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Medicine" (4th edition, Elsevier, 2008) Sebastian Kuepper email@example.com Contents Gastroenterology three reflux disease .......................................... ..... .................................................. ...................... 4 gastritis .......................... ......................................... ......... .................................................. gastroduodenal ulce r disease .......................................... ..... 5 ................... ............................... .6 Malassimilationssyndrom ..................... .......................... .................................................. .. ..... 7 colorectal cancer ........................................ ............. ..................................... ................... 8 Crohn's disease and ulcerative colitis ........................ .................................... .............. Hepatitis ........................ 9 ........................ ... ............................................... ................................ .................. .... 10 liver cirrhosis ..................................... ....... .................................................. cholecystolithiasis . ......................... 11 ...................... ............................ ...................... ......................................... 12 ....... panc reatitis .................................................. .................... .............................. Endocrinology 14 ................ 13 ............ .................. hyperthyroidism ............................................. ..... ....................................... 15 ......... hypothyroidism ...... ............................................ ................................... ............... ........... .................................... 16 Diabetes mel litus .................................................. ....................... ..... 17 .................... hyperparathyroidism .............................. .................... literature ................................. 19 20 2 GASTROENTEROLOGY Signs and symptoms of gastrointestinal disorders Dysphagia: subjective swallowing disorder (on solid food: mostly mechanical obst ruction, even in liquid: more neuromuscular). Causes: Esophageal Ca., Peptic str ictures in reflux, scleroderma, goiter, Zenker's diverticulum. Heartburn: a burn ing retrosternal pain, often accompanied by acid regurgitation. Dyspepsia: nonsp ecific upper abdominal discomfort associated with food intake. Causes: reflux, e sophageal motility disorder, ulcer, gastritis, gastric Ca., Pregnancy, gallstone s, delayed gastric emptying but functional in 50%! Indications for further investigation: warning signs (weight loss, performance b uckling, dysphagia), progression, spec. etiologic information (eg, heartburn), o lder patients (excluding tumor), longer than 1 month-long refractory symptoms. Nausea and vomiting: vagal stimulation (Hohlorgandehnung, peritonitis, mucosal i rritation, nephrogenic / pancreatic / hepatic / biliary afferents), Area-postrem a-triggering (toxins, opioids, cytotoxic drugs, "pregnancy hormone"), CNS-mediat ed (intracranial pressure, vestibular stimulation , migraine, meningitis, severe pain psychogenic). Diarrhoea: osmotically (laxatives, lactose, sorbitol / xylit ol chewing gum from), secretory (rotavirus bact. Toxin from S. aureus, C. perfri ngens or V. cholerae, endocrine tumors, fat and bile acids), inflammation (mucos al irritation at enteritis), motilitätsbedingt psychogenic (, hyperthyroidism, a fter vagotomy). Constipation: Chronic habit (low-fiber diet, low fluid), organic bowel disease with obstruction (strictures in IBD, stenosis in carcinoma), gang lionic motility (Hirschsprung), anal (pain-Defäkationsunterdrückung, eg anal fis
sure). Blood in the stool: at macroscopic melena (tarry) and Hämatochelazie (fre sh bleeding) and microscopic (occult). Causes: epistaxis, esophagitis, gastritis , ulcer, Crohn's disease, enteritis, intestinal polyps, NSAIDs, anticoagulants, and cancer. Abdominal pain is different, "visceral" (abdominal viscera can be tr ansferred to Headsche zones) and "somatic" pain (parietal peritoneum, act quickl y!). visceral pain, dull, painful, gnawing, wavy, convulsive or colicky poorly l ocalized, often median line, projection attempts in other parts of the body the patient by position change mitigation to provide output of entrails, elongation of hollow organs, inflammation, visceral hull somatic pain sharp, burning, conti nuous increasing duration of pain well localized (the patient can draufzeigen fi nger) Pat takes a posture, not moving breathing, flat output from the parietal p eritoneum and Mesenterialwurzeln e.g. Biliary colic,Constipation, liver capsule pain strain A hollow organ perforation, peritonitis, bleeding into the abdominal cavity Acute Abdomen Acute situation in the abdominal area: acute pain, guarding, decompensation. Cen tral question: OP indexed? Interdisciplinary diagnostics! Causes: appendicitis (55%), gallbladder (15%), mech. Ileus (10%), peritonitis (5 %), pancreatitis (5%), more rarely, diverticulitis, renal colic, gynecological E rkr., Testicular torsion, intestinal ischemia, Organruptur, Extraabdominal (hear t attack, pneumonia, porphyria). 3 Reflux disease General reflux of stomach contents (often stomach acid, rare alkali Galle-/Pankr eassekret) in the esophagus with mucosal irritation. Symptom: heartburn. Heartbu rn Clinic (mostly postprandial or lying), epigastric pain or restrosternale, Reg urgation, acid regurgitation. In 10% inflamed mucosa (reflux esophagitis). Compl ications: peptic stenosis (dysphagia for solid food), Barrett's esophagus (metap lasia: shattered plates is replaced by columnar epithelium, increased ulcer-and cancer risk), asthma (chronic stimulation of the vagus). Hoarseness. 10 rule: 10% with reflux esophagitis have, 10% with esophagitis develop Barrett, 10% with Barrett's develop cancer. Etiology and pathogenesis Inadequate resting pressure of the lower esophageal sp hincter (eg, scleroderma), prolonged relaxation phase, decrease of peristaltic n ightly cleaning, hiatal hernia (in 90% of severe erosive esophagitis-Pat.). Risk factors: obesity, sedentary activity, physical activity, coffee, alcohol, p regnancy, medications (anticholinergics, theophylline, nitro, opiates). Diagnostic pH monitoring (pH if pathol. while 7% of the time under 4), manometry (appreciation of Kardiakompetenz, eg for surgical planning), endoscopy (for sta ging). Stages of esophagitis: I-IV (single erythematous erosions in mucous membranes, c onfluent lesions, circular erosive lesions, ulcers / strictures / Barrett). Therapy General measures: weight loss, avoidance of nocturnal meals, healthy diet, diges tive stroll. Acid reduction: antacids, H2 blockers, proton pump inhibitors (eg o meprazole, best and fastest results). OP (at Therapieresitenz or severe esophagi tis): hiatal, Fundopexie or fundoplication. 4
GASTRITIS General gastritis. Classification by cause (A: autoimmune; B: bacteria, eg H. py lori, C: chemical, such as NSAIDs), histology (non-erosive = A + B vs. Erosive = C) and course (acute vs.. Chronic). Clinic erosive gastritis: usually asymptomatic. Possibly. Aversion to food, epigastric discomfort, dyspepsia. If bleeding: coffee-ground vomiting. In Ggs. to ulcer ble eding usually no serious bleeding. non-erosive gastritis: autoimmune gastritis i s asymptomatic, symptoms of pernicious anemia (lack of intrinsic factor, thereby Vit B12 deficiency), in Helicobacter: dyspepsia (acute), then usually asymptoma tic. "Real" symptoms until complications (peptic ulcer disease, malignant degene ration).
