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UNIT TWO The GI Tract.

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Presentation on theme: "UNIT TWO The GI Tract."— Presentation transcript:

1 UNIT TWO The GI Tract

2 Gastro-Intestinal Tract & Disorders

3 Objectives Review the A&P of the GI system
Discuss the significance of vitamins and our ability to absorb them Describe oral infections/inflammations and the nursing care. Discuss the pathophysiology of esophageal disorders and the treatment /nursing care (i.e. GERD, hiatal hernia) Discuss the pathophysiology of disorders of the stomach and upper small intestine (i.e. gastritis, upper GI bleed, peptic ulcer disease).

4 Selected Readings In Your text chapters chapters 34, 35, 36, 37
Readings from your syllabus

5 Can you imagine: Not to be able to eat anything with wheat in it? What condition? What it is like to live with an esophageal sphincter not closing? What condition? Living with part of your stomach in your esophagus? Being incontinent of stool or continuous diarrhea? Open Sores over your lips on most important occasions... Celiac Disease GERD: 3. HERNIA 4. Chron’s Disease 5. Herpes

6 The main functions of GI system:
Ingestion & propulsion: (movement )food done by mouth, pharynx , esophagus Digestion (mouth, stomach, small intestine) Absorption (mouth, stomach, small intestine) Elimination (large intestine) GI organs: liver, biliary tract & pancreas. GI tract approx. 30 feet (9 M) in length from mouth to anus Tract composed of four layers inside to outside: Mucosa Sub-mucosa Muscle Serosa Esophagus the outer coat is fibrous tissue rather than serosa. GI tract innervated by parasympathetic nervous system ( mainly excitatory )& sympathetic nervous system (inhibitory). Ex: peristalsis is increased by the parasympathetic stimulation & decreased by sympathetic system. GI tract has its own nervous system: enteric or intrinsic nervous system which has neurons that contribute to coordination of GI motor & secretory activities. The enteric NS is also known as the” gut brain.”- it controls movement and secretions of the GI tract. Circulation in GI system is unique as venous blood draining the GI tract organs empties into portal vein, then perfuses the liver. Upper portion GI tract receives blood from spanchnic artery. Small intestine receives blood from hepatic & superior mesenteric arteries. Large intestine recieves blood from superior & inferior mesenteric arteries. Since a large percentage of cardiac output (25-30%) perfuses these organs, GI tract is major source from which blood flow can be diverted during exercise or stress. GI tract 2 types of movements mixing (segementation) & propulsion (perstalsis). Secretions GI system: enzymes & hormones for digestion, mucous for protrction & luberication and water & electrolytes. The main functions of GI system: Ingestion & propulsion (movement )food done by mouth, pharynx , esophagus Digestion (mouth, stomach, small intestine) Absorption (mouth, stomach, small intestine) Elimination .(large intestine) GI organs: liver, biliary tract & pancreas.

7 Mouth & Ulcerative Colitis /Crohn’s &Celiac

8 Food & GI System: Food generally takes about four hours to make it from the mouth to the end of the small intestine. The non-digested residue normally spends one to three days in the large intestine but can be there for seven days. Foods high in insoluble fiber (whole grains, wheat and corn brans, some vegetables) speedup intestinal transit. This is desirable because it prevents constipation, hemorrhoids, and diverticular disease. Fats: Ingested fat travels virtually unaffected until it contacts bile in the duodenum. Bile softens the fat molecule, lowering surface tension & enabling use Pancreatic Lipase + Intestinal Lipase convert the “softened” fat into Fatty Acids + Glycerol. It is then absorbed by the lymph. **Fat is essential for life & is a form of stored energy** Most carbohydrates are absorbed in the intestine and broken down by pancreatic & intestinal enzymes. It is the greatest source of energy especially quick energy. It is important in the prevention of constipation, diverticulosis & colon cancer & is thought to lower blood lipid & glucose. Proteins: Essential for life & healing. It has an important role in building & maintaining structural body tissue such as muscle, bone matrix & connective tissue. It provides about 12% of energy to the body. The end product of protein hydrolysis is Amino Acids which are absorbed by the blood stream

9 Vitamins Fat Soluble (stored & need fat for absorption):
A: vision (fish, fruit, veg) D: bone (dairy products esp calcium) E: Antitoxins (dairy) K: Blood clotting (milk, gr leafy veg) Water Soluble (not stored): C: Connective tissue ascorbic acid, citrus, gr veg, tomatoes, broccoli B1, B2,B6, B12: energy, lips, GI, RBC, heart, skin, gait, eyes synthesis DNA/RNA (meat veg, dairy products) NB: Vitamin B12 needs intrinsic factor

10 Vitamin B12 Acts as antitoxidant
Essential to formation of the protein collagen facilitates iron absorption facilitates cholesterol conversion to bile acids essential to serotonin synthesis B12: water soluable & therefore destroyed by light & lost during cooking. Citrus fruits, strawberries, green peppers, cauliflower

11 Vitamin B12

12 Intrinsic factor Parietal cells in the stomach secrete the the intrinsic factor necessary for the absorption of vitamin B12 in the small intestine. A lack in Vitamin B12 results in pernicious anemia. Loss of intrinsic factor also leads to degeneration of nerves & spinal column

13 Pernicious Anemia:

14 Common Herbal Supplements
Side effects Allium sativum (Garlic) Anticlotting Heartburn, flatulence, caution if client is on ASA or anticoagulants Echinacea Immunostimulator Some allergies; contraindicated in several diseases Ginkgo Vasodilator, ↑ cerebral blood flow Headache, GI upset, dizziness, N/V decreased clotting time St. John’s Wort Antianxiety, antidepressant Allergies, photosensitivity, avoid concurrent use with MAO inhibitors, opioids Ginseng Living fossil, ↑ vitality, ↓stress Nervousness, excitation, skin eruptions, avoid with hypertension

15 GI Tract: Oral Problems

16 Oral Inflammations & Infections:
The person who is ill, on medication, or receiving radiation is subject to alterations in ecology of the mouth & subsequently to decay, periodontal disease, and injury to the oral mucosa. Identify oral stressors: mechanical, chemical, infectious, or due to local or systemic disorder Oral inflammations & infections maybe specific mouth diseases or due to systemic diseases such as leukemia or vitamin deficiency. Can severely impair ingestion food & fluids. Client who is immunosuppressed (had chemo /radiation) is most susceptible to oral infections. (candida)

