-Diverticular disease is the most common structural abnormality of the colon.

– A true diverticulum is a saclike herniation of the entire bowel wall, whereas a pseudo diverticulum involves only a protrusion of the mucosa and submucosa through the muscularis propria of the colon

-In Western countries, diverticula are predominantly left-sided, 95% involve the sigmoid colon while in the Eastern countries, they are predominantly right-sided.

only 20% of patients with diverticulosis develop diverticular disease

-the rectum is always spared

Uncomplicated Diverticulosis

-The majority of patients with diverticulosis are asymptomatic

Treatment: Most patients with diverticulosis do not require any specific treatment.

There are no medical treatments that will lead to the regression of diverticula, once present.

Asymptomatic diverticular disease is best managed by lifestyle changes. Recommend a high-fiber diet or fiber supplements such as psyllium or methylcellulose.

Refrain from smoking

Q: How does a high-fiber diet help in diverticular disease?

Fiber is fermented by gut bacteria producing fatty acids and gas. This results in shortened gut transit time and reduced intracolonic pressure.

Q: What is the most common location of diverticular disease? Sigmoid colon

Diverticulitis

Diverticulitis is inflammation of a diverticulum.

Symptoms & Signs:

Symptomatic Uncomplicated Diverticular Disease, SUDD: Fever, anorexia,leukocytosis, left lower quadrant abdominal pain, and obstipation

Complicated diverticulitis: Symptoms and signs listed above plus symptoms and signs associated with an abscess or perforation  and less commonly with a fistula.

Diagnosis:

Colonoscopy is relatively contraindicated in patients in whom acute diverticulitis is suspected, due to an increased risk of colonic perforation.

The diagnosis of diverticulitis is best made on CT: the presence of colonic diverticula and wall thickening, pericolic fat infiltration, inflammation within the pericolic fat,  abscess formation, or extraluminal air or contrast suggests diverticulitis.

Treatment:

Mild disease: clear liquid diet, selective use of antibiotics – augmentin, metronidazole + ciprofloxacin, rifaximin. Mesalamine to decrease inflammation.

Severe disease: nothing  by mouth, IV fluids, IV antibiotics

Antibiotics: oral penicillin/clavulanic acid, third generation penicillin such as piperacillin, third generation cephalosporin, ciprofloxacin and metronidazole.

A colonoscopy should be performed ~6 weeks after an attack of diverticular disease.

Prognosis: diverticulitis may lead to abscess formation which may lead to fistula formation

Q: What is the most common symptom of diverticular disease? Abdominal pain, usually localized in the left lower quadrant.

Q: Why is endoscopy contraindicated during the initial stages of an acute attack of diverticulitis? Because of the risk of free perforation.

Q: How do you differentiate severe diverticulitis from ulcerative colitis? Rectum is spared in Diverticular disease

T or F? Diverticulosis is not associated with an increased risk of colorectal cancer. True

Q: What do you suspect in a woman, who has a history of diverticular disease and hysterectomy, and reports passing gas or stool through her vagina? Colovaginal fistula

Appendicitis is caused by luminal obstruction of the vermiform appendix, typically by a fecalith. Other causes include obstruction by tumor, lymphatic tissue, gallstone or parasites.

-Approximately 9% of men and 7% of women will experience an episode during their lifetime.

-The most common abdominal surgical emergency

-It is most common in patients aged 10 to 19 years

– the most frequent cause of atraumatic abdominal pain in children >1 year old

– the most common non-obstetric surgical emergency in pregnancy

So, consider appendicitis in any patient with acute atraumatic abdominal pain without prior appendectomy.

Symptoms and Signs:

-Appendicitis usually begins with vague, often colicky periumbilical or epigastric pain. Within 12 hours the pain shifts to the right lower quadrant, manifested as a steady ache that is worsened by walking or coughing. Almost all patients have nausea with one or two episodes of vomiting.

-A worsening pain with deep inspiration may be present if there is peritoneal irritation. -Individuals may state that the trip to the hospital was painful, particularly when encountering bumps in the road.

-Low-grade fever (below 38°C) is typical.

–Flank pain, dysuria, or hematuria can occur, given the typical proximity of the appendix to the urinary tract.