Etiology and Pathogenesis erosive gastritis: tissue defect to only lamina propria to the exclusion of the muscularis mucosae (in contrast to the ulcer). Most exogenous (alcohol, NSAIDs), besides stress gastritis in Intensivpat., Portal hypertension, radiation. Chron ic erosive gastritis corresponds to type C gastritis. non-erosive gastritis: (a) autoimmune ("corpus gastritis") with autoantibodies to parietal cells, in 50% i n addition to intrinsic factor. In the long term reduction of principal cells (a trophic glands). Possibly. Association of Hashimoto, Addison. (B) bacteria ("ant ral gastritis") with Helicobacter pylori infection.
Diagnostic gastroscopy with biopsy. HP-proof means of urease test (piece of tiss ue is placed in medium, Helicobacter consumed urea, medium changes color), 13CHa rnstoff breath test (split orally recorded urea only in the presence of Helicoba cter detectable then exhaled 13CO2), histology (HE staining) or cultural culturi ng (consuming, expensive and rarely used). Therapy Type A (autoimmune): no specific therapy, it is treated the pernicious anemia. A nnual follow-up because of cancer risk. Type B (bacterial): Hp eradication alway s with complication (ulcer, lymphoma), giant folds gastritis (Menetrier's diseas e), NSAID-taking or erosions (rare). In asymptomatic patients without risk factors and complications is the Helicobac ter detection per se is not an absolute indication for eradication is due to the increased Karzinom-/Lymphomrisikos but often recommended. Type C (chemical, erosive): bleeding prophylaxis in Risikopat. (Sucralfate, H2Bl ocker), hemorrhage treatment (sucralfate with PPI, endoscopic hemostasis in diff use bleeding is not possible), discontinue NSAID if possible, not drinking alcoh ol. 5 Peptic Peptic ulcer peptic ulcer disease General Benign mucosal ulcers with circumscribed loss of substance, at least unt il reaching the muscularis mucosae in (as opposed to erosion). Differentiate acu
te ulcers (erosive gastritis, stress factors, such as OP combustion) and chronic recurrent ulcer (gastroduodenal ulcer disease =). Gastric ulcer: v.a. lesser curvature (immediately distal to the säureprod. Korpu smukosa), atypical location (eg, greater curvature) is karzinomverdächtig. Duode nal ulcer: duodenal bulb almost always, in Zollinger-Ellison syndrome and distal . Clinic Epigastric pain: gnawing, dull, hungerartig, rhythmic (intensity fluctuates with time of day / food intake), periodic (symptom change with symptomatic periods). Furthermore, dyspepsia, nausea, food intolerance. asymptomatic in 20%. Clinical ly, however, not diagnosed because symptoms nonspecific. Etiology and pathogenesis of Helicobacter pylori (4-fold increased risk) and NSA IDs (10% suffer ulcer, of which 10% with a complication, of which 10% fatal), ac ute physical stress, hypersecretion (gastrinoma). Imbalance between Protektiva ( mucus, blood flow, motility, prostaglandins) and Aggressiva (acid, pepsin, drugs such as NSAIDs and glucocorticoids). Obligatory: acid. Diagnostic endoscopy wit h sampling and Hp diagnostics. In 5-10% of ulcerated carcinoma! Therapy General measures: Nicotine waiver sell, NSAIDs. Acid reduction: proton pump inhi bitor. Helicobacter pylori eradication: PPI + clarithromycin + metronidazole (It alian) or PPI + clarithromycin + amoxicillin (French triple therapy) for 7-10 da ys. Complications Perforation: a breakthrough in the abdominal cavity, mostly open air (with duode nal ulcer may also retroperitoneal on the edge of the iliopsoas). Clinical: acut e abdomen. Diagnosis: Rom-Abdomenübersicht, endoscopy. Treatment: immediate surg ery. Penetration (= "subdued perforation): Breakthrough in another organ (pancre as, hepatoduodenal ligament, left lobe of the liver) with no leakage of air. Tre atment: Surgery. Bleeding: v.a. in NSAID dose. Mortality: 10%. Clinically vomiti ng blood (hematemesis, coffee grounds), melena (melena). Mostly conservative the rapy: Endoscopic Submucosal (adrenaline, fibrin glue), while PPI (eg omeprazole) .
