Peptic ulcer disease 2010

Views:
 
Category: Education
     
 

Presentation Description

No description available.

Comments

Presentation Transcript

Dyspepsia :

Dyspepsia

Slide 2:

Dyspepsia is a term used to describe a group of symptoms includes epigastric pain, heartburn or acid regurgitation (with or without bloating), nausea, or vomiting.

Slide 3:

Organic dyspepsia - the causes are GERD, PUD, chronic pancreatitis. Functional dyspepsia (nonulcer dyspepsia (NUD) – presenting of symptoms in the absence of any organic disease.

Functional dyspepsia:

Functional dyspepsia Criteria for Functional dyspepsia diagnosis, Rome II conference (all of the following): A duration of symptoms >= 12 cumulative weeks over the past 12 months (may or may not be consecutive). Persistent or recurrent discomfort or pain centered in the upper abdomen.

Criteria for Functional dyspepsia diagnosis, Rome II conference (all of the following)::

Criteria for Functional dyspepsia diagnosis, Rome II conference (all of the following): No evidence that the discomfort or pain is associated with the irritable bowel syndrome (not exclusively relieved by defecation, not associated with a change in stool frequency, and not associated with a change in stool form or consistency) No evidence of organic disease after a careful evaluation.

Subtypes of dyspepsia :

Subtypes of dyspepsia ulcer-like: chief complaint is pain centered in the upper abdomen dysmotility-like: chief complaint an unpleasant or troublesome discomfort in the upper abdomen (may be described as fullness, early satiety, bloating, nausea) nonspecific (dyspepsia not ulcer-like or dysmotility-like)

Severity of dyspepsia (De Luca et al.) :

Severity of dyspepsia (De Luca et al.) Symptoms evaluated: epigastric pain pain before meals or when hungry pain relieved by antacids and/or food abdominal pain or discomfort feeling of fullness in the upper abdomen discomfort in the upper abdomen heartburn acid regurgitation

Severity:

Severity None Mild Moderate S evere V ery severe

Tests :

Tests There is no specific test or investigation which will diagnose this condition and the diagnosis is usually made after ruling out other disorders e.g. peptic ulcer disease, gallstones or cancer of the stomach.

Tests:

Tests Biochemistry, urinalysis, hematology, stool for occult blood Upper endoscopy Ultrasound scan of the upper abdomen X-ray studies of the esophagus, stomach, duodenum; Esophageal pH monitoring

Slide 11:

Peptic ulcer disease (PUD)

Peptic ulcer disease:

Peptic ulcer disease PUD is a clinical-anatomical term, identifying a chronic relapsing disease with a trend to progression, caused by either pathological influences of the aggressive factors on gastroduodenal mucosa (the most important of these are acidic-peptic factors and H.Pylori) or decrease of the defense mechanisms of the mucosa.

Peptic ulcer disease (PUD):

Peptic ulcer disease (PUD) causes inflammatory injuries in either the gastric or duodenal mucosa, with extension beyond the submucosa into the muscularis mucosa.

Peptic ulcer disease:

Peptic ulcer disease

Causes :

Causes H pylori infection 70-80% of duodenal ulcers Nonsteroidal anti-inflammatory drugs

Causes:

Causes Severe physiologic stress CNS trauma Surgery Severe medical illness Hypersecretory states (uncommon) Gastrinoma (Zollinger-Ellison syndrome) or multiple endocrine neoplasia (MEN-I) Antral G cell hyperplasia

Gastrinoma (Zollinger-Ellison syndrome):

Gastrinoma (Zollinger-Ellison syndrome)

Causes:

Causes Diseases associated with an increased risk of PUD : cirrhosis, chronic pulmonary disease, renal failure. Miscellaneous causes: radiation-induced chemotherapy-induced ulcers. Lifestyle factors: smoking, alcohol use, caffeine intake Genetics: family history of duodenal ulcer blood type O not secrete ABO antigens in their saliva and gastric juice

Pathophysiology :