Pregnancy: A right lower quadrant location of pain remains the most common location of pain in pregnant women with appendicitis. However, abdominal organ displacement from a gravid uterus may lead to right upper quadrant tenderness in pregnancy.

-the classic migration of pain to the right lower quadrant, to McBurney’s point, located one third of the distance from the anterior superior iliac spine to the umbilicus.

-On physical examination, localized tenderness with guarding in the right lower quadrant can be elicited with gentle palpation with one finger. When asked to cough, patients may be able to precisely localize the painful area, a sign of peritoneal irritation.

The psoas sign: Pain on passive extension of the right hip causes pain along posterolateral back and hip, suggesting retrocecal appendicitis

The obturator sign: Pain with passive flexion and internal rotation of the right hip, suggesting the possibility of an inflamed appendix in the pelvis

The Rovsing’s sign: Palpating in the left lower quadrant causes pain in the right lower quadrant if the appendix is located there.

Gastroenteritis vs. Appendicitis: In GastroeNteritis, Nausea comes first, then abdominal pain. In Appendicitis, Abdominal pain comes first, then nausea.

All patients should undergo a rectal examination.

Diagnosis:

Labs: Moderate leukocytosis  with ‘left shift’ neutrophilia; inflamed appendix that abuts the ureter or bladder may cause pyuria or hematuria.  

Imaging:

Abdominal ultrasound: wall thickening, an increased appendiceal diameter, and the presence of free fluid.

CT Scanning: dilatation >6 mm with wall thickening, a lumen that does not fill with enteric contrast, and fatty tissue stranding or air surrounding the appendix

Every woman of childbearing age should have a pregnancy test.

Treatment:

Pain: Control severe pain with narcotics

Infection: Broad-spectrum antibiotics

Surgery: Surgical appendectomy

Prognosis: If untreated, gangrene and perforation develop within 36 hours.

Q: What is the most common symptoms of appendicitis? Abdominal pain.

Acute Paralytic Ileus

-Ileus is a condition in which there is neurogenic failure or loss of peristalsis in the intestine in the absence of any mechanical obstruction.

-It is commonly seen in hospitalized patients as a result of abdominal surgery, peritonitis, pancreatitis, hemorrhage, pneumonia, sepsis, diabetic ketoacidosis, electrolyte abnormalities, and medications which affect intestinal motility such as opioids, phenothiazines, anticholinergics).

Symptoms and Signs: nausea, vomiting, abdominal pain, abdominal distention, diminished to absent bowel sounds.

Diagnosis: Serum electrolytes, abdominal x ray shows distended gas-filled loops of the small and large intestine.

Treatment:

-Treat the primary surgical or medical illness which precipitated the ileus;

-Restriction of oral intake with gradual liberalization of diet; nasogastric suction, parenteral administration of fluids and electrolytes.

-Opioids exacerbate postoperative ileus through activation of mu-opioid receptors. -Peripherally acting mu-opioid receptor antagonists do not cross the blood-brain barrier, so they can reduce postoperative ileus without diminishing the analgesic effect of opioids.

-Alvimopan: a peripherally acting mu-opioid receptor antagonist that reverses opioid-induced inhibition of intestinal motility.

-Methylnaltrexone: useful to treat opioid-induced constipation.

Lactase deficiency is the lack of the activity of the enzyme lactase, which is required for digesting the disaccharide lactose, the primary carbohydrate in cow’s milk. Dietary lactose is hydrolyzed by small intestinal lactase to glucose and galactose on the microvillus membrane of the intestinal adsorptive cells.

It is the most common problem of carbohydrate digestion. It results mainly from the reduction of lactase activity in adults.

Genetic or familial lactase deficiency appears after 5 years of age.

Secondary lactase deficiency: The most common etiology is acute GI infection resulting in small intestinal injury with loss of lactase-containing epithelial cells at the tips of the villi

Symptoms & Signs

Diarrhea, abdominal distention, flatus, and abdominal pain after ingestion of milk or milk-containing products.

Diagnosis

-Diagnostic tests include genetic testing and lactose breath test.

-The most widely available test for the diagnosis of lactase deficiency is the hydrogen breath test.

-Resolution of symptoms with lactose-free diet

-Patients with diarrhea have a stool osmotic gap of >125 mOsm/kg due to the presence of unabsorbed carbohydrates within the intestinal lumen and a stool pH <6 due to bacterial fermentation of lactose in the colon.

