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Presentation on theme: "PROF.DR/ MAGD ABD EL-AZIZ"— Presentation transcript:


2 Outlines Introduction The Gastrointestinal Tract
How to Diagnose Gastrointestinal Problems Common GIT disorders: Hernia Oral cancer Peritonitis GERD Intestinal obstruction Hital hernia Hemorrhoids Gastritis Hepatitis Peptic ulcer disease Liver cirrhosis Upper GIT bleed Assessment & management of gastrointestinal disorders

3 Objectives At the end of this presentation the audience will be able to: Identify how to Diagnose Gastrointestinal Problems Determine Common GIT disorders such as; oral cancer, GERD, peptic ulcer,……. Apply Assessment & management of gastrointestinal disorders

4 Introduction It is estimated that some form of digestive disorder affects more than 100 million people in America. That is more than half of the U.S. population. (WHO ,2009) For some people, digestive disorders are a source of irritation and discomfort that may cause them to drastically limit their lifestyles and to frequently miss work. For others, the disorders may be extremely crippling and even fatal.

5 The Gastrointestinal Tract
The gastrointestinal tract (GIT) is a long muscular tube that functions as the food processor for the human body. The digestive system includes the following organs: Upper GIT (mouth, esophagus stomach and duodenum) . Accessory digestive organs (Gallbladder, liver, and pancreatic) . Lower GIT.

6 How to Diagnose Gastrointestinal Problems
Physical examination Endoscopy: by use a small camera to look at the lining of stomach, esophagus and initial part of small intestine. The camera inserts into mouth and progresses down the gastrointestinal tract. Fluoroscopy : to examine the moving body structures. This procedure consists of an x-ray which shows the body area being examined and projects images onto a monitor so the physician can observe the movements of the stomach, duodenum and esophagus.

7 (ERC) Endoscopic retrograde cholangiopancreato graph :can examine any problems with gallbladder, liver and pancreas. patient swallow the scope, and the doctor directs a camera to the spot where the ducts to the pancreas open into the duodenum. Then injects dye into the ducts to visualize the area and determine a course of treatment. liver biopsy: If patient have any issues with liver take biopsy to examine tissue and assess if there is any disease. This usually occurs after blood tests indicate a potential problem with liver. Fecal analysis : Fecal content is an indicator of the absorptive capacity of the gut

8 D-Xylose absorption test : D-Xylose, a monosaccharide, is absorbed in the small intestine and is used to assess malabsorption The client receives nothing by mouth (NPO) for 10 to 12 hours before the test. A blood sample and first-voided morning urine specimen are collected. After oral administration of a known quantity of D-Xylose mixed in water, blood and urine levels of D-Xylose are measured

9 Bernstein test (Esophageal acidity, esophageal manometry, acid perfusion): is measured to diagnosis problems of the lower esophageal sphincter and chronic reflux esophagitis. A catheter with a pH electrode is inserted into the esophagus through the mouth Barium swallow: To diagnosis esophageal varices, inflammation, ulcerations, hiatal hernia, foreign bodies, polyps, diverticula, and tumors of the esophagus, stomach, and duodenal bulb Client will drink ounces of a chalky liquid (barium sulfate before the exam and observing the movement of a contrast medium with a fluoroscope

10 Magnetic resonance imaging (MRI): To identify source of gastric bleeding
Gastric analysis: To evaluate gastric secretions and detect an increase or decrease of free hydrochloric acid ( fasting: mEq/per hour To conduct the gastric analysis, a nasogastric tube is inserted into the stomach and specimens are aspirated to evaluate gastric acidity

11 Common GIT disorders Hernia Oral cancer Peritonitis GERD
Intestinal obstruction Hital hernia Hemorrhoids Gastritis Hepatitis Peptic ulcer disease Liver cirrhosis Upper GIT bleed

12 Oral cancer Uncommon (5% of all cancers) but has high rate of morbidity, mortality. Highest among males over age 40. Risk factors include smoking and using oral tobacco, drinking alcohol, marijuana use, occupational exposure to chemicals

13 Pathophysiology Squamous cell carcinomas
Begin as painless oral ulceration or lesion with irregular, ill-defined borders Lesions start in mucosa and may advance to involve tongue, oropharynx, mandible, maxilla Non-healing lesions should be evaluated for malignancy after one week of treatment

14 Diagnosed by biopsy, CT, MRI
Based on age, tumor stage, general health and client’s preference, treatment may include surgery, chemotherapy, and/or radiation therapy Advanced carcinomas may necessitate radical neck dissection with temporary or permanent tracheostomy.