Pathophysiology A PUD occurs when an alteration occurs in the aggressive and/or protective factors increases gastric acidity (eg, individuals with increased maximal and basal acid output), decreases prostaglandin production (eg, nonsteroidal anti-inflammatory drugs), interferes with the mucous layer (eg, Helicobacter pylori infection)

Pathophysiologic defects: :

Pathophysiologic defects: gastric ulcer disease Decreased acid secretion, decreased parietal cell mass, back-diffusion of acid Chronic superficial and atrophic gastritis Increased concentration of bile acids and pancreatic juice in stomach (duodenogastric reflux) Delayed gastric emptying Inappropriately decreased pyloric sphincter pressure under basal conditions and in response to acid (secretin) or fat (cholecystokinin) in the duodenum

Pathophysiologic defects:

Pathophysiologic defects Duodenal ulcer disease Increased parietal cell mass Increased sensitivity of parietal cells to gastrin Increased secretory drive Decreased acid-induced inhibition of meal-stimulated gastrin release Increased gastric emptying Increased duodenal acid/pepsin loads Chronic active gastritis

Workgroups classification of PUD (usually used in practice):

Workgroups classification of PUD (usually used in practice) 1. Localisation: cardial, subcardial, fundal (mediogastric), prepyloric (antral), canalis pyloricus duodenal: located in bulbus; located in postbulbar zone combined ulcers with both duodenum, and stomach affection 2. Form: acute chronic: a) recurrent b) persistent 3. Phases: exacerbation, reducing exacerbation (subremission); remission 4. Complications: bleeding; perforation; penetration; gastroduodenal stenosis; malignisation 5. Disease course (exacerbations rate) Mild - once per 2-3 years or more rare Moderate - every year Severe - 2-3 times per year and more frequent 6. Gastric secretion: normal, reduced, increased.

Symptoms :

Symptoms Epigastric pain Gnawing or burning, may radiate into the back. Classic gastric ulcer pain: occurring shortly after meals, antacids provide minimal relief. Duodenal ulcer pain: occurs 2-3 hours after meals and awakens the patient at night , characteristically relieved with food or antacids. This pattern is believed to be the result of increased gastric acid secretion, which occurs after meals and during the late night and early morning hours when circadian stimulation of gastric acid secretion is the highest.

Symptoms:

Symptoms Nausea Vomiting Belching Bloating Distention Constipation Feeling of hunger (DU) Fatty food intolerance Heartburn Chest discomfort Anorexia W eight loss

Physical: :

Physical: tenderness over the epigastrium tenderness is present over the right upper quadrant (RUQ), left upper quadrant (LUQ), supraumbilical region Mendel’s symptom (painful percussion – viscerosensory reflex) – in 20-30% Local muscular tension (visceromotoric reflex) – usually in duodenal ulcers

Lab Studies: :

Lab Studies: complete blood cell count (detect anemia) iron studies stool for occult blood biochemistry, urinalysis (normal) serum gastrin (complicated PUD, to screen for Zollinger-Ellison syndrome) secretin stimulation test (to distinguish Zollinger-Ellison syndrome). measurement of acid secretion is not useful in the routine evaluation of PUD.

Gastric Analysis:

Gastric Analysis Gastric analysis is used to evaluate hyperchlorhydria (eg, Zollinger-Ellison syndrome) or hypochlorhydric states (eg, pernicious anemia, atrophic gastritis). A Levin nasogastric tube is passed. Gastric contents are aspirated and discarded. Four 15-min samples of gastric juice are collected by continuous manual aspiration (basal acid output [BAO]). Next, pentagastrin (6 µg/kg) is given sc, and again, four 15-min samples are obtained (maximal [or peak] acid output [MAO or PAO]). Samples are titrated with sodium hydroxide to calculate BAO and stimulated MAO secretory rates.

Imaging Studies and procedures: :

Imaging Studies and procedures: Double-contrast radiography “Recess” syndrome - focal protuberance on stomach or duodenum outline with barium retention. Folds convergention towards the scar, stomach or duodenum deformation in case of perigastritis and periduodenitis Increase of gastric secretion (fluid revealed in stomach, the investigation is performed before breakfast) Regional spasm Increase of certain focus motility Changes of process of stomach emptying, its tone and peristaltics De Kerven’s symptom=”finger symptom” – drawn in circulatory muscles at the controversial side.