Treatment

Dietary lactose restriction: Milk product avoidance

Enzyme replacement: Symptoms can be ameliorated by administration of commercial lactase preparations.

Calcium and Vitamin D: Patients who choose to restrict or eliminate milk products may have increased risk of osteoporosis. so, give calcium and vitamin D

Q: What does the breath hydrogen test measure? lactose malabsorption.

Q: Patient reports a recent history of Giardiasis, he was treated with metronidazole. Now, he reports abdominal pain, flatulence and diarrhea after milk products. What do you suspect? Lactose intolerance, which is a common complication of Giardiasis

Whipple disease (WD) is a rare systemic infectious disease, caused by the bacterium Tropheryma whipplei, that can potentially affect all organ systems, but has a predilection for both the GI tract and CNS.

-Invasion of the intestinal mucosa and lamina propria with a gram-positive bacillus, Tropheryma whippelii produces foamy macrophages with glycoprotein leading to lymphatic obstruction and malabsorption.

-It most commonly affects white men in the fourth to sixth decades.

Symptoms and Signs:

The clinical features may include virtually any of the body’s organ systems.However, in the classic presentation, gastrointestinal symptoms are usually striking.

Gastrointestinal: Weight loss, diarrhea, abdominal pain.

Cardiac: heart failure or valvular regurgitation.

Pulmonary: cough, pleural effusion

Neurological: dementia, lethargy, coma, seizures, myoclonus, or hypothalamic signs. Cranial nerve findings include ophthalmoplegia or nystagmus. A pathognomonic sign of CNS Whipple disease is oculomasticatory myorhythmia, where involuntary blinking occurs when the patient is talking or eating.

Rheumatological: migratory polyarthralgia with enlarged or warm joints

Ocular: Uveitis

Diagnosis:The diagnosis of Whipple disease is established in 90% of cases by endoscopic biopsy of the duodenum with histologic evaluation, which demonstrates infiltration of the lamina propria with numerous foamy PAS-positive, diastase-resistant macrophages that contain gram-positive rod-like bacilli (which are not acid-fast) and dilation of the lacteals. In suspected CNS involvement, PCR and cytology of cerebro- spinal fluid sediment are of major diagnostic value.

Treatment: Empiric treatment with antibiotics results in prompt improvement in most patients. A course of induction by penicillin or ceftriaxone for 2 weeks followed by trimethoprim-sulfamethoxazole or doxycycline continued for 1 year are the currently recommended regimens. Complete clinical response usually is evident within 1–3 months

Prognosis: If untreated, the disease is fatal.

Q: Describe the typical patient with Whipple Disease? White, middle-aged man

Q: What is the most common presenting symptom seen in Whipple disease? Weight loss

Q: What is the most common form of ocular disease seen in Whipple’s? Uveitis

Q: What is the most common site for relapse in Whipple Disease? CNS

Q:What is the most common skin lesion in Whipple Disease? Hyperpigmentation

Q:  What is the characteristic histologic finding in Whipple disease?  is the presence of PAS-positive macrophages

-Celiac disease (CD) is a chronic inflammatory, immunologic disease of the small intestine triggered by gluten and related proteins that are components of wheat, barley, and rye grain products.

-The hallmark of celiac disease is an abnormal small-intestinal biopsy.

-Celiac disease is associated with dermatitis herpetiformis, diabetes mellitus type 1, IgA deficiency, Down’s syndrome, and Turner’s syndrome.

-IgA deficiency is 10 to 15 times more common among patients with CD than in the general population.

Symptoms and Signs:  

Gastrointestinal: Chronic diarrhea, steatorrhea, abdominal distention, irritability, anorexia, vomiting, and poor weight gain are typical.

Non-gastrointestinal:  iron-deficiency anemia, decreased bone mineral density, osteoporosis, infertility, elevated liver function enzymes, arthritis, or epilepsy with cerebral calcifications, neurological symptoms such as ataxia, neuropathy, migraine or rash suggestive of dermatitis herpetiformis. Celica Crisis can produce dehydration, hypotension, and hypokalemia.

