4-MS 2-PRELIMS PDF

1 Anaerobic metabolism CARE OF CLIENTS WITH PROBLEMS IN  creation of energy through burning of NUTRITION AND GASTRO-INTESTINAL, carbohydrates in the absence of...

1 Anaerobic metabolism CARE OF CLIENTS WITH PROBLEMS IN  creation of energy through burning of NUTRITION AND GASTRO-INTESTINAL, carbohydrates in the absence of oxygen METABOLISM & ENDOCRINE, PERCEPTION & End product  lactic acid COORDINATION, (ACUTE & CHRONIC) BODY PROCESSES INVOLVED IN GETTING NOURISHMENT FROM FOOD BASIC CONCEPT  Ingestion- mouth 1.1 METABOLISM & ENERGY  Digestion- stomach  Absorption- small intestine METABOLISM  Transport- blood vessels, blood  Cell Metabolism- liver ❒ sum total of all the body’s physical and chemical processes. Includes both: MATERIAL  Excretion- large intestine CHANGES / ENERGY CHANGES REQUIREMENTS TO MAINTAIN INTERNAL 2 PHASES: BALANCE:  Adequate Nutrient Supply  Normal Functioning of Body Systems ANABOLISM  building up of more complex biochemical ENERGY IS LOST AS HEAT substances or synthesis of nutrients  Glycogenesis- conversion of glucose into ADENOSINE TRIPHOSPHATE (ATP) glycogen for storage CATABOLISM MEASURING ENERGY – HEAT used to Measure  break down of biochemical substances into Energy simplier substances (starvation)  KILOCALORIE – (KCAL) – Preferred Unit for  Glycogen is converted to glucose Energy Measurement  Glycogenolysis- break down of glycogen ➔ In a gram of protein= 4 kcal  Gluconeogenosis- ➔ In a gram of Carbohydrates- 4kcal ➔ In a gram of Fats- 9kcal ENERGY ❒ Capacity to do work. FACTORS DETERMINING INDIVIDUAL’S BASIC FUEL NUTRIENTS SUPPLYING ENERGY FOR ENERGY NEEDS METABOLISM A) B ASAL METABOLIC R ATE (BMR) = 1 Kcal/Kg Macronutrients: body weight/Hr Carbohydrates  breakdown enzymes in salivary gland- Salivary FACTORS AFFECTING BMR: Amylase 1. Sex- male  produce by pancreas- amylase 2. Body Surface Area- 3. Age and Growth- elderly- lower BMR children- Fats higher BMR  Lipase -responsible for the final breakdown of fats 4. Hormones- Thyroid Glands- thyroxine (T4), release by pancreas triiodothyronine (T3)  Bile- 5. Nutritional State 6. Body Temperature/Environmental temperature- Proteins increase temp-increase BMR  Trypsin- breakdown of protein 7. Diseases that Increase Cellular Activity 8. Muscular Activity- Small Intestine- duodenum Jejunum- absorption B) ACTIVITY LEVEL ❒ the higher a person’s activity level, the more Aerobic metabolism energy he needs  and the higher his/her BMR.  uses oxygen, process of extracting energy from Activity level can be expressed as calories carbohydrates used/minute or Metabolic Equivalent of a Task End product (METs) – expressed in Milliliters of Oxygen  carbon dioxide, water, heat consumed/ Kg/ body weight/ min Abigail marie  2 C) ENERGY FOR FOOD DIGESTION  Elimination of undigested unabsorbed food ❒ food intake increases energy expenditure and stuffs and other waste products. heat production. STOMACH OTHER FACTORS AFFECTING ENERGY NEEDS: 1. Heredity- obesity ❒ stores, secretes digestive juice and propels the 2. Set Point Theory-states that the body maintains its chyme (partially digested food mixed with gastric weight within a preferred range secretions) into the small intestine. 3. Appetite- 4. Environmental Influences- hot environment- Layers of Gastrointestinal Tract increase bmr Mucosa- inner most layer Submusocsa- HOW FOODS MEET BODY’S METABOLIC NEEDS: Muscularis layer- responsible for alternating Nutrients (as complex organic compounds) broken to Serosa- outermost layer simpler forms before absorption and use for energy.  (increase production→ peptic ulcer, ulceration) PHYSIOLOGIC FUNCTIONS PERFORMED BY 4 ANATOMIC REGIONS OF THE STOMACH: CARBOHYDRATES, PROTEINS & FATS: 1. Cardia – narrow portion  Furnish energy 2. Fundus - upper portion of stomach  Provide components for cell growth and 3. Corpus (body) – main storage area maintenance 4. Antrum (Pylorus) – distal portion  Supply material for the compounds that regulates body functions. Parietal cells  secretes HCL acid and produces intrinsic factors ANATOMIC and PHYSIOLOGIC OVERVIEW INTRINSIC FACTOR- responsible for the absorption of Vitamin B12 (responsible for maturation of RBC) I. ANATOMY OF THE GASTROINTESTINAL lack of B12→ Pernicious anemia SYSTEM:  exocrine glands- parietal cells  chief cells- res. Production of pepsin- The GI tract (23 – 26 foot-long/7 m to 7.9 m) extends  neck cells- gastric mucosa barriers- responsible from: for the production of mucus (protects the  Mouth stomach against acid)  Esophagus Bicarbonate- responsible for neutralization  Stomach Blood supply  Small (longest segment) and large intestines ➔ peptic ulcer (melena- black starry stool)  Duodenum  Jejunum SMALL INTESTINE  Ileum longest segment  Rectum  Anus 3 SECTIONS: 1. DUODENUM – proximal section Both the sympathetic and parasympathetic autonomic 2. JEJUNUM – middle section; most absorption takes nervous system innervates the GI tract. place 3. ILUEM – distal section Sympathetic(fight or flight) ➔ It terminates in the ILEO-CECAL valve  increase BP, PR. RR, decrease peristalsis ➔ APPENDIX – small structures, no known (decrease GI function- constipation), dry physiologic function. Parasympathetic (rest and digest) ➔ VILLI – small fingerlike projections  decrease BP, PR,RR, increase peristalsis  produce enzymes and absorb nutrients. (increase GI function- diarrhea), wet LARGE INTESTINES FUNCTION OF THE DIGESTIVE SYSTEM: extends from the ileo-cecal valve to the anus. Primary Functions:  Consists of an ascending segment, transverse  Breakdown of food particles into the molecular segment and descending segment form for digestion.  Sigmoid colon, rectum and anus – completes  Absorption into the bloodstream of small the terminal portion of the large intestine nutrient molecules produced by digestion  Absorbs water and electrolytes  Bacteria – major content – assist in completing the breakdown of waste material Abigail marie  3  MUCUS – protects the colonic mucosa and 1) Undigested Food Residue provide adherence for fecal mass 2) Metabolic Wastes 3) Dietary Excesses  Excess carbohydrates, proteins, fats and fat- METABOLIC PROCESSES soluble vitamins are not excreted but mainly stored as Adipose Tissue. 1. INGESTION – The act of Eating  HUNGER NURSING PROCESS  APPETITE  SATIETY A. ASSESSMENT OF THE GASTROINTESTINAL SYSTEM 2. DIGESTION  MECHANICAL- breaking down of food using ASSESSMENT: teeth, movement of food going to stomach ❒ To assess the clients’ digestive function and  CHEMICAL- hydrochloric acid for the nutritional assessment, nurses should conduct breakdown of food both health assessment (to collect subjective data) and physical assessment (to collect 3. ABSORPTION objective data).  