You are on page 1of 6

Overview of Anatomy & Physiology Gastro Intestinal Track System The primary function of GIT are the movement

t of food, digestion, absorption, elimination & provision of a continuous supply of the nutrients electrolytes & H2O. Upper alimentary canal: function for digestion Mouth Consist of lips & oral cavity Provides entrance & initial processing for nutrients & sensory data such as taste, texture & temperature Oral Cavity: contains the teeth used for mastication & the tongue which assists in deglutition & the taste sensation & mastication Salivary gland: located in the mouth produce secretion containing pyalin for starch digestion & mucus for lubrication Pharynx: aids in swallowing & functions in ingestion by providing a route for food to pass from the mouth to the esophagus Esophagus Muscular tube that receives foods from the pharynx & propels it into the stomach by peristalsis Stomach Located on the left side of the abdominal cavity occupying the hypochondriac, epigastric & umbilical regions Stores & mixes food with gastric juices & mucus producing chemical & mechanical changes in the bolus of food The secretion of digestive juice is stimulated by smelling, tasting & chewing food which is known as cephalic phase of digestion The gastric phase is stimulated by the presence of food in the stomach & regulated by neural stimulation via PNS & hormonal stimulation through secretion of gastrin by the gastric mucosa After processing in the stomach the food bolus called chyme is released into the small intestine through the duodenum Two sphincters control the rate of food passage Cardiac Sphincter: located at the opening between the esophagus & stomach Pyloric Sphincter: located between the stomach & duodenum Three anatomic division Fundus Body Antrum Gastric Secretions: Pepsinogen: secreted by the chief cells located in the fundus aid in CHON digestion Hydrocholoric Acid: secreted by parietal cells, function in CHON digestion & released in response to gastrin Intrinsic Factor: secreted by parietal cell, promotes absorption of Vit B12 Mucoid Secretion: coat stomach wall & prevent auto digestion 1st half of duodenum Middle Alimentary canal: Function for absorption; Complete absorption: large intestine Small Intestines Composed of the duodenum, jejunum & ileum Extends from the pylorus to the ileocecal valve which regulates flow into the large intestines to prevent reflux to the into the small intestine

Major function: digestion & absorption of the end product of digestion Structural Features: Villi (functional unit of the small intestines): finger like projections located in the mucous membrane; containing goblet cells that secrets mucus & absorptive cells that absorb digested food stuff Crypts of Lieberkuhn: produce secretions containing digestive enzymes Brunners Gland: found in the submucosaof the duodenum, secretes mucus

2nd half of duodenum Jejunum Ileum 1st half of ascending colon Lower Alimentary Canal: Function: elimination Large Intestine Divided into four parts: Cecum (with appendix) Colon (ascending, transverse, descending, sigmoid) Rectum Anus Serves as a reservoir for fecal material until defecation occurs Function: to absorb water & electrolytes MO present in the large intestine: are responsible for small amount of further breakdown & also make some vitamins Amino Acids: deaminated by bacteria resulting in ammonia which is converted to urea in the liver Bacteria in the large intestine: aid in the synthesis of vitamin K & some of the vitamin B groups Feces (solid waste): leave the body via rectum & anus Anus: contains internal sphincter (under involuntary control)& external sphincter (voluntary control) Fecal matter: usually 75% water & 25% solid wastes (roughage, dead bacteria, fats, CHON, inorganic matter) a. 2nd half of ascending colon b. Transverse c. Descending colon d. Sigmoid e. Rectum Accessory Organ Liver Largest internal organ: located in the right hypochondriac & epigastric regions of the abdomen Liver Loobules: functional unit of the liver composed of hepatic cells Hepatic Sinusoids(capillaries): are lined with kupffer cells which carry out the process of phagocytosis Portal circulation brings blood to the liver from the stomach, spleen, pancreas & intestines Function: Metabolism of fats, CHO & CHON: oxidizes these nutrient for energy & produces compounds that can be stored Production of bile Conjugation & excretion (in the form of glycogen, fatty acids, minerals, fat-soluble & watersolublevitamins) of bilirubin Storage of vitamins A, D, B12 & iron Synthesis of coagulation factors Detoxification of many drugs & conjugation of sex hormones Salivary gland