Procedures::

Procedures: Upper GI endoscopy Allows for biopsies and cytologic brushings in the setting of a gastric ulcer in order to differentiate a benign ulcer from a malignant lesion Allows for detection of H pylori infection

Other Tests: :

Other Tests: Detection of H pylori infection is essential in all patients with peptic ulcers.

Noninvasive laboratory tests:

Noninvasive laboratory tests Urea breath test (a sensitivity 90-95%): the patient ingests radiolabeled 13 C- or 14 C-labeled urea po. In an infected patient, the organism metabolizes the urea and liberates labeled CO 2, which is exhaled and can be quantified in breath samples taken 20 to 30 min after ingestion. Serology ( sensitivity 95% ): Enzyme-linked immunoassay (ELISA) can detect both immunoglobulin G (IgG) and immunoglobulin A (IgA) antibodies directed against H pylori . Fecal antigen test test helps identify bacterial antigens in stool. The test has been shown to be extremely accurate with a sensitivity of 89-98% and with a specificity of greater than 90% in helping to diagnose infection or to document eradication.

Endoscopic or invasive tests:

Endoscopic or invasive tests The rapid urease test : is performed by placing a gastric biopsy specimen onto a gel or membrane containing urea and a pH-sensitive color indicator. If H. pylori is present, the bacterial urease hydrolyzes urea and changes the color of the media. RUT has a sensitivity and specificity > 90%. Culture of tissue for the presence of H pylori . Histopathology . Histologic staining of gastric mucosal biopsies has a sensitivity and specificity > 90%.

Complications:

Complications Penetration (confined perforation): a peptic ulcer may penetrate the wall of the stomach or duodenum and enter the adjacent confined space (lesser sac) or organ (eg, pancreas, liver). Pain may be intense, persistent, referred to sites other than the abdomen (usually the back when caused by penetration of a posterior duodenal ulcer into the pancreas), and modified by body position. Radiographic evaluation with contrast study or CT is usually needed to confirm the diagnosis.

Complications:

Complications Hemorrhage : Symptoms: hematemesis (vomiting of fresh blood or "coffee ground" material); passage of bloody or black tarry stools (hematochezia and melena, respectively); weakness, orthostasis, syncope, thirst, sweating caused by blood loss. The physical examination: a digital rectal exam (DRE) to assess for evidence of GI bleeding. Melena is noted easily on such an examination.

Complications:

Complications Gastric outlet obstruction: Symptoms: fullness and bloating associated with nausea and emesis occurring several hours after food intake. The physical examination: upper abdominal distention, a succussion splash on auscultation.

Complications:

Complications Free perforation: Ulcers that perforate the peritoneal cavity are usually located in the anterior wall of the duodenum or, less commonly, in the stomach. The patient experiences sudden, intense, steady epigastric pain that spreads rapidly throughout the abdomen, often becoming prominent in the right lower quadrant and at times referred to one or both shoulders. The patient usually lies still because even deep breathing can worsen the pain.

Complications:

Complications Free perforation: Palpation of the abdomen is painful, rebound tenderness is prominent, abdominal muscles are rigid (boardlike), and bowel sounds are diminished or absent. Diagnosis is confirmed if an upright or a lateral decubitus x-ray of the abdomen shows free air under the diaphragm or in the peritoneal cavity, but the diagnosis is not excluded if no air is seen. Stomach cancer .

Slide 38:

Duodenal ulcer (DU). An elderly patient presents with melena and hypotension.

Slide 39:

Duodenal ulcer (DU). A 35-year-old woman presents with tarry stools and a hemoglobin level of 75 g/L.

Slide 40:

Gastric ulcer with punched-out ulcer base with whitish fibrinoid exudates.

Gastric cancer:

Gastric cancer The ancient Egyptian papyrus Ebers describes a patient with dysphagia in whom the stomach had the appearance of a shrivelled fetal face. This may well represent the first description by Egyptian physicians of a gastric carcinoma, a disease that is now a major health care and surgical problem.