15 Gastroesophageal Reflux Disease (GERD)
GERD is the backward flow of gastric content into the esophagus common, affecting 15 – 20% of adults 10% persons experience daily heartburn and indigestion symptoms may mimic other illnesses including heart problems because of location near other organs

16 Gastroesophageal reflux results from transient relaxation or incompetence of lower esophageal sphincter, or increased pressure within stomach which may result from: Increased gastric volume (post meals) Position pushing gastric contents close to gastroes-ophageal juncture (such as bending or lying down) Obesity or tight clothing Hiatal hernia

17 Manifestations Heartburn after meals, while bending over, or recumbent
May have regurgitation of sour materials in mouth, pain with swallowing Atypical chest pain Sore throat with hoarseness voice Bronchospasm and laryngospasm



20 Diagnostic Tests Barium swallow (evaluation of esophagus, stomach, small intestine) Upper endoscopy: direct visualization; biopsies may be done 24-hour ambulatory pH monitoring Esophageal manometry, which measure pressures of esophageal sphincter and peristalsis Esophageal motility studies

21 Medications Antacids for mild to moderate symptoms, e.g. Maalox, Mylanta, Gaviscon H2-receptor blockers: decrease acid production; e.g. cimetidine, ranitidine, famotidine, nizatidine Proton-pump inhibitors: reduce gastric secretions, promote healing of esophageal erosion and relieve symptoms, e.g. omeprazole (prilosec); lansoprazole (Prevacid) initially for 8 weeks; or 3 to 6 months Promotility agent: enhances esophageal clearance and gastric emptying, e.g. metoclopramide (reglan)

22 Dietary and Lifestyle Management
Elimination of acid foods (tomatoes, spicy, citrus foods, coffee) Avoiding food which relax esophageal sphincter or delay gastric emptying (fatty foods, chocolate, peppermint, alcohol) Maintain ideal body weight Eat small meals and stay upright 2 hours post eating; no eating 3 hours prior to going to bed Elevate head of bed on 30 degree to decrease reflux No smoking Avoiding bending and wear loose fitting clothing

23 Hiatal Hernia Part of stomach protrudes through the esophageal (hiatus of the diaphragm into thoracic cavity). Sliding hiatal hernia :gastro esophageal junction and funds of stomach slide through the esophageal hiatus Para esophageal hiatal hernia: the gastro esophageal junction is in normal place but part of stomach herniated through esophageal hiatus


25 Predisposing factors include:
Increased intra-abdominal pressure Increased age Trauma Congenital weakness Forced recumbent position Manifestations: Similar to GERD Diagnostic Tests Barium swallow Upper endoscopy Treatment surgery; usually Nissen fundoplication by thoracic or abdominal approach Anchoring the lower esophageal sphincter by wrapping a portion of the stomach around it to anchor it in place

26 Nissen fundoplication

27 Gastritis Inflammation of stomach lining from irritation of gastric mucosa Types Acute Gastritis: Disruption of mucosal barrier allowing hydrochloric acid and pepsin to have contact with gastric tissue: leads to irritation, inflammation, superficial erosions Progressive disorder beginning with superficial inflammation and leads to atrophy of gastric tissues

28 Causes Irritants include aspirin and other NSAIDS, corticosteroids, alcohol, caffeine Ingestion of corrosive substances: alkali or acid Effects from radiation therapy, certain chemotherapeutic agents Manifestations Mild: anorexia, mild epigastric discomfort, belching More severe: abdominal pain, nausea, vomiting, hematemesis, melena Erosive: not associated with pain; bleeding occurs 2 or more days post stress event If perforation occurs, signs of peritonitis

