The Stomach… IT’S a GUT FEELING

The Stomach… IT’S A GUT FEELING

MAUREEN STRESINSHE, BSN, RN SAY WHAT?

gizzard paunch OBJECTIVES 1. Describe the anatomy and physiology of the stomach . Structure of the stomach . Function of the stomach . Substances secreted by the by the stomach 2. Identifies disease of the stomach . Contributing factors . Symptoms . Diagnosis and treatment 3. Identifies pharmacological agents used to treat diseases of the stomach . Drug classifications . Mechanism of action . Therapeutic use What is it? J Red face when Knowblushing? YourYour stomach lining turns Anatomyred too! Cardia

. Upper opening of the stomach, where the esophagus enters . Cardiac mucosa primarily contains mucus-secreting cells that form a columnar epithelium . Just below the gastroesophageal junction . Transition point where the stratified squamous epithelium assumes the columnar structure Fundus

. The word “fundus” literally means “bottom” . Bulging part of the stomach above the level of the esophagus opening . Stores undigested food and gases released from chemical digestion Body

. Largest portion of the stomach . Mucosa of the body of the stomach has much deeper and less coiled gastric glands than that of the cardia. . Where mechanical and chemical digestive processes occur Antrum

. Lowermost part of the stomach which looks like a funnel. . Its wide end joins the lower part of the stomach body while the narrow part makes a connection with the pyloric canal. Pylorus

. Narrowest portion of the stomach . Measures roughly an inch in diameter with thick loops of smooth muscles surrounding it . Pyloric canal makes a connection of the stomach with the duodenum, measuring about 2 to 3 cm in length . Pyloric orifice is the opening or passage between the stomach and duodenum. Layers Serosa > Covers exterior of the stomach Muscle layers > • Comprised of 3 different types of muscle fibers • Contraction of these fibers responsible PERISTALSIS Submucosa > • Connective tissue, blood vessels, lymphatics & nerves Mucosa > • Secretes mucus https://upload.wikimedia.org/wikipedia/commons/6/64/Illu_stomach2.jpg Physiology

Hormonal Secretion • Food enters into stomach • Mechanical Digestion Control through the esophagus & • Chemical Digestion lower esophageal • Endocrine and exocrine • Regulate production sphincter functions stomach acid • Secretes acids, mucous & • Gradual release of food digestive enzymes into the small intestine

Storage Digestion • Hold an average of 1- 2 L of food & drink during the average meal • Can expand to hold 3 -4 L of food & drink when we overdo it • Stomach distention to its maximum size can make digestion difficult, not allowing for proper contractions • Stores food as digestion begins • Pyloric sphincter control gastric emptying and the release of chyme into duodenum, maximizing the digestion and absorption of nutrients in the intestines

STORAGE Gastric Juice • a mixture of mucus, hydrochloric acid, and digestive enzymes thatInner promotes stomach digestion. lining is covered Mucus with layers of • Spreads acrossfresh the surface mucus of the mucosa to coat the lining of the stomach with a thick, acid- and enzyme- resistant barrier.every 2 weeks • Stomach mucus is also rich in bicarbonate ions, which neutralize the pH of stomach acid.

EXOCRINE SECRETION Gastric Pit Produces Parietal Cells & Chief Cells

EXOCRINE SECRETION Parietal Cells (“fried egg”) • Intrinsic factor and Hydrochloric Acid • Intrinsic factor is a glycoprotein that binds to the vitamin B12 in the stomach and allows the vitamin to be absorbed in the small intestine. Vitamin B12 is an essential nutrient for the formation of red blood cells. • Hydrochloric acid protects the body by killing pathogenic bacteria naturally found in food. Helps to www.dreamstime.com digest proteins by denaturing them into an unfolded shape that is easier for enzymes to digest. The protein digesting enzyme pepsin is activated by exposure to hydrochloric acid inside the stomach. EXOCRINE SECRETION Chief Cells • Pepsinogen and Gastric Lipase • Pepsinogen is precursor molecule of the very potent protein-digesting enzyme pepsin. • Because pepsin would destroy the chief cells that produce it, it is secreted in its inactive pepsinogen form. When pepsinogen reaches the acidic pH found in the stomach thanks to hydrochloric acid, it changes shape and becomes the active enzyme pepsin. Pepsin then breaks dietary proteins into their amino acid building blocks. Hydrochloric acid protects the body by killing pathogenic bacteria naturally found in food. Helps to digest proteins by denaturing them into an unfolded shape that is easier for enzymes to digest. The protein digesting enzyme pepsin is activated by exposure to hydrochloric acid inside the stomach. • Gastric lipase is an enzyme that digests fats by removing a fatty acid from a triglyceride molecule. EXOCRINE SECRETION G Cells • Found at the bottom of the gastric pits. • Release the hormone gastrin into the bloodstream in response to many stimuli • signals from the vagus nerve; • presence of amino acids in the stomach from digested proteins • stretching of the stomach wall during a meal.

