Presentation on theme: "PROF.DR/ MAGD ABD EL-AZIZ"— Presentation transcript:
1 PROF.DR/ MAGD ABD EL-AZIZ GIT DISORDERSBYSAMAR FALTASUNDERSUPERVISION OFPROF.DR/ MAGD ABD EL-AZIZ
2 Outlines Introduction The Gastrointestinal Tract How to Diagnose Gastrointestinal ProblemsCommon GIT disorders:Hernia Oral cancerPeritonitis GERDIntestinal obstruction Hital herniaHemorrhoids GastritisHepatitis Peptic ulcer diseaseLiver cirrhosis Upper GIT bleedAssessment & management of gastrointestinal disorders
3 ObjectivesAt the end of this presentation the audience will be able to:Identify how to Diagnose Gastrointestinal ProblemsDetermine Common GIT disorders such as; oral cancer, GERD, peptic ulcer,…….Apply Assessment & management of gastrointestinal disorders
4 IntroductionIt 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 includesthe following organs:Upper GIT (mouth, esophagusstomach and duodenum) .Accessory digestive organs(Gallbladder, liver, and pancreatic) .Lower GIT.
6 How to Diagnose Gastrointestinal Problems Physical examinationEndoscopy: 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 malabsorptionThe 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 mouthBarium swallow: To diagnosis esophageal varices, inflammation, ulcerations, hiatal hernia, foreign bodies, polyps, diverticula, and tumors of the esophagus, stomach, and duodenal bulbClient 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 hourTo 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 obstructionHital herniaHemorrhoidsGastritisHepatitisPeptic ulcer diseaseLiver cirrhosisUpper GIT bleed
12 Oral cancerUncommon (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 bordersLesions start in mucosa and may advance to involve tongue, oropharynx, mandible, maxillaNon-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 therapyAdvanced 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 esophaguscommon, affecting 15 – 20% of adults10% persons experience daily heartburn and indigestionsymptoms 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 clothingHiatal hernia
17 Manifestations Heartburn after meals, while bending over, or recumbent May have regurgitation of sour materials in mouth, pain with swallowingAtypical chest painSore throat with hoarseness voiceBronchospasm and laryngospasm
20 Diagnostic TestsBarium swallow (evaluation of esophagus, stomach, small intestine)Upper endoscopy: direct visualization; biopsies may be done24-hour ambulatory pH monitoringEsophageal manometry, which measure pressures of esophageal sphincter and peristalsisEsophageal motility studies
21 MedicationsAntacids for mild to moderate symptoms, e.g. Maalox, Mylanta, GavisconH2-receptor blockers: decrease acid production; e.g. cimetidine, ranitidine, famotidine, nizatidineProton-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 monthsPromotility 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 weightEat small meals and stay upright 2 hours post eating; no eating 3 hours prior to going to bedElevate head of bed on 30 degree to decrease refluxNo smokingAvoiding bending and wear loose fitting clothing
23 Hiatal HerniaPart 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 hiatusPara 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 pressureIncreased ageTraumaCongenital weaknessForced recumbent positionManifestations: Similar to GERDDiagnostic TestsBarium swallowUpper endoscopyTreatmentsurgery; usually Nissen fundoplication by thoracic or abdominal approachAnchoring the lower esophageal sphincter by wrapping a portion of the stomach around it to anchor it in place
27 GastritisInflammation of stomach lining from irritation of gastric mucosaTypesAcute Gastritis: Disruption of mucosal barrier allowing hydrochloric acid and pepsin to have contact with gastric tissue: leads to irritation, inflammation, superficial erosionsProgressive disorder beginning with superficial inflammation and leads to atrophy of gastric tissues