Gastric cancer :

Gastric cancer Gastric cancer is the second most common cause of cancer-related death in the world. Gastric adenocarcinoma accounts for 95% of malignant tumors of the stomach; less common are lymphomas (which may be localized primarily in the stomach) and leiomyosarcomas.

Gastric cancer:

Gastric cancer Carcinoma of the stomach is closely correlated with age, occurring predominantly between the fifth and seventh decade and in people in the lower socioeconomic groups. It is universally more common in men than women.

SITE OF GASTRIC CARCINOMA :

SITE OF GASTRIC CARCINOMA Approximately 40% of cancers develop in the lower part, 40% in the middle part, and 15% in the upper part, and 10% involve more than one part of the organ. T umours in the fundus are more aggressive, with a greater tendency to submucosal invasion regardless of the histological type. The gross morphological difference in the fundus that may explain this is the thinner muscularis mucosa and the presence of tightly packed glands that might block lateral growth. Proximally placed tumours generally have a worse prognosis than those placed distally. This phenomenon may be a result of the features described above or because they tend to be at a more advanced stage at presentation.

Gastric cancer:

Gastric cancer Causes: Several factors are implicated in the development of gastric cancer, including diet, Helicobacter pylori infection, previous gastric surgery, pernicious anemia, adenomatous polyps, g astric ulcer, chronic atrophic gastritis, genetic factors, previous radiation therapy. Gastric cancer most likely represents the result of multiple events occurring in an appropriate environment.

Genetic:

Genetic There is clear evidence of familial clustering of carcinoma of the stomach, the most famous being that of the Bonapartes. Napoleon, his father, his grandfather, brother, and three sisters died of gastric carcinoma.

Environmental and dietary:

Environmental and dietary Various foodstuffs have been implicated in the aetiology of the disease, predominantly low quality diets poor in milk, animal protein, and vitamins but rich in starch. Heavily salted pickles favoured in Japan (tsukemono) have been implicated, as have the smoked fish and meats eaten in Iceland and Scandinavia: these smoked meats contain polycyclic hydrocarbons (such as benzopyrene) which are probable carcinogens. The decline in the incidence of the tumour in the United States has been attributed to the widespread use of refrigeration with a decline in food preservation by smoking or salting.

Causes::

Causes: Chronic atrophic gastritis and intestinal metaplasia G astric cancer results from gastric mucosa that has undergone a sequence of mutations and defined histopathological changes that may start in the first decade of life. The first lesion is atrophic gastritis followed by progressive intestinalization of the mucosa to intestinal metaplasia, then dysplasia and finally carcinoma.

Causes::

Causes: G astric cancer has been associated with Helicobacter pylori infection . This organism is associated with antral inflammation and gastritis. It is proposed that infection and inflammation may result in the production of an epidermal growth factor which may have an oncogenic action on gastric mucosa.

Causes:

Causes Benign gastric ulcers . There is debate over whether benign chronic gastric ulcers have malignant potential; the suggestion is that the regenerating mucosa around an ulcer is prone to become malignant. It is now accepted that the most important question on finding a gastric ulcer is to decide whether it is benign or malignant from the outset.

Causes:

Causes Gastric polyps . A denomatous polyps are truly premalignant. They are often larger (80 per cent greater than 2cm) and are tubulovillous or villous on microscopic examination. The frequency of malignant change increases with increasing size. In a large series, 38 per cent of patients with gastric adenomatous polyps had gastric carcinoma.

Pathology :

Pathology Gastric adenocarcinomas can be classified according to gross appearance: (1) Protruding--The tumor is polypoid or fungating, with a nodular polypoid surface with superficial ulceration . (2) Penetrating--The tumor has a sharp, well-circumscribed border and may be ulcerated.

Pathology:

Pathology (3) Spreading--The tumor shows superficial spread along the mucosa or infiltration within the wall. If an ulcer is present, its edge tends to be ill-defined or heaped up. Tumor infiltration of the stomach wall and an associated fibrous reaction may produce a "leather bottle" stomach (linitis plastica). (4) Miscellaneous--The tumor shows characteristics of two of the other types; this is the largest classification.