ENDOCRINE SECRETION These cells work together

Junqueira’s Basic Histology, Chapter 15 Mechanical digestion Chemical digestion of physically divides a large molecules into mass of food into small subunits smaller masses • Gastric lipase splits • Mixing action of smooth triglyceride fats muscles of stomach wall • Pepsin breaks down • Mix food bolus with proteins gastric juice > production • Completed when chyme of CHYME reaches intestines

MECHANICAL & CHEMICAL DIGESTION HORMONE ACTION

Produced by the G cells of the stomach. Increases activity of the stomach by stimulating increased gastric juice Gastrin production, muscle contraction, and gastric emptying through the pyloric sphincter. Produced by the mucosa of the duodenum. A hormone that acts to slow gastric emptying by contracting the Cholecystokinin (CCK) pyloric sphincter. CCK is released in response to food rich in proteins and fats, which are difficult for the body to digest. Produced by the duodenum's mucosa. Responds to the acidity of chyme entering the duodenum from the stomach. Travels through the bloodstream to the Secretin stomach where it slows the production of gastric juice by the exocrine glands of the mucosa. Promotes the production of pancreatic juice and bile. Protects the intestines from the damaging effects of acidic chyme.

Regulates the production of HORMONAL CONTROL stomach acid and the release of food into the duodenum. Most elders tell you MYTH OR not to swallow chewing gum because FACT? it stays in the stomach for 7 years

Our digestive tract cannot break down the chewing gum’s synthetic resin but it is highly efficient enough to it pass all the way through to the end Deranged function in an organ due to a disease.

Pathophysiology Gastritis Inflammation/Irritation/Erosion of the gastric mucosa

Excessive alcohol use Heavy use of NSAIDs Smoking Chemotherapeutic drugs Systemic Infection (Salmonella, CMV) Severe stress – trauma, surgery\ Ingestion of corrosives (acid/lye) Radiation

Classified according to inflammatory pattern: Acute, Chronic or part specialized condition Gastritis

Acute Gastritis > Erosive, hemorrhagic Serious illness Alcoholism Tobacco Use

Chronic Gastritis >Non-erosive, non-specific gastritis (NNG) Normal aging Gastric Ulcers Pernicious anemia Gastric cancer H. pylori Disease associated gastritis Ménétrier’s disease Eosinophilic gastritis Sarcoidosis Infections

http://www.journalnma.org/article/S0027-9684(15)30608-8/pdf Gastritis Nausea or recurring upset stomach Abdominal Bloating and/or Pain Vomiting Indigestion Burning or gnawing feeling in the stomach between meals or at night Hiccups Loss of appetite Vomiting blood or coffee ground-like material Black, tarry stools Many patients may have no symptoms Gastritis Diagnosis Upper Endoscopy Blood Tests – serum gastrin, gastric analysis

Treatment Review contributing factors patient medications, sepsis, H. pylori Stop smoking/alcohol intake Eliminate food triggers Antacids, Sucralfate, H2 Blockers, PPI, Antibiotics Antiemetics Gastritis Erosive Gastritis Stress Ulcers

Gastric mucosal stress erosions associated with serious illness

Severe trauma Sepsis Undergoing treatment for serious illness Have significant burn injury Sustained intracranial trauma – craniotomy/TBI (Cushing’s Ulcer) Chronic NSAID or alcohol use Stress Ulcer Cushing’s Ulcer