Classification of ulcer bleeding after Forrest I: active bleeding: spraying (a) vs. oozing (b). II: currently no bleeding, but reference to previous history of fresh bleeding: visible vessel (a) vs. Thrombus Ulcer (b) vs.. Residual blood in the stomach / duodenum (c). III: lesions witho ut bleeding, bleeding history. 6 MALASSIMILATIONSSYNDROM General disorders of digestion and absorption in the small intestine. Various ca uses. Clinic Chronic diarrhea (fermentation chairs with osmotically active undigested constit uents, fatty stools, watery in bile acid loss), weight loss, bloating (due to fe rmentation of indigestible disaccharides, eg lactase deficiency), deficiency (hy poproteinemia, lack of fat-soluble vitamins, iron deficiency, folate deficiency) . Etiology and Pathogenesis Maldigestion: pancreatic enzymes (chronic pancreatitis, cystic fibrosis), decrea
sed Gallensäurekonz. (Cholestasis, bacterial overgrowth, bile acid loss during r esection of the term. Ileum). Malabsorption: reduction of resorption (short bowe l syndrome, Crohn's disease), injury of resorption (infection and bact. Overgrow th, amyloidosis, celiac disease), intestinal enzyme (lactase deficiency), ischem ic bowel disease. Lymphatic obstruction: steatorrhea by abnormal chylomicron upt ake (lymphangiectasia, Whipple, lymphomas). Diagnosis Malassimilation: Inspection of the chair, laboratory values (deficiency symptoms , such as hypoproteinemia, anemia, prolonged bleeding time), stool examination ( stool fat determination, 1-antitrypsin as a marker protein loss). Malabsorptio n: inflammation, fermentation chairs, pathol. Schilling test (ileal-absorptive: oral administration of radioactive vitamin B12, vitamin B12 in the measurement o f the selected 24-hour urine excretion decreased in favor of decreased absorptio n), pathol. Xylose test (oral xylose in serum and urine decreased speaks for dis turbed absorption). Maldigestion: fatty stools, normal Schilling and xylose test . Breath tests: H2 is in the colon in bact. Metabolism of sugars formed. Malabsorption in the small intestine: sugar reaches the colon and increases H 2 production, eg with lactase deficiency. Overgrowth in the small intestine: H2 pr oduction increases immediately, because sugar is already verstoffwechst in the s mall intestine, without having to get into the colon. Diseases Celiac disease (gluten enteropathy): Autoimmune disease with hypersensitivity to gluten (wheat, barley, rye, oats). Diagnosis: Small intestine biopsy (zottenlos e mucosa). Therapy: elimination diet. M. Whipple: Infection with Tropheryma whip plei.Clinic: steatorrhea, abdominal pain, edema by protein loss, arthritis, myo carditis. Diagnosis: Small intestine biopsy. Therapy: intravenous antibiotic the rapy, followed for 1 year trimethoprim / sulfamethoxazole. Bile acid loss: Inter ruption of the enterohepatic circulation (decreased resorption bact. Overgrowth) . Clinic: watery diarrhea, psychologists, disorder Fettdigestion. Therapy: low-f at diet, resins, antibiotic treatment.
7 Colorectal CARCINOMA CARCINOMA General One of the most common malignancies in 25% already metastasized at diagn osis. Almost always adenocarcinoma, benign adenoma often proceeding. Hematogenou s metastasis in the liver and lung (), lymphatic para-aortic, inguinal and iliac LKS (). Infiltration of the bladder, ureter, prostate, uterus and ovaries possi ble (continuous growth). Clinic fatigue, buckling performance, due to lack of tu mor anemia. GI symptoms until late, and depending on the location: Melena and oc cult blood loss (prox. colon), change in bowel habits, diarrhea and hematochezia paradoxical (dist. colon). Location: rectum 60%, 20% Sigma, 10% caecum / colon ascend., 10% Rest of the col on. Etiology and Pathogenesis
Risk factors: age, colorectal adenoma, pos. Family history (2x greater risk), ul cerative colitis (5x) increases, family Adenopolyposis coli (FAP): 100% degenera tion. Genetically adenoma-carcinoma sequence for two special anchored responsible: Polyposis syndrome: juvenile polyposis (hamartomas in 10% malignancies), PeutzJe ghers (hamartomas, in 3% malignancies), FAP (in 100% malignancy), Gardner (= FAP with concurrent Knochen-/Weichteiltumoren). Lynch syndrome (HNPCC, hereditary n onpolyposis colon Ca.): This is the most proximal right colon, by 45 Year of lif e. Amsterdam criteria: at least three relatives affected, including a first Grad es used excluded disease in at least two successive generations, at least one <5 0 years, FAP.
