the oesophagus ending into the stomach under blunt His-angle (= oesophageal Angle) due to loosening of the ligamentary apparatus. Frequent gastroscopic finding ! Sliding hernia (axial hernia): With 90 % of cases the most frequent hiatal hernia: Dislocation of the cardia and the fornix of the stomach through the diaphragm hiatus into the thorax space under involvement of the peritoneum: cardia above the diaphragm. The occurrence of hiatus sliding hernias is increasing with age: 50 % of people > 50 yrs have a hiatal sliding hernia. Paraoesophageal hiatus hernia: Position of the cardia and function of the LES are normal. A part of the stomach pushes its way into the thorax with a peritoneal hernia sac close to the oesophagus. Extreme variation: so-called thorax stomach (upside-down-stomach ). Cl.: 1. Axial sliding hernia: pain due to reflux has a similar occurrence as among the normal population. (symptom-free axial sliding hernia without disease value) As a prominent Schatzki-ring, the upper edge of an axial hiatus hernia can become the cause of a rare bolus obstruction by a bigger piece of unchewed meat (= steakhouse syndrome) 2. Paraoesophageal hernia: Asymptomatic stage Uncomplicated stage: belch, feeling of pressure in the cardial area, esp. after eating Complication stage: passage failure, incarceration, erosion or ulcer at the ligature ring, chronic posthaemorrhagic anaemia x-ray Barium swallow in Trendelenburgs position + abdominal pressure, endoscopy Axial hernia: Necessity for treatment only in case of discomforts like reflux oesophagitis (see section on this topic) Paraoesophageal hernia: Indication for surgical procedure also in the asymptomatic stage because of danger from complications - method: transabdominal gastropexy (reduction and fixation of the stomach to the front abdominal wall).

Di.: Th.:

DIVERTICULA
Def.: Pouches in the digestive tract which either consist of the entire intestinal wall (true diverticulum) or represent only mucousal pouches through muscle gaps (pseudodiverticulum). Location: Oesophagus, duodenum, Meckel`s diverticulum in the ileum, colon (rarely stomach, small bowel); diverticula are often multiple, they are most frequently in the colon.

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Copyright 2010 by Dr. Gerd Herold, Cologne, Germany. All rights reserved. Original German Textbook by Gerd Herold Translation by Ralf Brcker, Bettina Mues, Hedwig Mller, Sylvia Mller Project coordination by Bjrn Gemein Volume One: 432 pages in total, Royal (6 x 9) Table of Contents: Evidence based medicine, Haematology, Cardiology, Pulmonology, Gastroenterology (part 1) ISBN 978-1-4467-6367-4 Price: 23.50 Volume Two: 408 pages in total, Royal (6 x 9) Table of Contents: Gastroenterology (part 2), Salt and water homeostasis, Nephrology, Rheumatology, Metabolic system disorders, Endocrinology, Angiology, Infectious diseases, , Reference intervals ISBN: 978-1-4467-6368-1 Price: 23.50 Digital Edition: 824 pages in total, DIN A4 Table of Contents: See Vol. 1 + 2 Available at Lulu.com, ID 9545211 Price: 35.00 The e-book requires Adobe Digital Editions
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