17 Infections & Inflammation of the Mouth
Gingivitis inflamed gingivae & interdental papillae, pus development, bleeding during brushing, formation of abscess with loosening of teeth. Vincent’s Infection painful, bleeding gingivae, bleeding ulcers, increased saliva with metallic taste, odor, fever, malaise & anorexia. Oral Candidiasis pearly, milk-curd like lesions on mucosa of mouth & larynx, sore, yeasty halitosis. Herpes Simplex lip & mouth lesions, vesicle formation, painful. Canker Sore ulcer mouth & lips, extreme pain, ulcer surrounded erythematous base. Parotitis inflammation parotid gland. Pain gland & ear, absence of salivation, purulent exudate from gland. Stomatitis inflammation of mouth with excessive salivation, halitosis, sore mouth

18 Herpes Simplex I Cold Sore
St. Vincent’s Oral Candidiasis Herpes Simplex I Cold Sore Stomatitis Gingivitis Parotitis

19 Oral Candidiasis . AIDS Immunosuppression for transplant recipients
Classical symptoms of oral candidiasis include the appearance of whitish velvety plaques on the mucous membranes of the mouth and tongue. If the whitish material is scraped away the base may be red (erythematous) with pinpoint bleeding. is an opportunistic organism that causes oral candidiasis and other forms of infection Oral candidiasis in adults should always be considered abnormal - know that it commonly occurs when conditions that depress the immune system are present. AIDS Immunosuppression for transplant recipients Individuals in chemotherapy Diabetes, advanced age, generalized poor health, and inherited abnormalities of the immune system Following antibiotic use

20 Oral Candidiasis Care:
Candidiasis: topical nystatin suspension (2 ml four times a day) or miconazole gel (5-10 ml four times daily, held in the mouth with dentures removed). Resistant candidacies: usually responds to systemic oral fluconazole (50 mg capsule daily for 7-14 days). Very frequent mouth care is essential

21 Herpes Simplex This close-up view of early herpes outbreak shows small, grouped blisters (vesicles) and lots of inflammation (erythema). By age five it is believed that 90% of population has had a HSV infection! Drug of choice is Acyclovir Transmission HSV Herpes (types 1 and 2) can be transmitted through skin to skin contact, kissing, sexual intercourse, and oral sex. The mucous membranes (mouth, nose, ears, throat, genitals, and anus) are most susceptible to infection with HSV The cervix and urethra are also high target areas. Also susceptible are any areas that may be subject to abrasion, and warm, moist areas such as the upper thighs, underarms, hairline, lower back, perineum, scrotum, and buttocks - any areas when sweating is common.

22 Transmission HSV: Herpes is most easily passed through inoculation from active lesions. The virus may also spread during times when there are no symptoms, and from sites that are seemingly inactive. There is a significant percentage of genital herpes infections resulting from oral to genital sexual contact. Most of these oral to genital transmissions will be of the type 1 variety, although type 2 incidence is not uncommon. Many times the partner who carries the virus is not even aware of an outbreak. In most cases, however, close examination reveals a history of symptoms.

23 Transmission HSV: Nurses when caring for clients with HSV beware of Herpetic whitlow (autoinoculation of herpes simplex virus to fingers).

24 Parotiditis- inflammation of parotid gland
Parotitis-inflammation parotid gland. Pain gland & ear, absence of salivation, purulent exudate from gland.

25 General Nursing Interventions for Oral Pain Relief:
Careful, regular, frequent mouth care Oral agents such as Lidocaine 2% viscous, Benadryl elixir, Antacid, & Kaopectate, Acetaminophen Topical agents such as coating agents Swishing agents providing topical & anti-inflammatory action analgesia Iced water or a dish of crushed ice (with spoon). Mouth sprays - a small hand-held spray filled with iced fruit juice is simple and effective. It can be easily used by client or relative Artificial saliva - frequent sips of `artificial saliva' may help some patients. An artificial saliva aerosol spray such as An artificial saliva spray such as Moistir is also available. Chilled fruit - chilled fruit jellies, ice lollipops, chilled slivers of pineapple Juices - fresh orange, lemon or grapefruit juices if able to tolerate. Sparkling water - tonic or soda water (may be frozen).

26 Oral Cancer Occur lips or anywhere within the mouth.
Smoking, excessive alcohol, chronic irritation from a jagged tooth, poor dental care, constant exposure to sun are predisposing factors Usually appears painless ulcer on lip Ca tongue ulcer or area of thickness, sore Biopsy to diagnose Treatment surgery, radiation, chemotherapy or combination. Mostly commonly occur lower lip. Also can occur lateral border & undersurface of tongue, buccal mucosa. More common males

27 Oral Cancer

28 Esophageal Disorders Mechanical : Tumor, Diverticulum, injury
CV: aneurysm, varices Neurogenic: Neuro, CVA

29 Esophageal Disorders GERD (Gastroesophageal Reflux Disease)
Hiatal Hernia Esophageal Cancer Esophageal Diverticula Esophageal Strictures Achalasia Esophageal Varices Gastro-esophageal reflux disease (GERD), a multi-factorial disease is a primary disorder of gut motility that is also linked to the presence of gastric acid in the esophagus. (Reflux of stomach & duodenal contents into the esophagus).

30 Common Signs & Symptoms of Esophageal Disorders
Problem swallowing * Pain * Hoarseness * Weight loss * Bleeding * Regurgitation (water brash) Heart burn Hiccups

31 GERD Syndrome No one single cause Factors causing GERD:
Impaired esophageal mobility Delayed gastric emptying Defective mucosal defense Reflux of gastric contents Lower Esophageal Sphincter (LES) dysfunction –main factor. 5-7% world’s population experience GERD. GERD results when defenses of the lower esophagus are overwhelmed by the reflux of stomach acidic contents into the esophagus. Hiatal hernia, incompetent LES, decreased esophageal clearance (ability to clear liquids or food from the esophagus into the stomach ) resulting from impaired esophageal mobility & decreased gastric emptying. Acidic Gastric secretions that reflux up into the lower esophagus causes esophageal irritation & inflammation. Additionally, gastric enzyme (pepsin) & intestinal enzyme (trypsin) & bile salts corrode the esophageal mucosa.