Staging :

Staging The 1997 American Joint Committee on Cancer (AJCC) Cancer Staging Manual presents the following TNM classification system for staging gastric carcinoma: Primary tumor TX = primary tumor (T) cannot be assessed T0 = no evidence of primary tumor Tis = carcinoma in situ, intraepithelial tumor without invasion of lamina propria T1 = tumor invades lamina propria or submucosa T2 = tumor invades muscularis propria or subserosa T3 = tumor penetrates serosa (ie, visceral peritoneum) without invasion of adjacent structures T4 = tumor invades adjacent structures

Staging:

Staging Regional lymph nodes : NX = regional lymph nodes (N) cannot be assessed N0 = no regional lymph node metastases N1 = metastasis in 1-6 regional lymph nodes N2 = metastasis in 7-15 regional lymph nodes N3 = metastasis in more than 15 regional lymph nodes

Staging:

Staging Distant metastasis : MX = distant metastasis (M) cannot be assessed M0 = no distant metastasis M1 = distant metastasis

History :

History Early disease has no associated symptoms . Patients may complain of indigestion, nausea or vomiting, dysphagia, postprandial fullness, loss of appetite, and weight loss , haematemesis and malaena, profound anorexia, early satiety, and flatulence . Satiety (fullness or distention) after a large meal is likely if the cancer partially obstructs the pyloric region, a common site. The pain may mimic angina pectoris, or may exhibit periodicity and be relieved by food, mimicking benign gastric disease.

Physical :

Physical All physical signs are late events, and almost invariably the signs develop too late for curative procedures. Signs may include a palpable enlarged stomach with succussion splash; primary mass (rare); and enlarged liver, Virchow nodes (ie, left supraclavicular), Sister Mary Joseph node. Some patients have signs of weight loss. Other patients may have pallor from bleeding and anemia.

Sister Joseph's nodule:

Sister Joseph's nodule Sister Joseph's nodule, named after a nurse at the Mayo Clinic who discovered the phenomenon, a visible and palpable secondary deposit at the umbilicus due to spread along the lymphatics around the falciform ligament, is a presentation of ovary tumor, tumor of the stomach and colon. It is a poor prognostic sign and the mean survival of patients in whom the primary lesion is gastric is only 3.5 months.

Troisier's sign:

Troisier's sign Troisier's sign, an enlarged lymph node in the left supraclavicular fossa (Virchow node), indicates lymphatic spread via the thoracic duct. Armand Trousseau (1801–1867), a Paris physician, first suspected he had a gastric cancer when he developed superficial thrombophlebitis on the legs (Trousseau's sign), but Trousseau's sign is also associated with pancreatic cancer.

Lab Studies: :

Lab Studies: The goal of obtaining laboratory studies is to assist in determining optimal therapy. A complete blood cell count can identify anemia, which may be caused by bleeding, liver dysfunction, or poor nutrition. Approximately 30% of patients have anemia. Electrolyte panels and liver function tests also are essential to better characterize the patient's clinical state.

Imaging Studies :

Imaging Studies Esophagogastroduodenoscopy - permits direct inspection and biopsy of suspicious areas. This procedure also is the primary method for obtaining a tissue diagnosis of suspected lesions. Cytology on gastric washings is helpful in some institutions . Double-contrast air/barium upper GI series Air and barium are introduced together to coat the mucosa with a thin layer of barium and enhance mucosal detail. The technique can be further refined by using high density barium, carbon dioxide, simethicone for gas dispersion, and glucagon to induce gastroparesis.

Imaging Studies:

Imaging Studies Chest radiograph: This is done to evaluate for metastatic lesions. CT scan or MRI of the chest, abdomen, and pelvis . These imaging studies assess the local disease process as well as evaluate potential areas of spread (ie, enlarged lymph nodes, possible liver metastases). Endoscopic ultrasound

Imaging Studies:

Imaging Studies Computerized tomography, ultrasonography, and magnetic resonance are most helpful in the diagnosis of metastatic disease. Attempts to improve the accuracy of preoperative lymph node involvement include localization with monoclonal targeted isotopes, endoscopic lymphography, endoluminal ultrasound, and dynamic CT.