28 CausesIrritants include aspirin and other NSAIDS, corticosteroids, alcohol, caffeineIngestion of corrosive substances: alkali or acidEffects from radiation therapy, certain chemotherapeutic agentsManifestationsMild: anorexia, mild epigastric discomfort, belchingMore severe: abdominal pain, nausea, vomiting, hematemesis, melenaErosive: not associated with pain; bleeding occurs 2 or more days post stress eventIf perforation occurs, signs of peritonitis
29 Diagnostic TestsGastric analysis: assess hydrochloric acid secretionHemoglobin, hematocrit, red blood cell indices: anemia including pernicious or iron deficiencySerum vitamin B12 levels: determine pernicious anemiaUpper endoscopy: visualize mucosa, identify areas of bleeding, obtain biopsies; may treat areas of bleeding with electro or laser coagulation or sclerosing agent
30 Peptic UlcerBreak 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 jejunumCommon in smokers, users of NSAIDS; familial pattern, alcohol, cigarettes
31 PathophysiologyUlcers or breaks in mucosa of GI tract occur withH. pylori infection (spread by oral to oral, fecal-oral routes) damages gastric epithelial cells reducing effectiveness of gastric mucusUse of NSAIDS: interrupts prostaglandin synthesis which maintains mucous barrier of gastric mucosaChronic with spontaneous remissions and exacerbations associated with trauma, infection, physical or psychological stress
32 Acid secretionGastric 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 mucosaDiagnosisEndoscopy with culturesLooking for H. PyloriUpper GI barium contrast studiesEGD-esophagogastroduodeno scopySerum and stool studies
36 ManifestationPain 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 lossComplication: GI hemorrhage or perforation of stomach or duodenum
37 Treatment Rest and stress reduction Nutritional management Pharmacological managementHistamine blockers (Tagamet, Zantac, Axid)Blocks gastric acid secretionCarafateForms protective layer over the siteMucosal barrier enhancers (colloidal bismuth, prostoglandins)Protect mucosa from injuryAntibiotics (Amoxicillin):Treat H. Pylori infection
38 Surgical intervention NG suctionSurgical intervention1. Minimally invasive gastrectomyPartial gastric removal with laproscopic surgery2. Bilroth I and IIRemoval of portions of the stomach3. VagotomyCutting of the vagus nerve to decrease acid secretion4.PyloroplastyWidens the pyloric sphincter5.Gastrectomy (roux-en-y)Remove antrum
45 ComplicationsHemorrhage: hematemesis, melena, hematochezia (blood in stool)weakness, fatigue, dizziness, orthostatic hypotension and anemiaGastric 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 shoulder2.Abdomen becomes rigid, board like with absent bowel sounds; symptoms of shock3.Older adults may present with mental confusion and non-specific symptoms
48 Signs and Symptoms Coffee ground vomitus Black, tarry stools Melena Decreased B/PVertigoDrop in Hct, HgbConfusionsyncope
49 Crystalloids- normal saline Blood transfusions NG lavage TreatmentsVolume replacementCrystalloids- normal salineBlood transfusionsNG lavageEndoscopic treatment of bleeding ulcerSclerotheraphy-injecting bleeding ulcer with necrotizing agent to stop bleedingSengstaken-Blakemore tubeUsed 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.
52 HerniaIt 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 herniaTypes of Hernia:Inguinal hernia.Femoral hernia.Umbilical hernia.Ventral or incision hernia
60 Surgical repair of hernias is usually recommended even if they are reducible. Two surgical procedures are used to repair hernias1. Herniorrhaphy:Surgical repair of the hernia through ligation and removal of the hernia defect2. Hernioplasty:Surgical repair of the hernia with reinforcement of the weakened musculature with fascia or a Dacron mesh.