32 GERD Normally, after a meal, the lower esophageal sphincter (LES) usually remains closed. Secondary peristalsis returns approx. 90% of the acid and food to the stomach. Once peristalsis ends, the LES closes again. The remaining acid in the esophagus is neutralized by successive swallows of saliva, which is alkaline in nature - it is then cleared into the stomach. When LES relaxes at inappropriate time, it allows acid and food particles to reflux into the esophagus. (GERD) Secondary peristalsis occurs in response to esophageal distention or irritation caused by gastric reflux, spreading from the point of irritation in the esophagus to the stomach. The condition is characterized by the failure of the LES to remain normally closed between swallows

33 LES & GERD Results in a decrease in pressure in distal portion of esophagus Thus gastric contents move from area of higher pressure (stomach) to area of lower pressure (esophagus) when client supine position or increased intra-abd pressure

34 LES & GERD Results in a decrease in pressure in distal portion of esophagus Thus gastric contents move from area of higher pressure (stomach) to area of lower pressure (esophagus) when client supine position or increased intra-abd pressure

35 Factors that Increase LES Pressure:
Reglan Urocholine Motilium Gastrin Nonfat milk Chewing gum helps GERD Therefore might help GERD.

36 Some Common Agents that Decrease LES Pressure:
Alcohol, Nicotine, ASA Anticholenergic drugs Beta-adrenergetic blocking drugs Calcium channel blockers Chocolate, Coffee, Fatty foods, Peppermint Demerol, Estrogen, Lidocaine, Morphine hinders GERD Therefore must avoid if client has GERD

37 Clinical Manifestations GERD
Heartburn very common due to gastroesophageal reflux chest pain Respiratory systems- wheezing, coughing, dyspnea Otolaryngologic symptoms- hoarseness, sore throat, feeling as though a lump in throat, choking Regurgitation common Gastric symptoms- early satiety, post meal bloating, N&V. Clinical Manifestations GERD are individual and vary. Heartburn normally occurs after a meal once a week is mild however heartburn occurring more frequently than once a week, becomes more severe or wakes a person at night is signs of more serious condition. Heartburn is often relieved with milk, alkaline substances or water. Regurgitation: food/gastric contents from stomach into esophagus or mouth- feeling as hot, bitter or sour liquid coming into throat or mouth.

38 Complications of GERD Esophagitis Barrett’s esophagus
Respiratory complications: bronchospasms, laryngospasms, pneumonia Dental erosion Esophagitis: inflammation esophagus due to gastric secretions on esophageal mucosa Barrett’s esophagus: esophageal metaplasia precancerous lesion increasing the risk for ca esophagus. Respiratory complications: bronchospasms, laryngospasms, pneumonia due to the irritation upper airway by gastric secretions. Dental erosion

39 Barrett’s Esophagus:

40 Diagnosing GERD Barium swallow /X-ray if protrusion upper part of stomach Esophageal Endoscopy Biopsies to determine ca stomach or Barrett’s esophagus Esophageal manometric studies- measure pressure esophagus & LES PH measuring devices to determine if acid in esophagus High-dose proton pump inhibitor (PPI) Endoscopy useful in assessing competence LES & extent inflammation, potential scarring & strictures Esophagus normally alkaline High-dose proton pump inhibitor (PPI) due to cost & discomfort of tests it is recommended that PPI be used (Drug therapy) for 2 weeks as a first step in diagnosis as PPI treatment should result in marked reduction or elimination of symptoms if client has GERD.

41 Barium Swallow X-ray Figure 1 shows the lower end of a normal esophagus with a smooth connection between the lower esophagus and stomach. Figure 2 shows the lower end of the esophagus with a small hiatal hernia, which occurs when a small portion of the stomach pushes up into the chest.

42

43 Esophageal Endoscopy This test involves passing an endoscope, a long, flexible black tube with a light and video camera on one end, through the mouth to examine the esophagus, stomach and the first part of the small intestine called the duodenum. The advantages of this test over the barium esophagram (x-ray test) are that the lining of the upper digestive tract can be directly viewed by the doctor and very small abnormalities seen. Endoscopic therapies (treatments) can be performed at the time of the procedure. Examples of such therapies include dilation of an esophageal stricture (stretching an esophageal narrowing with a tube) or treating a bleeding ulcer to stop the bleeding. Biopsies (taking small pieces of tissue) of any abnormality may also be done directly through the endoscope including biopsy of suspected Barrett's esophagus or duodenal and stomach ulcers. The patient should not eat or drink for 6 to 12 hours before the examination. Patient preparation includes helping the patient spray or gargle with a local anesthetic, and administering midazolam (Versed) intravenously just before the scope is introduced. Midazolam is a sedative that provides moderate sedation and relieves anxiety during the procedure. The nurse also may administer atropine to reduce secretions, and may give glucagon, if needed and prescribed, to relax smooth muscle. The nurse positions the patient on the left side to facilitate saliva drainage and to provide easy access for the endoscope. After the procedure, the nurse instructs the patient not to eat or drink until the gag reflex returns (in 1 to 2 hours), to prevent aspiration of food or fluids into the lungs. The nurse places the patient in the Sims' position until he or she is awake and then places the patient in the semi-Fowler's position until ready for discharge. After gastroscopy, assessment by the nurse includes observing for signs of perforation, such as pain, bleeding, unusual difficulty swallowing, and an elevated temperature. The nurse monitors the pulse and blood pressure for changes that can occur with sedation. The nurse can test the gag reflex by placing a tongue blade onto the back of the throat to see whether gagging occurs. After the patient's gag reflex has returned, the nurse can offer lozenges, saline gargle, and oral analgesics to relieve minor throat discomfort. Patients who were sedated for the procedure must stay on bed rest until fully alert. After moderate sedation, the patient must be accompanied and transported home if the procedure was performed on an outpatient basis. The nurse instructs the patient not to drive for 10 to 12 hours if sedation was used. NPO to prevent vomiting, aspiration Local spray anesthetic to prevent gagging, choking and numb the throat Suction and CPR equipment in case of aspiration, vasovagal response and perforation Withhold fluid and food post exam until gag reflex returns; usually 2-4 hours post procedure Moistir for throat discomfort Check for sore throat, gag reflex, choking, perforation, aspiration pneumonia

44 Esophageal Endoscopy NPO 6-10 hours pre examination. Why?
Why is a local spray anesthetic used? Why suction & CPR equipment ready? Why withhold fluid & food post exam? How long? What can you do for throat discomfort? What do you check for post procedure?