Verniform appendix Liver Pancreas: auto digestion Gallbladder: storage of bile Biliary System Consist of the gallbladder & associated ductal system (bile ducts) Gallbladder: lies under the surface of the liver Function: to concentrate & store bile Ductal System: provides a route for bile to reach the intestines Bile: is formed in the liver & excreted into hepatic duct Hepatic Duct: joins with the cystic duct (which drains the gallbladder) to form the common bile duct If the sphincter of oddi is relaxed: bile enters the duodenum, if contracted: bile is stored in gallbladder Pancreas Positioned transversely in the upper abdominal cavity Consist of head, body & tail along with a pancreatic duct which extends along the gland & enters the duodenum via the common bile duct Has both exocrine & endocrine function Function in GI system: is exocrine Exocrine cells in the pancreas secretes: Trypsinogen & Chymotrypsin: for protein digestion Amylase: breakdown starch to disacchardes Lipase: for fat digestion Endocrine function related to islets of langerhas Physiology of Digestion & Absorption Digestion: physical & chemical breakdown of food into absorptive substance Initiate in the mouth where the food mixes with saliva & starch is broken down Food then passes into the esophagus where it is propelled into the stomach In the stomach food is processed by gastric secretions into a substance called chyme In the small intestines CHO are hydrolyzed to monosaccharides, fats to glycerol & fatty acid & CHON to amino acid to complete the digestive process When chymes enters the duodenum, mucus is secreted to neutralized hydrocholoric acid, in response to release secretin, pancreas releases bicarbonate to neutralized acid chyme Cholecystokinin & Pancreozymin(CCKPZ) Are produced by the duodenal mucosa Stimulate contraction of the gallbladder along with relaxation of the sphincter of oddi (to allow bile flow fromcommon bile duct into the duodenum)& stimulate release of the pancreatic enzymes Salivary Glands 1. Parotid below & front of ear 2. Sublingual 3. Submaxillary Produces saliva for mechanical digestion 1200 -1500 ml/day - saliva produced

Excoriation / erosion of submucosa & mucosal lining due to: Hypersecretion of acid: pepsin Decrease resistance to mucosal barrier Caused by bacterial infection: Helicobacter Pylori

Doudenal Ulcer Most commonly found in the first 2 cm of the duodenum Characterized by gastric hyperacidity & a significant rate of gastric emptying Predisposing factor Smoking: vasoconstriction: effect GIT ischemia Alcohol Abuse: stimulates release of histamine: Parietal cell release Hcl acid = Ulceration Emotional Stress Drugs: Salicylates (Aspirin) Steroids Butazolidin S/sx Site Pain Gastric Ulcer Duodenal Ulcer Antrum or lesser Duodenal bulb curvature 30 min-1 2-4 hrs hr after after eating eating Left Mid epigastriu epigastri m um Gaseous Crampin & burning g& Not burning Usually usually relieved relieved by food & by food antacid & antacid 12 MN 3am pain Normal Increase gastric d gastric acid acid secretion secretion Common Not common Hematem Melena eis Weight Weight loss gain Stomach Perforati cause on Hemorrha ge 60 years 20 years old old

Hypersecreti on Vomiting Hemorrhage Weight Complicatio ns High Risk

Dx

Hgb & Hct: decrease (if anemic) Endoscopy: reveals ulceration & differentiate ulceration from gastric cancer Gastric Analysis: normal gastric acidity Upper GI series: presence of ulcer confirm

Disorder of the GIT Peptic Ulcer Disease(PUD) Gastric Ulcer Ulceration of the mucosal lining of the stomach Most commonly found in the antrum

Medical Management 1. Supportive: Rest Bland diet Stress management

2.

Drug Therapy: Antacids: neutralizes gastric acid Aluminum hydroxide: binds phosphate in the GIT & neutralized gastric acid & inactivates pepsin Magnesium & aluminum salt: neutralized gastric acid & inactivate pepsin if pH is raised to >=4

3. 4. 5.

Aluminum containing Antacids Magnesium containing Antacids Ex. Aluminum OH gel (Amphojel) Ex. Milk of Magnesia SE: Constipation SE: Diarrhea

Maintain patent IV line Monitor V/S, I&O & bowel sounds Complications: Hemorrhage: Hypovolemic shock: Late signs: anuria Peritonitis Paralytic ileus: most feared Hypokalemia Thromobphlebitis Pernicious anemia

Nursing 1. 2. 3.