Most nutrient absorption occurs in the first and second intestine segment. SIGNS OF NUTRITIONAL STATUS: System Good Nutrition Poor Nutrition MECHANISMS OF ABSORPTION INCLUDE: 1) Simple Diffusion- higher concentration to lower General Alert, energetic, Withdrawn, concentration good endurance, apathetic, easily 2) Carrier-Facilitated Diffusion- psychologically fatigued, irritable, stable, weight with over/underweight 3) Active Transport- uses energy to transport range of height, age 4) Pinocytosis- and body size Integumentary Glowing, good Dull, pasty, scaly,  FAT AND FAT-SOLUBLE VITAMIN – Absorbed as turgor, smooth, free dry, bruises, Mixed Micelles  Small Intestines ( Vit K, A D) of lesions, hair multiple lesion,  Chylomicrons – lipid droplet (contains shiny, lustrous. brittle hair, dull, mostly triglycerides) Minimal loss falls out easily  WATER, ALCOHOL, SOME MINERALS, SMALL Head, Eyes, Bright, clear, no Eyes dull, ears, Nose, fatigue circle, oral conjunctiva pale, GLOCUSE AMOUNTS Stomach Throat mucous membrane discoloration under  WATER, INDIGESTIBLE FOOD PARTS AND pink-red and moist, eyes, oral mucous SOME VITAMINS AND MINERALS  Colon gums pink, firm and membrane pale,  WATER-SOLUBLE NUTRIENTS – Dissolved in pink tongue, gums red, spongy plasma  enters Portal vein  Liver moderately smooth, and bleeds easily,  FAT-SOLUBLE VITAMINS – enter lymphatics as no swelling tongue bright to Chylomicrons  L Subclavian Vein  Heart  dark red, swollen Liver Abdomen Flat, firm Flaccid, distended Musculoskeletal Firm, well- Flaccid muscles. 4. TRANSPORT developed muscles, Wasted good posture, no appearance, LIVER skeletal changes stooped posture,  Upon arrival at the Liver  undergo either skeletal FURTHER METABOLISM OR DIRECT malformations TRANSPORT to Body cells  Interstitial Fluid via Neurologic Good attention Inattentive, easily span, good distracted, impaired arteries and capillaries  Transported across cell concentration, though process, membranes for Cellular metabolism astute/alert thought paresthesias, process, good reflexes diminished 5. CELL METABOLISM reflexes or hyperactive  Describes all Physical and Chemical Changes occurring within Body Cells 1. SUBJECTIVE DATA 6. EXCRETION  Final Nutrient-use Phase A) NURSING HISTORY – To include:  Through LARGE INTESTINES, KIDNEYS,  BIOGRAPHICAL/DEMOGRAPHIC DATA LUNGS and SKIN Abigail marie  4 Gerontologic Consideration: difficulty a) Mouth and Pharynx swallowing and chewing, heartburn and 1. Lips – color, moisture, swelling, cracks or reflux, malabsorption, constipation lesions.  CHIEF COMPLAINTS – Most common symptoms. 2. Teeth – completeness (20 in children, 32 in adults), caries, loose teeth, absence of teeth ➔ Common Symptoms: impair adequate chewing.  Pain – note character, duration, pattern, 3. Gums – color, redness, selling, bleeding, pain frequency, distribution of referred pain and time (gingivitis) of the pain. 4. Mucosa – color (light pink)  Dyspepsia – commonly called indigestion. Ex:  Examine for moisture, white spots or fatty foods patches, bleeding or ulcers  Intestinal gas- belching, flatulence (bloating,  White patches – due to candidiasis (oral distention, feeling full of gas) thrush)  Nausea and vomiting- indigested particles,  White patches within red patches may blood, bile & gastric juice indicate malignant lesions Etiology: infection, peritoneal irritation, 5. Tongue – color, mobility, symmetry, mechanical obstruction, CNS problems, ulcerations/nodules or lesions radiation, distended upper intestine 6. Pharynx – observe the uvula, soft palate,  Change in Bowel Habits and Stool tonsils, posterior pharynx Characteristics  Constipation ➔ Signs of inflammation (redness, edema,  Diarrhea ulcerations thick yellowish secretions), assess also  Melena for symmetry of uvula.  Hematochezia-bright red color  Greasy stool-steatorrhea b) Abdomen  Acholic stool ❒ Assess for the presence of tenderness and organ  Change in appetite enlargement, masses, spasms or rigidity of the abdominal muscles, fluid or air in the abdominal  Weight gain or loss cavity.  Dysphagia Anatomic Location of Organs:  PRESENT/CURRENT ILLNESS – COLDSPA  RUQ – liver, gallbladder, duodenum, right kidney,  PAST MEDICAL HISTORY hepatic flexure of colon.  Known GI Disorders  RLQ – cecum, appendix, ovary and fallopian tube  Possible Genetic or Environmental cause  LUQ – stomach, spleen, right kidney, pancreas,  Chronic Diseases splenic flexure of colon  Medications  LLQ–sigmoid colon, L ovary & tube  Allergies  Habits c) Rectum  FAMILY HISTORY ❒ Perineal skin and perianal skin  SOCIAL HISTORY ❒ Assess for the presence of pruritus, fissures,  DIETARY HISTORY external hemorrhoids, rectal prolapse. Digital Rectal exam (DRE) - performed with insertion of 2.2 OBJECTIVE DATA lubricated finger into the anal canal while the client bears down to note for sphincter tone, nodules or irregularities of the anal ring. A. BASELINE DATA– Vital signs / General Nutritional State / Body Build / Fat Distribution / Oral Cavity / Swallowing B. PHYSICAL EXAMINATION B.1 INSPECTION Physical Examination:  Skin changes, lesions, nodules, scarring,  When performing a focused assessment, you will discolorations (pale), inflammation, bruising or use at least one of the following four basic striae. techniques during your physical exam: inspection, auscultation, percussion, and  Abdominal Movement – Visible strong palpation. contractions / Undulating L  R movement  The physical examination includes assessment of  (Upper abdomen) / Pulsation (epigastric the mouth, abdomen, and rectum. area)(Cullen’s sign)  Abdominal Contour – Flat, Rounded, Scaphoid, Distended /Protuberant (Fats, Fluid, Feces, Fetus, Fibroids, Flatus) – Symmetrical / Asymmetrical Abigail marie  5 B.2 AUSCULTATION  Biliary Tract Disease  Bowel sounds (stet- diaphragm) / Vascular  DNA Testing sounds  Imaging Studies:  Normal B.S. – high pitched / gurgling – 5-34/min  Computed Tomography (CT)  Abnormal B.S.  Use: inflammatory conditions  Decreased/ Hypoactive- paralytic ileus  Pregnancy status  Increased / Hyperactive- borborygmus  Allergy  Absent –listen up to 5min to confirm -  Kidney function peritonitis / paralytic ileus  IV Na HCO3, 1hr before, 6hrs  Vascular sounds (stet- bell) after  Bruits- narrowing of blood vessels /  NACI artery – obstruction  hydration  Murmurs-  Magnetic Resonance Imaging (MRI)  Venous Hums- epigastric area /  Positron Emission Tomography (PET) umbilical area  Scintigraphy (radionuclide imaging)  Peritoneal Friction Rub- heard in lower  Radioactive isotopes right coastal area- hepatic abscess,  Change in organ size Infection in liver  Neoplasm  Radioactive tagging of RBCs B.3 PERCUSSION  Virtual Colonoscopy.  