45 Nursing Interventions for GERD
Assess cause Position-elevate head no lying down 2-3 hrs. post eating Nutrition Drugs as ordered Lifestyle- stop smoking, Weight loss Avoid factors that aggravate symptoms. Positioning: If symptoms occur at night, use extra pillows to prop up head and shoulders. If this fails, raise the head of bed about 10 cm (4 inches) to prevent acid reflux at night- if not contraindicated Nutrition: diet does not cause GERD but foods may aggravate, fatty foods (decrease rate gastric emptying & release CHolecystokinin hormone decreases LES pressure), chocolate, tea, coffee & pepermint decrease LES pressure Milk products as increases gastric secretion Recommend small frequent meals so not to overextend the stomach, avoid late eating, take fluid between meals to reduce gastric distension. Orange juice irritate esophagus Weight reduction to reduce intraabd. Pressure Losing weight nearly always cures it. Eating several very small meals each day instead of 2 or 3 large ones help. Have a light evening meal without alcohol and avoid heavy supper so that stomach is empty on retiring. It takes about 1 hour for the stomach to empty after a small feeding. stop smoking: smoking associated with decreased acid clearance from lower esophagus.

46 Drugs for GERD: Drugs for GERD focus on:
Improving LES function (urecholine) Increasing esophageal clearance (metoclopramide) Decreasing volume & acidity of reflux (H2 receptor blockers, PPI, maalox, mylanta) Protecting esophageal mucosa (gaviscon, carafate) If they do not work surgery maybe required Two approaches drug therapy: Step-up approach: start with antacid (Maalox) & OTC histamine 2 receptor (Zantac)blockers, increasing to prescription H2R (Tagamet) and finally PPI(Nexium, prevacid) Step-down approach-starting with PPI (nexium, Prevacid) and over time titrating down to prescription H2R (tagamet), then OTC H2R & antacids.(Zantac & Mylanta, Maalox). Anacaids: should be taken 1-3 hours post meals & hs Anisecretory agents decrease the secretion HCL acid by the stomach (tagamet, zantac, pepcid, axid. PPI’s (proton pump inhibitors) prilosec, nexium, prevacid decrease stomach HCL acid secretion. They inhibit the proton pump mechanism responsible for secretion H ions.

47 Nissen Fundoplication
Fundus is sutured around the esophagus An increase in pressure or volume in the stomach closes the cardia and blocks reflux into the esophagus Valve-like substitute sphincter to replace incompetent sphincter.

48 Angelchick antireflux Surgery
Angelchick antireflux Surgery In clients with severe reflux an Angelchick prosthesis maybe inserted. A laparotomy is performed, and a synthetic C shaped silicone prosthesis is tied around the distal esophagus. Prosthesis anchors the LES in place & reinforces sphincter pressure. Procedure has variable success depending on severity of problem. With severe reflux may not be successful. High rate of recurrance. Recently approved Stretta procedure to treat GERD Balloon-tipped four needle catheter delivers radiofrequency energy to smooth muscle of gastroesophageal junction for the management of GERD. Long term benefits are not yet determined. B Menu F

49 Hiatal Hernia

50 Normally: The stomach is below the diaphragm

51 Hiatal Hernia Is herniation of a portion of the stomach into the esophagus through an opening, or hiatus, in the diaphragm. The weakest part of the diaphragm is the opening through which the esophagus passes. Most common abnormality found on x-ray examination of upper GI tract Common older adults More common women than men There are two types sliding or rolling hiatal hernias A hiatus hernia occurs when the upper part of the stomach, which is joined to the esophagus moves up into the chest through an enlargement (called a hiatus) in the diaphragm.

52 Hiatal Hernia: Inside view of hiatal hernia

53 Sliding Hiatal Hernia A hiatus hernia occurs when the upper part of the stomach, which is joined to the esophagus moves up into the chest through an enlargement (called a hiatus) in the diaphragm. Gastroesophageal junction above the diaphgram 90% of hiatal hernia’s are sliding type Sliding: the junction of the stomach & esophagus is above the hiatus of the diaphragm & a part of the stomach slides through the hiatal opening in the diaphragm. The stomach slides into the thoracic cavity when the client is supine & usually goes back into the abdominal cavity when the client is standing upright. Most common type of hernia. Black, 2001 B Menu F

54 Sliding Hiatal Hernia/ Without Hernia
Turning the tip of the gastroscope up inside the stomach gives an excellent view of the fundus- and hiatus-region. In a patient with a sliding hiatal hernia, an opening to the hernia (x) can be seen, and it is easy to understand, that a situation like this can cause reflux to the oesophagus. In a normal patient (the picture to the right), the cardia region closes tightly around the gastroscope (G).

55 Rolling Hiatal Hernia B Menu F 10% of hiatal hernia’s are rolling type
The gastroesophageal junction stays below the diaphragm but the fundus & greater curvature of the stomach roll up through the diaphragm,forming a pocket alongside the esophagus. B Menu F

56 Sliding Rolling B Menu F

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58 Hiatal Hernia Causes: Structural causes such as weakening of muscles in diaphragm around the esophagogastric opening Factors that increase intrabd. pressure: obesity Pregnancy Ascites Tumors Tight corsets Intense physical exertion Heavy lifting continual basis Increased age Trauma Poor nutrition Forced recumbent position

59 Clinical Manifestation Hiatal Hernia
Maybe asymptomatic Heartburn after a meal or after lying supine Dysphagia Reflux & discomfort associated with position lying down Bending over may cause severe burning pain, relieved by standing Pain with large meals, alcohol, & smoking Heartburn at night common A painful burning sensation in the chest sometimes occurs, which can be felt in the throat. Other symptoms include belching, pain on swallowing hot fluids and a feeling of food sticking in the esophagus.

60 Complications of Hiatal Hernia:
GERD Hemorrhage from erosion Stenosis of esophagus Ulcerations of herniated portion of stomach Strangulation of the hernia Regurgitation with tracheal aspiration Increased risk for respiratory disease

61 Diagnosis of Hiatal Hernia
Barium swallow: may show protrusion of gastric mucosa through the esophagus X-rays Endoscopy: visualization of the lower esophagus provides info on the degree of mucosal inflammation or other abnormalities.