Maalox SE: fever Histamines (H2) receptor antagonist: inhibits gastric acid secretion of parietal cells Ranitidine(Zantac):has some antibacterial action against H. pylori Cimetidine(Tagamet) Famotidine(Pepcid) Anticholinergic: Atropine SO4: inhibit the action of acetylcholine at post ganglionic site (secretory glands) results decreases GI secretions Propantheline: inhibit muscarinic action of acetylcholine resulting decrease GI secretions Proton Pump Inhibitor: inhibit gastric acid secretion regardless of acetylcholine or histamine release Omeprazole(Prilosec): diminished the accumulation of acid in the gastric lumen & healing of duodenal ulcer Pepsin Inhibitor: reacts with acid to form a paste that binds to ulcerated tissue to prevent further destruction by digestive enzyme pepsin Sucralfate(Carafate): provides a paste like subs that coats mucosal lining of stomach Metronidazole & Amoxacillin: for ulcer caused by Helicobacter Pylori Surgery: Gastric Resection Anastomosis: joining of 2 or more hollow organ Subtotal Gastrectomy: Partial removal of stomach Before surgery for BI or BII Do Vagotomy (severing or cutting of vagus nerve)& Pyloroplasty (drainage) first Billroth II (Gastrojejunostomy) Removal of -3/4 of stomach & duodenal bulb &anastomostoses of gastric stump to jejunum.

Intervention Administer medication as ordered Diet: bland, non irritating, non spicy Avoid caffeine & milk / milk products: Increase gastric acid secretion 4. Provide client teaching & discharge planning a. Medical Regimen Take medication at prescribe time Have antacid available at all times Recognized situation that would increase the need for antacids Avoid ulcerogenic drugs: salicylates, steroids Know proper dosage, action & SE b. Proper Diet Bland diet consist of six meals / day Eat slowly Avoid acid producing substance: caffeine, alcohol, highly seasoned food Avoid stressfull situation at mealtime Plan rest period after meal Avoid late bedtime snacks c. Avoidance of stress-producing situation & development of stress production methods Relaxation techniques Exercise Biofeedback

3.

Dumping syndrome Abrupt emptying of stomach content into the intestine Rapid gastric emptying of hypertonic food solutions Common complication of gastric surgery Appears 15-20 min after meal & last for 20-60 min Associated with hyperosmolar CHYME in the jejunum which draws fluid by osmosis from the extracellular fluid into the bowel. Decreased plasma volume & distension of the bowel stimulates increased intestinal motility S/sx 1. 2. 3. 4. 5. 6. 7. Nursing 1. 2. 3. 4. Weakness Faintness Feeling of fullness Dizziness Diaphoresis Diarrhea Palpitations Intervention Avoid fluids in chilled solutions Small frequent feeding: six equally divided feedings Diet: decrease CHO, moderate fats & CHON Flat on bed 15-30 min after q feeding

Billroth I(Gastroduodenostomy) Removal of of stomach & anastomoses of gastric stump to the duodenum.

Nursing Intervention Post op 1. Monitor NGT output Immediately post op should be bright red Within 36-42 hrs: output is yellow green After 42 hrs: output is dark red 2. Administer medication Analgesic Antibiotic Antiemetics

Disorders of the Gallbladder Cholecystitis / Cholelithiasis Cholecystitis: Acute or chronic inflammation of the gallbladder Most commonly associated with gallstones Inflammation occurs within the walls of the gallbladder & creates thickening accompanied by edema

Consequently there is impaired circulation, ischemia & eventually necrosis Cholelithiasis: Formation of gallstones & cholesterol stones Inflammation of gallbladder with gallstone formation.

Predisposing Factor: 1. High risk: women 40 years old 2. Post menopausal women: undergoing estrogen therapy 3. Obesity 4. Sedentary lifestyle 5. Hyperlipidemia 6. Neoplasm S/sx: 1. 2. 3. 4. 5. 6. 7. 8. 9. Dx 1. 2. 3. 4. 5. 6. Medical 1. 2. 3. Direct Bilirubin Transaminase: increase Alkaline Phosphatase: increase WBC: increase Amylase: increase Lipase: increase Oral cholecystogram(or gallbladder series): confirms presence of stones Management Supportive Treatment: NPO with NGT & IV fluids Diet modification with administration of fat soluble vitamins Drug Therapy Narcotic analgesic:DOC: Meperdipine Hcl (Demerol): for pain (Morpine SO4: is contraindicated because it causes spasm of the Sphincter of Oddi) Antocholinergic: (Atrophine SO4): for pain (Anticholinergic: relax smooth muscles & open bile ducts) Antiemetics: Phenothiazide (Phenergan): with anti emetic properties Surgery: Cholecystectomy / Choledochostomy Intervention Administer pain medication as ordered & monitor effects Administer IV fluids as ordered Diet: increase CHO, moderate CHON, decrease fats Meticulous skin care: to relieved priritus Severe Right abdominal pain(after eating fatty food): Occurring especially at night Intolerance of fatty food Anorexia N/V Jaundice Pruritus Easy bruising Tea colored urine Steatorrhea

2. 3. 4. 5. 6. 7. 8. 9. 10. S/Sx: 1. 2. 3. 4. 5. 6. 7. 8. 9. Dx 1. 2. 3. 4. 5. 6.