Tympany / Dullness  Upper Gastrointestinal Tract Study:  Upper GI fibroscopy; Barium swallow B.4 PALPATION  Lower Gastrointestinal Tract Study:  RIGIDITY  Barium enema- left side position  Rebound Tenderness-  Gastrointestinal Motility Studies:  Murphy’s sign – gallbladder –acute cholecystitis  Radionuclide testing- tagged, rate of  Murphy’s punch – kidneys - pyelonephritis passing  Colonic transit studies- capsule with ASSESSMENT OF THE METABOLIC STATUS markers  Duration: 4-5 days, up to 10 days in NECESSARILY INCLUDE EXAMINATION OF constipation ANUS AND RECTUM, USING -  Endoscopic Studies:  Inspection Fibroscopy/Esophagogastroduodenoscopy (EGD);  Palpation – Digital exam  Small bowel endoscopy  Colonoscopy- larger, longer scopes DIAGNOSTIC STUDIES:  Watch our for: dysrhythmias, over/underhydration  Post-procedure: bowel perforation  Serum Laboratory Studies:  Sigmoidoscopy  CBC- hemoglobin & hematocrit- GI Bleeding  Proctosigmoidoscop  Prothrombin time  Anoscopy  Triglycerides- LDL  Endoscopy through an ostomy.  Liver Function tests ➔ Fibroscopy Endoscopic retrograde  Amylase and Lipase cholangiopancreatography  Stool Tests: Diagnostic or therapeutic  FOBT  Biopsy  ova and parasites  Removal of stones  fecal leukocytes  Sclerosing agents  Breath Tests ➔ Fibroscopy/ Esophagogastroduodenoscopy  Abdominal Ultrasonography: Endoscopic Ultrasonography (EUS)  Water soluble lubricant  NPO- 8-12 hrs, reduce gas  Nausea, gagging topical anesthetics moderate sedation  Gallbladder: fat-free meal  Risk for desaturation  Barium studies post- ultrasound Pre-procedure  Endoscopic Ultrasonography (EUS)  NPO for 8 hours  Moderate sedation  Local anesthetic gargle or spray  Evaluate submucosal lesions  Midazolam (Versed)- sedation  Barret esophagus  Portal hypertension  Pancreatitis, Ca Abigail marie  6  Atropine- anticholinergic agent= block  Diarrhea the parasympathetic = decrease  Vomiting secretions = SE: tachycardia  Glucagon- relaxes skeletal muscles PATHOPHYSIOLOGIC MECHANISM OF  Left lateral position Post-procedure SPECIFIC NUTRITIONAL-METABOLIC  LOC PROBLEMS DISTUBANCES OF THE  VS ESOPHAGUS:  O2 Saturation  Signs of perforation 1. GASTROESOPHAGEAL REFLUX DISEASE  (-) gag reflex initially (GERD)  Minor throat discomfort: lozenges, saline ❒ represents symptoms or tissue damage that gargle, and oral analgesic agents result from GER (Gastroesophageal Reflux)   Sedation-not allowed inflammatory changes → Hallmark of GERD.  Verbal or written instructions ❒ Also known as Reflux Esophagitis.  Manometry and Electrophysiologic Studies  Manometry- intraluminal pressure achalasia COMMON RISK FACTORS FOR GERD: 1. Obesity  Electrogastography- nerve dysfunction in 2. Peptic ulcers the stomach 3. Hiatal hernia  Defecography- 4. Pregnancy  Gastric Analysis, Gastric Acid Stimulation Test 5. Diabetes and pH Monitoring 6. Asthma  Gastric Analysis 7. Connective tissue disorders Prep: NPO 8-12 hours, X Smoking 8. Zollinger-Ellison syndrome  Pernicious anemia  Severe chronic atrophic gastritis PREDISPOSING FACTORS:  Gastric Ca 1. Position – bending/stooping  Gastric ulcer 2. Increased gastric pressure  Duodenal ulcer 3. Excessive ingestion of foods that relaxes LES.  Gastric Acid Stimulation Test 4. Drugs that relaxes LES. Medications: (q 15mins for 1 hour)  Histamine SQ PATHOPHYSIOLOGIC FACTORS:  Pentagastrin SQ 1. Inappropriate relaxation of the LES – most  “flush feeling” common cause.  pH Monitoring 2. Irritation from the refluxed material  Laparoscopy (Peritoneoscopy) 3. Delayed gastric emptying 4. Abnormal esophageal clearance PLANNING/NURSING DIAGNOSES: ASSESSMENT FINDINGS:  Imbalanced nutrition: less than body  Pyrosis requirements  Dyspepsia  Deficient fluid volume  Report of regurgitation  Nausea  Dysphagia or odynophagia  Impaired skin integrity  Hypersalivation  Acute Pain / Chronic Pain  Chronic cough at night when in recumbent  Risk for Infection position  Knowledge deficient  Substernal or retrosternal pain (atypical chest  Constipation pain)  Risk for Urinary Retention  Anxiety or Fear DIAGNOSTIC STUDIES:  Ineffective Coping 1. Barium Swallow  Disturbed Body Image 2. 2.Endoscopy (Esophagogastrodoudenoscopy)  Sleep pattern disturbance 3. 24 -36 Hr pH monitoring  Risk for sexual dysfunction 4. Bernstein test (Acid Perfusion Test)  Risk for Deficient Fluid Volume  Activity Intolerance MEDICAL MANAGEMENT:  Ineffective therapeutic regimen management 1. Non-Surgical Management:  Aspiration risk a) Diet therapy – Low protein, low fat; eliminate or limit foods that decreases LES pressure; restrict Abigail marie  7 spicy and acidic foods; teach client to eat 4- Types: 6x/day; avoid carbonated beverages; avoid a) Sliding hernia evening snacks – no eating 3 hours before going to bed.  most common type of hiatal hernia, accounts b) Lifestyle change – elevate head of bed by 6-8 for 90% of all hiatal hernias, a portion of the inches; sleep in L lateral position; decrease stomach slides upward through the diaphragm intra-abdominal pressure; avoid lifting heavy and into the chest. objects or straining, bending or stoop position; stop smoking/ avoid alcohol; control weight; Common Complication: Development of Esophageal bland diet; avoid evening snacks; avoid Reflux overeating c) Drug Therapy – antacids; H2 receptor b) Paraesophageal hernia antagonist, proton pump inhibitor; promotility  the gap in the phrenoesophageal and a agents. portion of the stomach herniates into the d) Endoscopic Therapies: chest alongside the esophagus and stays  Stretta Procedure – inhibits the activity of there, but the junction between the stomach the vagus nerve thus reducing discomfort and the esophagus remains below the of client. diaphragm.  Enteryx Procedure – tightens the LES, prevent reflux. ➔ ROLLING (Paraesophageal) HERNIA – the  Bard EndoCinch Suturing System fundus of the stomach rolls into the thorax (BESS) – tightens the LES. through a weakness in the diaphragm causing an herniation next to the esophagus. 2. Surgical Management: Antireflux surgery  Nissen Fundoplication – gold standard for Common Complication: Strangulation; Obstruction surgical management involves 360 degrees wrap of the fundus of the stomach around the INCIDENCE: distal esophagus.  Estimated as 5/1000 in general population &  Complication of Surgery: may be as high as 60% in clients over 60-year-  Small bowel obstruction old.  