29 Diagnostic Tests Gastric analysis: assess hydrochloric acid secretion Hemoglobin, hematocrit, red blood cell indices: anemia including pernicious or iron deficiency Serum vitamin B12 levels: determine pernicious anemia Upper endoscopy: visualize mucosa, identify areas of bleeding, obtain biopsies; may treat areas of bleeding with electro or laser coagulation or sclerosing agent

30 Peptic Ulcer Break in mucous lining of GI tract comes into contact with gastric juice often involves the deeper structures of the upper gastrointestinal tract e.g., esophagus, stomach, duodenum, or jejunum Common in smokers, users of NSAIDS; familial pattern, alcohol, cigarettes

31 Pathophysiology Ulcers or breaks in mucosa of GI tract occur with H. pylori infection (spread by oral to oral, fecal-oral routes) damages gastric epithelial cells reducing effectiveness of gastric mucus Use of NSAIDS: interrupts prostaglandin synthesis which maintains mucous barrier of gastric mucosa Chronic with spontaneous remissions and exacerbations associated with trauma, infection, physical or psychological stress

32 Acid secretion Gastric acid secreted by the parietal cell in the fundus at the stomach in response to: Gastrin (secreted by cells in the pyloric region ) Acetylcholine (cholinergic action of the vagus nerve) Histamine (found in cells throughout the gastric mucosa Diagnosis Endoscopy with cultures Looking for H. Pylori Upper GI barium contrast studies EGD-esophagogastroduodeno scopy Serum and stool studies

33 Stomach structure

34 Sites of ulcer

35 Peptic ulcer

36 Manifestation Pain is classic symptom: gnawing, burning, aching hunger like in epigastric region possibly radiating to back; occurs when stomach is empty and relieved by food (pain: food: relief pattern) Symptoms less clear in older adult; may have poorly localized discomfort, dysphagia, weight loss Complication: GI hemorrhage or perforation of stomach or duodenum

37 Treatment Rest and stress reduction Nutritional management
Pharmacological management Histamine blockers (Tagamet, Zantac, Axid) Blocks gastric acid secretion Carafate Forms protective layer over the site Mucosal barrier enhancers (colloidal bismuth, prostoglandins) Protect mucosa from injury Antibiotics (Amoxicillin):Treat H. Pylori infection

38 Surgical intervention
NG suction Surgical intervention 1. Minimally invasive gastrectomy Partial gastric removal with laproscopic surgery 2. Bilroth I and II Removal of portions of the stomach 3. Vagotomy Cutting of the vagus nerve to decrease acid secretion 4.Pyloroplasty Widens the pyloric sphincter 5.Gastrectomy (roux-en-y) Remove antrum

39 Bilroth I

40 Bilroth II

41 Bilroth I & Bilroth II

42 Vagotomy

43 Pyloroplasty

44 Gastrectomy

45 Complications Hemorrhage: hematemesis, melena, hematochezia (blood in stool) weakness, fatigue, dizziness, orthostatic hypotension and anemia Gastric outlet (pyloric sphincter) obstruction: edema surrounding ulcer blocks GI tract from muscle spasm or scar tissue leads to feelings of epigastric fullness, nausea, worsened ulcer symptoms

46 Perforation: ulcer erodes through mucosal wall and gastric or duodenal contents enter peritoneum leading to peritonitis; chemical at first (inflammatory) and then bacterial in 6 to 12 hours with the following: 1.severe upper abdominal pain radiating throughout abdomen and possibly to shoulder 2.Abdomen becomes rigid, board like with absent bowel sounds; symptoms of shock 3.Older adults may present with mental confusion and non-specific symptoms

47 Upper GI Bleed Mortality approx 10%
Predisposing factors include: drugs, esophageal varacies, esophagitis, peptic ulcer diseases, gastritis and carcinoma Diagnosis History Blood, stool, vomitus studies Endoscopy

48 Signs and Symptoms Coffee ground vomitus Black, tarry stools Melena
Decreased B/P Vertigo Drop in Hct, Hgb Confusion syncope