Diagnosis Investigation: possibly palpable mass in the lower abdomen, rectal examination, fecal occult blood. Colonoscopy with biopsy: method of choice. Staging: sonograp hy (liver!), CT. Labor: Tumor markers CEA and CA 19-9 (follow-up, not for primar y diagnosis!). UICC IA Dukes B1 T 1 2 N 0 M 0 0 0 5-year survival> 85% 90% Explanation tumor li mited to mucosa or submucosa invasion of muscularis II III IV B2 C D 3 each 4 each each 0 0 1 2 each 0 0 0 0 1 70-80% 35-65% <5% Infiltration of the subserosa infiltrated visc. Peritoneum / organs affected lym ph nodes metastases (UICC = International Union Against Cancer, 5-year survival = 5-year survival ra te in USA) Therapy OR (as advanced stages) benefit. Objective: Radical tumor resection with a safet y distance of 5cm, eliminating local LKS. Kontinenzerhaltend if at least 2 cm di stance remaining to the anus. Ileostomy: aggressive thinner chair, expensive car e, the patient significantly reduced. Colostomy: rather solid stool, easier main tenance. Radiotherapy / chemotherapy of minor importance. Indications for chemot herapy: UICC III (eg, adjuvant 5-fluorouracil, folinic acid and oxaliplatin afte r FOLFOX regimen). 8 Crohn's Disease General AND
Ulcerative Colitis Colitis Nonspecific, chronic inflammatory bowel disease (IBD) with loss of mucosal integ rity, decreased resorption and increased secretion and excretion. Differences in appearance and distribution pattern. Clinic Because inflammatory changes and th eir effects on the intestinal wall. Crohn's disease: General symptoms: weight loss, anorexia, weakness. Abdominal pain: diffuse, cram ping later, depending on location of infestation. Diarrhea (if colon affected): occasional admixture of blood. Obstruction (by entz. / fibrotic bowel wall thick ening): subileus-weight. Fistulae, abscesses, perianal changes (fissures, fistul as, abscesses). extraintestinal manifestations cholangitis, erythema nodosum, ar thritis. Diarrhea: bloody, slimy (and night), 10-20 per day, possibly tenesmus. no perianal changes, rare extraintestinal manifestations. Ulcerative colitis: Etiology and pathogenesis remains unclear. Genetic, immunologic and environmenta l factors. Crohn's entire GI tract can be affected: preferred ileum, colon (omitted rectum) segmental or diffuse distribution of discontinuous propagation ("skip lesions") affect all layers of the wall (transmural) ulcerative colitis to the colon boun ded (rectum always involved) diffuse distribution continuous propagation limited to mucosa At most slightly increased risk of cancer diagnosis Cancer risk increases Clinical, laboratory and endoscopy (with histology). Unambiguous assignment is n ot always poss. Crohn's disease: Lab: increased Entz.parameter, ASCA pos. (70%), KM-ray image: c razy paving; Endoscopy: "skip lesions and mouth ulcers. Ulcerative colitis: Lab: increased Entz.parameters, anemia, pANCA pos. (70%), KM-X-ray: mucosal ulcerati ons, pseudo polyps, Haustrenschwund (inner tube), endoscopy Rektumbefall obbliga to. Therapy acute phase: diet (possibly parenteral nutrition), glucocorticoids, azathioprine , cyclosporine, methotrexate, in Crohn's disease: infliximab (monoclonal TNF-ant ibody). Term therapy: 5-amino-salicylates (5-ASA). In ulcerative colitis as a last resort: colectomy (curative). Crohn's disease: n o cure. 9 HEPATITIS General Numerous causes (viruses, toxins, drugs) can lead to liver cell necrosis with infiltration of the tissue with inflammatory cells. Extremely variable cou rse. Classification: acute vs. Chronic (> 6 months) or cause (infectious, toxic, autoimmune, hereditary). Clinic of hepatitis virus
Prodromal stage (days to weeks) with nausea, vomiting, anorexia, fever, upper ab dominal pain, arthralgia, disturbed taste, cigarette aversion. Organ manifestati on (up to 8 weeks): liver tenderness, jaundice, itching. Forms: anicteric (especially Hep. C): in 50% of hepatitis, often completely asymptomati c course. cholestatic (especially Hep. A and B) in 5% of patients Stuhlentfärbun g, increased cholestasis (bilirubin, -GT and AP), AZ-significant reduction. bri lliant (especially Hep. B, pregnant women with Hep. E): progressive liver failur e: hepatic encephalopathy, cerebral edema, hypoglycemia, GI bleeding, respective ly. Insuff., Infection tendency. Histologically: bridging necrosis. Transplantat ion indexed! Chronic (Hep B, C and D):> 6 months existing transaminases increase . Clinically reduced performance, fatigue, intermittent anorexia. Diarrhea.