Hepatobilary disease Trauma Viral infection Penetrating duodenal ulcer Abscesses Obesity Hyperlipidemia Hyperparathyroidism Drugs: Thiazide, steroids, diuretics, oral contraceptives Severe left upper epigastric pain radiates from back & flank area: aggravated by eating with DOB N/V Tachycardia Palpitation: due to pain Dyspepsia: indigestion Decrease bowel sounds (+) Cullens sign: ecchymosis of umbilicus Hemorrhage (+) Grey Turners spots: ecchymosis of flank area Hypocalcemia Serum amylase & lipase: increase Urinary amylase: increase Blood Sugar: increase Lipids Level: increase Serum Ca: decrease CT Scan: shows enlargement of the pancreas

4. Nursing 1. 2. 3. 4.

Medical Management 1. Drug Therapy Narcotic Analgesic:for pain Meperidine Hcl(Demerol) Dont give Morphine SO4: will cause spasm of Sphincter of Oddi Smooth muscle relaxant: to relieve pain Papaverine Hcl Anticholinergic: to decrease pancreatic stimulation Atrophine SO4 Propantheline Bromide (Profanthene) Antacids: to decrease pancreatic stimulation Maalox H2 Antagonist: to decrease pancreatic stimulation Ranitidin(Zantac) Vasodilators: to decrease pancreatic stimulation Nitroglycerine (NTG) Ca Gluconate: to decrease pancreatic stimulation 2. Diet Modification 3. NPO (usually) 4. Peritoneal Lavage 5. Dialysis Nursing Intervention 1. Administer medication as ordered 2. Withhold food & fluid & eliminate odor: to decrease pancreatic stimulation / aggravates pain 3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation Complication of TPN Infection Embolism Hyperglycemia 4. Institute non-pharmacological measures: to decrease pain Assist client to comfortable position: Knee chest or fetal like position

Disorders of the Pancreas Pancreatitis An inflammatory process with varying degrees of pancreatic edema, fat necrosis or hemorrhage Proteolytic & lipolytic pancreatic enzymes are activated in the pancreas rather than in the duodenum resulting in tissue damage & auto digestion of pancreas Acute or chronic inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion Bleeding of Pancreas: Cullens sign at umbilicus Predisposing factors: 1. Chronic alcoholism

5.

Teach relaxation techniques & provide quiet, restful environment Provide client teaching & discharge planning Dietary regimen when oral intake permitted High CHO, CHON & decrease fats Eat small frequent meal instead of three large ones Avoid caffeine products Eliminate alcohol consumption Maintain relaxed atmosphere after meals Report signs of complication Continued N/V Abdominal distension with feeling of fullness Persistent weight loss Severe epigastric or back pain Frothy foul smelling bowel movement Irritability, confusion, persistent elevation of temperature (2 day)

4. 5. 6.

Antibiotics: for infection Antipyretics: for fever (PRN) Monitor VS, I&O, bowel sound Maintain patent IV line Complications: Peritonitis, Septicemia

Liver Cirrhosis Chronic progressive disease characterized by inflammation, fibrosis & degeneration of the liver parenchymal cell Destroyed liver cell are replaced by scar tissue, resulting in architectural changes & malfunction of the liver Lost of architectural design of liver leading to fat necrosis & scarring Types Laennecs Cirrhosis: Associated with alcohol abuse & malnutrition Characterized by an accumulation of fat in the liver cell progressing to widespread scar formation Postnecrotic Cirrhosis Result in severe inflammation with massive necrosis as a complication of viral hepatitis Cardiac Cirrhosis Occurs as a consequence of right sided heart failure Manifested by hepatomegaly with some fibrosis Biliary Cirrhosis Associated with biliary obstruction usually in the common bile duct Results in chronic impairment of bile excretion Fatigue Anorexia N/V Dyspepsia: Indigestion Weight loss Flatulence Change (Irregular) bowel habit Ascites Peripheral edema Hepatomegaly: pain located in the right upper quadrant Atrophy of the liver Fetor hepaticus: fruity, musty odor of chronic liver disease Aterixis: flapping of hands & tremores Hard nodular liver upon palpation Increased abdominal girth Changes in moods Alertness & mental ability Sensory deficits Gynecomastia Decrease of pubic & axilla hair in males Amenorrhea in female Jaundice Pruritus or urticaria Easy bruising Spider angiomas on nose, cheeks, upper thorax & shoulder Palmar erythema Muscle atrophy Liver enzymes: increase SGPT (ALT) SGOT (AST) LDH Alkaline Phosphate Serum cholesterol & Indirect bilirubin: increase CBC: pancytopenia