62 Conservative Treatment Hiatal Hernia
Keep to weight as ideal as possible Avoid stooping Avoid smoking Reduce alcohol and coffee Avoid tight clothing/under garments Adjust bed - elevate HOB Take antacid such as TUMS Have small meals especially at supper Avoid spicy food Avoid hot drinks Avoid gassy drinks

63 Other Esophageal Disorders
Esophageal Diverticula- saclike outpouchings of one or more layers of the esophagus Esophageal Strictures – narrowing of esophagus caused by acids or alkalis ingested and reflux of gastric juices Esophageal cancer-rare Achalasia- peristalsis of the lower two thirds of esophagus is absent. LES increased pressure & incomplete relaxation LES. Esophageal Varices- dilated veins occurring in lower portion of the esophagus as a result of portal hypertension. Common cirrhosis of liver. Esophageal Strictures can be dilated by endoscopy

64 DIGESTIVE SYSTEM The stomach, intestines, and digestive glands produce acid and various enzymes, including pepsin, that break down and digest the starch, fat, and protein in food. The stomach itself is composed mostly of protein and must be protected from the same acid and enzymes, or it too can be attacked and broken down The main function of the stomach is to process and transport food. Stomach functions to store food, mix the food with gastric secretions and empty contents into the small intestine at a rate at which digestion can occur. Stomach absorbs only a small amounts of water, alcohol & electrolytes & certain drugs. Stomach always containsgastric fluids & mucous. Three parts of stomach: Fundus, body & antrum. Pylorus is small portion of the antrum that lies proximal to the pyloric sphincter. Sphincter muscles (LES & pyloric sphincter) guard the entrance to & exit from the stomach. Cardiac orifice is opening between esophagus & stomach.

65

66 THE ANATOMY OF THE STOMACH
Anatomically, the stomach can be divided into three major regions: fundus (the most proximal), corpus and antrum Stomach functions to store food, mix the food with gastric secretions and empty contents into the small intestine at a rate at which digestion can occur. Stomach absorbs only a small amounts of water, alcohol & electrolytes & certain drugs. Stomach always contains gastric fluids & mucous. Three parts of stomach: Fundus, body & antrum. Pylorus is small portion of the antrum that lies proximal to the pyloric sphincter. Sphincter muscles (LES & pyloric sphincter) guard the enterance to & exit from the stomach. Cardiac orifice is opening between esophagus & stomach.

67 Disorders of Stomach & Upper Small Intestine
Gastritis Upper GI Bleeding Peptic Ulcer Disease Gastric Ulcers Duodenal Ulcers Gastric cancer Food Poisoning Manifestations of GI disorders are generally caused by excessive gastric secretions that erode the stomach mucosa, excessive motility, or retention of gastric contents. Manifestations include: Pain Anorexia Nausea/vomiting Bleeding Diarrhea indigestion

68 Gastritis Inflammation of gastric mucosa as a result of breakdown in normal gastric mucosal barrier. Most common problems affecting stomach Gastritis have tissue edema, disruption of capillary walls with loss of plasma into gastric lumen & possible hemorrhage. Broken mucosal barrier, autodigestion, HCL & pepsin cause gastritis. Can be acute or chronic (loss of intrinsic factor) Chronic further divided into three subtypes: auto-immune- involves body & fundus of stomach Diffuse antral-affects antrum Multifocal-diffuse throughout stomach Causes of gastritis & relationship to other disorders (H-pylori infection & gastric ca) are focus of research. The mucosal barrier normally protects stomach tissue from autodigestion by HCL acids & pepsin. A broken barrier, HCL acid diffuses back into the mucosa resulting in tissue edema, disruption of capillary walls with loss of plasma into gastric lumen & possible hemorrhage.

69 Causes of Gastritis Drugs- aspirin, corticosteroids, NSAIDS, digitalis
Diet-alcohol, spicy irritating foods Microorganisms-Helicobacter (H-Pylori), Salmonella, Staphylococcus organisms. Environmental-smoking, radiation Pathophysiologic Conditions- burns, lg. hiatal hernia, stress, reflux bile & pancreatic secretions, renal failure, sepsis, shock Other factors- endoscopic procedures, NG suction, psychologic stress aspirin, NSAIDS, digitalis- direct irritating effects on gastric mucosa. corticosteroids, NSAIDS also inhibit the synthesis of prostoglandins that are protective of gastric mucosa (more susceptible to damage) Taking warfarin with NSAIDS increases risk of gastritis, being female & over 60 also does. H-pylori infection-common in many adults & may be symptomatic. H-pylori thought to be acquired childhood & able to survive in gastric lumen. H-pylori causes breakdown of gastric mucosa barrier with certain triggers. 30% clients with h-pylori have antigastric antibodies.

70 Clinical Manifestation Gastritis:
Anoxeria N&V Epigastric tenderness Feeling of fullness Hemorrhage-common alcohol abuse Acute gastritis- self-limiting, lasts few hrs to few days, complete healing mucosa Chronic gastritis-loss of intrinsic factor Chronic gastritis-loss of intrinsic factor (substance secreted by gastric mucosa) can’t absorb B12 & have reduction in growth & maturation of RBC’s-anemia.

71 Diagnosis Gastritis Acute – based on history drugs & alcohol
Chronic- non-specific symptoms: endoscopic examination with BX CBC-anemia/bld. Loss/lack intrinsic factor Stools Occult blood gastric analysis- HCL present serum tests antibodies tissue BX- R/O gastric cancer Chronic-non-specific symptoms: dx maybe delayed or missed endoscopic examination with BX: to determine h-pylori

72 Nursing Management Gastritis
Acute Gastritis: eliminate cause Supportive care Vomiting-bedrest, npo, IV, antiemetics Severe V – NG Hemorrhage-V/S freq. check v blood Administer antacids (raise ph above 6), H2R blockers & PPI. H2R blockers- zantac, tagamet, PPI (prilosec, prevacid) Give Tritec (drug) reduces bleeding & promotes healing of erosive gastritis. Anti secretory agents such as Pepcid, Zantac & tagamet (H2 receptor antagonists) and Prevacid,& Prilosec (proton pump inhibitors Often combined with Pepto=Bismol ( suppresses H. pylori bacteria in the gastric mucosa and assists with the healing of mucosal lesions)

