Gastrointestinal and endocrine disorders
Script to gastro-intestinal and metabolic diseases
based on the "basic textbook of Internal Medicine" (4th edition, Elsevier, 2008)
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
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).
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
Stages of esophagitis: I-IV (single erythematous erosions in mucous membranes, c
onfluent lesions, circular erosive lesions, ulcers / strictures / Barrett).
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.
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).
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.
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.
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