Dermatitis herpetiformis is a form of gluten sensitivity characterized by a pruritic, papulovesicular rash that affects up to 20% of CD patients.  

Diagnosis:

The most sensitive and specific tests are antitissue transglutaminase (anti-tTG) or antiendomysial IgA antibodies. However, the gold standard of diagnosis is still demonstration of villous atrophy, flattening of the mucosa, increased intraepithelial lymphocytes on duodenal biopsy and a clinical response to a gluten-free diet.

-The preferred single, initial testing: A serologic test for IgA antitissue transglutaminase (tTG) antibodies.

-Genetic testing for HLA-DQ2 or DQ8 has strong negative predictive value and can help to rule out CD when the diagnosis is uncertain.

-Patients should be tested for deficiency of vitamins (A, D, E, B12), copper, zinc, carotene,folic acid, ferritin, and iron.

Treatment:

Diet: The mainstay of treatment for CD is lifetime adherence to a gluten-free diet. Avoid wheat, rye or barley.

Corticosteroids: Corticosteroids are indicated for celiac crisis with profound anorexia, edema, abdominal distention, and hypokalemia.

Nutrients: Iron, Folate, Calcium, Vitamin D

Vaccines: Pneumococcal vaccine to those with evidence of hyposplenism.

Prognosis: The most important complication of celiac disease is the development of cancer: T cell Lymphomas, gastrointestinal neoplasms such as small intestinal adenocarcinoma

Q: What is the most reliable, initial, noninvasive test to diagnose CD? Tissue transglutaminase (tTG) IgA antibodies

Q: What do you suspect in a patient with typical symptoms of CD who is negative for Immunoglobulin A (IgA) anti-tissue transglutaminase (tTG) antibody? IgA deficiency.

Q: What is the gold standard to establish the diagnosis of CD? Intestinal biopsy.

Q: What are the most important known genetic contributors to the pathogenesis of CD? genes encoding the MHC class II molecules, HLA-DQ2 or HLA-DQ8.

Q: Does Dermatitis herpetiformis respond to gluten withdrawal? Yes

Zollinger-Ellison syndrome (ZES) is characterized by peptic ulcers, diarrhea, and marked gastric acid hypersecretion in association with a gastrin-secreting non–β islet cell endocrine tumor (gastrinoma).

-The mean age of onset of symptoms is 41 years

-Multiple endocrine neoplasia syndrome type 1 (MEN 1) is present in approximately 20–25% of patients. It consists of pancreatic neuroendocrine tumors, pituitary tumors, and hyperparathyroidism.

-Most gastrinomas occur in the submucosa of the duodenum.

-Most patients have a typical duodenal ulcer.

Symptoms and Signs: Peptic ulcer disease, abdominal pain, and diarrhea, gastroesophageal reflux, nausea, weight loss, bleeding.  

Diagnosis:

When the diagnosis is suspected, a fasting gastrin is usually the initial test performed. Serum gastrin concentration >1000 pg/mL in combination with acidic stomach pH <2.0 is diagnostic.

The secretin stimulation test is the provocative test of choice used to differentiate patients with gastrinomas from other causes of hypergastrinemia and to establish the diagnosis of ZES.

In all patients with ZES, a serum PTH, Prolactin, LH, FSH, GH levels should be obtained to exclude MEN 1.

CT and MRI scans to identify the site of the primary tumor and whether there is metastasis.

Treatment:

Medical Treatment: PPIs are the drugs of choice, though H2 blocking drugs can also be used. Nasogastric aspiration of stomach acid stops the diarrhea.

-With long-term PPI use in ZES patients, vitamin B12 deficiency can develop; thus, vitamin B12 levels should be assessed during follow-up.

-Long-term PPI use may be associated with a number of side-effects including; an increased incidence of bone fractures;

Surgical Treatment: Tumor resection

In patients with MEN 1, surgical resection is recommended

Q: What are the most common symptoms experienced by ZES patients? Abdominal pain and diarrhea

Q: What do you suspect in patients who had peptic ulcers in unusual locations? ZES

Q: Who can have significant hypergastrinemia beside individuals with ZES? Patients taking PPIs, those with H pylori infection, chronic atrophic gastritis, pernicious anemia, hypochlorhydria

Q: What is the most sensitive method for identifying ZES? Demonstration of an increased fasting serum gastrin concentration.