49 Crystalloids- normal saline Blood transfusions NG lavage
Treatments Volume replacement Crystalloids- normal saline Blood transfusions NG lavage Endoscopic treatment of bleeding ulcer Sclerotheraphy-injecting bleeding ulcer with necrotizing agent to stop bleeding Sengstaken-Blakemore tube Used with bleeding esophageal varacies

50 Sengstaken-Blakemore tube
A tube used for the tamponade of bleeding esophageal varacies. It has three separate small tubes; One leads to a balloon inflated in the stomach, to keep the instrument in place and compress the vessels around the cardia; The second leads to a long narrow balloon that exerts pressure against the wall of the esophagus; The third is attached to a suction apparatus for aspirating the contents of the stomach.

51 Sengstaken-Blakemore tube

52 Hernia It is an abnormal protrusion of the intestine or other abdominal organ through a weakness or defect in the musculature into another cavity. Hernia is the protrusion of an organ or tissue out of the body cavity in which it normally lies. Caused by a congenital or acquired abdominal muscle weakness as Obesity, Pregnancy, or Occupations that involve heavy lifting

53 Pathophysiology: Muscles play an important role in keeping the abdominal organ in place. Increased intra-abdominal pressure with presence of abdominal muscle weakness allows a portion of intestine to push through the abdominal wall. Intra-abdominal pressure may increase due to lifting heavy objects, coughing, straining, pregnancy, and tumor

54 Ventral or incision hernia
Classification of Hernia: Reducible hernia: slips back into the abdominal cavity with gentle pressure or when the patient lies on his/her back. Irreducible hernia: is trapped and unable to be replaced in a normal position, and sometimes called incarcerated hernia Types of Hernia: Inguinal hernia. Femoral hernia. Umbilical hernia. Ventral or incision hernia

55 Inguinal hernia


57 Femoral hernia

58 Umbilical hernia

59 Ventral or incision hernia

60 Surgical repair of hernias is usually recommended even if they are reducible. Two surgical procedures are used to repair hernias 1. Herniorrhaphy: Surgical repair of the hernia through ligation and removal of the hernia defect 2. Hernioplasty: Surgical repair of the hernia with reinforcement of the weakened musculature with fascia or a Dacron mesh.

61 Hernioplasty & Herniorrhaphy

62 Peritonitis Inflammation of peritoneum lining
Enteric bacteria enter the peritoneal cavity through a break of intact GI tract (e.g. perforated ulcer, ruptured appendix) Causes include: Ruptured appendix Perforated bowel secondary to DU Gangrenous gall bladder Ulcerative colitis Trauma Peritoneal dialysis

63 Pathophysiology Peritonitis results from contamination of normal sterile peritoneal cavity with infections or chemical irritant Release of bile or gastric juices initially causes chemical peritonitis; infection occurs when bacteria enter the space Bacterial peritonitis usually caused by these bacteria (normal bowel flora): Escherichia coli, Klebsiella, Proteus, Pseudomonas Inflammatory process causes fluid shift into peritoneal space leading to hypovolemia, then septicemia

64 Manifestations Depends on severity and extent of infection, age and health of client Presents with “acute abdomen” -Abrupt onset of diffuse, severe abdominal pain - Pain may localize near site of infection (may have rebound tenderness) - Intensifies with movement Entire abdomen is tender with board like guarding or rigidity of abdominal muscle

65 Decreased peristalsis leading to paralytic ileus, bowel sounds are diminished or absent with progressive abdominal distention, pooling of GI secretions lead to nausea and vomiting Systemically: fever, malaise, tachycardia and tachypnea, restlessness, disorientation, oliguria with dehydration and shock

66 Diagnostic Tests WBC with differential: elevated WBC to 20,000 Blood cultures: identify bacteria in blood Liver and renal function studies, serum electrolytes: evaluate effects of peritonitis Abdominal x-rays: detect intestinal distension, air-fluid levels, free air under diaphragm (sign of GI perforation) Diagnostic paracentesis