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 appendixPerforated bowel secondary to DUGangrenous gall bladderUlcerative colitisTraumaPeritoneal dialysis
63 PathophysiologyPeritonitis results from contamination of normal sterile peritoneal cavity with infections or chemical irritantRelease of bile or gastric juices initially causes chemical peritonitis; infection occurs when bacteria enter the spaceBacterial peritonitis usually caused by these bacteria (normal bowel flora): Escherichia coli, Klebsiella, Proteus, PseudomonasInflammatory process causes fluid shift into peritoneal space leading to hypovolemia, then septicemia
64 ManifestationsDepends on severity and extent of infection, age and health of clientPresents with “acute abdomen”-Abrupt onset of diffuse, severe abdominal pain- Pain may localize near site of infection (may have rebound tenderness)- Intensifies with movementEntire 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 vomitingSystemically: fever, malaise, tachycardia and tachypnea, restlessness, disorientation, oliguria with dehydration and shock
66 Diagnostic TestsWBC with differential: elevated WBC to 20,000Blood cultures: identify bacteria in bloodLiver and renal function studies, serum electrolytes: evaluate effects of peritonitisAbdominal x-rays: detect intestinal distension, air-fluid levels, free air under diaphragm (sign of GI perforation)Diagnostic paracentesis
67 MedicationsAntibiotics1.Broad-spectrum before definitive culture results identifying specific organisms causing infection2.Specific antibiotics treating causative pathogensAnalgesics Intravenousfluids and electrolytes to maintain vascular volume and electrolyte balance with NPOBed rest in Fowler’s position to localize infection and promote lung ventilationIntestinal decompression with nasogastric tube or intestinal tube connected to suction
68 SurgeryLaparotomy 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 contaminantsOften 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.
71 Types of intestinal Obstruction Mechanical intestinal obstruction: Which accounts for 90% of intestinal obstructionNon- 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 strangulatedTumor or neoplasmValvulus: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 intestineLarge intestineonsetRapidGradualvomitingFrequentRarePainColic & crampingCramping & abdominal painBowelIntermittent feces for short timeAbsolute constipationAbd. distensionMinimally increasedGreatly increased
75 DiagnosisHistory and physical examinationAbdominal X-rays show the presence of gas and fluid in the intestineBarium enemas:Are helpful in locating large intestinal obstruction but not used when performing is suspectedColonoscopyLaboratory test: CBC, serum electrolyte, blood urea nitrogen then stool should be checked for occult blood
76 HemorrhoidsAre enlarge veins located within tissues of the lower portion of the rectum or anus.
77 Types of hemorrhoid1. 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 managementSclerotherapy :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 necrosisLigation: 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 necrosisHemorrhoidectomy
84 HepatitisThe 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 byPercutaneous(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 CirrhosisCirrhosis 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 chemical3.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.JaundicePortal –Systemic Encephalopathy (PSE) with hepatic coma: It is basically a disorder of protein metabolism and excretion
103 ASSESSMENT AND MANAGEMENT OF GASTROINTESTINAL DISORDERS Assessment: Done through the followingHistory (Health assessment interview)Physical examinationDiagnostic tests
104 History (Health assessment interview) Biographical and demographic data,Current health ; chief complain & symptoms focus on:Nausea & vomiting, Indigestion, DiarrheaAbdominal painAppetite and weight changePast health historyFamily healthDrug-nutrient interactions.