73 Histamine H2 Receptor Antagonists
Inhibits acid secretion

74 Proton Pump Inhibitors
Decreased acid secretion

75 Nursing Management Gastritis
Chronic Gastritis: evaluation & eliminating cause (cessation alcohol, abstance from drugs, H.pylori eradication) (Flagyl) Antibiotics & antisecretory agents –rid H-pylori Strict adherence drug regime Non-irritating diet Smoking cessation Close medical follow-up as increase incidence Gastric cancer

76 Upper GI Bleeding

77 Upper Tract GI Bleeding
Upper GI bleeding greater incidence older adults, esp. women using NSAID A sudden onset, insidious bleeding Can be venous, capillary or arterial Common sites esophagus, stomach & duodenum Types upper GI Beeding: Hematemesis- bldy vomit bright red or coffee-grounds Melena-black, tarry stools (foul smelling) Occult Blding- sm. Amt bld in gastric secretions, vomitus or stool not apparent by appearance. Bleeding arterial source profuse , bld bright red (indicates not been in contact with stomach’s acid secretions). Coffee grounds- vomit reveals bld & other contents have been changed by contact with gastric secretions. Massive upper GI bld loss 1500cc or 25% intravascular volumne. Melena indicates slow bleeding from upper GI source.

78 Common Causes Upper GI Bleeding
Drugs- Corticosteriods, NSAIDS, Salicylates (stimulate acid production, suppress mucous production and cause local damage) Esophagus- Varices, esophagitis, Mallory-Weiss tear (complication of Bulemia) Stomach & duodenum- gastric Ca, hemorrhagic gastritis, peptic ulcers, polyps, stress ulcer Systemic diseases-leukemia, renal failure (increase secretion gastric acid) Chronic esophagitis cause can be ingestion chemicals & irritating drugs, smoking & alcohol. Mallory –weiss tear- usually caused by severe retching & vomiting whereby a tear occurs in esophageal mucosa at junction of esophagus & stomach-severe blding. Esophageal varices usually secondary to cirrhosis- vessels are inelastic & engorged due to increased prssure of portal hypertension.; coughing, sneezing , vomiting can cause massive blding. Blding ulcers stomach & duoedeum accounts for majority of Upper GI bleeds. Erosion bld vessels .most blding ulcers due to H.pylori or drug use.(aspirin, NSAIDS cause irritation & disrupt mucosal barrier. Stress ulcers after severe burn, trauma, major surgery.

79 Upper GI Bleed: Emergency Assessment & Management
Immediate physical exam VS Q mins., capillary refill, check distension neck veins Abdominal exam (BS) & Resp assessment Labs- CBC, E+, PT, PTT, liver enzymes, ABG’s Assess stool, vomit bld. UA & specific gravity Start 2 IV’s (Bld & fluid replacement R/L) O2 & meds as ordred Foley indwelling (accurate measures urine ) May have Central line inserted (measure venous pressures) NG tube (mouth) removes bld from stomach & alleviates need to vomit & gastric lavage H2O or saline Some prefer endoscopy to NG 80-85% massive bld stop spontaneously. UA (tells presence bld.) & specific gravity (hydration status) gastric lavage H2O or saline so to ensure that blood will not interfere with emergency endoscopic visualization of gastric mucosa. Instill cc water or NS leave in several mins and allow gravity or low suction to drain- may repeat every mins. Administer drugs during endoscopy- epinephine –produce tissue edema & pressure on source of blding.

80 Diagnosis Upper GI Bleed
Endoscopy- identifies specific source bleeding. Angiography-when endoscopy not done. Invasive procedure catheter placed into gastric or superior mesenteric artery & advanced until site discovered. Barium Contrast- used after acute phase blding to detect lesion can’t verify blding source. Endoscopy- bleeding from severe gastritis can be determined from gastric or dueodenal ulcer by skilled Dr.

81 Nursing Management: Upper GI Bleeding
Accurate & thorough assessment VS History drugs, ulcers, previous bleeds, varcies Approach calm manner acute phase bleed Start IV I/O measurements draw bloods Administer meds as ordered

82 Nursing Diagnosis Upper GI Bleed
Fluid volume deficit re: acute loss blood Ineffective tissue perfussion re: loss circulatory volume Anxiety re: upper GI bleed, uncertain outcome Risk of aspiration re: active blding & altered LOC Decreased cardiac output re: loss of blood

83 Peptic Ulcer Disease

84 Peptic Ulcer Disease Condition characterized by erosion of GI mucosa resulting from the digestive action of HCL acid & pepsin. Can occur in any portion of GI tract comes in contact with gastric secretions Lower esophagus, stomach, duodenum, or jejunum after surgical procedure (gastroenterostomy) 10% males & 4% women will have ulcers during their lifetime An open sore/raw area in the lining of the upper part of the small intestine or the stomach Ulcers develop when an imbalance occurs between the digestive juices used by the stomach to breakdown food and the various factors that protect the lining of the stomach and the duodenum

85 Gastric Ulcer duodenal ulcer stress ulcer
Gastric –occur any portion stomach, more common lesser curvature close to the pylorus Duodenal-80% of ulcers, associated with high HCL acid secretion, mostly occur duodenum Stress Ulcers; Most occur in the proximal portion of the stomach. Often a result of medical crisis or trauma such as head injury, burn, respiratory failure, shock, or septic state. Gastric Ulcer duodenal ulcer

86 Peptic Ulcers In order for pepsin and HCL acid to cause damage to the stomach, the stomach defense system must be altered or damaged.

87 Facts Relating To Peptic Ulcers
Peptic ulcer Disease (PUD) is the most common stomach disorder. Peptic Ulcers are responsible for up to 50% of all upper GI bleeding episodes PUD is a chronic disorder

88 Types Peptic Ulcers: Acute- superficial erosion & minimal inflammation of mucosa. Short in duration & resolves quickly when cause identified & removed. Chronic-long duration, eroding through muscular wall & formation fibrous tissue. Gastric –occur any portion stomach, more common lesser curvature close to the pylorus. Duodenal-80% of ulcers, associated with high HCL acid secretion, mostly occur duodenum Stress – Most occur in the proximal portion of the stomach. Often a result of medical crisis or trauma such as head injury, burn, respiratory failure, shock, or septic state. depending on degree of mucosal involvement acute or chronic Chronic ulcer-present for many months or intermittently thurought a person’s life. 4X more common than acute.