Retching (involuntary effort to vomit)  Females tends to be more often affected than  Gas-Bloat syndrome males  Dumping syndrome c) “Mixed”  Complications related to Fundoplication: 1. Temporary dysphagia  In a combination of events, should the defect 2. Gas-bloat syndrome in the diaphragm become larger, the junction 3. Atelectasis between the stomach and the esophagus can 4. Obstructed NGT herniate through the diaphragm into the chest causing an hernia that is both paraesophageal and sliding. COMPLICATIONS OF GERD:  Esophagitis ETIOLOGY:  Respiratory symptoms: Aspiration Pneumonia  Hiatal hernias are related to muscle weakness in  Development of Barrett’s syndrome the esophageal hiatus which loosens the esophageal supports and allows the lower POSSIBLE NURSING DIAGNOSES: portion of the stomach to rise into the thorax.  Acute Pain  Knowledge Deficit PRIMARY PREVENTION:  Ineffective Management of Therapeutic  Losing weight; limit activities that increase intra- Regimen abdominal pressures. 2. HIATAL HERNIA (DIAPHRAGMATIC ASSESSMENT FINDINGS: Sliding Hernia HERNIA)  Heartburn 30 – 60 mins after meals; Reflux  ❒ A condition when part of the stomach protrudes Substernal pain through the diaphragm into the thorax. Rolling (Paraesophageal) Hernia RISK FACTORS:  No manifestation of reflux; Feeling of fullness  Aging / Trauma / Congenital Muscle weakness / after eating or have difficulty of breathing. Some Anything that increases intra-abdominal clients experienced chest pain similar to that of pressure / Surgery anginal pain. Abigail marie  8 DIAGNOSTIC STUDIES:  X-ray; Barium Swallow with Fluoroscopy; Chest ASSESSMENT FINDINGS: X-ray Achalasia: MEDICAL MANAGEMENT:  Chronic & progressive dysphagia  Chest pain (Substernal discomfort or a feeling of 1. Non-surgical management: fullness)  Diet therapy and drug – same with GERD  Regurgitation during meal or several hours after  Health teaching  Cough  Sleep with head elevated 6 inches.  Heartburn  Remain in upright position several hours after  Weight loss eating DES:  Avoid straining or excessive vigorous exercise.  Anterior chest pain  Refrain from wearing too tight clothing around  Heartburn the abdomen.  Odynophagia  Regurgitation 2. Surgical Management:  Aggravated often by large meals, hot and cold  Laparoscopic Nissen Fundoplication liquid.  Post-op Care: Monitor for bleeding, infection and organ injury. COMPARING C LINICAL MANIFESTATIONS : COMMON COMPLICATIONS : S/S Achalasia  Temporary dysphagia/ Gas-Bloat syndrome /  Dysphagia Atelectasis or Pneumonia.  Pain or discomfort in your chest  Weight loss POSSIBLE N URSING D IAGNOSES:  Heartburn  Risk for Aspiration R/T Reflux of gastric contents  Intense pain or discomfort after eating  Imbalanced Nutrition  Regurgitation or backflow.  Acute pain S/S Diffuse Esophageal Spasm  Knowledge Deficit  Chest pain  Anxiety / Fear  Heartburn  Painful swallowing 3. IMPAIRED ESOPHAGEAL MOTILITY  Regurgitation DISORDERS: DIAGNOSTIC TEST: a. ACHALASIA ACHALASIA: ❒ is a disorder characterized by progressively  Xray studies increasing dysphagia, with the client eventually  Ba swallow (barium esophagography) – “bird having great difficulty in swallowing and beak” narrowing expressing the feeling that “Something is stuck  Esophageal Manometry in the throat”. DES: ❒ OCCURRENCE : 40 y/o or older  Ba Esophagography – “Corkscrew or rosary bead”  Esophageal manometry – intermittent contraction b. DIFFUSE ESOPHAGEAL SPASM(DES): with episodes of normal peristalsis ❒ motor disorder non-propulsive, nonperistaltic tertiary contractions; LES functioning is normal. MEDICAL MANAGEMENT: ❒ Common: women – middle age ACHALASIA: PATHOPHYSIOLOGY:  Diet – Semi-solid warm food and liquid in 4-6 smaller meals. ACHALASIA:  Medications that relax LES or lower  Incomplete relaxation of the LES with esophageal pressure (Anticholinergic drugs, swallowing and failure in the lower two-thirds of nitrate, Calcium Channel blockers, Botox inj.). the esophagus – due to defective innervation of  Surgery: the involuntary muscles of the esophagus.  Esophageal Pneumatic Dilatation – for DES: severe cases  Unknown; stress Abigail marie  9  Esophagomyotomy (Heller’s myotomy)  Massive gastrointestinal bleeding can occur – used for those who do not respond to from hematologic disorders that decrease dilation. platelet numbers or function. DES:  Lower gastrointestinal bleeding is most often  Diet: Soft diet, small frequent feeding in upright caused by hemorrhoids and polyps of the colon. position.  Primary treatment: DRUGS such as: Calcium ➔ Symptoms of GI bleeding often first appear as Channel blockers & Nitrates; Sedatives blood in the vomit or stool, or black, tarry stools. The  Esophageal dilation person also may experience abdominal pain.  Myotomy – rarely used ➔ Symptoms associated with the blood loss, include: fatigue; weakness; pale skin; and shortness of NURSING MANAGEMENT: breath. 1. Improve nutritional status ➔ GI bleeding can usually be diagnosed by a digital 2. Promote comfort rectal exam, an endoscopy or colonoscopy, and lab 3. Monitor for post-op complications tests. ➔ Treatment for GI bleeding usually includes a. Teach client how to swallow: hospitalization because blood pressure may drop  Choose food with shape; moist to prevent and heart rate may increase and this needs to be crumbling stabilized. b. Use mugs and glasses with spouts or straws.  In some cases, IV fluids or blood transfusions c. Avoid sticky foods. are needed, and surgery may be required. d. Moistened dry food with gravy or broths; thickened juices with sherbets. IMMEDIATE INTERVENTIONS: e. Avoid tepid or room temperature foods.  Cardiac stabilization  Identification of the source of bleeding DURING MEALS:  Attempts to stop the bleeding a. Eat with head in the midline, forward, chin  Psychosocial support pointed downwards. b. Hold each bite for a few seconds, hold lips MEDICAL MANAGEMENT: together firmly, concentrate on swallowing the  Upper GI bleeding  NGT  Gastric lavage swallow.  Tamponade for bleeding esophageal varices – c. If with increased saliva during meal, collect application of pressure to the lower esophagus, a saliva with tongue and swallow in between the tube is inserted and dilated to control bleeding. bites throughout the meals. d. If with dry mouth – instruct to move tongue in circular motion inside the cheeks. POSSIBLE NURSING DIAGNOSES: e. Caution about talking during meal or with the  Fluid Volume Deficit mouth full of food.  Risk for Bleeding COMPLICATION: B. GASTRITIS  Lung problems ❒ Gastritis is an inflammation, irritation, or erosion  Weight Loss of the lining of the stomach. It can occur suddenly (acute) or gradually (chronic). POSSIBLE NURSING DIAGNOSES: ❒ It is an inflammation of the stomach lining from  Imbalanced Nutrition irritation of the gastric mucosa (normally  Pain protected from gastric acid and enzymes by  Knowledge Deficit mucosal barrier).  