105 2. Physical examination Inspect and palpate lips and oral mucosa intolerance of foods that are acidic, spicy, or fattyRegurgitation 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 hoarsenessHeartburn, presence of bright blood or “coffee-grounds” appearing material in vomitus
106 Drug-nutrient interactions Possible nutrient interactionsDrug classDecreased absorption of calcium, iron, magnesium, zincAntacidsCephalosporins: increased vitamin K depletionAntibioticsVitamin K antagonistAnticoagulantsDecreased folate and biotinAnticonvulsantsInterfere with metabolism of vitamin B6 and B12Antituberculosis drugs
107 Nonrenal losses of calcium, potassium, water CatharticsInhibition of fat digestion and absorptionSimvastatin: grapefruit juice may increase drug levelCholesterol-reducing drugsIncreased renal loss of potassium, calcium, magnesium, and zincDiureticsDecreased vitamin B12 absorptionH2 blockersInteract with tyramine-containing foods (cheese, smoked fish, wine, yeast)Monoamine oxidase inhibitors
108 Ineffective airway Clearance relate to oral surgery 2. Nursing managementCommon Nursing diagnosis:Ineffective airway Clearance relate to oral surgeryAltered comfortable related to gastritis, acidity as manifested by gastric painImbalanced 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 bleedKnowledge defect related to treatment & long term consequences of GERD problemsExcess fluid volume related to liver cirrhosis as manifested by ascitesActivity intolerance related to pain and weakness as manifested by inability to perform ADLsRisk for infection related to NGT
110 Ineffective airway Clearance relate to oral surgery as manifested by dyspnea Out comesPatient will demonstrate an effective respiratory rate, depth, clear airway and expanded chestInterventionAssess respiration for rate, depth, rhythm, and causes of dyspneaPut patient in comfortable positionAdminister O2 as prescribedApply suction frequently if patient on ventilatorAssess ABG frequently
111 Evaluation Apply chest physiotherapy Assess secretion color, amount if patient have productive coughGive patient prescribed medication in accurate dose, route and rate.EvaluationRespiratory with normal range, depth with normal ABG and dyspnea relivedPatient become comfortable
112 Altered comfortable related to gastritis, acidity as manifested by gastric pain Out comesComfortable level maintain.No signs & symptoms of restless and irritableInterventionUse pain scale(0-10) to assessing painAssess culture and beliefs about pain & pain reliefAssess patient pain toleranceGive prescribed analgesicsTry to keep patient in comfortable positionEliminate exercise according to patient ability and tolerance
113 EvaluationPatient reports adequate pain controlVital signs within normalNo 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 comesAdequate nutritionBody weight maintained within normalNormal serum electrolyteWound healing improvedInterventionAssess patient weight, general appearanceDaily weight and measure intake & outputAssess hemoglobin, hematocrit, serum albumin,Assess wound healingPrescribed 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 intakeKeep patient in clean environment away from offensive odors.Keep patient away from spicy and irritant foodsEvaluationPatient maintain adequate nutritionBody weight maintainedNormal serum albumin and electrolyte
116 Impaired skin integrity related to colostomy and surgical incision Out comesGood skin and stoma integrityNo signs of infection, vital signs within normalInterventionMonitor stoma color it should be pink, beefy red, and moist without cyanosis or bleeding and should extend about 2-3 cm from the abdominal wallAssess stoma functionEmpty 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., laxativesAssess 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 infectionEvaluationStoma pink and moistNo signs of wound infection.
118 Deficient fluid volume related to bowel obstruction, vomiting Out comesFluid balance maintainedVital signs within normalSkin moist, warm and pinkInterventionAssess 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 sequesteringAssess abdomen for bowel sounds and tendernessEvaluationFluid balanced maintainedNo signs of dry skin, hypertensiveAbdomen soft no increase in girth, bowel sound present.
120 Out comes Intervention Knowledge defect related to treatment & long term consequences of GERD problemsOut comesAble to verbalize lifestyle modificationUnderstand the chronic nature of the disease & long-term consequencesAware of the disease complication & how to deal with itInterventionTeach the importance of eating 4-6 small meals a day & to eliminate foods known to decrease lower esophageal sphincter pressure or cause irritationInstruct patient to avoid lying down after meals
121 Educate patient about medication regimen and possible side effects to improve adherence to medication regimenUse pain scale (0-10) to quantify pain and discomfort.EvaluationUnderstand the chronic nature of the disease & long-term consequencesPatient adapt to lifestyle modificationPatient 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 comesPatient will participate effectively in performing activity of daily livingInterventionAssess patient ability to tolerate activityMaintain balanced dietMake schedule of activity according to patient abilityMonitor vital signs during activityMaintain patient hygieneEvaluationPatient able to perform ADLs
123 Risk for infection related to NGT Out comesNo signs of infectionVital signs within normalInterventionMaintain low intermittent suctionCheck placement every 4 hours.Monitor skin integrity of nose for insertion site and provide skin care.Monitor bowel soundsMouth care at least every 2 hours.EvaluationNo signs of infection found