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90 Pathophysiology Peptic Ulcer disease
Caused by breakdown gastric muscosal barrier Acid back up resulting in diffusion into mucosa Destruction of mucosal cells Increase acid & pepsin release Further mucosal erosion, destruction blood vessels, bleeding, ulcerations , H-pylori: most common cause NSAIDs (Aspirin especially) Second leading cause of Peptic Ulcers Long-term use of NSAIDS is the second most common cause of peptic ulcers Common NSAIDS are aspirin, ibuprofen (advil), naproxen. NSAIDS are weak acids and non-ionized gastric pH NSAIDS reduce pain and inflammation by blocking an enzyme called cyclooxygenase (COX), which is involved in the production of prostaglandins. NSAIDS inhibit prostaglandins production, causing several changes in the gastric microenvironment leading to the breakdown of mucosal defense mechanisms Result in ulcer and Gastrointestinal bleeding Gastinoma (Zollinger-Ellison Syndrome)- duodenal ulcers a rare condition characterized by severe peptic ulcers, gastric acid secretion, elevated serum gastrin levels and gastroma pancreas or duodenum. Stress – impair wound healing, delay gastric motility.

91 Pathophysiology con’t
Drugs, aspirin, NSAIDs, Ischemia Gastinoma (Zollinger-Ellison Syndrome) Severe Stress Alcohol Radiation/chemo Bacterial or Viral Infection (H-pylori)

92 Helicobacter Pylori Most common cause of Peptic Ulcers
A short, spiral-shaped, microaerophillic gram-negative bacillus Live in the mucus layer of the stomach Secrete proteins that interact with the stomachs epithelial cells and attract macrophages and neutrophils cells that cause inflammation Secrete toxins that contribute to the formation of Peptic Ulcers Destruction of gastric mucosa by noxious agents such as drugs or smoking maybe enhanced by the presence of H-pylori, further promoting gastric mucosal destruction. Present in 70% of patients with gastric ulcers and 95% of patients with duodenal ulcers. Not usually associated with esophageal ulcers.

93 H-Pylori

94 Zollinger-Ellison Syndrome
The third leading cause of peptic ulcers A tumor in the pancreas produce excessive amounts of gastrin, a hormone that stimulates gastric acid formation Zollinger-Ellison syndrome is a disorder where increased levels of the hormone gastrin are produced, causing the stomach to produce excess hydrochloric acid. Often the cause is a tumor (gastrinoma) of the duodenum or pancreas producing the hormone gastrin. Gastrin then causes an excessive production of acid which can lead to peptic ulcers in almost 95% of patients.

95

96 Signs & Symptoms: Peptic Ulcers Disease
Anemia (Fatique, dyspnea) GI bleeding Dyspepsia – encompasses a wide variety of problems in the upper abdomen/epigastric dysfunction after meals. Pain Discomfort Bloating Nausea Heartburn Regurgitation Belching

97 Gastric Ulcers Commonly located lesser curvature close to pylorus
Normal to low secretion gastric acids but back diffusion of acid is greater (than with duodenal ulcers) Can be acute or chronic H-pylori 50-70% of patients NSAIDS, aspirin & corticosteroids cause acute gastric ulcers Chronic alcohol abuse, smoking Mortality rate gastric ulcer greater than duodenal ulcers due to peak incidence occurs in persons over 50. More common people of lower socioeconomic class & manual or unskilled workers more proned to than executives. Therefore the critical pathologic process in gastric ulcers may not be the amount of acid that is secreted but the amount that is able to penetrate the mucosal barrier Smoking- nicotine enhances reflux of duodenal contents into the antrum of the stomach.

98 Duodenal Ulcers Most common of all peptic ulcers
Associated with high acid secretion Increased risk with COPD, cirrhosis, chronic pancreatitis, CRF, Zollinger-Ellison Syndrome, alcohol & heavy smoking. H-pylori identified 90-95% Persons with blood type O have an increased incidence (genetic etiology) Develop in anyone regardless of socioeconomic factors 35-45 years of age, more men affected but steadily rising in women alcohol & heavy smoking: stimulates acid secretion Research is saying that not all people with H-pylori go to develop duodenal ulcers suggesting that additional factors are needed. H-pylori- survives in human Gi tract for a long time as a result of its ability to move in mucous & attach to mucosal cells. In addition it secretes urease which buffers the area around the bacterium & protects it from desrtuction in an acidic environment. Though that H-pylori occurs during childhood via transmission from family members possibly thru oral-fecal route or oral-oral route.

99 Stress Ulcers Acute ulcers
Develop following major physiologic insult trauma or surgery Form of erosive gastritis Gastric muscosa undergoes a period of transient ischemia in association of hypotension, severe injury, extensive burns & complicated surgery multiple superficial erosions may bleed Risk factors for developing stress ulcers bleeding, resp failure & coagulopathy Ischemia- due to decreased capillary bld flow or shunting bld.away from GI tract so that bld bypasses gastric mucosa.

100 Medications Antacids ( Maalox, Mylanta) -Neutralizes gastric acidity
H2 Receptor Antagonists (Pepcid, Zantac) – Inhibits acid secretion Proton Pump Inhibitors (Prevacid) – Inhibits the mechanism that pumps acid into stomach Gastrointestinal Agents (Carafate) – Prevent relapse Prostaglandins (Cytotec) – Prevention in Pt’s taking NSAIDS and may be used with NSAIDS in Pt’s at a high risk of complications

101 QUESTION What factors do you think the nurse should consider when conducting a nursing assessment of a client suspected of a peptic ulcer?

102 Patient Assessment Age & Sex Occupation/daily stressors
Diet- including caffeine and alcohol intake Use of Tobacco Medical and family History Medications History of when GI upset and pain occur

103 Three major Complications Peptic Ulcer Disease
Hemorrhage- most common complication. Erosion of granulation tissue at base of ulcer during healing or erosion through a major blood vessel- mostly duodenal Perforation- most lethal peptic ulcer. Large penetrating duodenal ulcers have not healed & posterior mucosal wall Gastric outlet obstruction- ulcers antrum & pyloric areas stomach & duodenum cause predisposition Narrowing pylorus due to edema, inflammation & spasms Long hx ulcer pain Relief from belching or self-induced vomiting (projectile) Hemorrhage-Most common complication duodenal ulcers Occurring 15-20% of clients Vomits bright red or coffee-ground blood (hematemesis) Black, tarry stool (melena) Occur most often in gastric ulcers and elderly Perforated gastric ulcers located lesser curvature of stomach. Even though duodenal ulcers perforate more freq., mortality rates are higher in gastric ulcers. Perforation: Most common complication Gastric Outlet obstruction-Occurs when the area surrounding the pylori sphincter becomes narrowed and stenosed b/c a scar tissue, edema, or muscle spasm. Manifested by vomiting caused by stasis and gastric dilation See swelling in upper abd, loud peristalsis & visible periistaltic waves paaing thru abd from left to right.