Laboratory findings Transaminases (usually 15-fold increase), GOT / GPT <1 (De Ritis ratio), bilirub in increased most strongly (directly and indirectly in equal proportion) in chol estatic course: in addition -GT and AP increased. Serology: detection of antibo dies against certain hepatitis viruses or their components. In addition, determi ning autoantibodies to exclude autoimmune hepatitis (ANA, AMA, LMA, LKM, SLA). Therapy 40% of clinically apparent viral hepatitis need treatment: abstinence fr om alcohol until normalization of liver function tests, no discontinuation of ur gently needed medications. Glucocorticoids indicated, as favoring a chron. Cours e! Forms of acute viral hepatitis Hepatitis A: fecal-oral, a typical tourist disease, asymptomatic in 50%. Diagnos is: Anti-HAV IgM-AK detectable after 14d. Therapy: general hygiene measures. Pre diction: in 99% healed within three months. Hepatitis B: common viral hepatitis, transmission perinatally, parenterally and sexually. Diagnosis: Anti-HBc-IgM Ab and HBs Ag is proof of acute infection. Anti-HBe and anti-HBs AK remain lifelon g. Treatment: none. Forecast: 90% inconsequential healing, 10% of asymptomatic c arrier state, 1% fulminant chronic (cancer risk), 1%. Hepatitis C: Transmission parenterally and sexually, usually asymptomatic course. Diagnosis: anti-HCV-AK, HCV-RNA detection. Therapy: early 24-week interferon therapy can prevent chronic in almost 100%. Forecast: untreated chronic course in 80%, 20% in liver cirrh osis with increased cancer risk. Hepatitis D: only when co-infection with hepati tis B pathogen. Diagnosis: anti-HDV-IgM-AK. 10 Cirrhosis General irreversible end-stage fibrotic scarring with destruction of the lobules and vascular structures, inflammatory fibrosis and Regeneratknotenbildung. Clin ical symptoms of portal hypertension (see below) and hepatocellular dysfunction: General symptoms: fatigue, reduced performance, weight loss. Skin: jaundice, spi der nevi, white nails, Lackzunge, skin atrophy, palmar erythema, caput medusae, petechiae, abdominal baldness, gynecomastia. Foetor hepaticus. Edema: by hypoalb uminemia. hepatic encephalopathy: grobschlägiges hands trembling ("flapping trem or"), consciousness disturbance, apraxia, apathy, coma. Etiology and pathogenesis of 50% alcohol, 25% of chronic viral hepatitis (B, C, D), other: autoimmune hepatitis, drug-toxic liver damage, biliary cirrhosis (PBC , Caroli's syndrome), M. Wilson, hemochromatosis, Budd-Chiari syndrome (hepatic
vein thrombosis). Alcohol: intermediate fatty liver and fatty liver hepatitis, t hen small nodular cirrhosis. For other causes: postnekrotische macronodular cirr hosis with nodes. Diagnosis Lab: Liver disease (decreased: CHE, vitamin K-dependent coagulation factors, Pro thrombin time, AT-III, proteins C and S, albumin, increased: GOT, GPT,-GT , Bil i, ammonia). Sonography: non-homogeneous pattern, rounded liver edge, irregular surface. Biopsy indicated: only in exceptional cases, since therapeutic result o n clinical examination. Therapy General measures: avoid noxious substances, protein and calorie diet, folic acid . If necessary. specific therapy,if not too advanced cirrhotic remodeling (blee ding in hemochromatosis, Immunsuppress. in autoimmune hepatitis, virus eliminati on). If necessary. Liver transplantation. Forecast: depending on Child-Pugh scor e (from albumin, ascites, bilirubin, Quick and encephalopathy formed a score tha t correlates with prognosis). Complications Ascites: an excellent distention, increased abdominal girth. Risk of spontaneous bacterial peritonitis. Washing out too quickly: hepatorenal syndrome. Portal hy pertension: gastric fundus and esophageal varices, portal gastropathy. Therapy: propranolol, nitrates (reduction of portal pressure), Terlipressin in bleeding, ligation / sclerotherapy after hemorrhage, transjugular intrahepatic porto-syste mic shunt (TIPS) allows connection between the hepatic and portal veins. Hepat. Neurotoxic encephalopathy: through enrichment. Substances (e.g. ammonia). 11 Cholecystolithiasis General prevalence to 15%, of which 1% / year operating restitutor symptoms, app roximately 75% asymptomatic. Clinic 75% asymptomatic ("silent stones"), nonspeci fic upper abdominal discomfort (bloating, flatulence, nausea, vomiting), acute b iliary colic (usually stone passage in the cystic duct): plötzl. beginning, an i ncrease of hours, broadcasting right shoulder. When thinking of jaundice in the common bile duct stone. Etiology and pathogenesis Increased cholesterol synthesi s or bile acid loss. Risk factors ("female, fat, forty, fertile, family"): highfat diet, obesity, female hormones, pregnancy, family history. Diagnosis History: character of the pain, previous history of colic, decolorized chair. In vestigation: bulging of the abdominal wall, careful palpation, jaundice, Murphy' s sign. Labor: CRP, cholestasis parameters ( -GT, alkal. phosphatase, bilirubin) increased in speed shutter, lipase and amylase increases associated with pancre atitis. Sonography: Stones (posterior acoustic shadow), inflammation (acute: thr ee layers, chronic: thickening of the wall), duct dilatation as an indication of stones in the passage. Therapy With simultaneous jaundice (bile duct = cap): rapid ERCP with papillotom y. asymptomatic: no treatment required. Colic: pain (spasmolysis with scopolamine, analgesia with metamizol, alternatively pethidine). Except not use pethidine mor phine (spasmogen!). symptom-free interval: Stone Removal (1st choice: laparoscop ic surgery; aka extracorporeal shock wave therapy). In acute cholecystitis: stabilization of the patient (fasting, Schmerzther., Ant ibiotics), then the OR. In perforation surgery within the next few hours! Compli cations acute cholecystitis with empyema, upper abdominal pain, severe malaise, fever, c
hills, leukocytosis. Clinical: Murphy's sign (deep inspiration is terminated by pain when palpating finger triggers gallbladder below the right costal margin). Ultrasound: three layers of the GB wall. . Chron Cholecystitis: non-specific sym ptoms (abdominal fullness, nausea), pressure in the upper abdomen, pain on deep palpation. Ultrasound: wall thickened. Perforation: biliary peritonitis (high mo rtality rate!), Possibly gallstone (when migrating through the stone in the duod enum or colon). Rom-abdomen: bile ducts. Porcelain GB: rock hard calcium deposit s with GB (increased cancer risk). acute biliary pancreatitis: with stone passag e until closure of the papilla and D. hepaticopancreaticus.