Cytology:

Cytology Cytological study of gastric aspirate for exfoliated malignant cells has been reported for patients with advanced disease, but has a variable accuracy of between 40 and 90 per cent. The cytological specimen may be collected by gastric washing, washing with addition of a mucolytic agent,

Spread patterns :

Spread patterns Cancer of the stomach can spread directly, via lymphatics, or hematogenously. Direct extension into the omenta, pancreas, diaphragm, transverse colon or mesocolon, and duodenum is common. If the lesion extends beyond the gastric wall to a free peritoneal (ie, serosal) surface, then peritoneal involvement is frequent.

Spread patterns:

Spread patterns The abundant lymphatic channels within the submucosal and subserosal layers of the gastric wall allow for easy microscopic spread. Lymphatic drainage is through numerous pathways and can involve multiple nodal groups (eg, gastric, gastroepiploic, celiac, porta hepatic, splenic, suprapancreatic, pancreaticoduodenal, paraesophageal, and paraaortic lymph nodes).

Spread patterns:

Spread patterns The cancer also spreads hematogenously. The most common sites for distant metastatic spread are the liver (49 per cent), lung (33 per cent), ovary (14 per cent), bones (11 per cent), and cervical and supraclavicular (Virchow) nodes (8 per cent).

Histologic Findings::

Histologic Findings: Adenocarcinoma of the stomach constitutes between 90% and 95% of all gastric malignancies. The second most common gastric malignancies are lymphomas. Leiomyosarcomas (2%), carcinoids (1%), adenoacanthomas (1%), and squamous cell carcinomas (1%) are the remaining tumor histologic types.

Histologic classification:

Histologic classification is based on the extent to which the cells are arranged into normal-appearing tubular glands and the degree of cell differentiation. Histologic classification correlates moderately with gross appearance and prognosis.

Morphovolumetric types :

M orphovolumetric types The ratio of the amount of muscle invasion to mucosa affected defines a funnel type (mucosal involvement greater than muscle: ratio less than 0.75), column type (equal involvement: ratio 0.75 to 1.25), and the mountain type (muscle greater than mucosal involvement: ratio over 1.25). The metastatic characteristics of these tumours are variable: the funnel type carry the best prognosis, with 62 per cent lymph node involvement, the column type (80 per cent lymph node metastasis), mountain type (lymph node metastasis in 85 per cent).

Treatment :

Treatment Surgical Care: a total gastrectomy (if required for negative margins), an esophagogastrectomy for tumors of the cardia and gastroesophageal junction, and a subtotal gastrectomy for tumors of the distal stomach.

Treatment:

Treatment Combined chemotherapy may be palliative for patients with metastases Radiotherapy , i ntraoperative radiotherapy radiotherapy with chemotherapy may be indicated for patients with locally unresectable tumors

Slide 74:

46 year-old man with no prior gastrointestinal symptoms, presented with five days of epigastric pain. Initial studies revealed iron-deficiency anemia and blood in the stool. Endoscopy demonstrated this lesion on the lesser curvature which appeared to be edematous folds with a central ulceration, but which on biopsy proved to be a poorly differentiated adenocarcinoma, signet ring cell type.

Slide 75:

87 year-old woman was found to be anemic and to have occult blood in the stool; she had no gastrointestinal symptoms of any kind. Endoscopy revealed this ulcerated, sessile, polypoid mass which proved to be adenocarcinoma on biopsy.

Slide 76:

82 year-old woman who presented with early satiety and postprandial vomiting, suggestive of gastric outlet obstruction, along with weight loss and anemia. Endoscopy demonstrated an ulcerated mass with prominent folds, which did not obstruct the gastric outlet. The lesion was an adenocarcinoma of the signet ring cell type.