Anxiety / Fear Types of Gastritis: a) Acute gastritis - may occur suddenly DISTURBANCES IN DIGESTION b) Chronic gastritis - appear slowly over time A. GASTROINTESTINAL BLEEDING: CAUSES OF GASTRITIS: a) Various Medications - Aspirin, NSAIDs, Prescription steroids, Potassium supplements, 3 MAJOR CAUSES: Iron tablets, Cancer chemotherapy medications. 1. Peptic Ulcer Disease b) Medical and Surgical Conditions – Eg. People 2. Gastritis who are critically ill or injured can develop 3. Esophageal Varices gastritis; After medical procedures such as endoscopy c) Physical and Psychological Stresses Abigail marie  10 d) Social Habits - Alcohol consumption, Caffeine,  Chronic Gastritis – Vague discomfort relieved Smoking by eating, fatigue, anorexia, nausea and e) Swallowing Chemicals and Objects, such as vomiting, heartburn after eating, belching, sour Corrosives (acid or lye), Swallowed foreign taste in the mouth and Vit. B 12 deficiency. bodies (paper clips or pins) f) Infections, such as Viral infections, Fungal DIAGNOSTIC STUDIES: (yeast) infections, Salmonella, Parasites and 1. Esophagogastrodoudenoscopy with biopsy worms, and Hpylori infection is the most – diagnostic test of choice. common. 2. Gastric Aspirate Analysis such as: a) Basal Acid Output Test – measures PATHOPHYSIOLOGY OF GASTRITIS the amount of Hcl acid secreted by the stomach. DRUGS/DIET/H.PYLORI b) Gastric Acid Stimulation – Measures ↓ the total acid output after Pentagastrin DISRUPTION OF MUCOSAL BARRIER injection. ↓ Hcl acid/PEPSIN IN CONTACT WITH GASTRIC LINING MEDICAL MANAGEMENT: ↓  In mild cases – antacids and rest IRRITATION/INFLAMMATION/LESION  In severe cases – parenteral fluid and ↓ electrolyte replacement, antiemetics S/SX (Compazine, Tigan)  In Erosive Cases – Antacids, H2 Blockers, 2 TYPES: Mucosal Barrier Fortifiers; Antibiotics if caused 1. Acute Gastritis – most common form, benign; by bacteria self-limiting disorder associated with ingestion of  In Atrophic Gastritis – Anticholinergic drug alcohol, aspirin, NSAIDS, caffeine or (Pro-banthine) and Vitamin B12 injections. contaminated food.  If due to H. Pylori – Triple therapy with:  Erosive gastritis (Stress Induced Bismuth Subsalicylates or Proton Pump Inhibitor Gastritis) and a combination of 2 antibiotics 2. Chronic Gastritis – common among elderly, (Metronidazole and Tetracyclines or chronic alcoholic and cigarette smokers, dietary Clarithromycin and Amoxicillin). factors such as caffeine, NSAID’s, chronic reflux DIET THERAPY COMMON COMPLICATION:  Soft Bland diet, small frequent feeding; Avoid  Pernicious Anemia, Gastric Cancer spicy foods, tea, paprika, coffee, cola chocolates, mustard and pepper. CLASSIFICATION OF CHRONIC GASTRITIS: STRESS REDUCTION TYPE A GASTRITIS  Diversional activities  also known as Autoimmune Atrophic Gastritis triggered by physical or psycho-emotional stressors. SURGICAL MANAGEMENT Affects the fundus and the body of the stomach.  Partial Gastrectomy, Pyloroplasty, Vagotomy or TYPE B GASTRITIS Total Gastrectomy  also known as Simple Atrophic Gastritis, strongly associated with colonization of the gastric mucosa Pyloroplasty by H. Pylori. It is often a symptomatic until atrophy is ❒ a surgical procedure in w/c pyloric valve at the well advanced; not relieved by antacids. Affects the lower portion of the stomach is cut & resutured, glands of the antrum but may involve the entire relaxing & widening its muscular opening into the stomach. duodenum. Vagotomy PATHOLOGIC CHANGES: ❒ is the surgical cutting of the vagus nerve to  Vascular congestion; Edema; Acute reduce acid secretion in the stomach. inflammation; Degenerative changes in the  Alternative treatments for acute gastritis, superficial epithelium of the stomach lining. such as slippery elm, myrrh, berberine, licorice, wild indigo, clove Oregon grape. ASSESSMENT FINDINGS:  Dietary Modifications – bland diet  Acute Gastritis – Dyspepsia, Epigastric pain/Abdominal discomfort/ pain, anorexia, nausea and vomiting, hematemesis, melena, headache, hiccup. Abigail marie  11 ALTERNATIVE TREATMENTS FOR CHRONIC 3. DUODENAL ULCER GASTRITIS  common in men during young adulthood &  such as Garlic, Cranberries, Ginger, Turmeric, middle age; due to increase secretion of HCL Probiotics, especially ones that acid in the gastric mucosa & increase rate of contain Lactobacillus or Bifidobacterium. gastric emptying. Usually occurs within 1.5 cm of the pylorus. POSSIBLE N URSING D IAGNOSES:  Pain ASSESSMENT FINDINGS:  Imbalanced Nutrition – Less than the Body 1. Pain – describe to be burning, aching, cramp like Requirements & gnawing.  with Gastric Ulcer – pain occurs at the  Fluid Volume Deficit upper epigastrium with localization in the  Deficient Knowledge (L) or midline; present with food intake; vomiting relieves pain; antacid is C. PEPTIC ULCER DISEASE ineffective.  with Duodenal Ulcer - pain is felt on an ❒ Peptic ulcers are sores that develop in the lining empty stomach and discomfort is relieved of the stomach, lower esophagus, or small with food intake and antacid. intestine. 2. Nausea and vomiting – common with gastric ❒ An ulcer in the lining of the stomach, duodenum, ulcer or esophagus 3. Massive GI bleeding: Duodenal ulcer - melena is ❒ A sore that forms when digestive juices wear more common; while with Gastric ulcer, away the lining of the digestive system. hematemesis is more common. ❒ PEPTIC ULCERS – a sharply defined break in the continuity of the tissue involving the mucosa, submucosa and muscular layers of the digestive DIAGNOSTIC TEST: tract exposed to acid (Hydrochloric acid and  X-rays / Endoscopy / CBC / Stool for occult / Pepsin). Gastric Analysis ❒ A peptic ulcer can occur in the lining of the stomach, duodenum, or lower part of the MEDICAL MANAGEMENT: esophagus. 1. Provide stomach rest ❒ They’re usually formed as a result of 2. Medications such as Hyposecretory drugs; inflammation caused by the bacteria H. pylori, as mucosal barrier fortifiers; antibiotics; antacids well as from erosion from stomach acids. 3. Dietary management – avoid caffeine, alcohol, milk ETIOLOGY: 4. Prevent and treat complications a. Prevent shock  Peptic ulceration depends on the defensive b. Replace fluid resistance of the mucosa relative to the c. Maintain rest aggressive force of the secretory activity. d. Maintain gastric pH Ulceration occurs when aggressive factors e. For Hemorrhage & Perforations - Surgical exceed the defensive ones. The aggressive Management: Vagotomy with pyloroplasty; factors relate to the presence of H. pylori Gastroenterostomy, Subtotal Gastrectomy bacteria and the volume of hydrochloric acid & biliary acid. NURSING DIAGNOSES: 1. Pain related to Gastric Mucosal Injury RISK FACTORS:  Administer medications as ordered.  