12 Pancreatitis Acute pancreatitis after switching off the trigger rule to expect healing. Sympt om: abdominal pain, possibly radiating to the back, elastic waist (elastic waist voltage). Clinic Abrupt onset, severe abdominal pain, often radiating a belt in the back, nausea, vomiting. Typical: rubber belly. Characters: petechial hemorrhage, target lesio ns (Cullen), or in the flanks (Grey-Turner). In advanced disease: somatic pain ( well localized, parietal peritoneum affected). Division Easy: moderate pain, enzyme rise, low Parenchymschäden (edema). Expert: local (n ecrosis, abscess, pseudocyst) or organ complications (ARDS, disseminated intrava scular coagulation, acute renal failure). Complications: pseudocyst, bacterial superinfection of necrosis, paralytic ileus , hyperglycemia, hypocalcemia (Ca2 +-binding in fat necrosis), sepsis. Causes Biliary and binge-drinking by far the most! Rare: medications (including diureti cs, steroids, interferon), post-ERCP, autoimmune, primary hyperparathyroidism. Laboratory diagnosis: Lipase (at least 10-fold increase) and -amylase (4x), CRP , leukocytosis. In severe cases: LDH increased, hypocalcemia, lactic acidosis. I n biliary etiology: Cholestasis. Sonography: edema, ascites, necrosis, pseudocys ts, bile (away) stones, possibly CT. Therapy ICU! In V.a.Biliary etiology: ERC (without pancreatic duct display), possibly w ith papillotomy. Treatment goals: Pancreas are quietly leave food and liquid, gastric tubes, PPI administration. P ain: Fighting procaine Perfusor, possibly in addition metamizol, pethidine. If n ecessary. Epidural catheter. Complications: Avoid parenteral fluid (5l/24h), sys temic antibiotics, heparin. Surgical indication (cautious, because high mortalit y rate!): Not under control, intensive care complications (infected necrosis, pa ncreatic pseudocyst). Chronic pancreatitis with inflammatory Progressive irreversible damage and incre ased cancer risk. Clinically relapse. Upper abdominal pain, nausea, malabsorptio n, fatty stools, diabetes mell. Reasons: in 2 / 3 alcohol, pancreatic duct obstr uction (tumor, inflammation), hereditary, and rare cystic fibrosis, prim. Hyperp arathyroidism, hyperlipidemia. Diagnosis: ultrasound, ERCP, CT. itis distinction between tumor and not always possible. Therapy: abstinence from alcohol, elimin
ate runoff barriers, symptomatic treatment: acute episodes such as acute pancrea titis, pain treatment, exocrine / endocrine insufficiency. 13 ENDOCRINOLOGY Classification of endocrine disorders Primary: disruption of the gland (= peripheral hormone). Secondary: fault on pit uitary level (= glandotropes hormone). Tertiary: fault on hypothalamic-level (= releasing). A disturbance is an autonomous, decoupled from the feedback inhibition of secret ion. Signs and symptoms of hormonal imbalances General: fatigue, weakness, depression, appetite / thirst, and thermal sensation changes, anxiety, palpitations, tremor. Changes in physique: height, weight. Sk in pigmentation, dryness, sweating, hair loss, hirsutism. Sexual organs: libido / potency changed, cycle disorder, gynecomastia. Diagnosis of hormonal disorders Basal levels due to daily fluctuations and variable protein binding is often dif ficult to interpret and susceptible. Alternative: provocation test. Stimulation test: parent hormone (glandotrop or releasing covers) decreased Sekr etionskapazität of the gland (hypothyroidism = on). Suppression test: peripheral hormone suppressed normally glandotropen via feedback inhibition of the secreti on of the parent or releasing hormone. Lack of suppression: Autonomy or ectopic tumor (= hyperthyroidism). To localize the fault: sonography, CT, MRI, scintigraphy. 14 Hyperthyroidism General almost always primary, rarely secondary / tertiary. Severity: latent / s ubclinical (TSH decreased, normal T3/T4), manifest (T3/T4 increased, most sympto ms), thyrotoxicosis (life threatening, eg after contrast with existing autonomy: sinus tachycardia, fever, vomiting, restlessness, delirium, shock , coma). Very variable clinic. Hypermetabolism (sweating, heat intolerance, weight loss), cat echolamine sensitivity increased (tachycardia, palpitations, arrhythmia), diarrh ea, palmar erythema, feinschlägiger finger tremor, restlessness, nervousness (up to psychosis!). Etiology and Pathogenesis functional autonomy: unifocal (= adenoma), multifocal or disseminated. Graves' d isease: autoantibodies against TSH receptor with receptor-term stimulation. Clin ically Merseburg triad of goiter, exophthalmos, tachycardia. In addition, thyroi d eye disease (Mobius, Grafe, Dalrymple-and Stellwag sign) and dermopathy. more rarely, subacute thyroiditis (de Quervain), Hashimoto's thyroiditis with transie nt (Hashi-Toxicity), TSH produze. Tumor, ectopic hormone formation (struma ovari i).