67 Medications Antibiotics 1.Broad-spectrum before definitive culture results identifying specific organisms causing infection 2.Specific antibiotics treating causative pathogens Analgesics Intravenous fluids and electrolytes to maintain vascular volume and electrolyte balance with NPO Bed rest in Fowler’s position to localize infection and promote lung ventilation Intestinal decompression with nasogastric tube or intestinal tube connected to suction

68 Surgery Laparotomy to treat cause (close perforation, removed inflamed tissue) Peritoneal Lavage: washing out peritoneal cavity with copious amounts of warm isotonic fluid during surgery to dilute residual bacterial and remove gross contaminants Often have drain in place and/or incision left unsecured to continue drainage

69 Intestinal obstruction
Normal function of the small and large intestine depends on the presence of an open lumen or passageway for the movement of contents; as well as adequate circulation and nervous innervations to sustain normal peristalsis; any factors or condition that either narrow that intestinal passageway or interfere with peristalsis can result intestinal obstruction.

70 Intestinal obstruction

71 Types of intestinal Obstruction
Mechanical intestinal obstruction: Which accounts for 90% of intestinal obstruction Non- mechanical Intestinal obstruction

72 Mechanical obstruction
Adhesion: is the most common small bowel obstruction after abdominal surgery for unknown reasons; perhaps related to inflammatory responses in the healing bowel. Hernias: if the abdominal wall defect through which the hernia protrudes becomes so tight that the bowel segment becomes strangulated Tumor or neoplasm Valvulus:A twisting of the bowel upon it self.

73 Non-mechanical May result from neuro-muscular or vascular disorder:
Paralytic illus: result a lack of neurogenic impairment, It is a common temporary problem after abdominal surgery; particularly if the bowel has been handled. Mesenteric vascular occlusion infarction: The most common causes are emboli and atherosclerosis of mesentic arteries

74 Clinical manifestation
Small intestine Large intestine onset Rapid Gradual vomiting Frequent Rare Pain Colic & cramping Cramping & abdominal pain Bowel Intermittent feces for short time Absolute constipation Abd. distension Minimally increased Greatly increased

75 Diagnosis History and physical examination Abdominal X-rays show the presence of gas and fluid in the intestine Barium enemas: Are helpful in locating large intestinal obstruction but not used when performing is suspected Colonoscopy Laboratory test: CBC, serum electrolyte, blood urea nitrogen then stool should be checked for occult blood

76 Hemorrhoids Are enlarge veins located within tissues of the lower portion of the rectum or anus.

77 Types of hemorrhoid 1. External hemorrhoids :Occur below the anal sphincter. And can be detected by the affected person. consists of small lumps of fibrous tissue and folds of anal skin that been stretched bulging of the hemorrhoid. 2. Internal hemorrhoids Those that occur above the anal sphincter. Are not directly apparent to the person unless they become so large that they prolepses through the anus


79 Surgical management Sclerotherapy :The injection method can be effective for small, bleeding internal hemorrhoids. A sclerosing solution such as 5% phenol in oil is injected into the sybmucous areolar tissue in which the hemorrhoid vein lie. It consider palliative and not curative, and injection may be required in the future



82 Cryosurgery: hemorrhoidectomy involves freezing hemorrhoidal tissue through a probe that carries liquid nitrogen are another agent for a sufficient time to cause tissue necrosis Ligation: Internal hemorrhoid may be treated by ligation with latex bands. The hemorrhoid is grasped with forceps and pulled down into a special instrument that, when the trigger handle is pressed, slips a latex band over it. The band constrict the circulation and cause necrosis Hemorrhoidectomy

83 Cryosurgery & Ligation

84 Hepatitis The word "hepatitis" means inflammation of the liver and also refers to a group of viral infections that affect the liver. The most common types are Hepatitis A, Hepatitis B, and Hepatitis C

85 Types of Hepatitis Hepatitis A (HAV):
HBV is an RNA virus that transmitted through the fecal oral route. It frequently occurs in small outbreaks caused by fecal contamination of food or drinking water by an infected food handler. It found in feces 2 or more weeks before the onset of symptoms and up to 1 week after the onset of jaundice. The virus is present in feces during the incubation period, so it can be carried and transmitted by persons who have undetectable, subclinical infections