Infection of H. pylori bacteria; Smoking  Avoidance of Strenuous physical activity, (Nicotine); Steroids; Aspirin; Caffeine; alcohol; decreases gastric secretions and Stress; Hepatic and Biliary disease. peristalsis.  Advise to eat small amounts of frequent, 3 TYPES OF PEPTIC ULCERS: regular intervals. 1. ESOPHAGEAL ULCERS  Discourage ingestion of alcohol, cola,  ulcers that develop inside he esophagus. tobacco, caffeine, milk & foods that cause discomfort. 2. GASTRIC ULCER Vagotomy  common in older age group of both sexes; due ❒ is the surgical cutting of the vagus nerve to to rapid diffusion of acid in the gastric mucosa. reduce acid secretion in the stomach. Tend to heal with in few weeks, form with in 1 inch of the pylorus of the stomach, area where DUMPING SYNDROME gastritis is common. ❒ a post-prandial problem due to rapid emptying of gastric contents into the intestines; self-limiting Abigail marie  12 that last for 6-12 months after surgery (Gastric  As the inflammation progresses  areas of the surgery or a form of vagotomy). bowel sloughs off  some parts of ulcerated areas heal with normal mucosa and others are MANIFESTATIONS: replaced with scar tissue.  Early Manifestation: 5-30 minutes after eating, involves Vasomotor disturbances: Vertigo; ASSESSMENT FINDINGS: Tachycardia; Syncope; Sweating; Pallor;  Diarrhea (10 to 20 liquid stools/day during the Palpitation; Diarrhea; Nausea acute stage) ; Lower left quadrant Abdominal  Intestinal Manifestation: Epigastric fullness; pain; intermittent tenesmus & rectal bleeding; Distention; Abdominal discomfort; Cramping; Anorexia; Vomiting; Weight loss & dehydration; Nausea and client experience tenesmus; may Pus in the stools; Fever; Anemia. include dizziness, light headedness, palpitations, diaphoresis and confusion. DIAGNOSTIC TEST:  Late manifestations: occurs 2 -3 hours after  stool for occult (+); stool for ova & parasite; Hgb eating. and Hct; wbc; albumin (decreased); electrolyte (imbalance); sigmoidoscopy/ MEDICAL MANAGEMENT: colonoscopy/Barium enema.  Decrease the amount of food taken one at a time; eliminate intake of liquids with meals; Give COMPLICATIONS: high protein, low carbohydrate, high fat dry diet.  Toxic Megacolon; Perforation; Bleeding  Position in recumbent or semi-recumbent; avoid lying down after meals. MEDICAL MANAGEMENT:  Avoid fluids 1 hour before, during and may give a) Diet therapy – Hi-caloric, Protein, Vitamins and 2 hours after meals. Minerals; Low in Fats and Fiber; Lactose- free,  Drug therapy with Antispasmodics and given in small frequent feedings; TPN in acute Sedatives stages; Cold foods & smoking are avoided, both  Surgery – if manifestation persist: Reducing the increases intestinal motility. size of gastroenterostomy or converting Billroth b) Drug therapy – Sulfasalazine (drug of choice), II resection to Billroth I. Antidiarrheal drugs, Corticosteroids, Immunosuppressive drugs; Antibiotics Gastroenterostomy c) Surgical Intervention – Ileostomy ❒ the creation of a passage between the body of the stomach and the jejunum. 2. CROHN’S DISEASE OR REGIONAL INFLAMMATORY BOWEL DISEASE ENTERITIS ❒ is a chronic inflammatory ulcerating disease TYPES: affecting any segment of the GI tract, most 1. ULCERATIVE COLITIS commonly in the distal ileum, not continuous, predominantly a submucosal inflammation, may ❒ A recurrent ulcerative and inflammatory disease involve the entire thickness of the bowel that spans the entire length of the colon that (Transmural). involves only the mucosal and submucosal layers of the colon and the rectum. CAUSES:  Unclear, tends to be familial or may be Genetic / CAUSES: Hereditary; considered as Autoimmune in  Infectious agent; Allergic reaction to milk protein; nature. Psychosomatic theory; Genetic predisposition; Altered immunologic mechanisms. PATHOPHYSIOLOGY: Lesions develop in separated segments of the bowel PATHOPHYSIOLOGY (Cobblestone markings)  Inflammation slowly spreads Beginning at the mucosa  submucosa, beginning in progressively in the mucosa  To entire intestinal walls the distal colon  spreading proximally  colonic  Small superficial ulcerations (Apthoid lesions) with mucosa which becomes engorged and very friable  granulomas and fissures  Fistula and abscess Bleeds easily. formation  Small intestines becomes congested in the process of inflammation; In chronic cases  Scarring  Multiple, irregular, superficial ulcerations and develops which narrows the lumen. crypt abscesses develop  increased mucous secretions. Bloody discharges and pus are ASSESSMENT FINDINGS: common.  Crampy abdominal pain (RLQ) and Diarrhea – soft, semi-liquid/bloody; Abdominal tenderness Abigail marie  13 and spasm; Fever; Anemia; Nausea and 2. Relieve pain vomiting; weight loss; Malabsorption with  Administer anticholinergic 30 minutes steatorrhea. before meals – to decrease intestinal motility CHRONIC SYMPTOMS:  Administer analgesic  DIARRHEA, abdominal pain, steatorrhea,  Change position anorexia, weight loss, nutritional deficits.  Encourage diversional activities 3. Maintain fluid intake MANIFESTATION OUTSIDE OF GIT:  Maintain optimal nutrition – low residue,  Joint disorders, skin lesions, conjunctivitis, oral low fat 4. Promote rest ulcers. 5. Reduce anxiety  Enhance coping measures MEDICAL MANAGEMENT: 6. Prevent skin breakdown  Bed rest - during acute phase  Replacement of fluids & electrolytes STRUCTURAL and OBSTRUCTIVE BOWEL MEDICATIONS: DISORDERS:  Antidiarrheal drugs such as Loperamide (Imodium) INTESTINAL OBSTRUCTIONS: Partial or Complete  Antispasmodic meds such as Propantheline Bromide (ProBanthine), Glycopyrrolaten TYPES OF OBSTRUCTION: (Robinul) 1) MECHANICAL – INTRALUMINAL / MURAL  Antimicrobial agents such as Sulfasalazine OBSTRUCTION.  Steroids 2) FUNCTIONAL - inability of the intestine to propel contents along the bowel  PARALYTIC ILEUS. DIETARY MANAGEMENT:  TPN for those who fails to respond to medical PATHOPHYSIOLOGY: interventions.  An obstruction in the intestinal lumen causes an  Elemental diets – Low residue, Low in Fat and accumulation of fluid and gas proximal to the digested in the upper jejunum. site of bowel  Distention of bowel Increases  Foods to avoid – Cocoa, Chocolate, Citrus intestinal fluid secretions but decreases juices, Cola or carbonated drinks, nuts, seeds, absorption  results in increased buildup of popcorn and alcohol. fluids  lumen is blocked, peristalsis increases in an attempt to push contents past obstruction. SURGICAL INTERVENTIONS:  Done only to treat the complication of the  With increasing distention  Venous return is disorder such as Perforation, hemorrhage, etc. diminished  Capillary fluid is lost in the  Ileotransverse Colectomy intestinal lumen, peritoneal cavity & bowel wall  Ileostomy edematous bowel becomes permeable causing bacteria and fluids within the lumen DIAGNOSTIC TEST: enter the peritoneal cavity  PERITONITIS.  