Apendicitis Inflammation of the appendix that prevents mucus from passing into the cecum Inflammation of verniform appendix If untreated: ischemia, gangrene, rupture & peritonitis May cause by mechanical obstruction (fecalith, intestinal parasites) or anatomic defect May be related to decrease fiber in the diet Predisposing factor: 1. Microbial infection 2. Feacalith: undigested food particles like tomato seeds, guava seeds etc. 3. Intestinal obstruction S/Sx: 1. 2. 3. 4. 5. 6. Dx 1. 2. 3. CBC: mild leukocytosis: increase WBC PE:(+) rebound tenderness (flex Right leg, palpate Right iliac area: rebound) Urinalysis: elevated acetone in urine Pathognomonic sign: (+) rebound tenderness Low grade fever N/V Decrease bowel sound Diffuse pain at lower Right iliac region Late sign: tachycardia: due to pain

S/sx

Medical Management Surgery: Appendectomy 24-45 hrs Nursing Intervention 1. Administer antibiotics / antipyretic as ordered 2. Routinary pre-op nursing measures: Skin prep NPO Avoid enema, cathartics: lead to rupture of appendix 3. Dont give analgesic: will mask pain Presence of pain means appendix has not ruptured 4. Avoid heat application: will rupture appendix 5. Monitor VS, I&O bowel sound Nursing Intervention post op 1. If (+) Pendrose drain(rubber drain inserted at surgical wound for drainage of blood, pus etc): indicates rupture of appendix 2. Position the client semi-fowlers or side lying on right: to facilitate drainage 3. Administer Meds: Analgesic: due post op pain Dx

ammonia: increase

PT: prolonged Hepatic Ultrasonogram: fat necrosis of liver lobules Nursing Intervention CBR with bathroom privileges Encourage gradual, progressive, increasing activity with planned rest period Institute measure to relieve pruritus Do not use soap & detergent Bathe with tepid water followed by application of emollient lotion Provide cool, light, non-constrictive clothing Keep nail short: to avoid skin excoriation from scratching Apply cool, moist compresses to pruritic area Monitor VS, I & O Prevent Infection Prevent skin breakdown: by turning & skin care Provide reverse isolation for client with severe leukopenia: handwashing technique Monitor WBC Diet: Small frequent meals Restrict Na! High calorie, low to moderate CHON, high CHO, low fats with supplemental Vit A, B-complex, C, D, K & folic acid Monitor / prevent bleeding Measure abdominal girth daily: notify MD With pt daily & assess pitting edema Administer diuretics as ordered Provide client teaching & discharge planning Avoidance of hepatotoxicity drug: sedative, opiates or OTC drugs detoxified by liver How to assess weight gain & increase abdominal girth Avoid person with upper respiratory infection Reporting signs of reccuring illness (liver tenderness, increase jaundice, increase fatigue, anorexia) Avoid all alcohol Avoid straining stool vigorous blowing of nose & coughing: to decrease incidence of bleeding Complications: Ascites: accumolation of free fluid in abdominal cavity Nursing Intervention Meds: Loop diuretics: 10-15 min effect Assist in abdominal paracentesis: aspiration of fluid Void before paracentesis: to prevent accidental puncture of bladder as trochar is inserted Bleeding esophageal varices: Dilation of esophageal veins Nursing Intervention Administer meds: Vit K Pitrisin or Vasopresin (IM) NGT decompression: lavage Give before lavage: ice or cold saline solution Monitor NGT output Assist in mechanical decompression Insertion of sengstaken-blackemore tube 3 lumen typed catheter Scissors at bedside to deflate balloon. Hepatic encephalopathy Nursing Intervention Assist in mechanical ventilation: due coma Monitor VS, neuro check Siderails: due restless Administer meds

Laxatives: to excrete ammonia

You might also like