86 HBV is a DNA virus is transmitted by Percutaneous
2. Hepatitis B (HBV): HBV is a DNA virus is transmitted by Percutaneous (e.g., IV drug use, accidental needle-stick punctures). Permucosal exposure to: Infectious blood, blood products: Other body fluids (e.g., semen, vaginal secretions, saliva) or other body fluids enter the body of a person who is not immune to the virus. Prenatal transmission from mother to infant can occur. (Approximately 90% of infants infected at birth go on to develop chronic hepatitis B. The HBV can live on a dry surface for at least 7 days.

87 3.Hepatitis C Virus: HCV is an RNA virus that is primarily transmitted percutancously. The major risk factor for infection is direct percutaneous exposure, such as: Injecting drugs, Transfusion infected blood products, Hemodialysis, High-risk sexual behavior (e.g., unprotected sex, multiple partners), Organ transplants, Exposure to blood and blood products by health care workers


89 4. Hepatitis D Virus (Delta virus)
Is a defective single-stranded RNA virus that cannot survive on its own. HDV requires the help function of HBV to replicate. The importance of HDV relates to its clinical virulence. HDV infection can be acquired as a co-infection with HBV

90 5.Hepatitis E Virus (HEV).
It is an RNA virus. It transmitted by the fecal-oral route. The most common mode of transmission is drinking contaminated water. It occurs primarily in developing countries. Epidemiology and clinical course similar to those of hepatitis A virus infection; enteric transmission

91 6.Hepatitis G Virus: The HGV is an RNA virus. Hepatitis G virus (HGV) is a recently recognized although poorly characterized parenterally and sexually transmitted virus. Whether it accounts for all of the forms of hepatitis that are not related to viruses A, B, C, D, or E is not known. It has been found in some blood donors and can be transmitted by transfusion. HGV often coexists with other hepatitis viruses, such as HCV.

92 7. Autoimmune-Hepatitis:
This form of hepatitis is idiopathic; that the cause is unknown. Many of these patients often have a number of systemic problems, including glomerulonephritis and arthritis, the disease is thought to be autoimmune. The presenting signs and symptoms are variable and similar to viral hepatitis. Unlike viral hepatitis, autoimmune hepatitis is treated with corticosteroids or other immunosuppressive agents.

93 Hepatitis may be classified into three phases
1. Preicteric or prodromal phase: It precedes jaundice and lasts from 1 to 21 days. This is the period of maximal infectivity for hepatitis (HAV). Hepatitis B patients who are HBs Ag positive and patients with HCV can be infective for years

94 2. Icteric Phase: It lasts 2 to 4 weeks and is characterized by jaundice. Jaundice results when bilirubin diffuses into the tissues. The urine may darken because of excess bilirubin being excreted by the kidneys. The stool will be light or clay colored, if conjugated bilirubin cannot flow out of the liver because of obstruction or inflammation of the bile ducts.

95 3. Posticteric Phase: The convalescent stage of the posticteric phase begins as jaundice is disappearing and lasts weeks to months, with an average of 2 to 4 months. During this period the patient’s major complaint is malaise and easy fatigability. Hepatomegaly remains for several weeks, but splenomegaly subsides during this period. Relapses may occur and the disappearance of jaundice does not mean the patient has totally recovered

96 Liver Cirrhosis Cirrhosis is a chronic progressive disease of the liver characterized by extensive degeneration and destruction of the liver parenchemal cells. Cirrhosis refers to the chronic, degenerative changes (diffuse fibrotic bands of connective tissue) which distort the liver’s normal architecture. Extensive degeneration and destruction of hepatocytes cell occur

97 Causes of Liver Cirrhosis:
Chronic hepatitis. Repeated exposure to toxic substances. Disease processes (such as sclerosing cholangitis , cancer. Chronic alcohol abuse. Alcohol abuse accounts for most cases of cirrhosis. The most common cause for cirrhosis in Egypt is bilharaziasis