Proctosigmoidoscopy; stool for occult; Ba enema – most conclusive; “STRING SIGN”;  Last stage of intestinal obstruction  Bursting of CBC (Hgb, Hct, decreased; WBC – increased); the intestines  Spilling of contents into the ESR(increased); albumin and protein peritoneum. In response to this foreign material (decreased)  The peritoneum becomes inflamed and secretes fluid faster than it can reabsorbed  COMPLICATIONS: ASCITIS.  Intestinal obstruction, Stricture formation, Perianal disease, F/E imbalance; Malnutrition; ASSESSMENT FINDINGS: Fistula and Abscess formation. a) Distention – immediate effect. b) Increased bowel sounds and severe, colicky abdominal pain. NURSING INTERVENTIONS: c) In partial obstruction – Diarrhea stools. 1. Maintain normal elimination pattern d) Fluid and electrolyte changes – such as  Administer antidiarrheal – as ordered dehydration and ascites.  Record frequency/consistency of the stool e) Vomiting – Bile-stained (obstruction is high up  Encourage bed rest – decreases the intestines); Fecal-stained (if obstruction is in peristalsis/conserve energy the ileum or lower colon). f) Peritonitis Abigail marie  14 g) Impaired oxygenation – due to ascites.  UMBILICAL h) Positive x-ray results – increased fluid and gas  INCISIONAL OR VENTRAL HERNIAS levels in an obstructed bowel. ASSESSMENT FINDINGS SMALL BOWEL OBSTRUCTION:  Protrusion or lump over the herniated area while in supine position; Pain (Incarcerated or ❒ Due to adhesions/ bands of scar tissue followed by hernias & neoplasms. strangulated); S/S of obstruction MANIFESTATION: MEDICAL MANAGEMENT  Abdominal distention crampy pain (colicky  Use of Truss; Surgery (Herniorrhaphy) abdominal pain) – initial symptom; Vomiting – if in the ileum – may contain fecal matter; Reverse 2) INTUSSUSCEPTION peristalsis (complete obstruction); Signs of ❒ The telescoping of one portion of the bowel dehydration; Bowel sound - borborygmi (early forming an obstruction, generally occurring on the stage); late stage – absent; Tenderness on second half of the first year. palpation. CAUSES COMPLICATION:  Idiopathic (For infants younger than 1 year); In  hypovolemia → hypovolemic shock; possible older children and adults – A “Lead Point” peritonitis; gangrene caused by polyp, Hyperplasia of Payer's patches or Meckel’s Diverticulum gets caught in the fecal LARGE BOWEL OBSTRUCTION: stream and causes the invagination. ❒ Most common cause: Volvulus; Cancer of the bowel; Diverticular disease; Fecal impaction; ASSESSMENT FINDINGS: Inflammatory disorders.  Pain; Vomiting – Contains bile; Blood in the stools – “Currant Jelly Stools”; Abdominal MANIFESTATIONS: distention; Increase in temperature (Necrosis);  Constipation and colicky abdominal pain; Peritoneal irritation (Abdominal tenderness and vomiting; distention; high-pitched bowel sound; Guarding); Tachycardia; Increased WBC localized tenderness; shape of stool is altered; weakness, weight loss, anorexia; loops of large MEDICAL MANAGEMENT: bowel visible through the abdominal wall. Barium enema (If there is no “Lead Point”; Surgery) DIAGNOSTIC TEST: 3) VOLVULUS  X-rays/ CT scan/ LAB TEST (CBC, ❒ The twisting of the intestines upon itself ELECTROLYTES, S. AMYLASE, ABG’s) commonly involving the small intestines, although  BA study – contraindicated redundant loops of the sigmoid may also twist around the mesentery. SMALL BOWEL OBSTRUCTION MAY BE DUE TO: RISK FACTORS  High Residue diet; Chronic constipation; Habitual abuse of laxatives and enemas; 1.) HERNIAS Previous abdominal surgeries ❒ protrusion of contents of peritoneal cavity through an opening or weakness in the abdominal wall. ASSESSMENT FINDINGS  S/Sx of abdominal obstructions CAUSES  Muscle weakness (Congenital or a part of the MEDICAL MANAGEMENT aging process) and increased abdominal  Surgery pressure. TYPES 4) ADHESIONS  REDUCIBLE ❒ Bands of scar tissues which may cause  INCARCERATED mechanical obstruction of the bowels.  STRANGULATED CAUSES ACCORDING TO LOCATION :  Surgery  INGUINAL – Direct or Indirect;  FEMORAL Abigail marie  15 ASSESSMENT FINDINGS  Colon Resection with a temporary colostomy.  Distention; Increased bowel sounds and severe, colicky abdominal pain in patients with NURSING MANAGEMENT: mechanical obstruction.  Metronidazole/Ciprofloxacin/Bactrim  IV therapy NURSING MANAGEMENT FOR INTESTINAL  Demerol – analgesic of choice. OBSTRUCTION:  Morphine IS contraindicated – increases  Decompression – to relieve distention through intraluminal pressure. NGT insertion and attached to an intermittent  Diet: high fiber – avoid food with seeds. suction.  Bulk-forming agents – Metamucil  Decompression and replacement of potassium –  Bowel rest during acute attack – NPO/NGT/TPN for adynamic ileus; changes in position; rectal  Laxative/enema – contraindicated. tube insertion for 20 to 30 minutes.  Fluid and electrolytes replacement SURGERY:  Medications – Neostigmine and Prostigmine  Bowel resection with anastomosis /ligation of the (cholenergics) sac.  Truss placed over hernia to keep it reduced.  Surgery such as Surgical decompression; NURSING INTERVENTIONS: Bowel resection; temporary or permanent  Increase fluid intake (2 L/day). colostomy; Herniorrhaphy  Soft high fiber  Set time for defecation/ establish schedule for NURSING DIAGNOSES: meals  Fluid Volume Deficit R/T vomiting, decreased  Stool softeners/oil retention enemas as intestinal absorption of fluid indicated.  