• Deep and of full-thickness • Prone to perforation • Ulcers are located in stomach lining • Due to elevated intracranial pressure, results in vagal nuclei stimulation causing elevated gastric acid secretion Stress Ulcer Curling’s Ulcer

• Acute gastric erosions • Complication of sever burns • Reduced plasma volume → ischemia and cell necrosis of gastric mucosa Stress Ulcers Symptoms Massive upper GI Bleeding Can occur within hours of initial injury Rarely cause ulcer S &S prior to start of bleeding Stress Ulcer Treatment  Control of Bleeding

 Correcting Shock

 Treatment of underlying disorder

 Endoscopy

 Angiographic embolization Gastric Varices (GV)  Portal Hypertension may lead to development of collateral circulation  Commonly a result of alcoholic cirrhosis  Compared with esophageal varices, gastric varices are larger, more extensive, and lie deeper in the submucosa.  2/3 of patients with esophageal varices also have gastric varices  Accounts for 10-30% of all variceal hemorrhage  High mortality rate  Large gastric varices located at the fundus 35-90% will experience recurrent bleeding Gastric Varices Management

 Hemodynamically stabilize the patient  Stop acute bleeding  Reduce portal pressure Gastric Varices Sarin Classification Gastric Varices Treatment

Gastric Variceal Band Ligation  Second alternative therapy to obturation  High rate of re-bleeding from feeding vessels  Repeat therapy at 1-2 week intervals until eradication Gastric Varices Treatment

Gastric Variceal Sclerotherapy  Due to high volume of blood flow less successful treatment than in esophageal varices (EV)  Typically requires larger volume of sclerosant than for EV leads to more side effects  Retrosternal/Abominal pain  Ulcerations (causes ~50% of re-bleeding)  Perforations  Control bleeding in 60-100% cases with re-bleeding rates up to 90%  Not appropriate for fundal varices d/t ↓ rate hemostasis Gastric Varices Treatment Gastric Variceal Obturation  Essentially “flushing glue” into the varix until it is hard to palpation  2-octyl cyanoacrylate has been approved by the FDA for skin closure and has also been used for the management of gastric varices → rapid polymerization on contact with living tissues  May be performed with endoscopic ultrasound guidance (↓complications)  Weeks to months after the injection, the mucosa overlying the glue cast sloughs off and the plug is extruded into the stomach.  Initial hemostasis rates of over 90% can be achieved.  Thrombotic complications: cerebral embolization & stroke, portal vein embolization, coronary & pulmonary emboli Gastric Varices Treatment Transjugular Intrahepatic Portosystemic Shunt (TIPS)  Considered for refractory GV bleeding  Primary hemostasis rate of TIPS for acute GV bleeding is 92.3%. Other studies showed initial hemostasis of TIPS for acute refractory GV bleeding is between 87% and 100%  Complications of TIPS are encephalopathy and shunt stenosis/occlusion, with post-TIPS encephalopathy occurring in 4-16% of patients Hiatal Hernia

 Weakening of the muscles of the diaphragm around the esophagus  Incidence increases with age  Approximately 60% of individuals aged 50 or older have a hiatal hernia  More common in women vs. men  Pregnancy, obesity, abdominal ascites can be contributing factors Hiatal Hernia Classifications “Sliding” Most common Widening of the muscular hiatal tunnel and circumferential laxity of the phrenoesophageal ligament Migration of GE junction into thoracic cavity Associated with reflux disease

https://clinanat.com/100-mtd/428-phrenoesophageal-ligament Hiatal Hernia Classifications

 Paraesophageal hiatal hernia  Herniation of gastric fundus into the thoracic cavity alongside the esophagus  Defect in the phrenoesophageal ligament & GE Junction remains fixed  Progressive enlargement Hiatal Hernia Classifications

Mix of Types I & II Phrenoesophageal ligament stretches Herniation of both GE Junctions and stomach “Sliding” element to Type II hernia Hiatal Hernia Classifications