Slide 77:

72 year-old man undergoing endoscopy for evaluation of abdominal pain. Endoscopy revealed a subtle, 2-3 cm focus of barely raised, nodular mucosa with normal color, on the posterior wall of the distal gastric body. The antrum and pylorus are visible in the background of this photo. Biopsies from the lesion revealed adenocarcinoma, and the patient was referred for surgical resection. The surgical specimen showed the lesion to be intra-mucosal, with invasion of the lamina propria but not into the muscularis mucosa.

Malabsorption syndromes :

Malabsorption syndromes Malabsorption is a clinical term that encompasses defects occurring during the digestion and absorption of food nutrients by the gastrointestinal tract

Pathophysiology :

Pathophysiology normal physiological process of digestion and absorption by the intestinal tract: the luminal phase - dietary fats, proteins, and carbohydrates are hydrolyzed and solubilized by secreted digestive enzymes and bile the mucosal phase - integrity of the brush-border membrane of intestinal epithelial cells to transport digested products from the lumen into the cells the postabsorptive phase - reassembled lipids and other key nutrients are transported via lymphatics and portal circulation from epithelial cells to other parts of the body Perturbation by disease processes in any of these phases frequently results in malabsorption.

Pathophysiology, Luminal phase:

Pathophysiology, Luminal phase Impaired nutrient hydrolysis pancreatic insufficie ncy, i nactivation of pancreatic enzymes by gastric hypersecretion ( Zollinger-Ellison syndrome ) i nadequate mixing of nutrients, bile, and pancreatic enzymes ( gastrojejunostomy ) Impaired micelle formation decreased bile salt synthesis (cirrhosis); impaired bile secretion (primary biliary cirrhosis, primary sclerosing cholangitis); impaired enterohepatic bile circulation ( small bowel resection ) ; bile salt deconjugation due to small bowel bacterial overgrowth Luminal availability and processing Luminal bacterial overgrowth - decrease in the availability of substrates, including carbohydrates, proteins, and vitamins (eg, B-12 and folate)

Pathophysiology, Mucosal phase :

Pathophysiology, Mucosal phase Impaired brush-border hydrolase activity (d isaccharidase deficiency ) Impaired nutrient absorptio n 1. i nherited defects ( glucose-galactose malabsorption, abetalipoproteinemia ) 2. acquired defects decreased absorptive surface area ( intestinal resection ) ; damaged absorbing surface ( celiac sprue, Crohn disease ) infiltrating disease of the intestinal wall ( lymphoma , amyloidosis ) 3. Postabsorptive phase Obstruction of the lymphatic system, both congenital and acquired, impairs the absorption of chylomicrons and lipoproteins

Symptoms and Signs :

Symptoms and Signs Diarrhea. Steatorrhea - the passage of pale, bulky, and malodorous stools; is the result of fat malabsorption Weight loss and fatigue Flatulence and abdominal distention , cramps. Edema (h ypoalbuminemia from chronic protein malabsorption ) Anemia : microcytic (iron deficiency), macrocytic (vitamin B-12 deficiency) Bleeding disorders ( vitamin K malabsorption, hypoprothrombinemia) Ecchymosis, melena, hematuria. Metabolic defects of bones : osteopenia, osteomalacia (Vitamin D deficiency) . Neurological manifestations : tetany (hypocalcemia and hypomagnesemia) ; motor weakness (pantothenic acid, vitamin D) , peripheral neuropathy (thiamine), a sense of loss for vibration and position (cobalamin), night blindness (vitamin A)

Lab Studies and Imaging Studies :

Lab Studies and Imaging Studies Hematological tests ( microcytic anemia , macrocytic anemia ) Electrolytes and chemistries (hypokalemia, hypocalcemia, hypomagnesemia, and metabolic acidosis, hypoproteinemia and hypoalbuminemia, low serum levels of triglycerides, cholesterol, and alpha- and beta-carotene, s erum iron and B-12 and folate levels , p rothrombin time ) Small bowel barium studies CT scan of the abdomen Endoscopic retrograde cholangiopancreatogram (ERCP) Plain abdominal x-ray film Upper endoscopy with small bowel mucosal biopsy