Alteration in Comfort – Pain R/T abdominal  Analgesic as ordered. distention  Monitor for perforation – most common  Impaired Gas Exchange R/T ascitis complication. DIVERTICULAR DISEASE: ANORECTAL DISORDERS DIVERTICULI HEMORRHOIDS ❒ acquired herniations of colon mucosa through ❒ varicosities of the hemorrhoidal plexus which weak areas of the colon musculature drains the rectum and anal canal; Perianal varicose veins. DIVERTICULOSIS TYPES ❒ presence of noninflamed outpouchings of the  Internal / External Hemorrhoids intestines CAUSES DIVERTICULITIS  Constipation with prolonged straining, obesity, ❒ a condition that results when outpouchings pregnancy, prolonged sitting and standing. become irritated, inflamed and tender and may produce a pericolic abscesses and fistulas. PATHOPHYSIOLOGY: Straining during a bowel movement  Increases intra- ASSESSMENT FINDINGS abdominal pressure  Distention of the Hemorrhoidal  Pain; Change in bowel habits; Increased flatus; Veins  Permanent dilatation of hemorrhoidal veins. Anorexia; Low-grade fever; Pus, Mucous or blood may appear in the stools. ASSESSMENT FINDINGS  Enlarged mass at the anus; Bleeding and MEDICAL MANAGEMENT: prolapse; Rectal itching; Constipation; Pain (if  In mild cases – High fiber diet; Prevention of there is thrombosis); Bloody stools. constipation with bran and bulk laxatives  In acute cases – NPO; NGT insertion; IV MEDICAL MANAGEMENT therapy  Preventing constipation through dietary  Medications – Antibiotics changes; Hot sitz bath; Medications such as  Surgery – for clients who develop complications Stool softeners (Colase, Laxoberal), Topical anesthetic or steroidal preparations; Surgery  Ligation and removal of sac or Resection of (Hemorrhoidectomy). involved bowel. Abigail marie  16 RUBBER BAND LIGATION OF HEMORRHOIDS ASSESSMENT FINDINGS:  To remove a hemorrhoid using rubber band  Pain in the RUQ or epigastric that last for 12 – ligation, your surgeon inserts a small tool called 18 hours a ligator through a lighted tube (scope) in the  Low grade fever anal canal and grasps the hemorrhoid with  Nausea & vomiting after a High Fat Diet forceps. Sliding the lIgator’s cylinder upward  Flatulence releases rubber bands around the base of the  Indigestion hemorrhoid. Rubber bands cut off the  Abdominal tenderness hemorrhoid's blood supply, causing it to wither  Palpable gallbladder (Murphy’s sign) and drop off.  Clay-colored, steatorrhea stools  Bile colored urine NURSING MANAGEMENT (POST –OP)  Promote healing; Prevent complications; Relieve COMPLICATIONS: pain.  Perforation, peritonitis, infection of biliary system, pancreatitis, intestinal obstruction, DISTURBANCES IN ACCESSORY ORGANS: fistula formation. GALLBLADDER, LIVER AND EXOCRINE MEDICAL MANAGEMENT:  PANCREATIC DISORDERS  Bed rest Fluid and electrolyte replacement  Drug therapy – Analgesics/antibiotic  Dietary Management – Low Fat diet A. DISORDERS OF THE BILIARY TRACT:  Surgery – Cholecystostomy/Cholecystectomy 2. Chronic Cholecystitis 1. CHOLECYSTITIS ❒ is a long-standing swelling and irritation of the ❒ is an acute inflammation of the gallbladder, which gallbladder  thickening of the walls  shrink. is the storage site for bile production from the ❒ long term intolerance to fatty foods liver. SYMPTOMS are vague, such as: CAUSES: 1. Chronic indigestion  Gallstones / Surgical trauma or injury to the 2. Vague abdominal pain gallbladder / Anatomical abnormalities 4. Nausea 5. Belching PATHOPHYSIOLOGY:  Originate from an obstruction of the cystic duct TREATMENT: either by a stone or by a bacterial invasion. As a 1. Surgery – Cholecystectomy result of the inflammation, the gallbladder wall 2. Diet – Low Fat becomes thickened & edematous & the diameter 3. Weight reduction of the cystic duct lumen increases in size. 4. Drug therapy – Acid-suppressing and  If the inflammation and edema spread to the Anticholenergic; Antacids. common duct, the temporary obstruction of bile elimination will result in jaundice. COMPLICATIONS:  If the cystic duct is completely occluded, the  Pancreatitis or Cancer of the gallbladder (rarely). gallbladder will become distended with inflammatory exudate and bile. Following the DIAGNOSTIC TEST: acute attack, the surface mucosa heals, scarring  CBC – WBC is elevated the gallbladder wall, affecting future gallbladder  Serum alkaline phophatase, AST functioning.  S. Bilirubin  S. Amylase and Lipase TYPES:  UTZ of abdomen – diagnostic test of choice 1. Acute cholecystitis a) Calculous Cholecystitis – is the cause of 90% of cases of acute cholecystitis. Gallbladder stones obstruct s bile flow  gangrene & perforation. b) Acalculous Cholecystitis – is the absence of obstruction by a gallstone. Abigail marie  17 2. GALL BLADDER STONE OR  Improve respiratory status – deep breathing; use (CHOLELITHIASIS) of incentive spirometer, early ambulation.  Promote skin care/biliary drainage – signs of ❒ presence of gall stones. infection, protect from irritation of bile, measure collected bile, never clamp T-tube, if clamped– CAUSES: note for color of stools.  Change in bile composition, Stasis, Infection,  Improve nutritional status – low fat, high Genetic carbohydrate and protein. ETIOLOGY AND RISK FACTORS : C ARE OF T-TUBE:  5F’s, age, obesity, familial tendency, rapid  Normal drain – post – op: 500 ml 1st 24 hours weight loss post-op – decreased to 200 in 2-3 days.  INITIALLY – GREEN GROUP OF GALLSTONE INCLUDES :  Report excessive drainage – may indicate  Cholesterol stones obstruction.  Pigment stones  Place in fowler’s position.  Mixed stones  Assess skin for bile leakage during change of dressing. Gallbladder with numerous stones. Their brownish and  Ensure that T-tube is properly connected to greenish colors suggest a cholesterol calculi. drainage (JP drain); keep it below level of surgical wound. ASSESSMENT FINDINGS:  Asymptomatic for a majority of persons; Biliary NURSING DIAGNOSES: colic; Jaundice in CBD obstruction; Nausea and  Alteration in Comfort R/T Biliary Spasms vomiting; Intolerance to fatty foods; vague upper  NGT insertion relieves biliary spasms abdominal discomfort. (contractions)  Positive results of diagnostic studies such as  Analgesics, except MS (causes Ultrasonography; CT scan; Oral contraction of the sphincter of Oddi); Cholecystography; Cholangiography; ERCP. NTG – relaxes smooth muscles thus decrease colic MEDICAL MANAGEMENT:  Relaxation technics, diversional  Nutritional and Supportive Therapy activities  Complete bedrest  Fluid Volume Deficit R/T Vomiting and NGT  NPO and NGT; Fluid and electrolyte suctioning replacement; Medications such as  Potential for Injury R/T Endoscopic Procedure Demerol, Anti-emetics, Antispasmodics, for stone removal Anticholinergics, Antibiotics.  Observe for S/S of bleeding &  Pharmacologic Therapy hemorrhage due to procedure.  Ursodeoxycholic acid (UDCA/URSO,  Knowledge deficit Actigall) and Chenodeoxycholic Acid (Chenodiol).  Nonsurgical Removal of Stones  Dissolving of stones – infusion of a solvent (Mono-octanoin or methyl tertiary butyl ether [MTBE]) into the gallbladder.  Stone Removal by Instrumentation a. ERCP b. Intracorporeal Lithotripsy c. Extracorporeal Shock Wave Lithotripsy (ESWL)  Surgical Management a. Laparoscopic Cholecystectomy b. Cholecystectomy c. Choledochostomy d. Surgical Cholecystostomy e. Percutaneous Cholecystostomy POST-OPERATIVE CARE:  Relieve pain – analgesic Abigail marie