98 Types of Liver Cirrhosis
1.Laennec’ cirrhosis (most common type) It is also called as alcohol induced nutritional or portal cirrhosis. Alcohol has a direct toxic effect on liver cells (hepatocytes), causing inflammation. The liver enlarged, firm and hard in early disease. The liver is smaller and nodular in end-stage disease

99 2. Postnecrotic cirrhosis:
It caused by massive hepatic cell necrosis. It is usually resulting from acute viral hepatitis or exposure to certain hepatotoxins such as industrial chemical 3.Biliary cirrhosis: It caused by chronic billiard obstruction, bile stasis, and inflammation. The liver becomes fibrotic, hepatic cells are destroyed.

100 4.Cardiac cirrhosis: / vascular cirrhosis:
It caused by severe or chronic heart failure. The liver becomes enlarged and congested with venous blood resulting in cell necrosis from anorexia

101 Complications of Cirrhosis:
Portal hypertension. Bleeding esophageal varices. Ascites. Coagulation defects. Jaundice Portal –Systemic Encephalopathy (PSE) with hepatic coma: It is basically a disorder of protein metabolism and excretion

102 Jaundice & Ascites

Assessment: Done through the following History (Health assessment interview) Physical examination Diagnostic tests

104 History (Health assessment interview)
Biographical and demographic data, Current health ; chief complain & symptoms focus on: Nausea & vomiting, Indigestion, Diarrhea Abdominal pain Appetite and weight change Past health history Family health Drug-nutrient interactions.

105 2. Physical examination Inspect and palpate lips and oral mucosa
intolerance of foods that are acidic, spicy, or fatty Regurgitation of acidic gastric juice; increased symptoms when bending over, lying down, or wearing tight clothing; difficulty swallowing. Abdominal assessment including appearance, bowel sounds, and Epigastric tenderness. Chest pain, dysphagia ,coughing or hoarseness Heartburn, presence of bright blood or “coffee-grounds” appearing material in vomitus

106 Drug-nutrient interactions
Possible nutrient interactions Drug class Decreased absorption of calcium, iron, magnesium, zinc Antacids Cephalosporins: increased vitamin K depletion Antibiotics Vitamin K antagonist Anticoagulants Decreased folate and biotin Anticonvulsants Interfere with metabolism of vitamin B6 and B12 Antituberculosis drugs

107 Nonrenal losses of calcium, potassium, water
Cathartics Inhibition of fat digestion and absorption Simvastatin: grapefruit juice may increase drug level Cholesterol-reducing drugs Increased renal loss of potassium, calcium, magnesium, and zinc Diuretics Decreased vitamin B12 absorption H2 blockers Interact with tyramine-containing foods (cheese, smoked fish, wine, yeast) Monoamine oxidase inhibitors

108 Ineffective airway Clearance relate to oral surgery
2. Nursing management Common Nursing diagnosis: Ineffective airway Clearance relate to oral surgery Altered comfortable related to gastritis, acidity as manifested by gastric pain Imbalanced nutrition: less than body requirements related to pain as manifested by anorexia. Impaired skin integrity related to colostomy and surgical incision

109 Deficient fluid volume related to bowel obstruction, vomiting
Disturbed sleep pattern related to upper GIT bleed Knowledge defect related to treatment & long term consequences of GERD problems Excess fluid volume related to liver cirrhosis as manifested by ascites Activity intolerance related to pain and weakness as manifested by inability to perform ADLs Risk for infection related to NGT

110 Ineffective airway Clearance relate to oral surgery as manifested by dyspnea
Out comes Patient will demonstrate an effective respiratory rate, depth, clear airway and expanded chest Intervention Assess respiration for rate, depth, rhythm, and causes of dyspnea Put patient in comfortable position Administer O2 as prescribed Apply suction frequently if patient on ventilator Assess ABG frequently

111 Evaluation Apply chest physiotherapy
Assess secretion color, amount if patient have productive cough Give patient prescribed medication in accurate dose, route and rate. Evaluation Respiratory with normal range, depth with normal ABG and dyspnea relived Patient become comfortable