Stool inspection and microscopic examination:

Stool inspection and microscopic examination presence of reducing substances , a cidic stool ( pH lower than 5.5 ) - carbohydrate malabsorption t he level of quantitative stool fat and the amount of fat intake should be measured and monitored for 3 days. Normal fat absorption is 95% or more. Moderate fat malabsorption ranges from 40-60%. Fat absorption of less than 40% - severe malabsorption. 3. E xamination of the stool for ova and parasites , t esting for Clostridium difficile , Cryptosporidium

Other Tests :

Other Tests Tests of fat malabsorption : 72-hour fecal fat collection D-xylose absorption test: urinary excretion is lower than normal. Carbohydrate malabsorption tolerance test : hydrogen breath test ( аn increase in the exhaled hydrogen concentration following ingestion of an oral carbohydrate load ) Test of bile salt absorption. The patient is given oral conjugated bile salt (glycine cholic acid); radioactively labeled elevated breath carbon dioxide level if interrupted enterohepatic circulation such as bacterial overgrowth, ileal resection is present. Vitamin B-12 malabsorption tolerance test ( Schilling tes t) used to differentiate ileum disease from the lack of intrinsic factor by measuring the urinary excretion of radioactive vitamin B-12 administered by mouth with and without intrinsic factor .

Malnutrition:

Malnutrition The World Health Organization defines malnutrition as " the cellular imbalance between supply of nutrients and energy and the body's demand for them to ensure growth, maintenance, and specific functions." Protein-energy malnutrition (PEM) is observed most frequently in developing countries. Undernutrition in which nutrients are undersupplied, Overnutrition , in which nutrients are oversupplied.

Clinical signs and symptoms :

Clinical signs and symptoms PEM : Poor weight gain Slowing of linear growth Behavioral changes - irritability, apathy, decreased social responsiveness, anxiety, and attention deficits Micronutrient deficiencies : Iron - fatigue, anemia, decreased cognitive function, headache, glossitis, and nail changes Iodine - goiter, developmental delay, and mental retardation Vitamin D - poor growth, rickets, and hypocalcemia Vitamin A - night blindness, xerophthalmia, poor growth, and hair changes Folate - glossitis, anemia (megaloblastic), and neural tube defects (in fetuses of women without folate supplementation)

Physical examination :

Physical examination skin: dryness, scaliness, atrophy, petechiae, ecchymoses, mouth: angular stomatitis, glossitis, depapillation of the tongue , swollen or bleeding gums, and decayed teeth. depigmentation of the hair and spooned nails Abdominal findings Abdominal distension secondary to poor abdominal musculature Hepatomegaly secondary to fatty infiltration musculature: size, strength, and tenderness neurologic examination: disorientation, w eakness and paresthesia of the legs , altered reflexes, and sensory or motor neuron abnormalities anthropometric measurements edema: the distal extremities, anasarca [generalized edema]

Laboratory tests :

Laboratory tests hematological studies Electrolytes and chemistries (serum albumin, retinol-binding protein, prealbumin, transferrin, plasma lipids and related lipoproteins , f at- and water-soluble vitamins , a bnormal electrolyte levels , creatinine, and BUN) Sensitive measures of nutritional status Height-for-age or weight-for-height measurements greater than 2 standard deviations below the mean for age Height-for-age or weight-for-height measurements more than 2 standard deviations less than the mean for age Height-for-age measurements less than 95% of expected value Weight-for-height measurements less than 90% of expected value Body mass index (BMI)

Syndromes in gastroenterology :

Syndromes in gastroenterology 1. G astroesophageal dysmotility: Heartburn Belch Chest pain Regurgitation Dysphagia 2. Local enteral syndrome Abdominal pain Diarrhea Meteorism 3. General enteral syndrome Weight loss Poor appetite Headache Giddiness 4. Nonulcer dyspepsia 5. Malabsorption 6. Malnutrition 7. Portal hypertension 8. Hepatic insufficiency 9. General symptoms General weakness Non-motivated fatigue Decreased work capacity Irritation Insomnia