104 Interventions Hemorrhage
Npo, IV Note changes in V/S NG maintain patency Assess abd distension infers blocked NG CBC- hgb & hct Administer meds as ordered IV

105 Interventions Perforation
Assessment sudden severe, severe abd pain Rigid, boardlike abd, severe generalized abd & shoulder pain, drawing up knees BS may diminish & become absent Q 15 min V/S Npo, IV Patient allergies know Initiate A/B Prep for surgery

106 Interventions for Outlet gastric Obstruction
Insert NG tube and prepare for iced saline lavage Prepare for surgery protocol Monitor vitals Arrange Hemoglobin and Hematocrit evaluation – determines blood loss status Withhold all oral foods and fluids –prepares bowel for surgery, decreases stimulus to the area

107 Diagnostic Tests Endoscopy-view entire gastric & duodenal mucosa, determine degree healing after Rx, tissue specimens (H.pyloir, ca) Cytology (H-pylori, CBC, liver enzymes, serum amylase) U/A & stool specimens (blood) Urea breath test Upper GI Series ( Barium swallow)- beneficial Dx gastric outlet obstruction Gastric analysis Dx measures depends upon presence & location of peptic ulcer Cytology: IgG, serum or whole bld antibody tests called IgG % sensitive H-Pylori. Urea breath test- determines presence active infection H_Pylori as urea byproduct of H-pylori metabolism ( Barium swallow)- are not accurate although widely used as barium fails to fill the ulcer craters. X-rays are also ineffective as in differientiating peptic ulcer from ca. Dx gastric outlet obstruction – 50% barium remains on follow-up fils 6 hours later. Gastric analysis- identifying Zollinger-Ellision Syndrome, degree gastric hyperacidity & evaluate results of therapy. Amylase- ordered for info. Pancreatic function in pts whom posterior penetration pancreas suspected.

108 QUESTION What are the main nursing diagnosis related to a client diagnosed with a peptic ulcer?

109 NURSING DIAGNOSIS Pain Potential for hemorrhage perforation
obstruction Constipation/ Diarrhea Potential altered health maintenance

110 Diagnosis cont’d Constipation/Diarrhea r/t effects of medication on bowel function Potential altered health maintenance r/t lack of knowledge of disease process, contraindications, S&S of complications, and treatment regimen

111 PAIN R/T GASTRIC & MUCOSAL INJURY
As manifested by : Epigastric to left upper quadrant Frequently described as burning May radiate to the back Usually occurs 1-5 hr after meals May be related by food, antacids (Duodenal), or vomiting (Gastric)

112 Intervention for Pain Administer antacids, anticholinergics, H2 blockers as directed by physician Encourage lifestyle changes such as diet, exercise, stress, smoking, alcohol, caffeine, etc. Teach rationale avoiding OTC drugs (aspirin) Antibiotics for H-Pylori Goals: Expected to experience a reduction or alleviation of pain after treatment Experience no complications of PUD

113 Nutrition PUD Have small and more frequent meals
Important! Have small and more frequent meals Avoid drinking liquids with meals Refrain from skipping meals Eliminate caffeine and alcohol Abstain from hot ,spicy foods If a smoker, QUIT Encourage client to use relaxation techniques such as yoga, biofeedback, exercise, humor, and imagery Nurses assess clients stressors in life

114 Surgery Ulcer surgery is a procedure used to cure PUD when medications and other interventions have failed Used to relieve a present PUD and to prevent recurrence Surgery is indicated : Perforated and overflowed into the abdomen Scarring or swelling causing bowel obstruction Acute bleeding Defied all other types of treatments Less than 20% clients require surgery. Also there is high recurrence rate duodenal & gastric ulcersIntractability: failure of ulcer to heal or recurrence after therapy Hemorrhage or increased risk blding during Rx Pyloric ulcers Concurrent condition severe burns, trauma or sepsis Multiple ulcer sites Drug-induced ulcers Possible existence of malignant ulcer obstruction

115 Types of Surgery PUD Vagotomy: Cutting of vagus nerve (decreases gastric motility & gastric emptying) Pyloroplasty: To widen the exit of the pylorus and facilitates emptying of stomach contents, done post vagotomy. Billroth I: (Gastroduodenostomy) – The distal portion of the stomach is removed and the remainder is anastomosed to the duodenum. Billroth II (Gastrojejunostomy) – The lower portion of the stomach is removed and the remainder is anastomosed to the jejunum

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117 Surgery Cont’d Total Gastrectomy
remove the stomach from the level of the lower esophagus to the jejunum Gastric cancer

118 Total Gastrectomy

119 Post-op Complications
Effects of surgery: Dumping syndrome Reoccurrence Reflux gastritis: prolonged contact with bile causes damage to gastric mucosa. Delayed gastric emptying Dumping syndrome: occurs commonly after Billroth –meals having a hyperosmolar composition. N gastric chyme enters the small intestine in small amounts & shifts fld from extracellular space is minimal. However, after stomach surgery the stomach no longer has control over amt chyme entering small intestine. Therefore, a large bolus hypertonic fluid enters the intestine & results in fluid being drawn into the bowel lumen, causing a decrease in plasms volume. Approx 1/3 to ½ clients with PU surgery have. End of meal or 15-30mins generalized weakness, sweating, palpitations & dizziness., abd cramping, increased peristalsis & urge to defecate. Lasts an hour after meal Reflux gastritis- prolonged contact with bile causes damage to gastric mucosa. After a meal: V. Questran po med binds with bile salta seems to help.

120 Dumping Syndrome

121 Read on Gastric cancers:
Clinical manifestations Nursing care Food Poisoning Next Class: Lower GI


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