Q: What is the most important predictor of survival in ZES?  The presence of hepatic metastases.

Complications of peptic ulcer disease include bleeding, ulcer perforation, penetration, and gastric outlet obstruction.

Bleeding: Most common complication. Treat with fluid resuscitation to correct hypovolemia; blood transfusions as necessary; early, high-dose intravenous PPI.

Ulcer Perforation:

Perforation usually elicits a sudden, severe upper abdominal pain. The patient appears severely distressed, lying quietly with the knees drawn up and breathing shallowly to minimize abdominal motion. Pain may radiate to the top of the right shoulder or to both shoulders.In the second phase (usually 2 to 12 hours after onset), abdominal pain may lessen. Board-like abdominal rigidity. Plain x-ray or CT scan of the abdomen reveals free subdiaphragmatic air. Up to 40% of ulcer perforations seal spontaneously; treat with fluids, nasogastric suction,IV PPIs, antibiotics.

Penetration: Ulcer perforates into contiguous structures such as pancreas. The pain becomes more severe and constant, may radiate to the back. Treat with IV PPIs, surgery.

Gastric Outlet obstruction: Least common complication; Presents with new onset of early satiety, nausea, vomiting, increase of postprandial abdominal pain, and weight loss. Prolonged vomiting and poor fluid intake may lead to prerenal azotemia, hyponatremia, and a hypokalemic, hypochloremic metabolic alkalosis.

On physical examination, a succussion splash may be heard in the epigastrium, which indicates retained fluid in the stomach.

Diagnosis: Nasogastric aspiration of a large amount of foul-smelling fluid; Endoscopy

Treat with dilation of the gastric obstruction by hydrostatic balloons passed through the endoscope, surgery. Malignancy is a more common cause of gastric outlet obstruction and must be excluded.

Q: What is the most common complication observed in PUD? GI bleeding.

Q: What is the most common cause of ulcer-related death? Bleeding

A peptic ulcer is a defect in the gastric or duodenal mucosa that extends through the muscularis mucosa into the deeper layers of the wall.

Causes: H.pylori infection, NSAIDS, aspirin, Zollinger-Ellison syndrome, Hyperparathyroidism, Crohn disease, burns, head injury, organ failure

Symptoms and Signs: 70 percent of peptic ulcers are asymptomatic; Symptoms include epigastric pain, early satiety, nausea

Gastric Ulcer (GU): Occur later in life, 55-70 years; Eating exacerbates pain; Nausea and weight loss occur more commonly in GU patients than DU patients. Should be biopsied because 5% of gastric ulcers are malignant.

Duodenal Ulcer (DU): Younger age of onset, 30-55 years; Eating relieves pain; The typical pain pattern in DU occurs 90 min to 3 h after a meal and is frequently relieved by antacids or food. Awakens the patient at night. Do not require biopsy because DUs are virtually never malignant and do not require biopsy.

Q: What is the most discriminating symptom in DU? it awakes the patient from sleep (between midnight and 3 A.M)

Ulcer complications: Bleeding, gastric outlet obstruction, fistulization, perforation

Diagnosis: Upper endoscopy or radiologic studies, Testing for Helicobacter pylori: Urea breath test, stool antigen test, serologic testing

Treatment:

Removal of offending factors.

Antacids: rarely used by physicians. Most often used by patients. Aluminum hydroxide can produce constipation and phosphate depletion; magnesium hydroxide may cause loose stools.

H₂ receptor antagonists: cimetidine, ranitidine, famotidine, nizatidine. Cimetidine can cause reversible gynecomastia and impotence.

Proton Pump Inhibitors: Omeprazole, Esomeprazole, Lansoprazole, Rabeprazole, Pantoprazole etc

Cytoprotective agents: Sucralfate

Bismuth-Containing Preparations: Bismuth subsalicylate

Prostaglandin analogues: Misoprostol (contraindicated in women who may be pregnant)

Surgery: Vagotomy and drainage

H.pylori treatment:

Clarithromycin Triple: PPI + Clarithromycin + Amoxicillin for 14 days, Approved by FDA.

Bismuth Quadruple: PPI + Bismuth subsalicylate + Tetracycline + Metronidazole for 10-14 days, not approved by FDA

Levofloxacin Triple: PPI + Levofloxacin + Amoxicillin for 5-7 days, not approved by FDA.