Diagnosis basal TSH (if normal, hyperthyroidism excluded if decreased: T measure 3/T4), in Graves' disease: TSH receptor antibodies, often anti-TPO, and Sono-sc intigraphy. Therapy Functional Autonomy: Bridging: thyreostatic, definitely: Surgery, radioiodine. G raves' disease: antithyroid for 1-2 years, then TSH. If necessary. OP / radioiod ine. Antithyroid are thionamides (Favistan, Carbimazole) or perchlorate (Irenat). Thy rotoxic crisis (ICU!): High dose thyroid antagonists, beta-blockers, glucocortic oids, acute subtotal Thyreodektomie at Iodkontamination, possibly plasmapheresis (removal eiweißgebundener hormones). Comments Graves' disease usually speaks we ll to antithyroid and leads in 40% to permanent remission. In functional autonom y is preferred OP (before seeking euthyroidism!), In hyperthyroidism iodinduzier ter immediately OP. Postoperative: possibly hypothyroidism, which are permanentl y treated with thyroid hormone (Euthyrox) must. After radioiodine therapy, it is common to hypothyroidism (50% after 20 years). Complications after surgery: N. relapsing-injury (chronic unilaterally. hoarseness, both sides: vocal cord paral ysis), hypoparathyroidism with tetany (Ca2 +-control post-operative) in Mitentfe rnung of the parathyroid glands, hypothyroidism. 15 Hypothyroidism General lack of thyroid hormone in the target organs. The most common cause in a dults: Hashimoto's thyroiditis. Rare: secondary, rarity: tertiary. Creeping clin ic. Hypometabolism (cold intolerance, weight gain, apathy), catecholamine sensit ivity decreased (bradycardia), pasty skin, muscle weakness, diminished reflexes, constipation, depression. In children: failure to thrive. Myxedema (subcutaneous mucopolysaccharides): pericardial effusion, bloated body, edema does not leave any dents (in contrast to cardiac edema). Myxedema coma (e xtremely rare): hypoventilation, hypothermia, hypotension. Most in-HVL failure. Etiology and Pathogenesis congenital (heterogeneous, eg, thyroid aplasia, Iodverwertungsstörung): Macroglo ssia, constipation, jaundice neonatorum prolongatus, developmental disabilities, cretinism. acquired: the final state after all inflammations (especially Hashim oto, rarely Basedow), iatrogenic (treatment of hyperthyroidism) or excessive iod ine deficiency, and lithium. Diagnosis basal TSH (if normal: hypothyroidism excluded if: increase measure T4) . T3 can be low or normal (through increased conversion). In Hashimoto: AntiTPO antibodies, occasionally associated with type I diabetes, sprue, myasthenia grav is. Almost always, life-long substitution therapy with L-thyroxine (Euthyrox). E xceptions: transient forms such as antithyroid-induced hypothyroidism or thyroid itis de Quervain's (viral or parainfectious). Objectives: Beschwerdfreiheit, nor malization of TSH. 16 DIABETES General MELLITUS In industrialized countries most common cause of blindness and dialysis. Disturb ance of glucose, fat and protein metabolism due to insufficient insulin action i
n liver, fat and muscle cells (type I: lack of insulin, Type II: insulin resista nce, both types) to take. Insulin secretion in adults: 40 IU / day (high to food , low in hunger). Secretion: Basal secretion (Maximum early morning / late afternoon) and pro-secretory facto rs: -adrenergic stimulation, leucine, mannose (glucose-dependent) and GIP, chol ecystokinin, secretin, gastrin, lysine, fatty acids, ketone bodies, ACh (vagus), GLP1 (amplification of the glucose effect on the B-cell). Inhibition of secretion: Insulin (negative feedback), ukosekonz. 2-adrenergic stimulation, chronically elevated Gl
Effect of insulin: Increase anabolism (glycogen, lipid and protein synthesis), inhibition of catabo lism (glycolysis, lipolysis, proteolysis, gluconeogenesis) and influx of K +. Insulin antagonists: Glucagon, epinephrine, norepinephrine, glucocorticoids, growth hormone. Clinic Type I: <40 years, mostly acute hyperglycemia symptoms: polyuria, polydipsia, de hydration, weight loss, fatigue, immune deficiency (UTI, thrush, itching), coma. Type II: older patient, usually damages: neuropathy, nephropathy, stroke. Etiology and Pathogenesis Type I (insulin deficiency): autoimmune-mediated destruction of B-cells (trigger unknown), clinically significantly from 80% cell death, HLA association. Type I I (insulin resistance): genetic predisposition, no HLA association, overeating, lack of exercise. Hyperglycemia leads to tissue damage (microcirculation in type II also macroangi opathy by atherosclerosis and hypertension). Diagnosis fasting normal OGTT 2 h value <110 mg / dl (6.1 mmol / l) <140 mg / dl (7.8 mmol / l) impaired Gluk.toleranz 1 10-126 mg / dL 140-200 mg / dl diabetes> 126 mg / dl (7 , 0 mmol / l)> 200 mg / dl (11.1 mmol / l) or: casual-BZ> 200 mg / dl with polydipsia, polyuria, and une xplained weight loss, metabolic syndrome: Type II-Diabetes/gestörte glucose tole rance / insulin resistance (at least . one of them) + hypertension / obesity / d yslipidemia / microalbuminuria (at least 2 of them). Always look for Folge-/Begl eiterkrankungen: renal function (creatinine, U-status), lipid status, fundus is angiological investigation (PAD), vibratory (neuropathy), thyroid (type I diabet es associated with autoimmune thyroiditis). 17 Therapy Goals: Avoid long-term damage by the closest possible BZ-setting and consistent treatment of concomitant diseases (hypertension, dyslipidaemia). Intensified ins ulin therapy with HbA1C <7% is superior to the standard insulin therapy clearly! Lifestyle: regular meals, avoid movement, other vascular risks. Metabolic self-r egulation: BZ-control crucial determining prognosis. Diet: weight loss (type II) , full balanced mixed diet (no special diabetic diet, but on three main distribu
ted-and three snacks), avoid high glucose index (table sugar), rather, complex c arbohydrates. BE-need per day: 14 (normal), 28 (hard working), 7-10 (weight loss ). Drugs: Insulin or oral antidiabetic agents.