Upside down stomach Large defect in the phrenoesophageal ligamenet Colon, spleen, pancreas and small intestine may enter the hernia sac. Hiatal Hernia Symptoms

Asymptomatic Asymptomatic Mechanical Obstruction OR OR Dyspnea GERD Vague/intermittent GERD Dysphagia r/t ischemia or obstruction Dyspepsia Chronic cough Epigastric/substernal pain Substernal Pain Regurgitation Postprandial fullness Substernal fullness Nausea Retching Anemia Hiatal Hernia Diagnosis Endoscopy CXR Esophagram/Barium Swallow Esophageal Manometry pH Capsule > Hiatal Hernia Type I Courtesy of David Y. Graham, MD CBC → anemia Hiatal Hernia Complications  Iron deficiency anemia r/t intermittent bleeding from associated  esophagitis  erosions (Cameron ulcers)  discrete esophageal ulcer  Incarcerated hiatal hernia Hiatal Hernia No treatment Treatment Elevate head of bed 6 inches Avoid lying down after meals Avoid foods that trigger heartburn (chocolate, onions, spicy foods, citrus fruits and tomato- based foods. Avoid alcohol Stop smoking Weight loss Stress reductions Proton Pump Inhibitors & H2 receptor blockers Surgical Intervention Nissen Fundoplicaiton Gastric Antral Vascular Ectasia (GAVE) Gastric Antral Vascular Ectasia Symptoms

Gastrointestional Bleeding

Anemia

Hematemesis

Melena Gastric Antral Vascular Ectasia

Exact cause unknown

 Often associated with other chronic conditions (autoimmune diseases, atrophic gastritis, cirrhosis, scleroderma, pernicious anemia, portal hypertension, vascular disease, diabetes mellitus, chronic renal failure)

Absence of cirrhosis: 71% female, average age 73, presenting with occult blood loss leading to transfusion-dependent chronic iron-deficiency anemia, severe acute upper gastrointestinal bleeding, and nondescript abdominal pain. Gastric Antral Vascular Ectasia Diagnosis

Visualized through endoscopy

 Other tests may be used to help confirm diagnosis  CT Scan and/or tagged red blood cell scan  Endoscopic Ultrasound Gastric Antral Vascular Ectasia Treatment

Argon plasma coagulation at site of bleeding

Treat underlying cause

 http://www.gastrointestinalatlas.com/english/Watermelon_Stomach.html Treat resulting anemia – possible blood transfusions Motor Dysfunctions: Dumping Syndrome

Rapid gastric emptying that may start 15-30 minutes post meal Causes: Can result from gastric surgeries that include vagotomy Symptoms: anxiety, weakness, dizziness, tachycardia, diaphoresis, flushing, abdominal cramping, diarrhea. Reactive hypoglycemia approximately 90- 120 minutes post meal lead to decreased level of consciousness. Treatment: focuses on slowing intestinal delivery of nutrients/minimizing release of endogenous vasoactive peptides Recommendations: High fat/high protein/low carbohydrate meals, minimal fluids while eating Motor Dysfunctions: Gastroparesis  Delayed gastric emptying

 Idiopathic or commonly associated with diabetes Pacemaker Region Causes: Outlet obstruction of stomach (tumor/ulcer) Neurological defect to pyloric sphincter Dysrhythmic contractions of stomach Symptoms: nausea and vomiting, vague stomach pain, early satiety, weight loss, fluctuating blood sugar Diagnosis: endoscopy, barium swallow, radioisotope gastric emptying scan Treatment: eat several small meals low in fat/fiber/roughage, pro-motility agent (Reglan), jejunal feeding tube, gastric pacemaker Bezoars: Continuous and prolonged ingestion of indigestible materials Phytobezoar

 Composed of indigestible fruit and vegetable fibers  Occur in patients with impaired gastric motility or digestion, following gastric surgery, low gastric acidity, and loss of normal pyloric function can all contribute to phytobezoar formation. Symptoms: epigastric pain or discomfort, N&V, early satiety, weight loss, diarrhea, dysphagia, or upper gastrointestinal ulcerations and hemorrhage. Treatment: Cellulase/Papain, Reglan, surgical removal, endoscopic mechanical fragmentation Bezoars:

Trichobezoar Continuous and prolonged ingestion of indigestible materials

 Composed of hair  90% occur in women under age 20  Referral for a psychiatric consultation

Pantoprazol (Protonix)

Esomeprazole (Nexium)

Lansoprazole (Prevacid)

Dexlonsprazole (Dexilant)

Omeprazol (Prilosec) Proton Pump Inhibitors (PPI’s)

 Work by reducing the production of acid by blocking the enzyme in the wall of the stomach that produces acid.  Different PPI’s are similar in action but may differ in how they are metabolized by the liver. Generally well tolerated.  Most common side effects include:  Headache, diarrhea, constipation, abdominal pain, fever, nausea, rash  Complications:  C. difficile, osteoporosis related hip/wrist/spine fractures, ↓ Vit. B12 absorption, hypomagnesemia Proton Pump Inhibitors (PPI’s)

Drug Interactions:  Ketoconazole and Digoxin need stomach acid to be present. PPI’s reduce absorption & blood concentration of Ketonconazole and increase concentration of digoxin (toxicity)  May reduce liver metabolization of some drugs leading to an increased blood concentration. Omeprazole most likely to interfere with Diazepam, Warfarin and Phenytoin. Also blocks the conversion of Clopidogrel (Plavix) to its active form. Proton Pump Inhibitors (PPI’s) -Indications Pantaprazole Lansoprazole Esomeprazole Dexlonsprazole Omeprazole

GERD GERD GERD GERD Errosive Esophagitis Erosive Esophagitis Erosive Esophagitis Erosive Esophagitis Erosive Esophagitis GERD Zollinger-Ellison Duodenal Ulcer NSAID ulcer risk Heartburn Heartburn Gastric Ulcer reduction Bengin Gastric Ulcer NSAID gastric ulcer Peptic ulcer - H.Pylori Duodenal Ulcer Peptic ulcer - H.Pylori eradication Zollinger-Ellison eradication H-2 Receptor Antagonists

Ranitidine (Zantac)

Cimetidine (Tagamet)

Famotidine (Pepcid)

Nizatidine (Axid) H-2 Receptor Antagonists

 Works by blocking the action of histamine on the parietal cells, reducing the production of acid.  Most common side effects include:  Diarrhea, headache, dizziness, fatigue, muscle pain, rash, impotence, mild gynecomastia, leukopenia, thrymbocytopenia  Complications:  Drinking alcoholic beverages while taking an H2-receptor antagonist has been reported to increase the blood levels of alcohol  Cigarette smoking tends to decrease the effect of H2-blockers by increasing the amount of acid produced by the stomach H-2 Receptor Antagonists - Indications

Famotidine Cimetidine Ranitidine Nizatidine

GERD GERD Esophageal Reflux GERD Esophagitis Heartburn Esophagitis Heartburn Duodenal Ulcer Duodenal Ulcer Peptic Ulcer Disease Acid Indigestion Zollinger-Ellison Gastric Ulcer Duodenal Ulcer Peptic Ulcer Disease (pathological Zollinger-Ellison Duodenal Ulcer hypersecretory conditions) Antacids

Neutralize stomach acid Contain ingredients such as aluminum, calcium, or magnesium which act as bases (alkalis) to counteract the stomach acid and lower pH. Mylanta, Milk of Magnesia, TUMS, Caltrate, Gavison, Maalox Work to reduce acid reflux, heartburn or dyspepsia May not be suitable for sodium restricted diets Short term use Carafate (Sulcarafate) – Anti-ulcer

Works mainly in the lining of the stomach by adhering to ulcer sites and protecting them from acids, enzymes, and bile salts. Sucralfate can heal an active ulcer, but it will not prevent future ulcers from occurring. Take Carafate on an empty stomach, at least 1 hour before or 2 hours after a meal Avoid taking any other medications within 2 hours before or after taking Carafate  Common Carafate side effects may include: nausea, vomiting, upset stomach; stomach pain; constipation, diarrhea; mild itching or skin rash; sleep problems (insomnia);dizziness, drowsiness, spinning sensation; headache; or back pain.