-In patients treated for H. pylori, eradication of infection should be confirmed four or more weeks after the completion of therapy. Tests to confirm eradication: urea breath test, fecal antigen test, or upper endoscopy

-Approximately 60 percent of peptic ulcers heal spontaneously but with eradication of H. pylori infection, ulcer healing rates are >90 percent.

Potential Adverse effects of Proton Pump Inhibitor Drugs:

-Chronic kidney disease, acute kidney disease, acute interstitial nephritis, hypomagnesemia, Clostridium difficile, Community-acquired pneumonia, bone fracture

-Long-term acid suppression, especially with PPIs, has been associated with a higher incidence of community-acquired pneumonia as well as community and hospital acquired Clostridium difficile–associated disease.

– long-term use of PPIs was associated with the development of hip fractures in older women.

Q: What is the most commonly identified risk factor for peptic ulcer bleeding? NSAIDS use

Q: What is the most frequent finding on physical examination in patients with GU or DU? Epigastric tenderness.

Q: What is the procedure of choice for the diagnosis of duodenal and gastric ulcers? Upper Endoscopy  

Q: What are the antisecretory drugs of choice for treating NSAID-related ulcers? PPIs

Q: What is the most common complication associated with peptic ulcers? GI bleeding

T or F?The majority of patients with peptic ulcers may be asymptomatic.True

-Esophageal varices are dilated submucosal veins that develop in patients with underlying portal hypertension.

-About half of the patients with cirrhosis develop esophageal varices.

-They may result in upper gastrointestinal bleeding.

Symptoms and Signs: When bleeding, the varices present with acute gastrointestinal hemorrhage, hypovolemia.

Treatment: Most patients with cirrhosis should undergo diagnostic endoscopy to document the presence or absence of varices and to determine their risk for variceal hemorrhage.

Prophylactic Treatment: Nonselective beta blockers, nitrates, endoscopic variceal ligation, cyanoacrylate injection of gastric varices

Acute hemorrhage: Variceal hemorrhage is life-threatening. Hemodynamic resuscitation using IV fluids, Fresh frozen plasma, platelets.

Vasoactive drugs: Portal hypertension is a consequence of liver disease. Drugs designed to reduce portal hypertension are useful to treat variceal hemorrhage: Somatostatin and their analogues (terlipressin, octreotide), Vasopressin

Endoscopic Treatment: Endoscopic variceal ligation, sclerotherapy

Shunt procedures: Transjugular intrahepatic portosystemic shunt (TIPS), Emergency Shunt Surgery  

Balloon procedures: Balloon Tamponade, Balloon-Occluded Retrograde Transvenous Obliteration (BRTO)

Antibiotic prophylaxis: fluoroquinolones or cephalosporins

Q: What are the most common cause of gastrointestinal bleeding due to portal hypertension? Esophageal varices

Q: What is the most common cause of portal hypertension? Cirrhosis

Q: What is the definitive treatment of choice for active variceal hemorrhage? Endoscopic therapy.

Q: Which medications seems to be effective for both primary and secondary prophylaxis of variceal hemorrhage? Nonselective beta blockers

-Acute lower gastrointestinal (GI) bleeding refers to blood loss of recent onset originating from the colon.

-Upper GI bleeding presents with melena or hematemesis, whereas lower GI bleeding produces passage of bright red or maroon stools

Common causes: Diverticulosis, malignancy, polyps, colitis, hemorrhoids, anal fissures

Less common: angiodysplasia, ulcers,malignancy

Physical examination: Look for signs of hypovolemia (hypotension, tachycardia)

Laboratory tests: complete blood count, serum chemistries, liver tests, and coagulation studies

Diagnosis: Anoscopy, sigmoidoscopy, colonoscopy, radionuclide imagine, CT angiography,

Treatment: Fluid resuscitation, blood transfusions, therapeutic colonoscopy, intra-arterial embolization, surgery.

Q: What is the most common cause of major lower tract bleeding? Diverticulosis

Q: What is the initial examination of choice for the diagnosis and treatment of acute lower GI bleeding? Colonoscopy

Acute upper gastrointestinal bleeding

-Upper GI bleeding is defined as bleeding above the ligament of Treitz.