Insulin therapy Indication: all Type I diabetics, therapy-refractory type II diabetics. conventional: 2x dailyMisch-/Verzögerungsinsulin (2 / 3 breakfast, 1 / 3 dinner ). intensified (basal-bolus): 1-2x daily insulin delay, additional short-acting insulin before meals. Expensive, more frequent self-regulation, training! Insulin preparations: fast-acting (Lys-Pro insulin, insulin), delay insulin (int ermediate-and long-acting), mixed insulin (intermediate-plus insulin). "After 40 correct" rule means that if current fuel cell above the target (eg 200 instead of 120 mg / dl), shall be injected in the region above the target value for each 40 mg / dl glucose 1 IU insulin (here: two IE). Which diabetic insulin per unit which reacts with BZ-reduction is to be tried individually and needs. So there are also patients, to correct for either 30 or 50 rule. Therapy with oral antidiabetic 1st Choice for recruitment of type II diabetes when diet has not helped. Biguanides (eg metformin): delayed glucose absorption (intestine), inhibition of gluconeogenesis (liver) and increased glucose uptake (muscle cell). Advantages: no hypoglycemia, no Insulinmast, lowering triglycerides. Disadvantages: GIStöru ngen, lactic acidosis (before OPs sell!), Blood count changes. Glitazones (such as Actos): Insulinsensitizer (fat, muscle and liver tissues, so extrapancreatic) . Cheap endothelial effects and lipid lowering. Sulphonylurea analogues (eg Novo Norm): glucose-InsulinsekretionsSteigerung, possible combination with metformin. Sulfonylureas (eg glibenclamide): protracted hypoglycemia in older specimens. M etab. Syndrome is more likely to increase, so use caution.
Acute complications Hyperglycemia: hyperosmolar non-ketotic syndrome (mostly Type II), diabetic keto acidosis (type I). Both are called "diabetic coma", also mixed forms are possibl e. Hypoglycaemia: e.g. Insulin overdose. Early symptoms of beta-blockers veiled! Comments patient education (nutrition, BZ-self-measurement, recognize symptoms o f hypoglycemia, foot care to avoid, risk factors), HbA1C control (depending on t he laboratory: from 4 to 6.2%) every three months, at every doctor visit walk-ex amination. 18 Hyperparathyroidism General parathyroid hormone (PTH) is produced in four parathyroid glands (back o f the thyroid). Function: Prevent Hypocalcaemia (antagonist: Calcitonin). Effect s: release of Ca2 + and PO43-(skeletal), increasing the Ca2 +-absorption, PO43 VitaminD3 excretion and synthesis (kidney). Primary hyperparathyroidism is rela tively common, in addition to malignancy most common cause of hypercalcemia, usu ally sporadic, rarely in the context of a multiple endocrine neoplasia (MEN synd rome). Causes: solitary adenoma (80%), hyperplasia (20%) or parathyroid carcinom a (<1%).
Clinic In 50% asymptomatic, often found as part of the routine laboratory (hypercalcaem ia). Renal and osseous symptoms in the foreground. Renal: nephrolithiasis, nephrocalcinosis ("stone"). bony: osteopenia, pathologic al fractures, Maximalform: osteitis fibrosa cystica Generalisata Recklinghausen ("leg"). Gastrointestinal: ulceration due to increased Gastrinproduktion ("Magen pein"). psychological: psychosis, depression. Neurological: proximal muscle weak ness, fasciculations. general: polyuria, polydipsia, nausea, constipation, rapid fatigue. Diagnosis Laboratory: serum intact PTH increased, hypercalcemia, elevated alkaline phospha tase. Therapy Only curative option: surgical removal of the affected parathyroid gland (s). Po stoperative risk of hypocalcemia, so regular laboratory checks. Secondary hyperp arathyroidism typical complication of chronic renal failure, rarely in malabsorp tion. Cause: hypocalcemia and / or vitamin D deficiency. Clinic: Bone pain, spon taneous fractures. (No nephrolithiasis, because no hypercalcaemia!) Diagnosis: i ntact PTH and alkaline phosphatase increased, normal calcium / low, often hyperp hosphatemia. Therapy: reduction of phosphate, vitamin-D substitution, possibly P arathyreodektomie. Objective: Normalization of calcium and phosphate levels, pre venting extraosseous calcifications. Tertiary hyperparathyroidism autonomous hyp erfunction of the parathyroid glands in secondary hyperparathyroidism many years (PTH secretion independent of Ca2 + levels, disturbed neg feedback mechanism). Most dialysis patients after long-standing renal insufficiency. Absolute Surgica l Indications! 19 LITERATURE General Classen M, Diehl V, Kochsiek K et al. (2004): Internal Medicine. 5th Edition. Lo ndon: Elsevier. Kasper DL, Braunwald E, Fauci AS et al. (2008): Harrison's Princ iples of Internal Medicine. 17th Edition. New York: McGraw-Hill. Renz H-pads, Kr autzig S (2008): Basic Textbook of Internal Medicine. 4th Edition. London: Elsev ier. Gastroenterology Feldman M, Friedman LS,Brandt LJ (2006): Sleisinger & Fordtran's Gastrointestin al and Liver Disease. 8th Edition. Philadelphia: Saunders. Yamada T, Alpers DH ( 2008): Textbook of Gastroenterology. 5th Edition. Philadelphia: Lippincott Willi ams & Wilkins. Endocrinology Kronenberg HM, Melmed S, Polonsky KS et al. (2007): Williams Textbook of Endocri nology. 11th Edition. Philadelphia: Saunders. is the current version of this script are available for download at the address http://www.harvey-semester.de/
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