112 Altered comfortable related to gastritis, acidity as manifested by gastric pain
Out comes Comfortable level maintain. No signs & symptoms of restless and irritable Intervention Use pain scale(0-10) to assessing pain Assess culture and beliefs about pain & pain relief Assess patient pain tolerance Give prescribed analgesics Try to keep patient in comfortable position Eliminate exercise according to patient ability and tolerance

113 Evaluation Patient reports adequate pain control Vital signs within normal No restless or irritability

114 Out comes Intervention
Imbalanced nutrition: less than body requirements related to removal of part of stomach as manifested by weight loss. Out comes Adequate nutrition Body weight maintained within normal Normal serum electrolyte Wound healing improved Intervention Assess patient weight, general appearance Daily weight and measure intake & output Assess hemoglobin, hematocrit, serum albumin, Assess wound healing Prescribed medication giving for nausea, pain before meals

115 Provide patient with favorite foods or have family bring home-prepared feed if patient able to eat to increase patient nutrition intake Keep patient in clean environment away from offensive odors. Keep patient away from spicy and irritant foods Evaluation Patient maintain adequate nutrition Body weight maintained Normal serum albumin and electrolyte

116 Impaired skin integrity related to colostomy and surgical incision
Out comes Good skin and stoma integrity No signs of infection, vital signs within normal Intervention Monitor stoma color it should be pink, beefy red, and moist without cyanosis or bleeding and should extend about 2-3 cm from the abdominal wall Assess stoma function Empty the push when it not too full to avoid leakage. Apply a protective skin barrier under the pouch to prevent

117 Report abnormal assessment findings such as poor stoma color, bulging or retracted stoma, or rash around the stoma. Teach patient to notify health care provider if there is a change in the stoma or if a rash develops in the skin surrounding the stoma. Assess patient knowledge of stoma care, what medications to avoid e.g., laxatives Assess surgical incision for bleeding, redness and drainage at least ever 4 hours. Change dressing as ordered to keep the incision clean and dry to prevent wound infection Evaluation Stoma pink and moist No signs of wound infection.

118 Deficient fluid volume related to bowel obstruction, vomiting
Out comes Fluid balance maintained Vital signs within normal Skin moist, warm and pink Intervention Assess frequent and amount of vomiting. Monitor vital signs especially blood pressure. Monitor and record intake & output. Administer IV fluids as prescribed to replace fluid loss. Assess skin color, temperature, and character at least every 4 hours

119 Measure abdominal girth at least every 8 hours to determine increasing distention and possible fluid sequestering Assess abdomen for bowel sounds and tenderness Evaluation Fluid balanced maintained No signs of dry skin, hypertensive Abdomen soft no increase in girth, bowel sound present.

120 Out comes Intervention
Knowledge defect related to treatment & long term consequences of GERD problems Out comes Able to verbalize lifestyle modification Understand the chronic nature of the disease & long-term consequences Aware of the disease complication & how to deal with it Intervention Teach the importance of eating 4-6 small meals a day & to eliminate foods known to decrease lower esophageal sphincter pressure or cause irritation Instruct patient to avoid lying down after meals

121 Educate patient about medication regimen and possible side effects to improve adherence to medication regimen Use pain scale (0-10) to quantify pain and discomfort. Evaluation Understand the chronic nature of the disease & long-term consequences Patient adapt to lifestyle modification Patient Aware of the disease complication & how to deal with it

122 Activity intolerance related to pain and weakness as manifested by inability to perform ADLs
Out comes Patient will participate effectively in performing activity of daily living Intervention Assess patient ability to tolerate activity Maintain balanced diet Make schedule of activity according to patient ability Monitor vital signs during activity Maintain patient hygiene Evaluation Patient able to perform ADLs

123 Risk for infection related to NGT
Out comes No signs of infection Vital signs within normal Intervention Maintain low intermittent suction Check placement every 4 hours. Monitor skin integrity of nose for insertion site and provide skin care. Monitor bowel sounds Mouth care at least every 2 hours. Evaluation No signs of infection found


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