-Patients with acute upper gastrointestinal (GI) bleeding commonly present with hematemesis (vomiting of blood or coffee-ground-like material) and/or melena (black, tarry stools)

-Upper GI bleeds are 4–8 times more common than lower GI bleeds.Peptic ulcer disease accounts for at least 50% of upper GI bleeds.

-The most common presentation of upper gastrointestinal bleeding –

Hematemesis: either red blood or coffee-ground emesis (proximal to ligament of Treitz)

Melena: black, tarry stool (proximal to ligament of Treitz)

Hematochezia: red or maroon blood in the stool, usually due to lower GI bleeding (distal to ligament of Treitz)

Causes of GI bleeding:

Common Causes

-Peptic ulcers account for 40% of major upper gastrointestinal bleeding.

-Portal hypertension from esophageal varices, gastric, duodenal varices.

-Mallory-Weiss tears: lacerations of the gastroesophageal junction.

Less common: Angiodysplasia, gastritis, malignancy, esophagitis.

Specific causes of upper GI bleeding and their symptoms

●Peptic ulcer: Upper abdominal pain

●Esophageal ulcer: Odynophagia, gastroesophageal reflux, dysphagia

●Mallory-Weiss tear: Emesis, retching, or coughing prior to hematemesis

●Variceal hemorrhage or portal hypertensive gastropathy: Jaundice, abdominal distention (ascites)

●Malignancy: Dysphagia, early satiety, involuntary weight loss, cachexia

Physical examination: Symptoms: light-headedness, shortness of breath, abdominal pain. Signs of hypovolemia (hypotension, tachycardia), blood in the stool.

Q: What is the diagnostic modality of choice for acute upper GI bleeding: Upper endoscopy.

Q: Can you order upper GI barium studies in the setting of acute upper GI bleeding? No, they are contraindicated.

Q: What do you suspect in a patient with hematemesis, severe abdominal pain, rebound tenderness and guarding? Perforation.

Treatment includes Fluid repletion with IV fluids, transfuse packed red cells, endoscopy, IV proton pump inhibitors, prokinetics (metoclopramide, erythromycin), antibiotics for patients with cirrhosis, IV octreotide to reduce portal blood pressure in variceal bleeding, intra-arterial embolization, Transvenous Intrahepatic portosystemic shunts (TIPS)

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-Irritable bowel syndrome (IBS) is a functional disorder of the gastrointestinal tract characterized by chronic abdominal pain and altered bowel habits.

-The most common diagnosis made by gastroenterologists.

-Affects predominantly women (70% of patients).

-The location and character of the pain can vary widely.

-The severity of the pain may range from mild to severe.

-The pain is frequently related to defecation.

-Symptoms of IBS include diarrhea, constipation, alternating diarrhea and constipation, or normal bowel habits alternating with either diarrhea and/or constipation.

Rome IV criteria for IBS – According to the Rome IV criteria, IBS is defined as recurrent abdominal pain, on average, at least one day per week in the last three months, associated with two or more of the following criteria:Related to defecation, Associated with a change in stool frequency, Associated with a change in stool form (appearance).

IBS subtypes: IBS with predominant constipation, IBS with predominant diarrhea, IBS with mixed bowel habits, IBS unclassified.

The physical examination is usually normal in patients with IBS.

There is no definitive diagnostic laboratory test for IBS. The diagnosis of the disorder is based on clinical presentation.  The purpose of laboratory testing is primarily to exclude an alternative diagnosis:  CBC, C-reactive protein and/or fecal calprotectin, serologic testing for celiac disease, colonoscopy etc.

Treatment: Reassurance, dietary modification, In patients with constipation, treat with fibers like psyllium/ispaghula, laxatives like polyethylene glycol, Lubiprostone, Guanylate cyclase agonists (Linaclotide, Plecanatide). In patients with diarrhea, use antidiarrheal agents like loperamide, Eluxadoline (mu-opioid receptor agonist), bile acid sequestrants like cholestyramine, colestipol, colesevelam; 5-hydroxytryptamine-3 receptor (5HT-3) antagonists like Alosetron; In patients with abdominal pain, use antispasmodic agents like Dicyclomine, Hyoscyamine.